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We are indebted to the National Eating Disorder Association (NEDA) for the following eating disorder terms and definitions. We supply them for purposes of helping parents, families, coaches, educators and provider better understand the nature and symptoms of eating disorders in children and assist in securing eating disorder help for their loved ones.
In the context of treatment for eating disorders, a treatment that does not use drugs or bring uncon- scious mental material into full consciousness. For example yoga, guided imagery, expressive therapy, and massage therapy are considered alternative therapies.
The absence of at least three consecutive menstrual cycles.
Slang for anorexia or anorexic.
ANAD (National Association of Anorexia Nervosa and Associated Disorders):
A nonprofit corporation that seeks to alleviate the problems of eating disorders, especially anorexia nervosa and bulimia nervosa.
A disorder in which an individual refuses to maintain minimally normal body weight, intensely fears gaining weight, and exhibits a significant disturbance in his/her perception of the shape or size of his/her body.
The use of excessive exercise to lose weight. [Ed. Note: This is not an officially recognized diagnosis under DSM V. Excessive exercise is a classic symptom of anorexia nervosa.]
used to prevent or treat convulsions.
used to prevent or treat nausea and vomiting.
A persistent feeling of dread, apprehension, and impending disaster. There are several types of anxiety disorders, including: panic disorder, agoraphobia, obsessive-compulsive disorder, social and specific phobias, and post-traumatic stress disorder. Anxiety is a type of mood disorder (see Mood Disorders).
Feeding disorder of infancy or early childhood has been renamed avoidant/restrictive food intake disorder (ARFID).
An alteration in the normal rhythm of the heartbeat.
A form of expressive therapy that uses visual art to encourage a patient’s growth of self awareness and self esteem to make attitudinal and behavioral changes.
A new group of medications used to treat psychiatric conditions, e.g. Olanzapine (brand name Zyprexa). These drugs may have fewer side effects than older classes of drugs used to treat the same psychiatric conditions.
An abbreviation used for binge eating and purging in the context of bulimic behavior.
Behavior Therapy (BT):
A type of psychotherapy that uses principles of learning to increase the frequency of desired behaviors and/or decrease the frequency of problem behaviors. When used to treat an eating disorder, the focus is on modifying behavioral abnormalities of the disorder by teaching relaxation techniques and coping strategies that affected individuals can use instead of restricting, binge eating and/or purging. Subtypes of BT include dialectical behavior therapy (DBT), exposure and response prevention (ERP), and hypno-behavioral therapy.
Binge Eating (also Bingeing):
Consuming an amount of food that is considered much larger than the amount that most individuals would eat under similar circumstances within a discrete period of time. Also referred to as “binge eating.”
The recipient of benefits from an insurance policy.
A technique that measures bodily functions, like breathing, heart rate, blood pressure, skin temperature, and muscle tension. Biofeedback is used to teach people how to alter bodily functions through relaxation or imagery. Typically, a practitioner describes stressful situations and guides a person through using relaxation techniques. The person can see how their heart rate and blood pressure change in response to being stressed or relaxed.
Body Dysmorphic Disorder or Dysmorphophobia:
A mental condition defined in the DSM-V in which the patient is preoccupied with a real or perceived defect in his/her appearance (see DSM-V).
The subjective opinion about one’s physical appearance based on self perception of body size and shape and the reactions of others.
Body Mass Index (BMI):
A formula used to calculate the ratio of a person’s weight to height. BMI is expressed as a number that is used to determine whether an individual’s weight is within normal ranges for age and sex on a standardized BMI chart. The U.S. Centers for Disease Control and Prevention Web site offers BMI calculators and standardized BMI charts.
A disorder defined in the DSM-V in which a patient binges on food an average of twice weekly in a three-month time period, followed by compensatory behavior aimed at preventing weight gain. This behavior may include excessive exercise, vomiting, or the misuse of laxatives, diuretics, other medications, and enemas.
A term used incorrectly to describe individuals who engage alternately in bulimic behavior and anorexic behavior. The correct diagnosis would be restricting anorexia, purging sub-type. "Bulimic behavior" (e.g. purging) is not a diagnosis but rather a symptom and one that can occur with anorexia as well as bulimia.
An approach to patient care in which a case manager working for an insurance company mobilizes people to organize appropriate services and supports for a patient’s treatment. A case manager coordinates mental health, social work, educational, health, vocational, transportation, advocacy, respite care, and recreational services, as needed. The case manager ensures that the changing needs of the patient and family members supporting that patient are met.
A federal act in 1985 that included provisions to protect health insurance benefits coverage for workers and their families who lose their jobs. The landmark Consolidated Omnibus Budget Reconciliation Act of 1985 (COBRA) health benefit provisions became law in 1986. The law amends the Employee Retirement Income Security Act (ERISA), the Internal Revenue Code, and the Public Health Service Act to provide continuation of employer-sponsored group health coverage that otherwise might be terminated. The U.S. Centers for Medicare & Medicaid Services has advisory jurisdiction for the COBRA law as it applies to state and local government (public sector) employers and their group health plans.
Cognitive Therapy (CT):
A type of psychotherapeutic treatment that attempts to change a patient’s feelings and behaviors by changing the way the patient thinks about or perceives his/her significant life experiences. Subtypes include cognitive analytic therapy and cognitive orientation therapy.
Cognitive Analytic Therapy (CAT):
A type of cognitive therapy that focuses its attention on discovering how a patient’s problems have evolved and how the procedures the patient has devised to cope with them may be ineffective or even harmful. CAT is designed to enable people to gain an understanding of how the difficulties they experience may be made worse by their habitual coping mechanisms. Problems are understood in the light of a person’s personal history and life experiences. The focus is on recognizing how these coping procedures originated and how they can be adapted.
Cognitive Behavior Therapy (CBT):
A treatment that involves three overlapping phases when used to treat an eating disorder. For example, with bulimia, the first phase focuses on helping people to resist the urge to binge eat and purge by educating them about the dangers of their behavior. The second phase introduces procedures to reduce dietary restraint and increase the regularity of eating. The last phase involves teaching people relapse-prevention strategies to help them prepare for possible setbacks. A course of individual CBT for bulimia nervosa usually involves 16 to 20 hour-long sessions over a period of 4 to 5 months. It is offered on an individual, group, or self-managed basis. The goals of CBT are designed to interrupt the proposed bulimic cycle that is perpetuated by low self-esteem, extreme concerns about shape and weight, and extreme means of weight control.
Cognitive Orientation Therapy (COT):
A type of cognitive therapy that uses a systematic procedure to understand the meaning of a patient’s behavior by exploring certain themes such as aggression and avoidance. The procedure for modifying behavior then focuses on systematically changing the patient’s beliefs related to the themes and not directly to eating behavior.
Multiple physical and/or mental conditions existing in a person at the same time (see Dual Diagnosis).
Crisis Residential Treatment Services:
Short-term, round-the-clock help provided in a non-hospital setting during a crisis. The purposes of this care are to avoid inpatient hospitalization, help stabilize the individual in crisis, and determine the next appropriate step.
The treated condition or disorder is permanently gone, never to return in the individual who received treatment. Not to be confused with “remission” (see Remission).
Also known as tooth decay. The teeth of people with bulimia who using vomiting as a purging method may be especially vulnerable to developing cavities because of the exposure of teeth to the high acid content of vomit.
Depression (also called Major Depressive Disorder):
A condition that is characterized by one or more major depressive episodes consisting of two or more weeks during which a person experiences a depressed mood or loss of interest or pleasure in nearly all activities. It is one of the mood disorders listed in the DSM-V (see Mood Disorders).
Diabetic Omission of Insulin:
A non-purging method of compensating for excess calorie intake that may be used by a person with diabetes and an eating disorder.
Dialectical Behavior Therapy (DBT):
A type of behavioral therapy that views emotional deregulation as the core problem in bulimia nervosa. It involves teaching people with bulimia nervosa new skills to regulate negative emotions and replace dysfunctional behavior. A typical course of treatment is 20 group sessions lasting 2 hours once a week (see Behavioral Therapy).
Term used to describe any atypical eating behavior.
Behaviors that include any or all of the following: replacing food consumption with excessive alcohol consumption; consuming food along with sufficient amounts of alcohol to induce vomiting as a method of purging and numbing feelings. [Ed. Note: this is not a recognized medical term, but rather one popularized in the lay media.]
The fifth (and most current as of 2014) edition of the Diagnostic and Statistical Manual for Mental Disorders V published by the American Psychiatric Association (APA). This manual lists mental diseases, conditions, and disorders, and also lists the criteria established by APA to diagnose them. Several newly created eating disorders diagnoses are listed in this edition, including Avoidant/Restrictive Food Intake Disorder (see ARFID).
Two mental health disorders in a patient at the same time, as diagnosed by a clinician. For example, a patient may be given a diagnosis of both bulimia nervosa and obsessive-compulsive disorder or anorexia and major depressive disorder.
Eating Disorders Anonymous (EDA):
A fellowship of individuals who share their experiences with each other to try to solve common problems and help each other recover from their eating disorders.
Eating Disorders Not Otherwise Specified (ED-NOS):
Any disorder of eating that does not meet the criteria for anorexia nervosa or bulimia nervosa. This diagnosis has been discontinued under the DSM-V.
Eating Disorder Inventory (EDI):
A self-report test that clinicians use with patients to diagnose specific eating disorders and determine the severity of a patient’s condition.
Eating Disorder Inventory-2 (EDI-2):
Second edition of the EDI.
(slang) Eating disorder.
Acronym for eating disorder.
A physical condition that occurs when ionized salt concentrations (commonly sodium and potassium) are at abnormal levels in the body. This condition can occur as a side effect of some bulimic compensatory behaviors, such as vomiting. Severe electrolyte imbalance can be fatal.
A class of drugs that induces vomiting. Emetics may be used as part of a bulimic compensatory behavior to induce vomiting after a binge eating episode.
The injection of fluid into the rectum for the purpose of cleansing the bowel. Enemas may be used as a bulimic compensatory behavior to purge after a binge eating episode.
A treatment program in which people interact with horses and become aware of their own emotional states through the reactions of the horse to their behavior.
An individualized exercise plan that is written by a doctor or rehabilitation specialist, such as a clinical exercise physiologist, physical therapist, or nurse. The plan takes into account an individual’s current medical condition and provides advice for what type of exercise to perform, how hard to exercise, how long, and how many times per week.
Exposure and Response Prevention (ERP):
A type of behavior therapy strategy that is based on the theory that purging serves to decrease the anxiety associated with eating. Purging is therefore negatively reinforced via anxiety reduction. The goal of ERP is to modify the association between anxiety and purging by preventing purging following eating until the anxiety associated with eating subsides (see Behavioral Therapy).
A non-drug, non-psychotherapy form of treatment that uses the performing and/or visual arts to help people express their thoughts and emotions. Whether through dance, movement, art, drama, drawing, painting, etc., expressive therapy provides an opportunity for communication that might otherwise remain repressed.
Eye Movement Desensitization and Reprocessing (EMDR):
A non-drug and non-psychotherapy form of treatment in which a therapist waves his/her fingers back and forth in front of the patient’s eyes, and the patient tracks the movements while also focusing on a traumatic event. It is thought that the act of tracking while concentrating allows a different level of processing to occur in the brain so that the patient can review the event more calmly or more completely than before.
A form of psychotherapy that involves members of a nuclear or extended family. Some forms of family therapy are based on behavioral or psychodynamic principles; the most common form is based on family systems theory. This approach regards the family as the unit of treatment and emphasizes factors such as relationships and communication patterns. With eating disorders, the focus is on the eating disorder and how the disorder affects family relationships. Family therapy tends to be short-term, usually lasting only a few months, although it can last longer depending on the family circumstances.
A technique in which the patient is directed by a person (either in person or by using a tape recording) to relax and imagine certain images and scenes to promote relaxation, promote changes in attitude or behavior, and encourage physical healing. Guided imagery is sometimes called visualization. Sometimes music is used as background noise during the imagery session (see Alternative Therapy).
Health Insurance Portability and Accountability Act (HIPAA):
A federal law enacted in 1996 with a number of provisions intended to ensure certain consumer health insurance protections for working Americans and their families and standards for electronic health information and protect privacy of individuals’ health information. HIPAA applies to three types of health insurance coverage: group health plans, individual health insurance, and comparable coverage through a high-risk pool. HIPAA may lower a person’s chance of losing existing coverage, ease the ability to switch health plans, and/or help a person buy coverage on his/her own if a person loses employer coverage and has no other coverage available.
Health Insurance Reform for Consumers:
Federal law has provided to consumers some valuable–though limited–protections when obtaining, changing, or continuing health insurance. Understanding these protections, as well as laws in the state in which one resides, can help with making more informed choices when work situations change or when changing health coverage or accessing care. Three important federal laws that can affect coverage and access to care for people with eating disorders are listed below:
• Consolidated Omnibus Budget Reconciliation Act of 1985 (COBRA)
• Health Insurance Portability and Accountability Act of 1996 (HIPAA)
• Mental Health Parity Act of 1996 (MHPA)
• Patient Protection and Accountable Care Act of 2010 (aka Obamacare)
Health Maintenance Organization (HMO):
A health plan that employs or contracts with primary care physicians to write referrals for all care that covered patients obtain from specialists in a network of healthcare providers with whom the HMO contracts. The patient’s choice of treatment providers is usually limited.
The vomiting of blood.
A type of behavioral therapy that uses a combination of behavioral techniques such as self- monitoring to change maladaptive eating disorders and hypnotic techniques intended to reinforce and encourage behavior change.
An abnormally low concentration of glucose in the blood.
In-network benefits Health insurance benefits that a benefi- ciary is entitled to receive from a designated group (network) of healthcare providers. The “network” is established by the health insurer that contracts with certain providers to provide care for beneficiaries within that network.
A health insurance plan that reimburses the member or healthcare provider on a fee-for-service basis, usually at a rate lower than the actual charges for services rendered, and often after a deductible has been satisfied by the insured.
Independent Living Services:
Services for a person with a medical or mental health-related problem who is living on his/ her own. Services include therapeutic group homes, super- vised apartment living, monitoring the person’s compliance with prescribed mental and medical treatment plans, and job placement.
Intake Screening An interview conducted by health service providers when a patient is admitted to a hospital or treatment program.
International Classification of Diseases (ICD-10):
The World Health Organization lists international standards used to diagnose and classify diseases. The listing is used by the healthcare system so clinicians can assign an ICD code to submit claims to insurers for reimbursement for services for treating various medical and mental health conditions in patients. The code is periodically updated to reflect changes in classifications of disease or to add new disorders.
Interpersonal Therapy (IPT):
Also called interpersonal psychotherapy, IPT is designed to help people identify and address their interpersonal problems, specifically those involving grief, interpersonal role conflicts, role transitions, and interpersonal deficits. In this therapy, no emphasis is placed directly on modifying eating habits. Instead, the expectation is that the therapy will enable people to change as their interpersonal functioning improves. IPT usually involves 16 to 20 hour-long, one-on-one treatment sessions over a period of 4 to 5 months.
Ketosis A condition characterized by an abnormally elevated concentration of ketones in the body tissues and fluids, which can be caused by starvation. It is a complication of diabetes, starvation, and alcoholism.
Level of Care:
The care setting and intensity of care that a patient is receiving (e.g. inpatient hospital, outpatient hospital, outpatient residential, intensive outpatient, residential). Health plans and insurance companies correlate their payment structures to the level of care being provided and also map a patient’s eligibility for a particular level of care to the patient’s medical/psychological status.
(See Major Depressive Disorder)
Major Depressive Disorder:
A condition that is characterized by one or more major depressive episodes that consist of periods of two or more weeks during which a patient has either a depressed mood of loss of interest or pleasure in nearly all activities. (See Depression)
One or more slit-like tears in the mucosa at the lower end of the esophagus as a result of severe vomiting.
Treatment program for eating disorders based on the idea that psychiatric symptoms of people with eating disorders emerge as a result of poor nutrition and are not a cause of the eating disorder. A Mandometer is a computer that measures food intake and is used to determine a course of therapy.
(See State Mandates)
A generic term for any of a number of various types of therapeutic touch in which the practitioner massages, applies pressure to, or manipulates muscles, certain points on the body, or other soft tissues to improve health and well-being. Massage therapy is thought to relieve anxiety and depression in patients with an eating disorder.
A family-centered treatment program with three distinct phases. The first phase for a patient who is severely underweight is to regain control of eating habits and break the cycle of starvation or binge eating and purging. The second phase begins once the patient’s eating is under control with a goal of returning independent eating to the patient. The goal of the third and final phase is to address the broader concerns of the patient’s development.
Mealtime Support Therapy:
Treatment program developed to help patients with eating disorders eat healthfully and with less emotional upset.
Mental Health Parity Laws:
Federal and State laws that require health insurers to provide the same level of healthcare benefits for mental disorders and conditions as they do for medical disorders and conditions. For example, the federal Mental Health Parity Act of 1996 (MHPA) may prevent a group health plan from placing annual or lifetime dollar limits on mental health benefits that are lower, or less favorable, than annual or lifetime dollar limits for medical and surgical benefits offered under the plan.
(slang) For bulimia or bulimic.
Modified Cyclic Antidepressants:
A class of medications used to treat depression.
Monoamine Oxidase Inhibitors:
A class of medications used to treat depression. Mood Disorders Mental disorders characterized by periods of depression, sometimes alternating with periods of elevated mood. People with mood disorders suffer from severe or prolonged mood states that disrupt daily functioning. Among the general mood disorders classified in the Diagnostic and Statistical Manual of Mental Disorders (DSM-V) are major depressive disorder, bipolar disorder, and dysthymia (see Anxiety and Major Depressive Disorder).
Motivational Enhancement Therapy (MET):
A treatment is based on a model of change, with focus on the stages of change. Stages of change represent constellations of intentions and behaviors through which individuals pass as they move from having a problem to doing something to resolve it. The stages of change move from “pre-contemplation,” in which individuals show no intention of changing, to the “action” stage, in which they are actively engaged in overcoming their problem. Transition from one stage to the next is sequential, but not linear. The aim of MET is to help individuals move from earlier stages into the action stage using cognitive and emotional strategies.
The psychotherapeutic use of movement as a process that furthers the emotional, cognitive, social, and physical integration of the individual, according to the American Dance Therapy Association.
Any of a number of behaviors engaged in by a person with bulimia nervosa to offset potential weight gain from excessive calorie intake from binge eating. Non-purging can take the form of excessive exercise, misuse of insulin by people with diabetes, or long periods of fasting.
Therapy that provides patients with information on the effects of their eating disorder. For example, therapy often includes, as appropriate, techniques to avoid binge eating, and advice about making meals and eating. The goals of nutrition therapy for individuals with anorexia and bulimia nervosa differ according to the disorder. With bulimia, for example, goals are to stabilize blood sugar levels, help individuals maintain a diet that provides them with enough nutrients, and help restore gastrointestinal health.
Obsessive-compulsive Disorder (OCD):
Mental disorder in which recurrent thoughts, impulses, or images cause inappropriate anxiety and distress, followed by acts that the sufferer feels compelled to perform to alleviate this anxiety. Criteria for mood disorder diagnoses can be found in the DSM-IV.
An eating disorder in which a person obsesses about eating only “pure” and healthy food to such an extent that it interferes with the person’s life. This disorder is not a diagnosis listed in the DSM-IV.
A type of drug therapy that interferes with the brain’s opioid receptors and is sometimes used to treat eating disorders.
A condition characterized by a decrease in bone mass with decreased density and enlargement of bone spaces, thus producing porosity and brittleness. This can sometimes be a complication of an eating disorder, including bulimia nervosa and anorexia nervosa.
Healthcare obtained by a beneficiary from providers (hospitals, clinicians, etc.) that are outside the network that the insurance company has assigned to that beneficiary. Benefits obtained outside the designated network are usually reimbursed at a lower rate. In other words, beneficiaries share more of the cost of care when obtaining that care “out of network” unless the insurance company has given the beneficiary special written authorization to go out of network.
(see Mental Health Parity Laws)
Partial Hospitalization (Intensive Outpatient):
For a patient with an eating disorder, partial hospitalization is a time-limited, structured program of medical and psychotherapy services provided through an outpatient hospital or community mental health center. The goal is to resolve or stabilize an acute episode of mental/behavioral illness.
Inflammation of the esophagus caused by reflux of stomach contents and acid.
Use of drugs for treatment of a mental or emotional disorder.
Treatment of a disease or condition using clinician-prescribed drugs.
Phenethylamine Monoamine Reuptake Inhibitors:
A class of drugs used to treat depression.
A health problem that existed or was treated before the effective date of one’s health insurance policy.
A healthcare facility (e.g., hospital, residential treat- ment center), doctor, nurse, therapist, social worker, or other professional who provides care to a patient.
An intensive, nondirective form of psychodynamic therapy in which the focus of treatment is exploration of a person’s mind and habitual thought patterns. It is insight-oriented, meaning that the goal of treatment is for the patient to increase understanding of the sources of his/her inner conflicts and emotional problems. Scientific evidence and research has clearly shown psychoanalysis to be ineffective in treating eating disorders such as anorexia.
A method of psychotherapy in which patients enact the relevant events in their lives instead of simply talking about them.
Psychodynamic theory views the human personality as developing from interactions between conscious and unconscious mental processes. The purpose of all forms of psychodynamic treatment is to bring unconscious mental material and processes into full consciousness so that the patient can gain more control over his/her life.
Psychodynamic Group Therapy:
Psychodynamic groups are based on the same principles as individual psychodynamic therapy and aim to help people with past difficulties, relation- ships, and trauma, as well as current problems. The groups are typically composed of eight members plus one or two therapists.
The treatment of mental and emotional disorders through the use of psychological techniques (some of which are described below) designed to encourage communication of conflicts and insight into problems, with the goal being relief of symptoms, changes in behavior leading to improved social and vocational functioning, and personality growth.
A treatment intended to teach people about their problem, how to treat it, and how to recognize signs of relapse so that they can get necessary treatment before their difficulty worsens or recurs. Family psycho-education includes teaching coping strategies and problem-solving skills
to families, friends, and/or caregivers to help them deal more effectively with the individual.
Psychopathological Rating Scale Self-Rating Scale for Affective Syndromes (CPRS-SA):
A test used to estimate the severity of depression, anxiety, and obsession in an individual
To evacuate the contents of the stomach or bowels by any of several means. In bulimia, purging is used to compensate for excessive food intake. Methods of purging include vomiting, enemas, and excessive exercise.
A technique involving tightly contracting and releasing muscles with the intent to release or reduce stress.
A period in which the symptoms of a disease are absent. Remission differs from the concept of “cure” in that the disease can return. The term “cure” signifies that the treated condition or disorder is permanently gone, never to return in the individual who received treatment.
Services delivered in a structured resi- dence other than the hospital or a client’s home.
Residential Treatment Center:
A 24-hour residential environ- ment outside the home that includes 24-hour provision or access to support personnel capable of meeting the client’s needs.
Selective Serotonin Re-uptake Inhibitors (SSRI):
A class of antidepressants used to treat depression, anxiety disorders, and some personality disorders. These drugs are designed to elevate the level of serotonin, a neurotransmitter . A low level of serotonin is currently seen as one of several neuro-chemical symptoms of depression. Low levels of serotonin in turn can be caused by an anxiety disorder, because serotonin is needed to metabolize stress hormones. Serotonin is derived from food, which is why someone with a restricting eating disorder will not benefit from SSRI therapy in the absence of adequate weight restoration.
A personality trait that comprises self- confidence, reliability, responsibility, resourcefulness, and goal- orientation.
Self-guided Cognitive Behavior Therapy:
A modified form of cognitive behavior therapy in which a treatment manual is provided for people to proceed with treatment on their own, or with support from a nonprofessional. Guided self-help usually implies that the support person may or may not have some professional training, but is usually not a specialist in eating disorders. The important characteristics of the self-help approach are the use of a highly structured and detailed manual-based CBT, with guidance as to the appropriateness of self-help, and advice on where to seek additional help.
An itemized written test in which a person rates his/her feeling towards each question; the test is designed to categorize the personality or behavior of the person.
A type of psychoanalysis that views anorexia and bulimia as specific cases of pathology of the self. According to this viewpoint, for example, people with bulimia nervosa cannot rely on human beings to fulfill their self-object needs (e.g., regulation of self-esteem, calming, soothing, vitalizing). Instead, they rely on food (its consumption or avoidance) to fulfill these needs. Self psychological therapy involves helping people with bulimia give up their pathological preference for food as a self-object and begin to rely on human beings as self-objects, beginning with their therapist.
A proclamation, order, or law from a state legislature that issues specific instructions or regulations. Many states have issued mandates pertaining to coverage of mental health benefits and specific disorders the state requires insurers to cover.
Use of a mood or behavior-altering substance in a maladaptive pattern resulting in significant impairment or distress of the user.
Substance Use Disorders:
The fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-V) defines a substance use disorder as a maladaptive pattern of substance use leading to clinically significant impairment or distress, as manifested by one (or more) of the following, occurring within a 12-month period: (1) recurrent substance use resulting in a failure to fulfill major role obligations at work, school, or home; (2) recurrent substance use in situations in which it is physically hazardous; and (3) recurrent substance-related legal, social, and/ or interpersonal problems.
Sub-threshold Eating Disorder:
Condition in which a person exhibits disordered eating but not to the extent that it fulfills all the criteria for diagnosis of an eating disorder.
Supportive Residential Services:
(see Residential Treatment Center)
Psychotherapy that focuses on the management and resolution of current difficulties and life decisions using the patient’s strengths and available resources.
A type of psychotherapy provided over the telephone by a trained professional.
A class of drugs used to treat depression.
Therapeutic Foster Care:
A foster care program in which youths who cannot live at home are placed in homes with foster parents who have been trained to provide a structured environ- ment that supports the child’s learning, social, and emotional skills.
(slang) Photographs, poems, or any other stimulus that influences a person to strive to lose weight.
An organization that provides health insurance benefits and reimburses for care for beneficiaries.
A multidisciplinary care plan for each beneficiary in active case management. It includes specific services to be delivered, the frequency of services, expected duration, community resources, all funding options, treatment goals, and assessment of the beneficiary environment. The plan is updated monthly and modified when appropriate.
A class of drugs used to treat depression. Trigger A stimulus that causes an involuntary reflex behavior. A trigger may cause a recovering person with bulimia to engage in bulimic behavior again.
Thyroid Medication Abuse:
Excessive use or misuse of drugs used to treat thyroid conditions; a side effect of these drugs is weight loss.
Usual and Customary Rate (aka UCR):
An insurance term that indicates the amount the insurance company will reimburse for a particular service or procedure deemed "out of network". This amount is often less than the amount charged by the service provider. The patient is usually liable to the provider for the difference.
Programs that teach skills needed for self-sufficiency.
A system of physical postures, breathing techniques, and meditation practices to promote bodily or mental control and well-being. | <urn:uuid:738e3e14-7bdb-42b8-820e-cd6cd0ae35d5> | {
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Posttraumatic stress disorder[note 1] (PTSD) is a severe anxiety disorder that can develop after exposure to any event that results in psychological trauma. This event may involve the threat of death to oneself or to someone else, or to one's own or someone else's physical, sexual, or psychological integrity, overwhelming the individual's ability to cope. As an effect of psychological trauma, PTSD is less frequent and more enduring than the more commonly seen acute stress response. Diagnostic symptoms for PTSD include re-experiencing the original trauma(s) through flashbacks or nightmares, avoidance of stimuli associated with the trauma, and increased arousal— such as difficulty falling or staying asleep, anger, and hypervigilance. Formal diagnostic criteria (both DSM-IV-TR and ICD-10) require that the symptoms last more than one month and cause significant impairment in social, occupational, or other important areas of functioning. Psychological trauma PTSD is believed to be caused by experiencing any of a wide range of events which produces intense negative feelings of "fear, helplessness or horror" in the observer or participant. Sources of such feelings may include (but are not limited to): experiencing or witnessing childhood or adult physical, emotional, or sexual abuse; experiencing or witnessing physical assault, adult experiences of sexual assault, accidents, drug addiction, illnesses, medical complications; employment in occupations exposed to war (such as soldiers) or disaster (such as emergency service workers); or getting a diagnosis of a life-threatening illness. Children or adults may develop PTSD symptoms by experiencing bullying or mobbing. Approximately 25% of children exposed to family violence can experience PTSD. Preliminary research suggests that child abuse may interact with mutations in a stress-related gene to increase the risk of PTSD in adults. Multiple studies show that parental PTSD and other posttraumatic disturbances in parental psychological functioning can, despite a traumatized parent's best efforts, interfere with their response to their child as well as their child's response to trauma. Parents with violence-related PTSD may, for example, inadvertently expose their children to developmentally inappropriate violent media due to their need to manage their own emotional dysregulation. Clinical findings indicate that a failure to provide adequate treatment to children after they suffer a traumatic experience, depending on their vulnerability and the severity of the trauma, will ultimately lead to PTSD symptoms in adulthood. DSM-5 proposed diagnostic criteria changes In preparation for the May 2013 release of the DSM-5, the fifth version of the American Psychiatric Association's diagnostic manual, draft diagnostic criteria was released for public comment, followed by a two-year period of field testing. Proposed changes to the criteria (subject to ongoing review and research) include the following: Criterion A (prior exposure to traumatic events) is more specifically stated, and evaluation of an individual's emotional response at the time (current criterion A2) is dropped. Several items in Criterion B (intrusion symptoms) are rewritten to add or augment certain distinctions now considered important. Special consideration is given to developmentally appropriate criteria for use with children and adolescents. This is especially evident in the restated Criterion B – intrusion symptoms. Development of age-specific criteria for diagnosis of PTSD is ongoing at this time. Criterion C (avoidance and numbing) has been split into "C" and "D": Criterion C (new version) now focuses solely on avoidance of behaviors or physical or temporal reminders of the traumatic experience(s). What were formerly two symptoms are now three, due to slight changes in descriptions. New Criterion D focuses on negative alterations in cognition and mood associated with the traumatic event(s) and contains two new symptoms, one expanded symptom, and four largely unchanged symptoms specified in the previous criteria. Criterion E (formerly "D"), which focuses on increased arousal and reactivity, contains one modestly revised, one entirely new, and four unchanged symptoms. Criterion F (formerly "E") still requires duration of symptoms to have been at least one month. Criterion G (formerly "F") stipulates symptom impact ("disturbance") in the same way as before. The "acute" vs "delayed" distinction is dropped; the "delayed" specifier is considered appropriate if clinical symptom onset is no sooner than 6 months after the traumatic event(s). | <urn:uuid:ee949ad5-d584-464a-bf50-524b0d3ab2b0> | {
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Epidemiology of Trauma
According to the principles of medicine, trauma is a “disease” rather than an injury and, as such, is no different from malaria, heart disease, or cancer. It has degrees of severity and morbidity/mortality statistics just like other diseases. It is important to understand the epidemiology of trauma as it applies to different populations of people.
There is descriptive epidemiology, which looks at the distribution of the disease over time, place, and over different subgroups of people. There is also analytical epidemiology, which looks at the causation of the trauma/disease. The environment can be a physical one or a sociocultural one. How these factors interact determines the epidemiology of trauma. Knowing these things can help public policy and laws designed to protect people from injury secondary to trauma.
The transfer of physical/mechanical energy accounts for three-fourths of all traumas. The rest are due to chemicals, heat, electricity, and ionizing radiation. Injuries become severe and life-threatening when they fall outside the range of human tissue tolerance.
William Haddon in the 1960s first came up with the idea that trauma is a public health issue. He came up with three phases of trauma: 1) pre-event; 2) event; and 3) post-event. He invented the “Haddon Matrix”, which identified pre-event occurrences like avoidance of alcohol and the use of proper restraint. Speed limits are also a part of that. Event occurrences include the use of safety belts, the deployment of an airbag, and impact-absorbing barriers. Post-event occurrences include bystander care, assessment of the vehicle, and access to emergency care.
Epidemiology of Trauma in the US
Injuries account for a quarter of all deaths in the US per year in all age groups. It is the leading cause of death in children. About 150,000 people die per year as a result of an injury. This is about 54 people out of 100,000 individuals in the US. There are 400 injury deaths per day and 50 of these deaths occur in kids. A total of 80 percent of all deaths in people aged 15-24 are attributable to injuries.
Some declines in deaths have occurred over the years because of better restraint laws and the use of airbags. Workplace safety has saved some lives, while things like homicide fluctuate over time. Suicide deaths are relatively stable.
Intentional and unintentional deaths have accounted for more than 30 percent of potential lives lost under the age of 65. This means that injuries account for more premature deaths when compared to cancer, HIV, and heart disease.
Most deaths occur within minutes of the injury—at the scene, enroute to the hospital, or in the emergency rooms. Most deaths occur from central nervous system/head injuries. The immediate deaths are from massive hemorrhage, neurological injury or both. Even the best emergency medical systems can’t prevent or stop these deaths from occurring. There are fewer deaths from massive infection or end-organ damage because of better later trauma care.
The best way to stop deaths from trauma are to deal with prevention-related items like airbags, seatbelts, and better car design. Another thing is to help improve access of injured patients to higher levels of emergency care, such as level III trauma centers. Research into infection, hemorrhage, and trauma will eventually reduce the number of deaths, especially delayed deaths from trauma.
Deaths are only part of the injury burden. More than 1.5 million trauma victims are hospitalized in the US each year. These patients survive to the point of discharge from the hospital. About 28 million people are treated and eventually discharged from emergency rooms or urgent care centers. Injuries make up 6 percent of all discharges from the hospital and 30 percent of all emergency department visits per year. These injuries are far more than they look because they lead to things like disability and a decreased quality of life.
In dollar amounts, the cost of fatal and nonfatal accidents in any given year is about 406 billion dollars to the overall economy. The costs related to deaths account for a disproportionate share of the costs spent on injury care. Deaths account for only 1 percent of injuries but account for 30 percent of the total costs incurred. The rest, about 70 percent, are related to the treatment of nonfatal injuries. These include hospital costs and the other costs related to healthcare as part of the injury. A total of 41 percent of the costs are from permanent and temporary disability. This doesn’t take into account the losses spent by family and loved ones as part of the ongoing trauma-related expenses.
Injuries and deaths from trauma are most likely a problem of young males and older individuals. Seventy percent of deaths and half of all injuries not leading to death are seen in males. In all age groups, except for the age of 0-9, the rate of injury in males is more than twice that of females. In non-fatal injuries, males are only 1.3 times more likely to be affected. This trend reverses in the elderly, where females have a 1.3 times incidence of nonfatal injury when compared to men.
The peak of death is from 16-40 and from the over 65 group where trauma is concerned. People under the age of 45 have 53 percent of all fatalities from injuries and half of all hospitalizations. They accounted for about 80 percent of emergency department visits. Hospitalizations and nonfatal injuries follow this same bimodal pattern, especially when it comes to males.
The elderly person is less likely to be injured but more likely to be hospitalized and die from their injuries. The rate of death in the 65 and older population is 113 out of 100,000 persons and for those older than 75, the rate of death is 169 out of 100,000 persons. So it seems the elderly are overrepresented when it comes to injury fatalities in which approximately 14 percent were related to traffic injury deaths. Less than one percent of the deaths in the elderly were from firearms. Burns account for two percent of injury-related deaths and 1.4 percent of nonfatal events reported to the Centers for Disease Control.
In 2004, alone, there were 167,000 deaths due to trauma. There were 1.9 million hospital discharges from the hospital secondary to trauma. There were 3.1 million visits to the emergency room due to injuries. And there were 35 million initial visits to private physician clinics because of injury-related events.
Statistics show that 93 percent of nonfatal injuries were unintentional, whereas 68 percent of fatal injuries were unintentional. Thirty percent of deaths due to injury were related to violence. In 2007 alone, about 18,000 people were killed because of homicide. More than 34,000 deaths were related to the successful completion of suicide. This accounted for 66 percent of all violent deaths.
Injury in the workplace is common. About 5000 fatalities were reported in 2008 as a result of injuries sustained at the workplace. This means that there were 3.6 per million full time workers per year. Transportation-related deaths accounted for 40 percent of all workplace deaths. Assaults and violence accounted for 16 percent of all fatalities, whereas 18 percent of fatalities were because of contact with equipment. Falls accounted for 13 percent. A total of 10 percent of workplace deaths were because of homicide. Eighty percent of these were firearm-related deaths. Five percent of all workplace deaths were self-inflicted.
The Division of Labor Statistics reported about 4.6 million nonfatal work-related injuries. This amounts to 3.6 people out of 100 workers. A total of 71 percent of these injuries were in the service industry. Half of all injuries produced some kind of disability.
Distribution of Injuries
It is important to catalog injuries by severity and nature. There are several systems available for cataloguing injuries by nature and severity. ICD-10 codes are important in cataloguing the various injuries and their nature. Death certificate data is the best way to identify injury-related deaths. There can be variations in the way that these injuries are presented.
The National Trauma Database is another way to categorize injuries and deaths from trauma. They use a non-scientific sampling of various trauma centers that voluntarily submit data on trauma victims they see. Like death certificates, these voluntary submissions vary as to the completeness and accuracy of data provided. Some information is gleaned from coroner’s reports and autopsy reports. The autopsy results aren’t perfect but they do indicate a trend toward neurological injuries as a cause of death in many injuries. CNS-related deaths account for 40-50 percent of all fatalities found in fatal accidents. The second highest cause of death is hemorrhage, accounting for 30-35 percent of deaths.
According to the CDC, neurological trauma accounts for the most deaths in trauma. This is a serious public health issue in the US today. Traumatic brain injuries account for many deaths and a great deal of disability when it comes to injury. Traumatic brain injury can be mild or severe, and many of the mild cases are missed. There are about 1.7 million visits to the emergency room, deaths and hospitalizations directly related to traumatic brain injury. Traumatic brain injury accounts for 1/3 of all injury-related deaths or about 52,000 deaths per year.
The distribution of nonfatal injuries and fatal injuries is different from one another. There are many injuries associated with body areas that are not considered lethal. Even among nonfatal hospitalized injuries, only a fourth have Abbreviated Injury Scores of 3 or more on a scale of 0-6.
Injuries to the upper and lower extremities involve the leading cause of emergency department visits and hospitalizations among injured people. They account for over half of all non-fatal injuries and 47 percent of hospitalizations because of injuries. More than a third of all moderately severe or severe injuries are for injuries with an Abbreviated Injury Scores of 3 or more. Recovery can take a long time and can be costly. The best of treatment can result in disability and permanent impairment of the individual.
The second most common type of nonfatal injuries that are hospitalized are due to head injuries. It accounts for 10-15 percent of all hospitalizations because of injuries. Mild head injuries are usually treated as an outpatient. The make up 2-5 percent of all trips to the emergency room visits.
About 80 percent of these patients are treated and released from the emergency department. The actual number of head injuries may be under-represented due to the large number of them treated at outpatient centers and urgent care facilities. The total estimate of head injuries ranges from 152 to 367 people out of 100,000 individuals. Most head injuries are mild but about 70,000 to 90,000 are classified as severe and can result in long term disability. Head injuries from recreational activities are not uncommon, accounting for 300,000 injuries per year.
Spinal cord injuries represent a small proportion of injuries from trauma. They account for 10,000 to 15,000 hospitalizations per year. Motor vehicle injuries make up 30-60 percent of all spinal cord injuries. Falls account for 20-30 percent of spinal cord injuries. About 5-10 percent of all spinal cord injuries are from diving accidents. There is a huge financial cost incurred as a result of spinal cord injuries, many of which are nonfatal but result in major disability.
Distribution of Injuries as related to Geographic Location
There is a varying amount of injuries as stratified across different areas of the country and between rural and urban areas. Unintentional injuries are highest in rural populations. In these areas, homicide accounts for many times more deaths than in suburban and urban populations. Death rates for unintentional injuries are greater in the Southern states and Western states. Suicide rates are higher in the west and homicide rates are greater in the south. When things like access to care, educational climate, and economics are factored in, the differences in death among the different geographic locations become nonexistent.
Things that Influence Results
There are a number of confounding factors that play into the results from trauma assessments and epidemiology. There are things such as race, socioeconomic factors, culture, access to healthcare, alcohol abuse, drug abuse, and ethnicity that cannot all be controlled for when looking at trauma data. This means that caution must be observed when interpreting trauma data.
There is a lot of data missing regarding pre-hospital care and post-hospital care of injuries, including rehabilitation. There have been many pre-hospital databases developed over the years. Only 26 states supply data to the NEMSIS program, the “National Emergency Medical Services Information System” database. At least 12 states are considering legislation to have the states contribute to this system, which will help make the data more accurate. Many professional organizations are pushing for change that allows EMS systems to provide data that is NEMSIS-compliant.
Long term care data is essential when it comes to recognizing the long term financial implications of trauma. There is the Uniform Data System for Medical Rehabilitation or UDSMR that evaluates the effectiveness of rehab programs for the trauma patient. This has given us the most comprehensive data on rehabilitation from injuries. These data do not, however, translate well to prevention programs for injury/trauma patients.
Death certificate data doesn’t always provide accurate information for all injury-related deaths. Medical examiner and coroner reports help augment these data but they are not a hundred percent accurate either. Autopsy data is not perfect and tends to be skewed toward homicide-related trauma. Hospital-related data is also skewed and don’t often include data on those patients that were treated and released for their injuries. Trauma registries are skewed toward major trauma and exclude those patients who survive but are in the hospital less than three days. There is a great need for a single database that can link prehospital care, care in the emergency room, care in the hospital, and rehabilitative care altogether.
Injury imposes a heavy burden on society at many levels, including morbidity, mortality, and cost of care. What isn’t recognized is that many of these injuries are completely preventable using specific strategies. Because of this, there isn’t the public outcry about injury deaths, as there is about illnesses such as cancer, HIV, and heart disease. These other diseases are much talked about yet contribute far less to the burden on society as trauma-related injuries and deaths.
Most injuries are unintentional and most of the unintentional injury deaths occur in the elderly. Suicide greatly outnumbers homicide in this population. The risk of death greatly varies according to occupation. The US compares poorly when compared to other countries when it comes to firearm-related deaths. Elderly women make up the vast majority of hospitalizations from injuries sustained. Teens and young adults make up the majority of emergency department visits, with most injuries occurring around the home.
There has been a slight reduction in injury related deaths when comparing 1985 to 2004. Some causes of death are increasing while others are decreasing. Injury morbidity has dropped in every population except for the elderly. Alcohol and drug use continues to be related to several types of traumas.
Trauma remains a great public health issue. Prevention and treating these injuries better will continue to be the focus of healthcare providers across the nation. The priority should be on prevention programs. Accurate data continues to be the focus of agencies trying to determine who gets injured and how to prevent these injuries from occurring.
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Health Status: Mental Health
In recognition of the need to highlight issues of quality of life and rights of people with mental disorders, in 1992 the National Mental Health Strategy was developed and in 1996 mental health was designated as a National Health Priority Area.
Types of mental health disorders
The prevalence of mental disorder was similar for men and women (17% and 18% respectively). However, there were differences in the prevalence of mental disorders of different types among men and women and at different ages. Women were more likely to have experienced anxiety disorders (12% for women compared to 7% for men) and affective disorders (7% compared to 4%). On the other hand, men were more than twice as likely as women to have had a substance use disorder (11% compared to 4%).
The prevalence of anxiety disorders for women aged 18-44 ranged between 12% to 15%. Women aged 45-54 had the highest rate of anxiety disorders, 16%, which steadily declined in older age groups to 5% for those aged over 64. For men, the prevalence of anxiety disorders varied little with age until age 55, after which it declined. The prevalence of affective disorders was highest at 11% for women aged 18-24, more than three times the rate for men of this age. For women, the prevalence of affective disorders generally declined with age, while for men, rates increased in the middle years before declining after age 55.
Men aged 18-24 had the highest rate of substance use disorders, particularly from excessive alcohol intake, with more than one in five being affected (22%). The equivalent rate for women in this age group was half this (11%). For men and women, the prevalence of substance use disorders declined steadily with age. Alcohol use disorders were about three times more common than any other substance use disorder (7% compared to 2%).
The presence of a mental disorder may predispose individuals to other disorders. For example, people who experience social phobia may also experience depression and alcohol dependence. People with an affective disorder were the most likely to have more than one mental disorder. Of those with an affective disorder, 61% also had an anxiety or substance use disorder. In comparison, 43% of those with an anxiety disorder also had an affective or substance use disorder and 31% of those with a substance use disorder had an affective or anxiety disorder.
PREVALENCE OF MENTAL DISORDERS(a), 1997
(a) During the 12 months prior to interview.
Source: Mental Health and Wellbeing Profile of Adults, Australia 1997 (cat. no. 4326.0).
Impact on daily life
People with a mental disorder (or physical condition) are not necessarily restricted in their day to day activities. However, the presence of mental and/or physical conditions in combination often increases the likelihood of disability, compounding the difficulties that these people face.
The 1997 National Survey of Mental Health and Wellbeing used the Brief Disability Questionnaire (BDQ), based on a standard international questionnaire, as a measure of disability. The BDQ asks participants whether they are limited in a number of activities, and whether they have cut down or stopped activities they were expected to do as part of their routine. Participants were then allocated a score characterising them as having a mild, moderate or severe disability, or none.
People who reported physical conditions only were more likely to have a disability than those who reported mental disorders only (55% compared to 30%). This may partly reflect the emphasis the BDQ places on the physical rather than the mental aspects of disability. Even so, adults with mental disorders, were on average more likely to be disabled than adults in general (44% compared to 34%).
MENTAL DISORDERS AND PHYSICAL CONDITIONS(a) BY DISABILITY STATUS(b), 1997
(b) During the four weeks prior to interview, according to the Brief Disability Questionnaire.
Source: Mental Health and Wellbeing Profile of Adults, Australia, 1997 (cat. no. 4326.0).
Health service use
Some people experience a mental disorder once and fully recover. For others, it recurs throughout their lives or in episodes. The vast majority of mental illnesses are able to be treated if they have access to appropriate care and services2.
Of those with mental disorders in 1997, 38% used a health service for their mental health problems in the previous 12 months. Women were more likely than men to use health services (46% of women compared to 29% of men). The most commonly used health service for both men and women was consulting a general practitioner (22% and 37% respectively).
The likelihood of using health services for a mental health problem was closely related to the type of mental disorder. Of those with affective disorders only, 56% used health services, compared to 28% of those with anxiety only and 14% of those with substance use disorders only. Those with combinations of mental disorders were the most likely to use services for mental health problems (66%).
For those with a disability, service use for mental disorders increased with the severity of the disability. A small proportion of people with no mental disorders also used services for mental health problems (5%). These people may have consulted a health professional for a sub-clinical mental disorder such as stress, or for a mental disorder not included in the analysis of the National Survey of Mental Health and Wellbeing.
Overall, the proportion of people with a mental disorder decreased as the number of people living in the household increased. This may reflect the difficulties that some of these people have in forming and maintaining relationships.
After adjusting for age, the prevalence of mental disorder was highest for both men and women living alone. This was the case for anxiety, affective and substance use disorders individually.
Age standardised rates were higher among people who were separated or divorced (24% of men and 27% of women) compared to people who were married, widowed or never married. In particular, people who were separated or divorced had higher rates of anxiety or affective disorders (18% and 12% respectively) than the other groups. People who had never married also had higher rates of mental disorder than those who were married. In particular, this group, had higher rates of substance use disorders (14%).
People with mental disorders not only find it more difficult to obtain jobs (see Australian Social Trends 1997, Employment of people with a handicap), but unemployment may also contribute to their disorder. Higher unemployment rates among people with mental disorders could be the result of a combination of factors including the disabling effects of mental disorders, lack of training and negative employer attitudes.
After adjusting for age, rates of mental disorders were highest for men and women who were unemployed or not in the labour force. In particular, unemployed people had relatively high rates of substance use disorders (19% of men and 11% of women) compared to employed people and people not in the labour force. It is unclear whether substance use predisposes people to unemployment, unemployment predisposes people to substance use, or both.
Unemployed women also had relatively high rates of anxiety disorders (20%) compared to employed women and women not in the labour force.
PROPORTION OF PEOPLE WITH A MENTAL DISORDER(a) BY LABOUR FORCE STATUS, 1997
Source: Mental Health and Wellbeing Profile of Adults, Australia 1997, (cat. no. 4326.0).
Suicide is thought to be higher among people with mental disorders. However, the incidence of suicide among people with mental disorders is not known.
Results from the 1997 Survey of Mental Health and Wellbeing indicate that people with a mental disorder were nearly four times as likely to have thought about suicide since the age of 18 as people without a mental disorder (37% compared to 9%). Furthermore, they were nearly 7 times more likely to have attempted suicide (10% compared to 1.5%).
1 World Health Organisation (WHO) 1992, The ICD-10 Classification of Mental and Behavioural Disorders, Clinical Descriptions and Diagnostic Guidelines, WHO, Geneva.
2 National Mental Health Strategy brochure 1997, Mental illness - facts, AGPS, Canberra. | <urn:uuid:1e8e47f4-38ed-4a5f-b631-3440a6a8c87d> | {
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|Classification and external resources|
|ICD-9||307.42, 307.41, 327.0, 780.51, 780.52|
Insomnia, or sleeplessness, is a sleep disorder in which there is an inability to fall asleep or to stay asleep as long as desired. While the term is sometimes used to describe a disorder demonstrated by polysomnographic or actigraphic evidence of disturbed sleep, this sleep disorder is often practically defined as a positive response to either of two questions: "Do you experience difficulty sleeping?" or "Do you have difficulty falling or staying asleep?"
Insomnia is most often thought of as both a medical sign and a symptom that can accompany several sleep, medical, and psychiatric disorders characterized by a persistent difficulty falling asleep and/or staying asleep or sleep of poor quality. Insomnia is typically followed by functional impairment while awake. Insomnia can occur at any age, but it is particularly common in the elderly. Insomnia can be short term (up to three weeks) or long term (above 3–4 weeks); it can lead to memory problems, depression, irritability and an increased risk of heart disease and automobile related accidents.
Those who are having trouble sleeping sometimes turn to sleeping pills, which can help when used occasionally but may lead to substance dependency or addiction if used regularly for an extended period.
Insomnia can be grouped into primary and secondary, or comorbid, insomnia. Primary insomnia is a sleep disorder not attributable to a medical, psychiatric, or environmental cause. It is described as a complaint of prolonged sleep onset latency, disturbance of sleep maintenance, or the experience of non-refreshing sleep. A complete diagnosis will differentiate between free-standing primary insomnia, insomnia as secondary to another condition, and primary insomnia co-morbid with one or more conditions.
- 1 Classification
- 2 Causes and comorbidity
- 3 Diagnosis
- 4.1 Non-pharmacological
- 4.2 Medications
- 4.3 Alternative medicine
- 5 Epidemiology
- 6 Society
- 7 See also
- 8 References
- 9 Bibliography
DSM-5 criteria for insomnia
The DSM-5 criteria for insomnia include the following:
Predominant complaint of dissatisfaction with sleep quantity or quality, associated with one (or more) of the following symptoms:
- Difficulty initiating sleep. (In children, this may manifest as difficulty initiating sleep without caregiver intervention.)
- Difficulty maintaining sleep, characterized by frequent awakenings or problems returning to sleep after awakenings. (In children, this may manifest as difficulty returning to sleep without caregiver intervention.)
- Early-morning awakening with inability to return to sleep.
- The sleep disturbance causes clinically significant distress or impairment in social, occupational, educational, academic, behavioral, or other important areas of functioning.
- The sleep difficulty occurs at least 3 nights per week.
- The sleep difficulty is present for at least 3 months.
- The sleep difficulty occurs despite adequate opportunity for sleep.
- The insomnia is not better explained by and does not occur exclusively during the course of another sleep-wake disorder (e.g., narcolepsy, a breathing-related sleep disorder, a circadian rhythm sleep-wake disorder, a parasomnia).
- The insomnia is not attributable to the physiological effects of a substance (e.g., a drug of abuse, a medication).
- Coexisting mental disorders and medical conditions do not adequately explain the predominant complaint of insomnia.
note: The DSM-5 criteria for insomnia is intended for use by general mental health and medical clinicians (those caring for adult, geriatric, and pediatric patients).
Types of insomnia
Insomnia can be classified as transient, acute, or chronic.
- Transient insomnia lasts for less than a week. It can be caused by another disorder, by changes in the sleep environment, by the timing of sleep, severe depression, or by stress. Its consequences – sleepiness and impaired psychomotor performance – are similar to those of sleep deprivation.
- Acute insomnia is the inability to consistently sleep well for a period of less than a month. Insomnia is present when there is difficulty initiating or maintaining sleep or when the sleep that is obtained is non-refreshing or of poor quality. These problems occur despite adequate opportunity and circumstances for sleep and they must result in problems with daytime function. Acute insomnia is also known as short term insomnia or stress related insomnia.
- Chronic insomnia lasts for longer than a month. It can be caused by another disorder, or it can be a primary disorder. People with high levels of stress hormones or shifts in the levels of cytokines are more likely than others to have chronic insomnia. Its effects can vary according to its causes. They might include muscular fatigue, hallucinations, and/or mental fatigue. Chronic insomnia can cause double vision.
Patterns of insomnia
Symptoms of insomnia:
Sleep-onset insomnia is difficulty falling asleep at the beginning of the night, often a symptom of anxiety disorders. Delayed sleep phase disorder can be misdiagnosed as insomnia, as sleep onset is delayed to much later than normal while awakening spills over into daylight hours.
It is common for patients who have difficulty falling asleep to also have nocturnal awakenings with difficulty returning to sleep. Two thirds of these patients wake up in middle of the night, with more than half having trouble falling back to sleep after a middle of the night awakening.
Early morning awakening is an awakening occurring earlier (more than 30 minutes) than desired with an inability to go back to sleep, and before total sleep time reaches 6.5 hours. Early morning awakening is often a characteristic of depression.
Poor sleep quality
Poor sleep quality can occur as a result of, for example, restless legs, sleep apnea or major depression. Poor sleep quality is caused by the individual not reaching stage 3 or delta sleep which has restorative properties.
Some cases of insomnia are not really insomnia in the traditional sense. People experiencing sleep state misperception often sleep for normal durations, yet severely overestimate the time taken to fall asleep. They may believe they slept for only four hours while they, in fact, slept a full eight hours.
Causes and comorbidity
Symptoms of insomnia can be caused by or be co-morbid with:
- Use of psychoactive drugs (such as stimulants), including certain medications, herbs, caffeine, nicotine, cocaine, amphetamines, methylphenidate, aripiprazole, MDMA, modafinil, or excessive alcohol intake.
- Withdrawal from anti-anxiety drugs such as benzodiazepines or pain-relievers such as opioids.
- Previous thoracic surgery.
- Heart disease.
- Deviated nasal septum and nocturnal breathing disorders.
- Use of fluoroquinolone antibiotic drugs is associated with more severe and chronic types of insomnia.
- Restless legs syndrome, which can cause sleep onset insomnia due to the discomforting sensations felt and the need to move the legs or other body parts to relieve these sensations.
- Periodic limb movement disorder (PLMD), which occurs during sleep and can cause arousals of which the sleeper is unaware.
- Pain An injury or condition that causes pain can preclude an individual from finding a comfortable position in which to fall asleep, and can in addition cause awakening.
- Hormone shifts such as those that precede menstruation and those during menopause.
- Life events such as fear, stress, anxiety, emotional or mental tension, work problems, financial stress, birth of a child and bereavement.
- Gastrointestinal issues such as heartburn or constipation.
- Mental disorders such as bipolar disorder, clinical depression, generalized anxiety disorder, post traumatic stress disorder, schizophrenia, obsessive compulsive disorder, and dementia. or ADHD
- Disturbances of the circadian rhythm, such as shift work and jet lag, can cause an inability to sleep at some times of the day and excessive sleepiness at other times of the day. Chronic circadian rhythm disorders are characterized by similar symptoms.
- Certain neurological disorders, brain lesions, or a history of traumatic brain injury.
- Medical conditions such as hyperthyroidism and rheumatoid arthritis.
- Abuse of over-the counter or prescription sleep aids (sedative or depressant drugs) can produce rebound insomnia.
- Poor sleep hygiene, e.g., noise or over-consumption of caffeine
- A rare genetic condition can cause a prion-based, permanent and eventually fatal form of insomnia called fatal familial insomnia.
- Physical exercise. Exercise-induced insomnia is common in athletes in the form of prolonged sleep onset latency.
Sleep studies using polysomnography have suggested that people who have sleep disruption have elevated nighttime levels of circulating cortisol and adrenocorticotropic hormone They also have an elevated metabolic rate, which does not occur in people who do not have insomnia but whose sleep is intentionally disrupted during a sleep study. Studies of brain metabolism using positron emission tomography (PET) scans indicate that people with insomnia have higher metabolic rates by night and by day. The question remains whether these changes are the causes or consequences of long-term insomnia.
Steroid hormones and insomnia
Studies have been conducted with steroid hormones and insomnia. Changes in levels of cortisol, progesterone in the female cycle, or estrogen during menopause are correlated with increased occurrences of insomnia. Those with differing levels of cortisol often have long-term insomnia, where estrogen is onset insomnia catalyzed by menopause, and progesterone is temporary insomnia within the monthly female cycle.
Cortisol is typically thought of as the stress hormone in humans, but it is also the awakening hormone. Analyzing saliva samples taken in the morning has shown that patients with insomnia wake up with significantly lower cortisol levels when compared to a control group with regular sleeping patterns. Further studies have revealed that those with lower levels of cortisol upon awakening also have poorer memory consolidation in comparison to those with normal levels of cortisol. Studies support that larger amounts of cortisol released in the evening occurs in primary insomnia. In this case, drugs related to calming mood disorders or anxiety, such as antidepressants, would regulate the cortisol levels and help prevent insomnia.
Many postmenopausal women have reported changes in sleep patterns since entering menopause that reflect symptoms of insomnia. This could occur because of the lower levels of estrogen. Lower estrogen levels can cause hot flashes, change in stress reactions, or overall change in the sleep cycle, which all could contribute to insomnia. Estrogen treatment as well as estrogen-progesterone combination supplements as a hormone replacement therapy can help regulate menopausal women’s sleep cycle again.
Low levels of progesterone throughout the female menstruation cycle, but primarily near the end of the luteal phase, have also been known to correlate with insomnia as well as aggressive behavior, irritability, and depressed mood in women. Around 67% of women have problems with insomnia right before or during their menstrual cycle. Lower levels of progesterone can, like estrogen, correlate with insomnia in menopausal women.
A common misperception is that the amount of sleep required decreases as a person ages. The ability to sleep for long periods, rather than the need for sleep, appears to be lost as people get older. Some elderly insomniacs toss and turn in bed and occasionally fall off the bed at night, diminishing the amount of sleep they receive.
Insomnia affects people of all age groups but people in the following groups have a higher chance of acquiring insomnia.
- Individuals older than 60
- History of mental health disorder including depression, etc.
- Emotional stress
- Working late night shifts
- Travelling through different time zones
In medicine, insomnia is widely measured using the Athens insomnia scale. It is measured using eight different parameters related to sleep, finally it is represented as an overall scale which assess an individual's sleep pattern
A qualified sleep specialist should be consulted in the diagnosis of any sleep disorder so the appropriate measures can be taken. Past medical history and a physical examination need to be done to eliminate other conditions that could be the cause of the insomnia. After all other conditions are ruled out a comprehensive sleep history should be taken. The sleep history should include sleep habits, medications (prescription and non-prescription), alcohol consumption, nicotine and caffeine intake, co-morbid illnesses, and sleep environment. A sleep diary can be used to keep track of the individual's sleep patterns. The diary should include time to bed, total sleep time, time to sleep onset, number of awakenings, use of medications, time of awakening and subjective feelings in the morning.
Workers who complain of insomnia should not routinely have polysomnography to screen for sleep disorders. This test may be indicated for patients with symptoms in addition to insomnia, including sleep apnea, obesity, a risky neck diameter, or risky fullness of the flesh in the oropharynx. Usually, the test is not needed to make a diagnosis, and insomnia especially for working people can often be treated by changing a job schedule to make time for sufficient sleep and by improving sleep hygiene.
Some patients may need to do a sleep study to determine if insomnia is present. The sleep study will involve the assessment tools of a polysomnogram and the multiple sleep latency test and will be conducted in a sleep center or a designated hotel. Specialists in sleep medicine are qualified to diagnose the many different sleep disorders. Patients with various disorders, including delayed sleep phase syndrome, are often mis-diagnosed with primary insomnia. When a person has trouble getting to sleep, but has a normal sleep pattern once asleep, a delayed circadian rhythm is the likely cause.
In many cases, insomnia is co-morbid with another disease, side-effects from medications, or a psychological problem. Approximately half of all diagnosed insomnia is related to psychiatric disorders. In depression in many cases "insomnia should be regarded as a co-morbid condition, rather than as a secondary one;" insomnia typically predates psychiatric symptoms. "In fact, it is possible that insomnia represents a significant risk for the development of a subsequent psychiatric disorder."
Knowledge of causation is not necessary for a diagnosis.
It is important to identify or rule out medical and psychological causes before deciding on the treatment for insomnia. Cognitive behavioral therapy (CBT) "has been found to be as effective as prescription medications are for short-term treatment of chronic insomnia. Moreover, there are indications that the beneficial effects of CBT, in contrast to those produced by medications, may last well beyond the termination of active treatment." Pharmacological treatments have been used mainly to reduce symptoms in acute insomnia; their role in the management of chronic insomnia remains unclear. Several different types of medications are also effective for treating insomnia. However, many doctors do not recommend relying on prescription sleeping pills for long-term use. It is also important to identify and treat other medical conditions that may be contributing to insomnia, such as depression, breathing problems, and chronic pain.
Non-pharmacological strategies have comparable efficacy to hypnotic medication for insomnia and they may have longer lasting effects. Hypnotic medication is only recommended for short-term use because dependence with rebound withdrawal effects upon discontinuation or tolerance can develop.
Non pharmacological strategies provide long lasting improvements to insomnia and are recommended as a first line and long term strategy of management. The strategies include attention to sleep hygiene, stimulus control, behavioral interventions, sleep-restriction therapy, paradoxical intention, patient education and relaxation therapy. Reducing the temperature of blood flowing to the brain slows the brain's metabolic rate thereby reducing insomnia. Some examples are keeping a journal, restricting the time spending awake in bed, practicing relaxation techniques, and maintaining a regular sleep schedule and a wake-up time. Behavioral therapy can assist a patient in developing new sleep behaviors to improve sleep quality and consolidation. Behavioral therapy may include, learning healthy sleep habits to promote sleep relaxation, undergoing light therapy to help with worry-reduction strategies and regulating the circadian clock.
Sleep hygiene is a common term for all of the behaviors which relate to the promotion of good sleep. These behaviors are used as the basis of sleep interventions and are the primary focus of sleep education programs. Behaviors include the use of caffeine, nicotine and alcohol consumption, maximizing the regularity and efficiency of sleep episodes, minimizing medication usage and daytime napping, the promotion of regular exercise, and the facilitation of a positive sleep environment. Exercise can be helpful when establishing a routine for sleep but should not be done close to the time that you are planning on going to sleep. The creation of a positive sleep environment may also be helpful in reducing the symptoms of insomnia. In order to create a positive sleep environment one should remove objects that can cause worry or distressful thoughts from view.
Stimulus control therapy is a treatment for patients who have conditioned themselves to associate the bed, or sleep in general, with a negative response. As stimulus control therapy involves taking steps to control the sleep environment, it is sometimes referred interchangeably with the concept of sleep hygiene. Examples of such environmental modifications include using the bed for sleep or sex only, not for activities such as reading or watching television; waking up at the same time every morning, including on weekends; going to bed only when sleepy and when there is a high likelihood that sleep will occur; leaving the bed and beginning an activity in another location if sleep does not result in a reasonably brief period of time after getting into bed (commonly ~20 min); reducing the subjective effort and energy expended trying to fall asleep; avoiding exposure to bright light during nighttime hours, and eliminating daytime naps.
A component of stimulus control therapy is sleep restriction, a technique that aims to match the time spent in bed with actual time spent asleep. This technique involves maintaining a strict sleep-wake schedule, sleeping only at certain times of the day and for specific amounts of time to induce mild sleep deprivation. Complete treatment usually lasts up to 3 weeks and involves making oneself sleep for only a minimum amount of time that they are actually capable of on average, and then, if capable (i.e. when sleep efficiency improves), slowly increasing this amount (~15 min) by going to bed earlier as the body attempts to reset its internal sleep clock. Bright light therapy, which is often used to help early morning wakers reset their natural sleep cycle, can also be used with sleep restriction therapy to reinforce a new wake schedule. Although applying this technique with consistency is difficult, it can have a positive effect on insomnia in motivated patients.
Paradoxical intention is a cognitive reframing technique where the insomniac, instead of attempting to fall asleep at night, makes every effort to stay awake (i.e. essentially stops trying to fall asleep). One theory that may explain the effectiveness of this method is that by not voluntarily making oneself go to sleep, it relieves the performance anxiety that arises from the need or requirement to fall asleep, which is meant to be a passive act. This technique has been shown to reduce sleep effort and performance anxiety and also lower subjective assessment of sleep-onset latency and overestimation of the sleep deficit (a quality found in many insomniacs).
Meditation has been recommended for the treatment of insomnia. The meditation teacher Siddhārtha Gautama, 'The Buddha', is recorded as having recommended the practice of 'loving-kindness' meditation, or mettā bhāvanā as a way to produce relaxation and thereby, sound sleep – putting it first in a list of the benefits of that meditation. More recently, studies have concluded that: a mindfulness practice reduced mental and bodily restlessness before sleep and the subjective symptoms of insomnia; and that mindfulness-based cognitive behavioural therapy reduced restlessness, sleep effort and dysfunctional sleep-related thoughts including worry.
Cognitive behavioral therapy
There is some evidence that cognitive behavioural therapy for insomnia is superior in the long-term to benzodiazepines and the nonbenzodiazepines in the treatment and management of insomnia. In this therapy, patients are taught improved sleep habits and relieved of counter-productive assumptions about sleep. Common misconceptions and expectations that can be modified include: (1) unrealistic sleep expectations (e.g., I need to have 8 hours of sleep each night), (2) misconceptions about insomnia causes (e.g., I have a chemical imbalance causing my insomnia), (3) amplifying the consequences of insomnia (e.g., I cannot do anything after a bad night's sleep), and (4) performance anxiety after trying for so long to have a good night's sleep by controlling the sleep process. Numerous studies have reported positive outcomes of combining cognitive behavioral therapy for insomnia treatment with treatments such as stimulus control and the relaxation therapies. Hypnotic medications are equally effective in the short-term treatment of insomnia but their effects wear off over time due to tolerance. The effects of CBT-I have sustained and lasting effects on treating insomnia long after therapy has been discontinued. The addition of hypnotic medications with CBT-I adds no benefit in insomnia. The long lasting benefits of a course of CBT-I shows superiority over pharmacological hypnotic drugs. Even in the short term when compared to short-term hypnotic medication such as zolpidem (Ambien), CBT-I still shows significant superiority. Thus CBT-I is recommended as a first line treatment for insomnia. Metacognition is also a recent trend in approach to behaviour therapy of insomnia.
Insomnia can be short-term or long-term. Prevention of the sleep disorder may include maintaining a consistent sleeping schedule, such as waking up and sleeping at the same times every day. Also, one should avoid caffeinated drinks during the 8 hours before sleeping time. While exercise is essential and can aid the process of sleeping, it is important to not exercise right before bedtime, therefore creating a calm environment. Lastly, one's bed should only be for sleep and sex. These are some of the points included in sleep hygiene. Going to sleep and waking up at the same time every day can create a steady pattern, which may help against insomnia.
Despite the therapeutic effectiveness and proven success of CBT, treatment availability is significantly limited by a lack of trained clinicians, poor geographical distribution of knowledgeable professionals, and expense. One way to potentially overcome these barriers is to use the Internet to deliver treatment, making this effective intervention more accessible and less costly. The Internet has already become a critical source of health-care and medical information. Although the vast majority of health websites provide general information, there is growing research literature on the development and evaluation of Internet interventions.
These online programs are typically behaviorally-based treatments that have been operationalized and transformed for delivery via the Internet. They are usually highly structured; automated or human supported; based on effective face-to-face treatment; personalized to the user; interactive; enhanced by graphics, animations, audio, and possibly video; and tailored to provide follow-up and feedback.
A number of Internet interventions for insomnia have been developed and a few of them have been evaluated as part of scientific research trials.
A paper published in 2012 reviewed the related literature and found good evidence for the use of Internet interventions for insomnia.
Many insomniacs rely on sleeping tablets and other sedatives to get rest. In some places medications are prescribed to over 95% of insomniac cases. The percentage of adults using a prescription sleep aid increases with age. During 2005–2010, about 4% of U.S. adults aged 20 and over reported that they took prescription sleep aids in the past 30 days. Prevalence of use was lowest among the youngest age group (those aged 20–39) at about 2%, increased to 6% among those aged 50–59, and reached 7% among those aged 80 and over. More adult women (5.0%) reported using prescription sleep aids than adult men (3.1%). Non-Hispanic white adults reported higher use of sleep aids (4.7%) than non-Hispanic black (2.5%) and Mexican-American (2.0%) adults. No difference was shown between non-Hispanic black adults and Mexican-American adults in use of prescription sleep aids. As an alternative to taking prescription drugs, some evidence shows that an average person seeking short-term help may find relief from taking over-the-counter antihistamines such as diphenhydramine or doxylamine. Certain classes of sedatives such as benzodiazepines and newer nonbenzodiazepine drugs can also cause physical dependence, which manifests in withdrawal symptoms if the drug is not carefully tapered down. The benzodiazepine and nonbenzodiazepine hypnotic medications also have a number of side-effects such as day time fatigue, motor vehicle crashes, cognitive impairments and falls and fractures. Elderly people are more sensitive to these side-effects. The non-benzodiazepines zolpidem and zaleplon have not adequately demonstrated effectiveness in sleep maintenance. Some benzodiazepines have demonstrated effectiveness in sleep maintenance in the short term but in the longer term are associated with tolerance and dependence. Drugs that may prove more effective and safer than existing drugs for insomnia is an area of active research.
Benzodiazepines and nonbenzodiazepines have similar efficacy that is not significantly more than for antidepressants. Benzodiazepines did not have a significant tendency for more adverse drug reactions. Chronic users of hypnotic medications for insomnia do not have better sleep than chronic insomniacs not taking medications. In fact, chronic users of hypnotic medications have more regular nighttime awakenings than insomniacs not taking hypnotic medications. A further review of the literature regarding benzodiazepine hypnotic as well as the nonbenzodiazepines concluded that these drugs cause an unjustifiable risk to the individual and to public health and lack evidence of long-term effectiveness. The risks include dependence, accidents, and other adverse effects. Gradual discontinuation of hypnotics in long-term users leads to improved health without worsening of sleep. It is preferred that hypnotics be prescribed for only a few days at the lowest effective dose and avoided altogether wherever possible in the elderly.
The antihistamine diphenhydramine is widely used in nonprescription sleep aids such as Benadryl. The antihistamine doxylamine is used in nonprescription sleep aids such as Unisom (USA) and Unisom 2 (Canada). In some countries, including Australia, it is marketed under the names Restavit and Dozile. It is the most effective over-the-counter sedative currently available in the United States, and is more sedating than some prescription hypnotics.
While the two drugs mentioned above are available over the counter in most countries, the effectiveness of these agents may decrease over time, and the incidence of next-day sedation is higher than for most of the newer prescription drugs. Anticholinergic side-effects may also be a draw back of these particular drugs. While addiction does not seem to be an issue with this class of drugs, they can induce dependence and rebound effects upon abrupt cessation of use.
The most commonly used class of hypnotics prescribed for insomnia are the benzodiazepines. Benzodiazepines all bind unselectively to the GABAA receptor. But certain benzodiazepines (hypnotic benzodiazepines) have significantly higher activity at the α1 subunit of the GABAA receptor compared to other benzodiazepines (for example, triazolam and temazepam have significantly higher activity at the α1 subunit compared to alprazolam and diazepam, making them superior sedative-hypnotics – alprazolam and diazepam in turn have higher activity at the α2 subunit compared to triazolam and temazepam, making them superior anxiolytic agents). Modulation of the α1 subunit is associated with sedation, motor-impairment, respiratory depression, amnesia, ataxia, and reinforcing behavior (drug-seeking behavior). Modulation of the α2 subunit is associated with anxiolytic activity and disinhibition. For this reason, certain benzodiazepines are better suited to treat insomnia than others. Hypnotic benzodiazepines include drugs such as temazepam, clonazepam, lorazepam, oxazepam, diazepam, flunitrazepam, triazolam, flurazepam, midazolam, nitrazepam, and quazepam. These drugs can lead to tolerance, physical dependence, and the benzodiazepine withdrawal syndrome upon discontinuation, especially after consistent usage over long periods of time. Benzodiazepines, while inducing unconsciousness, actually worsen sleep as they promote light sleep while decreasing time spent in deep sleep. A further problem is, with regular use of short-acting sleep aids for insomnia, daytime rebound anxiety can emerge. Benzodiazepines can help to initiate sleep and increase sleep time, but they also decrease deep sleep and increase light sleep. Although there is little evidence for benefit of benzodiazepines in insomnia and evidence of major harm, prescriptions have continued to increase. There is a general awareness that long-term use of benzodiazepines for insomnia in most people is inappropriate and that a gradual withdrawal is usually beneficial due to the adverse effects associated with the long-term use of benzodiazepines and is recommended whenever possible.
Nonbenzodiazepine sedative-hypnotic drugs, such as zolpidem (Ambien), zaleplon, zopiclone (Imovane), and eszopiclone (Lunesta), are a class hypnotic medications indicated for mild to moderate insomnia. Their effectiveness at improving time to sleeping is slight.
Suvorexant is a recently FDA approved treatment for insomnia, characterized by difficulties with sleep onset and/or sleep maintenance. It exerts its therapeutic effect in insomnia through antagonism of orexin receptors. The orexin neuropeptide signaling system is a central promoter of wakefulness. Blocking the binding of wake-promoting neuropeptides orexin A and orexin B to receptors orexin receptor type 1 and orexin receptor type 2 is thought to suppress wake drive. Two other dual orexin antagonists currently in clinical trials are Filorexant and SB-649,868.
Some antidepressants such as amitriptyline, doxepin, mirtazapine, and trazodone can have a sedative effect, and are prescribed to treat insomnia. Amitriptyline and doxepin both have antihistaminergic, anticholinergic, and antiadrenergic properties, which contribute to their side effect profile, while mirtazapine's side effects are primarily antihistaminergic, and trazadone's side-effects are primarily antiadrenergic. Some also alter sleep architecture. As with benzodiazepines, the use of antidepressants in the treatment of insomnia can lead to withdrawal effects; withdrawal may induce rebound insomnia.
Agomelatine a novel melatonergic antidepressant with sleep-improving qualities that does not cause daytime drowsiness, is licensed for marketing in the European Union and TGA Australia. After trials in the United States its development for use there was discontinued in October 2011 by Novartis, who had bought the rights to market it there from the European pharmaceutical company Servier.
Evidence for ramelteon looks promising. It and tasimelteon, increase sleep time due to a melatonin rhythm shift with no apparent negative effects on the next day. Although thus far there has been little evidence of abuse, but most melatonin drugs have not been highly tested for longitudinal side effects because of the lack of approval, except for Ramelteon, from the Food and Drug Administration, concluding that all the risks are not known at this time. It is recommended that people who take melatonin take it at night right before going to bed.
Studies have also shown that children who are on the Autism spectrum or have learning disabilities, Attention-Deficit Hyperactivity Disorder (ADHD) or related neurological diseases can benefit from the use of melatonin. This is because they often have trouble sleeping due to their disorders. For example, children with ADHD tend to have trouble falling asleep because of their hyperactivity and, as a result, tend to be tired during most of the day. Children who have ADHD then, as well as the other disorders mentioned, are given melatonin before bedtime in order to help them sleep. The sleep cycle regulates for these children when given the melatonin supplement.
Alcohol is often used as a form of self-treatment of insomnia to induce sleep. However, alcohol use to induce sleep can be a cause of insomnia. Long-term use of alcohol is associated with a decrease in NREM stage 3 and 4 sleep as well as suppression of REM sleep and REM sleep fragmentation. Frequent moving between sleep stages occurs, with awakenings due to headaches, the need to urinate, dehydration, and excessive sweating. Glutamine rebound also plays a role as when someone is drinking; alcohol inhibits glutamine, one of the body's natural stimulants. When the person stops drinking, the body tries to make up for lost time by producing more glutamine than it needs. The increase in glutamine levels stimulates the brain while the drinker is trying to sleep, keeping him/her from reaching the deepest levels of sleep. Stopping chronic alcohol use can also lead to severe insomnia with vivid dreams. During withdrawal REM sleep is typically exaggerated as part of a rebound effect.
Opioid medications such as hydrocodone, oxycodone, and morphine are used for insomnia that is associated with pain due to their analgesic properties and hypnotic effects. Opioids can fragment sleep and decrease REM and stage 2 sleep. By producing analgesia and sedation, opioids may be appropriate in carefully selected patients with pain-associated insomnia. However, dependence on opioids can lead to suffering from long time disturbance in sleep.
The use of antipsychotics for insomnia, while common, is not recommended as the evidence does not demonstrate a benefit and the risk of adverse effects is significant. Concerns regarding side effects is greater in the elderly.
Some insomniacs use herbs such as valerian, chamomile, lavender, cannabis, hops, Withania somnifera, and passion-flower. Purified valerian extract has undergone multiple studies and appears to be modestly effective. L-Arginine L-aspartate, S-adenosyl-L-homocysteine, and delta sleep-inducing peptide (DSIP) may be also helpful in alleviating insomnia. A 1973 study published in Psychopharmacologia found that orally administered THC significantly reduced sleep latency and frequency of sleep interruptions in 9 healthy subjects. A 20 mg dose of THC was found to be most effective, reducing sleep latency by over an hour on average. A 2010 study published in Anesthesia and Analgesia found that synthetic THC was more effective than the antidepressant amitriptyline at improving sleep quality in patients with fibromylagia.
A survey of 1.1 million residents in the United States found that those that reported sleeping about 7 hours per night had the lowest rates of mortality, whereas those that slept for fewer than 6 hours or more than 8 hours had higher mortality rates. Getting 8.5 or more hours of sleep per night increased the mortality rate by 15%. Severe insomnia – sleeping less than 3.5 hours in women and 4.5 hours in men – also led to a 15% increase in mortality. However, most of the increase in mortality from severe insomnia was discounted after controlling for co-morbid disorders. After controlling for sleep duration and insomnia, use of sleeping pills was also found to be associated with an increased mortality rate.
The lowest mortality was seen in individuals who slept between six and a half and seven and a half hours per night. Even sleeping only 4.5 hours per night is associated with very little increase in mortality. Thus, mild to moderate insomnia for most people is associated with increased longevity and severe insomnia is associated only with a very small effect on mortality.
As long as a patient refrains from using sleeping pills, there is little to no increase in mortality associated with insomnia, but there does appear to be an increase in longevity. This is reassuring for patients with insomnia in that, despite the sometimes-unpleasantness of insomnia, insomnia itself appears to be associated with increased longevity. It is unclear why sleeping longer than 7.5 hours is associated with excess mortality.
Insomnia is 40% more common in women than in men.
The National Sleep Foundation's 2002 Sleep in America poll showed that 58% of adults in the U.S. experienced symptoms of insomnia a few nights a week or more. Although insomnia was the most common sleep problem among about one half of older adults (48%), they were less likely to experience frequent symptoms of insomnia than their younger counterparts (45% vs. 62%), and their symptoms were more likely to be associated with medical conditions, according to the poll of adults between the ages of 55 and 84.
As explained by Thomas Roth, estimates of the prevalence of insomnia depend on the criteria used as well as the population studied. About 30% of adults report at least one of the symptoms of insomnia. When daytime impairment is added as a criterion, the prevalence is about 10%. Primary insomnia persisting for at least one month yields estimates of 6%.
- Al Herpin, American insomniac, known as the "Man Who Never Slept"
- Fatal familial insomnia
- Sleep deprivation
- Thai Ngoc, Vietnamese insomniac, claimed to be awake for 33 years
- Golub, R. M. (2012). "Insomnia". JAMA: the Journal of the American Medical Association 307 (24): 2653–2653.
- Roth, T. (2007). "Insomnia: Definition, prevalence, etiology, and consequences". Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine 3 (5 Suppl): S7–10.
- Hirshkowitz, Max (2004). "10, Neuropsychiatric Aspects of Sleep and Sleep Disorders (pp. 315–340)". In Stuart C. Yudofsky and Robert E. Hales. Essentials of neuropsychiatry and clinical neurosciences (4 ed.). Arlington, Virginia, USA: American Psychiatric Publishing.
- Wilson, Jennifer F. (2008). "Insomnia". Annals of Internal Medicine 148: ITC1.
- Zahn, Dorothy (2003). "Insomnia: CPJRPC". The Canadian Pharmaceutical Journal.
- Schacter, D. L., Gilbert, D. T., & Wegner, D. M. (2010). Psychology. 2nd ed. p. 195. New york: Worth Publishers, ISBN 1429237198.
- "Dyssomnias" (PDF). WHO. pp. 7–11. Retrieved 2009-01-25.
- Buysse, Daniel J. (2008). "Chronic Insomnia". Am J Psychiatry 165 (6): 678–86.
Erman, Milton K. (2007). "Insomnia: Comorbidities and Consequences". Primary Psychiatry 14 (6): 31–35.
Two general categories of insomnia exist, primary insomnia and comorbid insomnia.
- World Health Organization (2007). "Quantifying burden of disease from environmental noise" (PDF). p. 20. Retrieved 2010-09-22.
- Riemann, Dieter; Ulrich Voderholzer (2002). "Consequences of Chronic (Primary) Insomnia: Effects on Performance, Psychiatric and Medical Morbidity – An Overview". Somnologie – Schlafforschung und Schlafmedizin 6 (3): 101–108.
- "Sleep Wake Disorders ." Diagnostic and statistical manual of mental disorders: DSM-5.. 5th ed. Washington, D.C.: American Psychiatric Association, 2013. -. Print.
- Roth, T.; Roehrs, T. (2003). "Insomnia: Epidemiology, characteristics, and consequences". Clinical cornerstone 5 (3): 5–15.
- "Insomnia – sleeplessness, chronic insomnia, acute insomnia, mental ...". Archived from the original on March 29, 2008. Retrieved 2008-04-29.
- "Acute Insomnia – What is Acute Insomnia". Sleepdisorders.about.com. Retrieved 2013-03-10.
- Simon, Harvey. "In-Depth Report: Causes of Chronic Insomnia". New York Times. Retrieved 4 November 2011.
- Kertesz, R. S.; Cote, K. A. (2011). "Event-Related Potentials During the Transition to Sleep for Individuals with Sleep-Onset Insomnia". Behavioral Sleep Medicine 9 (2): 68–85.
- Doghramji, Karl (2007). Clinical Management of Insomnia. Caddo, OK: Professional Communications, Inc. p. 28.
- Morin, Charles (2003). Insomnia: A Clinician's Guide to Assessment and Treatment. New York, New York: Kluwer Academic/Plenum Publishers. p. 16.
- Adler, C. H.; Thorpy, M. J. (2005). "Sleep issues in Parkinson's disease". Neurology 64 (12 Suppl 3): S12–S20.
- Insomnia > Complications. Mayo Clinic. Retrieved on May 5, 2009
- "Insomnia". University of Maryland Medical Center. Retrieved 11 July 2013.
- Comorbidity of chronic insomnia with medical problems, Sleep,
- "Excessive daytime slepiness and insomnia". Arch Otolaryngol. Retrieved 14 June 2014.
- Lawrence, K. R.; Adra, M.; Keir, C. (2006). "Hypoglycemia-induced anoxic brain injury possibly associated with levofloxacin". Journal of Infection 52 (6): e177–e180.
- "Insomnia Causes". Mayo Clinic. Retrieved 11 July 2013.
- "Restless Legs Syndrome/Periodic Limb Movement Disorder". National Heart Lung and Blood Institute. Retrieved 11 July 2013.
- Ramakrishnan, K.; Scheid, D. C. (2007). "Treatment options for insomnia". American family physician 76 (4): 517–526.
- "What causes insomnia?". National Heart, Lung, and Blood Institute. Retrieved 11 July 2013.
- Gelder, M., Mayou, R. and Geddes, J. (2005). Psychiatry. 3rd ed. New York: Oxford. p. 167, ISBN 0198528639.
- Bendz, L. M.; Scates, A. C. (2009). "Melatonin Treatment for Insomnia in Pediatric Patients with Attention-Deficit/Hyperactivity Disorder". Annals of Pharmacotherapy 44 (1): 185–191.
- Ouellet, M. C.; Beaulieu-Bonneau, S.; Morin, C. M. (2006). "Insomnia in patients with traumatic brain injury: Frequency, characteristics, and risk factors". The Journal of head trauma rehabilitation 21 (3): 199–212.
- Mendelson WB (2008). "New Research on Insomnia: Sleep Disorders May Precede or Exacerbate Psychiatric Conditions". Psychiatric Times 25 (7).
- Schenkein, J.; Montagna, P. (2006). "Self management of fatal familial insomnia. Part 1: What is FFI?". MedGenMed : Medscape general medicine 8 (3): 65.
- The epidemiological survey of exercise-induced insomnia in chinese athletes Youqi Shi, Zhihong Zhou, Ke Ning, Jianhong LIU. Athens 2004: Pre-Olympic Congress.
- Teran-Perez, G.; Arana-Lechuga, Y.; Esqueda-Leon, E.; Santana-Miranda, R.; Rojas-Zamorano, J.A.; Velazquez Moctezuma (2012). "Steroid Hormones and Sleep Regulation". Mini reviews in medicinal chemistry 12 (11): 1040–8.
- Backhaus, J.; Junghanns, K.; Hohagen, F. (2004). "Sleep disturbances are correlated with decreased morning awakening salivary cortisol". Psychoneuroendocrinology 29 (9): 1184–91.
- Backhaus, J.; Junghanns, K.; Born, J.; Hohaus, K.; Faash, F.; Hohagen, F. (2006). "Impaired Declarative Memory Consolidation During Sleep in Patients With Primary Insomnia: Influence of Sleep Architecture and Nocturnal Cortisol Release". Biological Psychiatry 60 (12): 1324–30.
- Rodenbeck, A.; Cohrs, S.; Jordan, W.; Huether, G.; Ruther, E.; Hajek, G. (Dec 2003). "The sleep-improving effects of doxepin are paralleled by normalized plasma cortisol secretion in primary insomnia: A placebo-controlled, double-blind, randomized, cross-over study followed by an open treatment over 3 weeks". Psychopharmacology (Berl) 170 (4): 423–8.
- Saletu-Zyhlarz, G.; Anderer, P.; Gruber, G.; Mandl, M.; Gruber, D.; Metka, M.; Huber, J.; Oattel, M.; Graser, T.; Abu-Bakr, M.H.; Gratzhofer, E.; Saletu, B. (2003). "Insomnia related to postmenopausal syndrome and hormone replacement therapy: Sleep laboratory studies on baseline differences between patients and controls and double-blind, placebo-controlled investigations on the effects of a novel estrogen-progesterone combination (Climodien, Lafamme) versus estrogen alone". Journal of Sleep Research 12 (3): 239–54.
- Ziomkiewicz, A.; Pawlowski, B.; Ellison, P.T.; Lipson, S.F.; Thune, I.; Jasienska, G. (2012). "Higher luteal progesterone is associated with low levels of premenstrual aggressive behavior and fatigue". Biological Psychology 91 (3): 376–82.
- Michaud, E.; Bain, J. (2013). Menstrual Insomnia. Reader’s Digest.
- American Family Physician: Chronic Insomnia: A Practical Review. Aafp.org (1999-10-01). Retrieved on 2011-11-20.
- Athens Insomnia Scale: validation of an instrument based on ICD-10 criteria
- Passarella, S, Duong, M. "Diagnosis and treatment of insomnia." 2008.
- Wilson, S.; Nutt, D.; Alford, C.; Argyropoulos, S.; Baldwin, D.; Bateson, A.; Britton, T.; Crowe, C.; Dijk, D. -J.; Espie, C.; Gringras, P.; Hajak, G.; Idzikowski, C.; Krystal, A.; Nash, J.; Selsick, H.; Sharpley, A.; Wade, A. (2010). "British Association for Psychopharmacology consensus statement on evidence-based treatment of insomnia, parasomnias and circadian rhythm disorders". Journal of Psychopharmacology 24 (11): 1577–1601.
- Wortelboer, U.; Cohrs, S.; Rodenbeck, A.; Rüther, E. (2002). "Tolerability of hypnosedatives in older patients". Drugs & aging 19 (7): 529–539.
- "NIH State-of-the-Science Conference Statement on manifestations and management of chronic insomnia in adults". NIH consensus and state-of-the-science statements 22 (2): 1–30. 2005.
- Merrigan, Jill M.; Buysse, Daniel J.; Bird, Joshua C. and Livingston, Edward H. (2013). "Insomnia". JAMA 309 (7): 733.
- National Prescribing Service (2010-02-01). "Addressing hypnotic medicines use in primary care". NPS News, Vol 67.
- Kirkwood, C. K. (1999). "Management of insomnia". Journal of the American Pharmaceutical Association (Washington,D.C. : 1996) 39 (5): 688–696; quiz 696–4.
- Hagan, Pat (14 July 2009). "The blast of cold air that cures insomnia.". MailOnline. Retrieved 14 July 2009.
- Lake, James A. (31 October 2006). Textbook of Integrative Mental Health Care. Thieme Medical Publishers. p. 313.
- Ellis, J. J., Hampson, S. E., & Cropley, M. M. "Sleep hygiene or compensatory sleep practices: an examination of behaviors affecting sleep in older adults". 2002
- Lande, R. G.; Gragnani, C. (2010). "Nonpharmacologic approaches to the management of insomnia". The Journal of the American Osteopathic Association 110 (12): 695–701.
- Kierlin, L. (2008). "Sleeping Without a Pill: Nonpharmacologic Treatments for Insomnia". Journal of Psychiatric Practice 14 (6): 403–407.
- Anguttara Nikaya XI.16. Metta Sutta. Good Will. University of Western Florida
- Cincotta, Andrea; Gehrman, Philip; Gooneratne, Nalaka S.; Baime, Michael J. (2009). "The effects of a mindfulness-based stress management program on pre-sleep arousal and insomnia symptoms: A pilot study". Stress and Health 27 (3): e299.
- Ong, J. C.; Shapiro, S. L.; Manber, R. (2008). "Combining Mindfulness Meditation with Cognitive-Behavior Therapy for Insomnia: A Treatment-Development Study". Behavior Therapy 39 (2): 171–182.
- Yook, K.; Lee, S. H.; Ryu, M.; Kim, K. H.; Choi, T. K.; Suh, S. Y.; Kim, Y. W.; Kim, B.; Kim, M. Y.; Kim, M. J. (2008). "Usefulness of Mindfulness-Based Cognitive Therapy for Treating Insomnia in Patients with Anxiety Disorders". The Journal of Nervous and Mental Disease 196 (6): 501–503.
- Mitchell, M. D.; Gehrman, P.; Perlis, M.; Umscheid, C. A. (2012). "Comparative effectiveness of cognitive behavioral therapy for insomnia: A systematic review". BMC Family Practice 13: 40.
- Jacobs, G. D.; Pace-Schott, E. F.; Stickgold, R.; Otto, M. W. (2004). "Cognitive behavior therapy and pharmacotherapy for insomnia: a randomized controlled trial and direct comparison". Archives of Internal Medicine 164 (17): 1888–1896.
- Morin, C. M.; Colecchi, C.; Stone, J.; Sood, R.; Brink, D. (1999). "Behavioral and pharmacological therapies for late-life insomnia: A randomized controlled trial". JAMA : the journal of the American Medical Association 281 (11): 991–999.
- Miller, K. E. (2005). "Cognitive Behavior Therapy vs. Pharmacotherapy for Insomnia". American Family Physician. Archived from the original on 2011-06-06.
- Ong, J. C.; Ulmer, C. S.; Manber, R. (2012). "Improving sleep with mindfulness and acceptance: A metacognitive model of insomnia". Behaviour Research and Therapy 50 (11): 651–660.
- Edinger, J. D.; Means, M. K. (2005). "Cognitive–behavioral therapy for primary insomnia". Clinical Psychology Review 25 (5): 539–558.
- Fox S, Fallows D. (2005-10-05) Internet health resources. Washington, DC: Pew Internet & American Life Project; 2003.
- Rabasca L. (2000). "Taking telehealth to the next step". Monitor on Psychology 31: 36–37.
- Marks IM, Cavanagh K, Gega L. (2007) Hands-on Help: Computer-Aided Psychotherapy. Hove, England and New York: Psychology Press, ISBN 184169679X.
- Ritterband, L. M.; Gonder-Frederick, L. A.; Cox, D. J.; Clifton, A. D.; West, R. W.; Borowitz, S. M. (2003). "Internet interventions: In review, in use, and into the future". Professional Psychology: Research and Practice 34 (5): 527.
- L. Ritterband et al., 2011; L. M. Ritterband et al., 2009; Ström, Pettersson, & Andersson, 2004; Vincent & Lewycky, 2009
- Cheng, S. K.; Dizon, J. (2012). "Computerised Cognitive Behavioural Therapy for Insomnia: A Systematic Review and Meta-Analysis". Psychotherapy and Psychosomatics 81 (4): 206–216.
- Harrison C, Britt H (2009). "Insomnia". Australian Family Physician 32: 283.
- Chong Y., Fryar, C.D., and Gu, Q. (2013). Prescription Sleep Aid Use Among Adults: United States, 2005–2010. Hyattsville, Md.: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Health Statistics.
- Glass, J.; Lanctôt, K. L.; Herrmann, N.; Sproule, B. A.; Busto, U. E. (2005). "Sedative hypnotics in older people with insomnia: Meta-analysis of risks and benefits". BMJ 331 (7526): 1169.
- Rosenberg, R. P. (2006). "Sleep Maintenance Insomnia: Strengths and Weaknesses of Current Pharmacologic Therapies". Annals of Clinical Psychiatry 18 (1): 49–56.
- Buscemi, N.; Vandermeer, B.; Friesen, C.; Bialy, L.; Tubman, M.; Ospina, M.; Klassen, T. P.; Witmans, M. (2007). "The Efficacy and Safety of Drug Treatments for Chronic Insomnia in Adults: A Meta-analysis of RCTs". Journal of General Internal Medicine 22 (9): 1335–1350.
- Ohayon, M. M.; Caulet, M. (1995). "Insomnia and psychotropic drug consumption". Progress in neuro-psychopharmacology & biological psychiatry 19 (3): 421–431.
- "What's wrong with prescribing hypnotics?". Drug and therapeutics bulletin 42 (12): 89–93. 2004.
- DrugBank: DB00366 (Doxylamine). Drugbank.ca. Retrieved on 2011-11-20.
- Temazepam. Websters-online-dictionary.org. Retrieved on 2011-11-20.
- Tsoi, W. F. (1991). "Insomnia: Drug treatment". Annals of the Academy of Medicine, Singapore 20 (2): 269–272.
- Montplaisir, J. (2000). "Treatment of primary insomnia". CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne 163 (4): 389–391.
- Carlstedt, Roland A. (13 December 2009). Handbook of Integrative Clinical Psychology, Psychiatry, and Behavioral Medicine: Perspectives, Practices, and Research. Springer. pp. 128–130.
- Lader, Malcolm Harold; P. Cardinali, Daniel; R. Pandi-Perumal, S. (22 March 2006). Sleep and sleep disorders: a neuropsychopharmacological approach. Georgetown, Tex.: Landes Bioscience/Eurekah.com. p. 127.
- Authier, N.; Boucher, A.; Lamaison, D.; Llorca, P. M.; Descotes, J.; Eschalier, A. (2009). "Second Meeting of the French CEIP (Centres d'Évaluation et d'Information sur la Pharmacodépendance). Part II: Benzodiazepine Withdrawal". Thérapie 64 (6): 365–370.
- Huedo-Medina, T. B.; Kirsch, I.; Middlemass, J.; Klonizakis, M.; Siriwardena, A. N. (2012). "Effectiveness of non-benzodiazepine hypnotics in treatment of adult insomnia: Meta-analysis of data submitted to the Food and Drug Administration". BMJ 345: e8343.
- ""Highlights of prescribing information"".
- Bertschy, G.; Ragama-Pardos, E.; Muscionico, M.; Aït-Ameur, A.; Roth, L.; Osiek, C.; Ferrero, F. O. (2005). "Trazodone addition for insomnia in venlafaxine-treated, depressed inpatients: A semi-naturalistic study". Pharmacological Research 51 (1): 79–84.
- Winokur, A.; Demartinis Na, 3.; McNally, D. P.; Gary, E. M.; Cormier, J. L.; Gary, K. A. (2003). "Comparative effects of mirtazapine and fluoxetine on sleep physiology measures in patients with major depression and insomnia". The Journal of clinical psychiatry 64 (10): 1224–1229.
- Schittecatte, M.; Dumont, F.; Machowski, R.; Cornil, C.; Lavergne, F.; Wilmotte, J. (2002). "Effects of mirtazapine on sleep polygraphic variables in major depression". Neuropsychobiology 46 (4): 197–201.
- Strat YL; Gorwood, P (September 2008). "Agomelatine, an innovative pharmacological response to unmet needs". Journal of Psychopharmacology 22 (suppl. 7): 4–8.
- "Summary of Product Characteristics" (PDF). European Medicine Agency. Retrieved 2013-10-14.
- "VALDOXAN® Product Information" (PDF). TGA eBusiness Services. Servier Laboratories Pty Ltd. 2013-09-23. Retrieved 2013-10-14.
- Novartis drops future blockbuster agomelatine. Scrip Intelligence, Oct 25 2011 (retrieved Oct 30, 2011).
- Bentham, Clara (2006-03-29). "Servier and Novartis sign licensing agreement for agomelatine, a novel treatment for depression". Servier UK. Archived from the original on 16 April 2009. Retrieved 2009-05-15.
- Ferguson, S. A.; Rajaratnam, S. M.; Dawson, D. (2010). "Melatonin agonists and insomnia". Expert Review of Neurotherapeutics 10 (2): 305–318.
- Liu, J.; Wang, L. -N. (2012). "Ramelteon in the treatment of chronic insomnia: Systematic review and meta-analysis". International Journal of Clinical Practice 66 (9): 867–873.
- Conn, D. K.; Madan, R. (2006). "Use of Sleep-Promoting Medications in Nursing Home Residents". Drugs & Aging 23 (4): 271–287.
- "Melatonin, Web M.D.". Retrieved 2 October 2012.
- Reilly, T (2009). "How can travelling athletes deal with jet lag?". Kinesiology 41.
- Sánchez-Barceló, Emilio; Mediavilla, Maria; Reiter, Russel J. (2011). "Clinical Uses of Melatonin in Pediatrics". International Journal of Pediatrics 2011: 1.
- Perry, Lacy. (2004-10-12) HowStuffWorks "How Hangovers Work". Health.howstuffworks.com. Retrieved on 2011-11-20.
- Lee-chiong, Teofilo (24 April 2008). Sleep Medicine: Essentials and Review. Oxford University Press, USA. p. 105.
- Asaad, T. A.; Ghanem, M. H.; Abdel Samee, A. M.; El–Habiby, M. M. (2011). "Sleep Profile in Patients with Chronic Opioid Abuse". Addictive Disorders & Their Treatment 10: 21.
, which cites
- "Consensus Development Conference on Antipsychotic Drugs and Obesity and Diabetes". Diabetes Care 27 (2): 596–601. 1 February 2004.
- Maglione, M; Maher, AR; Hu, J; Wang, Z; Shanman, R; Shekelle, PG; Roth, B; Hilton, L; Suttorp, MJ; Ewing, BA; Motala, A; Perry, T (Sep 2011). "Off-Label Use of Atypical Antipsychotics: An Update".
- Nasrallah, HA (Jan 2008). "Atypical antipsychotic-induced metabolic side effects: insights from receptor-binding profiles.". Molecular psychiatry 13 (1): 27–35.
- Coe, HV; Hong, IS (May 2012). "Safety of low doses of quetiapine when used for insomnia". The Annals of pharmacotherapy 46 (5): 718–22.
- Conn, DK; Madan, R (2006). "Use of sleep-promoting medications in nursing home residents : risks versus benefits". Drugs & aging 23 (4): 271–87.
- Donath, F.; Quispe, S.; Diefenbach, K.; Maurer, A.; Fietze, I.; Roots, I. (2000). "Critical Evaluation of the Effect of Valerian Extract on Sleep Structure and Sleep Quality". Pharmacopsychiatry 33 (2): 47–53.
- Morin, C. M.; Koetter, U.; Bastien, C.; Ware, J. C.; Wooten, V. (2005). "Valerian-hops combination and diphenhydramine for treating insomnia: A randomized placebo-controlled clinical trial". Sleep 28 (11): 1465–1471.
- Meolie, A. L.; Rosen, C.; Kristo, D.; Kohrman, M.; Gooneratne, N.; Aguillard, R. N.; Fayle, R.; Troell, R.; Townsend, D.; Claman, D.; Hoban, T.; Mahowald, M.; Clinical Practice Review Committee; American Academy of Sleep Medicine (2005). "Oral nonprescription treatment for insomnia: An evaluation of products with limited evidence". Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine 1 (2): 173–187.
- Billiard, M, Kent, A (2003). Sleep: physiology, investigations, medicine. pp. 275–7.
- Cousens K, DiMascio A (1973). "THC as an hypnotic". Psychopharmacologia 33 (4): 355–64.
- Ware MA, Fitzcharles MA, Joseph L, Shir Y (Feb 2010). "The effects of nabilone on sleep in fibromyalgia: results of a randomized controlled trial". Anesth Analg. 110 (2): 604–10.
- Kripke, D. F.; Garfinkel, L.; Wingard, D. L.; Klauber, M. R.; Marler, M. R. (2002). "Mortality associated with sleep duration and insomnia". Archives of general psychiatry 59 (2): 131–136.
- "Several Sleep Disorders Reflect Gender Differences". Psychiatric News 42 (8): 40. 2007.
- "2002 Sleep in America Poll". National Sleep Foundation. Archived from the original on June 14, 2008. Retrieved 2008-08-13.
- Summers-Bremner, Eluned (2010). Insomnia : a cultural history. London: Reaktion.
- Brigitte Steger (2009). "Insomnia: A Cultural History (review)". Bulletin of the History of Medicine 83 (2): 385–386.
- Ellis, J. J., Hampson, S. E., & Cropley, M. M. (2002). Sleep hygiene or compensatory sleep practices: an examination of behaviours affecting sleep in older adults. Psychology, Health & Medicine, 7(2), 156-161. doi:10.1080/13548500120116094
- Passarella, S., & Duong, M. (2008). Diagnosis and treatment of insomnia. American Journal Of Health-System Pharmacy, 65(10), 927-934. doi:10.2146/ajhp060640 | <urn:uuid:dc85a747-e5bf-4c4d-820d-2f15d526c9e0> | {
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July 18, 2011
Coding for Aortic Conditions
For The Record
Vol. 23 No. 13 P. 28
The aorta is the largest artery in the body, originating at the left ventricle in the heart and ending in the abdominal area where the aorta divides into the two iliac arteries. The two most common problems that can affect the aorta are aneurysms and dissections, which may be caused by conditions such as atherosclerosis, hypertension, Marfan syndrome, connective tissue disorders, and injury.
An aneurysm is a weak area of the artery wall where the diseased tissue does not stretch and contract well, causing a localized enlargement. The diameter of the enlargement determines whether it is considered an aneurysm. Typically, a permanent dilation of 4 cm in diameter is considered an aneurysm; anything less may be described as bulging, ballooning, or dilated. Other physicians may classify it as an aneurysm if the permanent enlargement is at least 1.5 times greater than its normal size.
Aneurysms are described according to location, size, and shape. Shapes include fusiform and saccular. Fusiform is when the aneurysm is enlarged equally in all directions; saccular is when the bulge or sac occurs on only one side of the aorta. Possible locations of an aortic aneurysm are as follows:
• Ascending (441.2); if ruptured, use 441.1;
• Arch (441.2); if ruptured, use 441.1;
• Descending, not otherwise specified (NOS) (441.9); if ruptured, use 441.5;
• Thoracic descending (441.2); if ruptured, use 441.1;
• Abdominal descending (441.4); if ruptured, use 441.3;
• Thoracoabdominal (441.7); if ruptured, use 441.6;
• Abdominal (441.4); if ruptured, use 441.3.
An abdominal aortic aneurysm is the most common type. If an aortic aneurysm is documented but not specified as to site, assign code 441.9. A ruptured aortic aneurysm, NOS is classified to code 441.5. A pseudoaneurysm (false aneurysm) is an aneurysm that does not have some or all of the aortic wall layers. Often due to an injury of inner aortic wall and an infection, a pseudoaneurysm is unpredictable and may rupture at smaller sizes. Pseudoaneurysm is classified to the same codes as the other aneurysms, depending on location.
Aortic tissue may tear even without an aneurysm. Dissection is the tearing of the inner layer of a vessel that allows blood to leak between the inner and outer layers, possibly causing severe back or chest pain, pallor, pulselessness, paresthesiae, and paralysis. This life-threatening condition usually occurs in the ascending or descending part of the thoracic aorta but may also occur in the abdominal aorta. The physician may document this condition as dissecting aneurysm.
Dissecting aortic aneurysm or aortic dissection is classified to ICD-9-CM code 441.0x. The following fifth-digit subclassifications identify the site of the dissection:
• 441.00, Unspecified site;
• 441.01, Thoracic;
• 441.02, Abdominal; and
• 441.03, Thoracoabdominal.
Aortic dissections may be classified as type A or B. Type A is defined as involving the ascending aorta and usually requires surgical treatment. Type B does not involve the ascending aorta and may be managed medically.
The type of aortic dissection does not affect code assignment. The code assignment is only based on the site of the dissecting aneurysm (AHA Coding Clinic for ICD-9-CM, 1989, fourth quarter, page 10).
Diagnosis and Treatment
Aortic diseases are diagnosed using echocardiogram, transthoracic echocardiogram, transesophageal cardiogram, a CT scan, or MRI.
The treatment for aortic aneurysm and dissection depends on the location, size, and type. The condition may be treated with medications to control blood pressure. Common medications given include beta blockers, anticholergenic inhibitors, and calcium channel blockers.
Surgical treatment may involve resection of the aneurysm with replacement with a Dacron graft. The aortic valve may also be repaired or replaced. An endovascular repair may also treat aneurysms.
Coding and sequencing for aortic conditions are dependent on the physician documentation in the medical record and application of the Official Coding Guidelines for inpatient care. Also, use specific AHA Coding Clinic for ICD-9-CM and American Medical Association CPT Assistant references to ensure complete and accurate coding.
— This information was prepared by Audrey Howard, RHIA, of 3M Consulting Services. 3M Consulting Services is a business of 3M Health Information Systems, a supplier of coding and classification systems to more than 5,000 healthcare providers. The company and its representatives do not assume any responsibility for reimbursement decisions or claims denials made by providers or payers as the result of the misuse of this coding information. More information about 3M Health Information Systems is available at www.3mhis.com or by calling 800-367-2447.
ICD-10-CM Coding for Aortic Aneurysm and Dissection
The index and tabular list for aortic aneurysm and dissection is very similar in ICD-10-CM as in ICD-9-CM. The ICD-10-CM code assignments are as follows:
• I71.00, Dissection of unspecified site of aorta;
• I71.01, Dissection of thoracic aorta;
• I71.02, Dissection of abdominal aorta;
• I71.03, Dissection of thoracoabdominal aorta;
• I71.1, Thoracic aortic aneurysm, ruptured;
• I71.2, Thoracic aortic aneurysm, without rupture;
• I71.3, Abdominal aortic aneurysm, ruptured;
• I71.4, Abdominal aortic aneurysm, without rupture;
• I71.5, Thoracoabdominal aortic aneurysm, ruptured;
• I71.6, Thoracoabdominal aortic aneurysm, without rupture;
• I71.8, Aortic aneurysm of unspecified site, ruptured; and
• I71.9, Aortic aneurysm of unspecified site, without rupture.
The only difference is that “dissecting” is no longer a subterm under aneurysm in the ICD-10-CM index. Therefore, it would stand to reason that if a patient experienced a dissecting aortic aneurysm, two codes should be assigned to identify the entire diagnosis: one for the dissection and one for the aneurysm.
— Audrey Howard | <urn:uuid:9bcf7cd2-3489-4f0b-a6c5-1b283d1d1f17> | {
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Medical billing and coding are considered important aspects of the healthcare industry. These practices ensure the involvement of those parts of the services must be according to their performance. Medical billers and medical coders are related to healthcare professionals who take care of the patients by processing their data, treatment record, and insurance information. It is the duty of medical billers and medical coders to code patients according to their diagnosis as well as receive payment from the insurance company of the patients. Both professionals are involved in the reimbursement cycle that assures the fact that health care providers are paid according to their services. It is crucial to review the primary and responsibilities these professions carry out in the healthcare industry.
The work of medical coding requires reviewing clinical statements and issues standard codes such as CPT, ICD-10-CM MAD HCPCS LEVEL II. It is an essential part of medical coding to translate medical reports in form code that can be utilized within the premises of healthcare. In simple words, medical code summarizes reports and medical services. In this regard, these medical codes provide aid to medical coders to maintain the record of the patient’s condition and also inform healthcare providers of relevant information related to the patient. For instance, patient s with different types of illness consults the doctors, and for this, they are required to go through certain types of medical test. In this respect, whenever patients visit the doctor, and doctors and health care providers maintain the record. Here, medical coders are required to translate each, and the doctors prescribe every information related to the diagnosis. The recommendation of treatment is coded in the form of numeric and alphanumeric codes, and lather, they are used in billing procedure. In this regard, medical coders need to be aware of the number of sets and subsets. These codes, also known as the universal language, is shared between doctors, hospitals, insurance companies, government agencies, clearinghouses, and organizations related to the healthcare sector. It is important to note that these codes carry significant guidelines and rules that tell about the pre-existing condition of patients. Furthermore, coding procedures come to its end when the medical coder enters the specific codes in the software program. In this way, once the report is submitted, it goes directly to medical billing.
The term medical billing seems simple and easy where medical billers are required to take the information from medical code submitted by medical coders and make a bill that they send to the insurance company known as a claim. In respect of healthcare, the procedure is carried out by medical billers is not that simple the way, as it seems. For instance, the patient visits the doctor after an appointment who carries the symptoms of cough and producing mucus. Now from here, medical billing starts its function. In this respect, it becomes convenient for medical billers to check the codes to determine the nature of the visit, the symptoms, and the diagnosis carried out by the doctor for further treatment. In this regard, a medical biller can also check the prescription of the doctor to claim a form already uploaded. This claim is further sent to the insurance company for evaluation and returns it. This claim gain comes in the hand of the medical biller to evaluate the return claim to acknowledge that the amount of the bill patient owes after taking out the insurance. It has been observed that those affected with issues like bronchitis, their bill will be comparatively low as compared to those diagnosed in terms of other harmful diseases. The medical biller considers all the aspects and creates a bill according to the nature of the condition. On the other hand, sometimes, some patients are not willing to pay the bill. The medical biller has to hire a collection agency to assure that health care providers are adequately paid.
Medical Billing and Coding Training
Training is an important aspect of the profession of medical billing and coding. These training programs teach medical billers and coders the technical element that enhances their skills and knowledge essential in the revenue cycle. It helps medical billers and coders to understand the nature of payment and payer requirements and also learn to maintain records of the patients in different types of codes that can determine the nature of illness and helpful for medical billers to prepare bill accordingly.About Complete Controller® – America’s Bookkeeping Experts Complete Controller is the Nation’s Leader in virtual bookkeeping, providing service to businesses and households alike. Utilizing Complete Controller’s technology, clients gain access to a cloud-hosted desktop where their entire team and tax accountant may access the QuickBooks™️ file, critical financial documents, and back-office tools in an efficient and secure environment. Complete Controller’s team of certified US-based accounting professionals provide bookkeeping, record storage, performance reporting, and controller services including training, cash-flow management, budgeting and forecasting, process and controls advisement, and bill-pay. With flat-rate service plans, Complete Controller is the most cost-effective expert accounting solution for business, family-office, trusts, and households of any size or complexity. | <urn:uuid:5eb3572b-1160-476a-9bad-97cba7ae8f06> | {
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Our review of HIPAA history begins on August 21, 1996, when the Healthcare Insurance Portability and Accountability Act (HIPAA) was enacted into law, but why was the HIPAA Act formulated?
The HIPAA Act was formulated to “improve the portability and accountability of health insurance coverage” for workers moving between jobs. Other objectives of the Act were to address waste, fraud and abuse in health insurance and healthcare delivery. The Act also included passages to encourage the use of medical savings accounts by creating tax breaks, provides coverage for employees with pre-existing medical conditions and streamlines the administration of health insurance.
The processes for simplifying the administration of health insurance became a way to encourage the healthcare industry to computerize patients’ medical records. This specific part of the Act spawned the Health Information Technology for Economic and Clinical Health Act (HITECH) in 2009, which then resulted in the introduction of the Meaningful Use incentive program – described by leaders in the healthcare sector as “the most important piece of healthcare legislation to be passed in the last 20 to 30 years”.
The HIPAA Privacy and Security Rules Begin to Evolve
Once HIPAA had been enacted into law, the US Department of Health and Human Services set about developing the first HIPAA Privacy and Security Rules. The Privacy Rule had an actual compliance date of April 14, 2003, and it referred to Protected Health Information (PHI) as “any information held by a covered entity which is related to health status, the provision of healthcare, or payment for healthcare that can be linked to an individual”.
Instructions were made available on how PHI should be shared and that permission should be received from patients before using their personal data for marketing, fundraising or research. It also gave patients the permission to withhold information about their healthcare from health insurance providers when their treatment is privately financed.
The HIPAA Security Rule became enforceable two years after the original legislation on April 21, 2005. Referring specifically to electronically stored PHI (ePHI), the Security Rule laid down three security measures – administrative, physical and technical – that must be complied with completely in order to comply with HIPAA. The security measures had these goals:
- Administrative – to develop policies and processes set up to clearly indicate how the entity will comply with the act.
- Physical – to manage physical access to areas of data storage to protect against improper access
- Technical – to safeguard communications including PHI when sent electronically across open networks
When Did HIPAA Become Enforceable?
In what year was HIPAA enacted into law? HIPAA was enacted into law on August 21, 1996, but there have been major amendments to HIPAA over the last 20 years: The introduction of the Privacy Rule, Security Rule, Breach Notification Rule, and the Omnibus Final Rule.
The most significant effective dates are: April 14, 2003 for the HIPAA Privacy Rule, although there was an extension of 12 months for small health plans, that were required to adhere with the HIPAA Privacy Rule provisions by April 14, 2004.
The effective compliance date for the HIPAA Security Rule was April 21, 2005. Similar to the HIPAA Privacy Rule, small health plans were given an extra year to adhere with the provisions of the HIPAA Security Rule and had an actual compliance date of April 21, 2006.
The HIPAA Breach Notification Rule became enforceable on September 23, 2009 and the Omnibus Final Rule became enforceable on March 26, 2013.
The Enactment of the Enforcement Rule
The failure of many covered outfits to fully adhere with the HIPAA Privacy and Security Rules lead to the introduction of the Enforcement Rule in March 2006. The Enforcement Rule gave the Department of Health and Human Services the power to look into complaints against covered entities for failing to comply with the Privacy Rule, and to fine covered outfits for avoidable breaches of ePHI due to not following the security measure laid down in by the Security Rule.
The Department’s Office for Civil Rights was also given the authority to bring criminal charges against repeat offenders who do not introduce corrective measures within 30 days. People also have the right to take a civil legal action against the covered entity if their personal healthcare information has been shared without their permission if it causes them to come to “serious harm”.
HITECH 2009 and the Breach Notification Rule
HIPAA history gathered pace in 2009 with the introduction of the Health Information Technology for Economic and Clinical Health Act (HITECH). HITECH had the main goal of compelling healthcare authorities to put in place the use of Electronic Health Records (EHRs) and enacted the Meaningful Use incentive program. Stage one of Meaningful Use was introduced the following year, incentivizing healthcare groups to maintain the Protected Health Information of patients in electronic format, instead of paper files.
With the incentive program also came an extension of HIPAA Rules to Business Associates and third-party suppliers to the healthcare sector, and the introduction of the Breach Notification Rule – which stated that all breaches of ePHI affecting more than 500 individuals must be made known to the Department of Health and Human Services’ Office for Civil Rights. The criteria for reporting breaches of ePHI were then extended in the Final Omnibus Rule of March 2013.
The Final Omnibus Rule of 2013
The last act of legislation in HIPAA history was the Final Omnibus Rule of 2013. The rule did not really introduce any new legislation, but addressed gaps in existing HIPAA and HITECH regulations – for example, specifying the encryption standards that need to be applied in order to make ePHI unusable, undecipherable and unreadable in the event of a breach occurring.
Many definitions were changed or extended to address grey areas – for example the definition of “workforce” was changed to make it clear that the term includes employees, volunteers, trainees, and other persons whose conduct, in the performance of work for a covered entity or Business Associate, is under the direct management of the covered entity or Business Associate.
The Privacy and Security Rules were also changed to permit allow patient’s health information to be held indefinitely (the previous legislation had stated it be held for 50 years), while new procedures were added to the Breach Notification Rule. New penalties were also applied – as dictated by HITECH – to covered outfits that fell afoul of the HIPAA Enforcement Rule.
Amendments were also included to take in to account changing work practices brought about by technological advances, covering the use of mobile devices in particular. A major number of healthcare professionals are now using their own mobile devices to view and share ePHI, and the Final Omnibus Rule included new administrative procedures and policies to account for this, and to include scenarios which could not have been predicted in 1996. The complete text of the Final Omnibus Rule can be found here.
After a number of delays, the deadline for the United States to use Clinical Modification ICD-10-CM for diagnosis coding and Procedure Coding System ICD-10-PCA for inpatient hospital procedure coding was finally established as October 1, 2015. All HIPAA covered outfits must use ICD-10-CM. Another requirement is these of EDI Version 5010.
HIPAA History Significant Dates
- August 1996 – HIPAA Enacted by President Bill Clinton.
- April 2003 – Effective Date of the HIPAA Privacy Rule.
- April 2005 – Effective Date of the HIPAA Security Rule.
- March 2006 – Effective Date of the HIPAA Breach Enforcement Rule.
- September 2009 – Effective date of HITECH and the Breach Notification Rule.
- March 2013 – Effective Date of the Final Omnibus Rule.
Some CEs and BAs were given a period of time to adhere with the provisions of each Rule. For instance, despite the effective date of the Final Omnibus Rule being March 2013, CEs and BAs were given 180 days to comply.
Final Omnibus Rule Impact
What the Final Omnibus Rule accomplished more than any earlier legislation was to make covered entities more aware of HIPAA safeguards that they had to comply with. Many healthcare outfits – who had been in breach of HIPAA for almost 20 years – implemented a number of measures to comply with the regulations, such as using data encryption on portable devices and computer networks, using secure messaging solutions for internal communications with care teams, setting up web filters and taking more care to archive emails securely.
The financial penalties now being sanctioned for data breaches along with the huge costs of issuing breach notifications, providing credit monitoring services and conducting damage mitigation makes investment in new technology to safeguard data appear cheap by comparison.
The HIPAA Compliance Audit Program
In 2011, the Office for Civil Rights began a series of pilot compliance audits to review how well healthcare providers were complying with HIPAA Privacy and Security Rules. The first found of audits was finished in 2012 and highlighted the shocking state of healthcare compliance.
Audited groups recorded many violations of the HIPAA Breach Notification Rule, Privacy Rule and Security Rule, with the latter leading to the most violations. The OCR issued action plans to help those organizations achieve compliance; however for the second phase of audits it is not expected to be as lenient.
Audits are predicted to focus on specific areas which proved problematic for so many healthcare providers, while a permanent audit plan is being planned to ensure ongoing HIPAA compliance. The age of lax security standards has now passed and the healthcare arena, like the financial sector before it, must improve standards to ensure confidential data remains private.
Any covered entity that does not adapt the necessary controls faces financial penalties, sanctions, potential loss of license and even criminal convictions for failing to secure ePHI.
How to Ensure Full HIPAA Compliance
Our “HIPAA Compliance Checklist” covers the facets of the Health Insurance Portability and Accountability Act relating to the storage, transmission and disposal of electronic Protected Health Information, the actions outfits must take to address a breach and the policies and procedures which must be used to achieve full compliance.
HIPAA regulations may be stringent, yet covered outfits are allowed some flexibility on the privacy and security measures used to protect data. Data encryption, for example, must be addressed but not necessarily implemented if other controls allow for the required protection. | <urn:uuid:07d8979c-1abd-41e6-a646-b22a7846eb68> | {
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[Ejection Fraction] What is an ejection fraction? Can I code an ejection fraction of 0% as with occlusion?
A: Now, ejection fraction just happens to be part of a cardiology aspect as well. You have ejection fractions for your gallbladder but you also have ejection fraction as most commonly known for cardiology. It’s pretty exciting. When I saw this question, I looked at and I thought, “OK, what is an ejection fraction?” and first of all, I spelled it wrong when I was thinking of it, I spelled it like injection, you give somebody an injection. But this is actually spelled with an “e” and they’re saying, “Can I code an ejection fraction of 0% as with occlusion?”
Well, let’s talk about what it is. By definition, ejection fraction is a measurement of the percentage of blood leaving your heart each time it contracts. So, picture your heart, you’ve got the two chambers at the top, and you have the two chambers at the bottom. The two chambers at the bottom are called ventricles. You have a right ventricle and a left ventricle. It just so happens that the left ventricle is the one that has the most power, fills up with the most blood. So, they can check both of them, but usually they start with the left ventricle.
What happens is when that contracts, it pushes out the blood, so then when it opens back up, the blood pushes into that ventricle. You have a certain capacity that that ventricle, that chamber can hold; and as it contracts and pushes that blood up pass the valve into the atrium, the ejection fraction is the amount of blood that pushes that gets out of the chamber, but some of that blood is left in the ventricle. So, let’s say that you’re never going to get 100% of the blood to go up into the atrium, there will be a little bit left, so they take how much went up there, let’s say, 85%; so then that’s how they measure that. It’s not what’s left in the ventricle, it’s how much got pushed through. There are guidelines that tell you how much is normal; so it’s measured.
Since the left ventricle (LV) is the main one that is the one measured. An LV ejection fraction of 55% or higher is for the most part considered normal. That’s what you’re looking at. So, 55% of the blood goes from the ventricle and whooshes up into the atrium, goes through that valve. If you’re 50% -55%, it might be considered “borderline.” But there are some studies and different physicians consider certain things 50, 51; 50 might not be borderline for them.
Medical Coding Ejection Fraction Diagnosis -Video
We’re going to see what are the reasons for an ejection fraction to be low, it might not be what you thought. It’s weakness of the heart so they might have dilated cardiomyopathy (again, on this term, if you don’t know what cardiomyopathy means, you need to go Google it. You need to go look it up). Maybe a former MI (meaning they’d had a heart attack).
Just a little tidbit in ICD-9, it was like six week’s out, I think, they will be considered an old MI. In ICD-10, it’s only four weeks; so there’s a big change there.
It might be a heart valve disease. As that goes through, the valve isn’t working properly, so that ejection of blood up into the atrium may not be a good amount that it should be. And they might just have uncontrolled hypertension, they may have had it for a long time. Those are all things that could give you low ejection fraction.
So, how did they figure this out? What did they do? Well, they can do several tests. They do echocardiograms, they do cardiac catheterizations, they may do an MRI, they do CT scans, and they do a nuclear medicine scan. All of those are ways that they can tell and see how much fluid and track that, that blood that’s getting up into the atrium from the left ventricle. And they can do the right ventricle too, but usually what they do is they focus on the left ventricle because that’s kind of the powerhouse of the heart.
Now, what I want to state, to answer the question that was given: occlusion has to be documented. So, occlusion isn’t necessary, if we’ve gotten zero percent ejection fraction, that doesn’t necessarily mean there’s an occlusion. I would say the answer to your question is no, it has to state that… it has to be documented for you to call it an occlusion because there are several other reasons why it could be that low.
This is an image of what they’re doing. There’s the left ventricle, you can always tell if you’re looking at the back or the front of the heart by the apex is looking; so if that apex, the little V part of the heart is facing this way, we’re looking at the front of the heart. If it’s facing off to the other side, we’re looking at the back of the heart. FYI. There we’ve got the percentage of blood ejected up into the atrium and that’s the left ventricle.
Right there at the last, I added: Normal – 50-65%, Below Normal – 36-49%. Anything below 35% is just real bad news; so what happens? It usually means they get, like, afib; and so then, you can treat that. But if you have a low ejection fraction, they’re absolutely going to run more tests to find out what’s going on and you’ll probably, they can give you a pacemaker maybe, but you results in afib medication and stuff could be given.
Most of this information I got was from the Mayo Clinic and there’s the website: www.mayoclinic.org/ejection-fraction/expert. I love the Mayo Clinic, lots of good stuff there.
Alicia has been working in the medical field for over 20 years. She first learned about medical coding while working in a medical records department at a resort town hospital near where she was raised. Through the years she has held several jobs in the medical field from, CNA, EMT, Pharmacy technician and Medial Records Abstractor and Analyst. Outside of the medical field she has worked as a Real Estate agent, and owned her own on-line retail business. The medical field has always been where she felt the most comfortable.
Alicia has taught medical coding, billing and medical law and ethics at a private college. She also did contract work in HCC Risk Adjustment and discovered she really enjoyed ICD work. Because she loves to learn Alicia is working towards her Masters in Health Care Administration with an emphasis on education. Having taken many online classes through the years to complete her degree she feels very comfortable with both face to face and on-line learning. Alicia will tell you that not only does she love medical coding but she has a passion for teaching it. Alicia lives in the middle of Texas with her husband who is a Pastor, five of her six children, three dogs and two cats. | <urn:uuid:126858dc-5003-4209-8510-59f823e69cad> | {
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|Other names||Tourette's syndrome, Tourette's disorder, Gilles de la Tourette syndrome (GTS)|
|Georges Gilles de la Tourette (1857–1904), namesake of Tourette syndrome|
|Specialty||Lua error in Module:WikidataIB at line 665: attempt to index field 'wikibase' (a nil value).|
|Usual onset||Typically in childhood|
|Causes||Genetic with environmental influence|
|Diagnostic method||Based on history and symptoms|
|Treatment||Education, behavioral therapy|
|Medication||Usually none, occasionally antipsychotics|
|Prognosis||Improvement to disappearance of tics beginning in late teens|
Tourette syndrome (TS or simply Tourette's) is a common neuropsychiatric disorder with onset in childhood, characterized by multiple motor tics and at least one vocal (phonic) tic. These tics characteristically wax and wane, can be suppressed temporarily, and are typically preceded by an unwanted urge or sensation in the affected muscles. Some common tics are eye blinking, coughing, throat clearing, sniffing, and facial movements. Tourette's does not adversely affect intelligence or life expectancy.
Tourette's is defined as part of a spectrum of tic disorders, which includes provisional, transient and persistent (chronic) tics. While the exact cause is unknown, it is believed to involve a combination of genetic and environmental factors. There are no specific tests for diagnosing Tourette's; it is not always correctly identified because most cases are mild and the severity of tics decreases for most children as they pass through adolescence. Extreme Tourette's in adulthood, though sensationalized in the media, is a rarity; tics are often unnoticed by casual observers.
In most cases, medication for tics is not necessary. Education is an important part of any treatment plan, and explanation and reassurance alone are often sufficient treatment. Many individuals with Tourette's go undiagnosed or never seek medical care. Among those who are seen in specialty clinics, attention-deficit hyperactivity disorder (ADHD) and obsessive–compulsive disorder (OCD) are present at higher rates. These co-occurring diagnoses often cause more impairment to the individual than the tics; hence, it is important to correctly identify associated conditions and treat them.
About 1% of school-age children and adolescents have Tourette's. It was once considered a rare and bizarre syndrome, most often associated with coprolalia (the utterance of obscene words or socially inappropriate and derogatory remarks), but this symptom is present in only a small minority of people with Tourette's. The condition was named by Jean-Martin Charcot (1825–1893) on behalf of his resident, Georges Albert Édouard Brutus Gilles de la Tourette (1857–1904), a French physician and neurologist, who published an account of nine patients with Tourette's in 1885.
Tics are sudden, repetitive, nonrhythmic movements (motor tics) and utterances (phonic tics) that involve discrete muscle groups. Motor tics are movement-based tics, while phonic tics are involuntary sounds produced by moving air through the nose, mouth, or throat.
Tourette's was classified by the fourth version of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR) as one of several tic disorders "usually first diagnosed in infancy, childhood, or adolescence" according to type (motor or phonic tics) and duration (transient or chronic). Transient tic disorders consisted of multiple motor tics, phonic tics or both, with a duration between four weeks and twelve months. Chronic tic disorder was either single or multiple, motor or phonic tics (but not both), which were present for more than a year. Tourette's is diagnosed when multiple motor tics, and at least one phonic tic, are present for more than a year. The fifth version of the DSM (DSM-5), published in May 2013, reclassified Tourette's and tic disorders as motor disorders listed in the neurodevelopmental disorder category, and replaced transient tic disorder with provisional tic disorder, but made few other significant changes.
Tic disorders are defined only slightly differently by the World Health Organization International Statistical Classification of Diseases and Related Health Problems, ICD-10; code F95.2 is for combined vocal and multiple motor tic disorder [de la Tourette].
Although Tourette's is the more severe expression of the spectrum of tic disorders, most cases are mild. The severity of symptoms varies widely among people with Tourette's, and mild cases may be undetected.
Tics are movements or sounds "that occur intermittently and unpredictably out of a background of normal motor activity", having the appearance of "normal behaviors gone wrong". The tics associated with Tourette's change in number, frequency, severity and anatomical location. Waxing and waning—the ongoing increase and decrease in severity and frequency of tics—occurs differently in each individual. Tics may also occur in "bouts of bouts", which vary for each person.
Coprolalia (the spontaneous utterance of socially objectionable or taboo words or phrases) is the most publicized symptom of Tourette's, but it is not required for a diagnosis of Tourette's and only about 10% of Tourette's patients exhibit it. Echolalia (repeating the words of others) and palilalia (repeating one's own words) occur in a minority of cases, while the most common initial motor and vocal tics are, respectively, eye blinking and throat clearing.
In contrast to the abnormal movements of other movement disorders (for example, choreas, dystonias, myoclonus, and dyskinesias), the tics of Tourette's are temporarily suppressible, nonrhythmic, and often preceded by an unwanted premonitory urge. Immediately preceding tic onset, most individuals with Tourette's are aware of an urge, similar to the need to sneeze or scratch an itch. Individuals describe the need to tic as a buildup of tension, pressure, or energy which they consciously choose to release, as if they "had to do it" to relieve the sensation or until it feels "just right". Examples of the premonitory urge are the feeling of having something in one's throat, or a localized discomfort in the shoulders, leading to the need to clear one's throat or shrug the shoulders. The actual tic may be felt as relieving this tension or sensation, similar to scratching an itch. Another example is blinking to relieve an uncomfortable sensation in the eye. These urges and sensations, preceding the expression of the movement or vocalization as a tic, are referred to as "premonitory sensory phenomena" or premonitory urges. Because of the urges that precede them, tics are described as semi-voluntary or "unvoluntary", rather than specifically involuntary; they may be experienced as a voluntary, suppressible response to the unwanted premonitory urge. Published descriptions of the tics of Tourette's identify sensory phenomena as the core symptom of the syndrome, even though they are not included in the diagnostic criteria.
|Video clips of tics|
While individuals with tics are sometimes able to suppress their tics for limited periods of time, doing so often results in tension or mental exhaustion. People with Tourette's may seek a secluded spot to release their symptoms, or there may be a marked increase in tics after a period of suppression at school or at work. Some people with Tourette's may not be aware of the premonitory urge. Children may be less aware of the premonitory urge associated with tics than are adults, but their awareness tends to increase with maturity. They may have tics for several years before becoming aware of premonitory urges. Children may suppress tics while in the doctor's office, so they may need to be observed while they are not aware they are being watched. The ability to suppress tics varies among individuals, and may be more developed in adults than children.
Although there is no such thing as a "typical" case of Tourette syndrome, the condition follows a fairly reliable course in terms of the age of onset and the history of the severity of symptoms. Tics may appear up to the age of eighteen, but the most typical age of onset is from five to seven. A 1998 study published by Leckman and colleagues from the Yale Child Study Center showed that the ages of highest tic severity are eight to twelve (average ten), with tics steadily declining for most patients as they pass through adolescence. The most common, first-presenting tics are eye blinking, facial movements, sniffing and throat clearing. Initial tics present most frequently in midline body regions where there are many muscles, usually the head, neck and facial region. This can be contrasted with the stereotyped movements of other disorders (such as stims and stereotypies of the autism spectrum disorders), which typically have an earlier age of onset, are more symmetrical, rhythmical and bilateral, and involve the extremities (e.g., flapping the hands). Tics that appear early in the course of the condition are frequently confused with other conditions, such as allergies, asthma, and vision problems: pediatricians, allergists and ophthalmologists are typically the first to see a child with tics.
Most cases of Tourette's in older individuals are mild and almost unrecognizable. When symptoms are severe enough to warrant referral to clinics, obsessive–compulsive disorder (OCD) and attention-deficit hyperactivity disorder (ADHD) are often associated with Tourette's. In children with tics, the additional presence of ADHD is associated with functional impairment, disruptive behavior, and tic severity. Compulsions resembling tics are present in some individuals with OCD; "tic-related OCD" is hypothesized to be a subgroup of OCD, distinguished from non-tic related OCD by the type and nature of obsessions and compulsions. Not all persons with Tourette's have ADHD or OCD or other comorbid conditions, although in clinical populations, a high percentage of patients presenting for care do have ADHD. One author reports that a ten-year overview of patient records revealed about 40% of patients with Tourette's have "TS-only" or "pure TS", referring to Tourette syndrome in the absence of ADHD, OCD and other disorders. Another author reports that 57% of 656 patients presenting with tic disorders had uncomplicated tics, while 43% had tics plus comorbid conditions. People with "full-blown Tourette's" have significant comorbid conditions in addition to tics.
The exact cause of Tourette's is unknown, but it is well established that both genetic and environmental factors are involved. Genetic epidemiology studies have shown that the overwhelming majority of cases of Tourette's are inherited, although the exact mode of inheritance is not yet known and no gene has been identified. In other cases, tics are associated with disorders other than Tourette's, a phenomenon known as tourettism.
A person with Tourette's has about a 50% chance of passing the gene(s) to one of his or her children, but Tourette's is a condition of variable expression and incomplete penetrance. Thus, not everyone who inherits the genetic vulnerability will show symptoms; even close family members may show different severities of symptoms, or no symptoms at all. The gene(s) may express as Tourette's, as a milder tic disorder (provisional or chronic tics), or as obsessive–compulsive symptoms without tics. Only a minority of the children who inherit the gene(s) have symptoms severe enough to require medical attention. Gender appears to have a role in the expression of the genetic vulnerability: males are more likely than females to express tics.
Non-genetic, environmental, post-infectious, or psychosocial factors—while not causing Tourette's—can influence its severity. Autoimmune processes may affect tic onset and exacerbation in some cases. In 1998, a team at the US National Institute of Mental Health proposed a hypothesis based on observation of 50 children that both obsessive–compulsive disorder (OCD) and tic disorders may arise in a subset of children as a result of a poststreptococcal autoimmune process. Children who meet five diagnostic criteria are classified, according to the hypothesis, as having Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal infections (PANDAS). This contentious hypothesis is the focus of clinical and laboratory research, but remains unproven.
Some forms of OCD may be genetically linked to Tourette's. A subset of OCD is thought to be causally related to Tourette's and may be a different expression of the same factors that are important for the expression of tics. The genetic relationship of ADHD to Tourette syndrome, however, has not been fully established.
The exact mechanism affecting the inherited vulnerability to Tourette's has not been established, and the precise cause is unknown. Tics are believed to result from dysfunction in cortical and subcortical regions, the thalamus, basal ganglia and frontal cortex. Neuroanatomic models implicate failures in circuits connecting the brain's cortex and subcortex, and imaging techniques implicate the basal ganglia and frontal cortex. After 2010, the role of histamine and the H3-receptor came into focus in the pathophysiology of TS, as "key modulators of striatal circuitry". A reduced level of histamine in the H3-receptor may disrupt other neurotransmitters, causing tics.
According to the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5), Tourette’s may be diagnosed when a person exhibits both multiple motor and one or more vocal tics over the period of a year; the motor and vocal tics need not be concurrent. The onset must have occurred before the age of 18, and cannot be attributed to the effects of another condition or substance (such as cocaine). Hence, other medical conditions that include tics or tic-like movements—such as autism or other causes of tourettism—must be ruled out before conferring a Tourette's diagnosis. Since 2000, the DSM has recognized that clinicians see patients who meet all the other criteria for Tourette's, but do not have distress or impairment.
There are no specific medical or screening tests that can be used in diagnosing Tourette's; it is frequently misdiagnosed or underdiagnosed, partly because of the wide expression of severity, ranging from mild (the majority of cases) or moderate, to severe (the rare, but more widely recognized and publicized cases). Coughing, eye blinking, and tics that mimic unrelated conditions such as asthma are commonly misdiagnosed.
The diagnosis is made based on observation of the individual's symptoms and family history, and after ruling out secondary causes of tic disorders. In patients with a typical onset and a family history of tics or obsessive–compulsive disorder, a basic physical and neurological examination may be sufficient.
There is no requirement that other comorbid conditions (such as ADHD or OCD) be present, but if a physician believes that there may be another condition present that could explain tics, tests may be ordered as necessary to rule out that condition. An example of this is when diagnostic confusion between tics and seizure activity exists, which would call for an EEG, or if there are symptoms that indicate an MRI to rule out brain abnormalities. TSH levels can be measured to rule out hypothyroidism, which can be a cause of tics. Brain imaging studies are not usually warranted. In teenagers and adults presenting with a sudden onset of tics and other behavioral symptoms, a urine drug screen for cocaine and stimulants might be necessary. If a family history of liver disease is present, serum copper and ceruloplasmin levels can rule out Wilson's disease. Most cases are diagnosed by merely observing a history of tics.
Secondary causes of tics (not related to inherited Tourette syndrome) are commonly referred to as tourettism. Dystonias, choreas, other genetic conditions, and secondary causes of tics should be ruled out in the differential diagnosis for Tourette syndrome. Other conditions that may manifest tics or stereotyped movements include developmental disorders, autism spectrum disorders, and stereotypic movement disorder; Sydenham's chorea; idiopathic dystonia; and genetic conditions such as Huntington's disease, neuroacanthocytosis, pantothenate kinase-associated neurodegeneration, Duchenne muscular dystrophy, Wilson's disease, and tuberous sclerosis. Other possibilities include chromosomal disorders such as Down syndrome, Klinefelter syndrome, XYY syndrome and fragile X syndrome. Acquired causes of tics include drug-induced tics, head trauma, encephalitis, stroke, and carbon monoxide poisoning. The symptoms of Lesch-Nyhan syndrome may also be confused with Tourette syndrome. Most of these conditions are rarer than tic disorders, and a thorough history and examination may be enough to rule them out, without medical or screening tests.
Although not all people with Tourette's have comorbid conditions, most Tourette's patients presenting for clinical care at specialty referral centers may exhibit symptoms of other conditions along with their motor and phonic tics. Associated conditions include attention-deficit hyperactivity disorder (ADD or ADHD), obsessive–compulsive disorder (OCD), learning disabilities and sleep disorders. Disruptive behaviors, impaired functioning, or cognitive impairment in patients with comorbid Tourette's and ADHD may be accounted for by the comorbid ADHD, highlighting the importance of identifying and treating comorbid conditions. Disruption from tics is commonly overshadowed by comorbid conditions that present greater interference to the child. Tic disorders in the absence of ADHD do not appear to be associated with disruptive behavior or functional impairment, while impairment in school, family, or peer relations is greater in patients who have more comorbid conditions and often determines whether therapy is needed.
Because comorbid conditions such as OCD and ADHD can be more impairing than tics, these conditions are included in an evaluation of patients presenting with tics. "It is critical to note that the comorbid conditions may determine functional status more strongly than the tic disorder," according to Samuel Zinner, MD. The initial assessment of a patient referred for a tic disorder should include a thorough evaluation, including a family history of tics, ADHD, obsessive–compulsive symptoms, and other chronic medical, psychiatric and neurological conditions. Children and adolescents with TS who have learning difficulties are candidates for psychoeducational testing, particularly if the child also has ADHD. Undiagnosed comorbid conditions may result in functional impairment, and it is necessary to identify and treat these conditions to improve functioning. Complications may include depression, sleep problems, social discomfort, self-injury, anxiety, personality disorders, oppositional defiant disorder, and conduct disorders.
The treatment of Tourette's focuses on identifying and helping the individual manage the most troubling or impairing symptoms. Most cases of Tourette's are mild, and do not require pharmacological treatment; instead, psychobehavioral therapy, education, and reassurance may be sufficient. Treatments, where warranted, can be divided into those that target tics and comorbid conditions, which, when present, are often a larger source of impairment than the tics themselves. Not all people with tics have comorbid conditions, but when those conditions are present, they often take treatment priority.
There is no cure for Tourette's and no medication that works universally for all individuals without significant adverse effects. Knowledge, education and understanding are uppermost in management plans for tic disorders. The management of the symptoms of Tourette's may include pharmacological, behavioral and psychological therapies. While pharmacological intervention is reserved for more severe symptoms, other treatments (such as supportive psychotherapy or cognitive behavioral therapy) may help to avoid or ameliorate depression and social isolation, and to improve family support. Educating a patient, family, and surrounding community (such as friends, school, and church) is a key treatment strategy, and may be all that is required in mild cases.
Medication is available to help when symptoms interfere with functioning. The classes of medication with the most proven efficacy in treating tics—typical and atypical neuroleptics including risperidone (trade name Risperdal), ziprasidone (Geodon), haloperidol (Haldol), pimozide (Orap) and fluphenazine (Prolixin)—can have long-term and short-term adverse effects. The antihypertensive agents clonidine (trade name Catapres) and guanfacine (Tenex) are also used to treat tics; studies show variable efficacy, but a lower side effect profile than the neuroleptics. Stimulants and other medications may be useful in treating ADHD when it co-occurs with tic disorders. Drugs from several other classes of medications can be used when stimulant trials fail, including guanfacine (trade name Tenex), atomoxetine (Strattera) and tricyclic antidepressants. Clomipramine (Anafranil), a tricyclic, and SSRIs—a class of antidepressants including fluoxetine (Prozac), sertraline (Zoloft), and fluvoxamine (Luvox)—may be prescribed when a Tourette's patient also has symptoms of obsessive–compulsive disorder. Several other medications have been tried, but evidence to support their use is unconvincing.
Because children with tics often present to physicians when their tics are most severe, and because of the waxing and waning nature of tics, it is recommended that medication not be started immediately or changed often. Frequently, the tics subside with explanation, reassurance, understanding of the condition and a supportive environment. When medication is used, the goal is not to eliminate symptoms: it should be used at the lowest possible dose that manages symptoms without adverse effects, given that these may be more disturbing than the symptoms for which they were prescribed.
Cognitive behavioral therapy (CBT) is a useful treatment when OCD is present, and there is increasing evidence supporting the use of habit reversal (HRT) in the treatment of tics. There is evidence that HRT reduces tic severity, but there are methodological limitations in the studies, and a need for more trained specialists and better large-scale studies.
Relaxation techniques, such as exercise, yoga or meditation, may be useful in relieving the stress that may aggravate tics, but the majority of behavioral interventions (such as relaxation training and biofeedback, with the exception of habit reversal) have not been systematically evaluated and are not empirically supported therapies for Tourette's. Deep brain stimulation has been used to treat adults with severe Tourette's that does not respond to conventional treatment, but it is regarded as an invasive, experimental procedure that is unlikely to become widespread.
Tourette syndrome is a spectrum disorder—its severity ranges over a spectrum from mild to severe. The majority of cases are mild and require no treatment. In these cases, the impact of symptoms on the individual may be mild, to the extent that casual observers might not know of their condition. The overall prognosis is positive, but a minority of children with Tourette syndrome have severe symptoms that persist into adulthood. A study of 46 subjects at 19 years of age found that the symptoms of 80% had minimum to mild impact on their overall functioning, and that the other 20% experienced at least a moderate impact on their overall functioning. The rare minority of severe cases can inhibit or prevent individuals from holding a job or having a fulfilling social life. In a follow-up study of thirty-one adults with Tourette's, all patients completed high school, 52% finished at least two years of college, and 71% were full-time employed or were pursuing higher education.
Regardless of symptom severity, individuals with Tourette's have a normal life span. Although the symptoms may be lifelong and chronic for some, the condition is not degenerative or life-threatening. Intelligence is normal in those with Tourette's, although there may be learning disabilities. Severity of tics early in life does not predict tic severity in later life, and prognosis is generally favorable, although there is no reliable means of predicting the outcome for a particular individual. The gene or genes associated with Tourette's have not been identified, and there is no potential "cure". A higher rate of migraines than the general population and sleep disturbances are reported.
Several studies have demonstrated that the condition in most children improves with maturity. Tics may be at their highest severity at the time that they are diagnosed, and often improve with understanding of the condition by individuals and their families and friends. The statistical age of highest tic severity is typically between eight and twelve, with most individuals experiencing steadily declining tic severity as they pass through adolescence. One study showed no correlation with tic severity and the onset of puberty, in contrast with the popular belief that tics increase at puberty. In many cases, a complete remission of tic symptoms occurs after adolescence. However, a study using videotape to record tics in adults found that, although tics diminished in comparison with childhood, and all measures of tic severity improved by adulthood, 90% of adults still had tics. Half of the adults who considered themselves tic-free still displayed evidence of tics.
Many people with TS may not realize they have tics; because tics are more commonly expressed in private, TS may go unrecognized or undetected. It is not uncommon for the parents of affected children to be unaware that they, too, may have had tics as children. Because Tourette's tends to subside with maturity, and because milder cases of Tourette's are now more likely to be recognized, the first realization that a parent had tics as a child may not come until their offspring is diagnosed. It is not uncommon for several members of a family to be diagnosed together, as parents bringing children to a physician for an evaluation of tics become aware that they, too, had tics as a child.
Children with Tourette's may suffer socially if their tics are viewed as "bizarre". If a child has disabling tics, or tics that interfere with social or academic functioning, supportive psychotherapy or school accommodations can be helpful. Because comorbid conditions (such as ADHD or OCD) can cause greater impact on overall functioning than tics, a thorough evaluation for comorbidity is called for when symptoms and impairment warrant.
A supportive environment and family generally gives those with Tourette's the skills to manage the disorder. People with Tourette's may learn to camouflage socially inappropriate tics or to channel the energy of their tics into a functional endeavor. Accomplished musicians, athletes, public speakers, and professionals from all walks of life are found among people with Tourette's. Outcomes in adulthood are associated more with the perceived significance of having severe tics as a child than with the actual severity of the tics. A person who was misunderstood, punished, or teased at home or at school will fare worse than children who enjoyed an understanding and supportive environment.
Tourette syndrome is found among all social, racial and ethnic groups and has been reported in all parts of the world; it is three to four times more frequent among males than among females. The tics of Tourette syndrome begin in childhood and tend to remit or subside with maturity; thus, a diagnosis may no longer be warranted for many adults, and observed prevalence rates are higher among children than adults. As children pass through adolescence, about one-quarter become tic-free, almost one-half see their tics diminish to a minimal or mild level, and less than one-quarter have persistent tics. Only 5 to 14% of adults experience worse tics in adulthood than in childhood.
Up to 1% of the overall population experiences tic disorders, including chronic tics and transient tics of childhood. Chronic tics affect 5% of children, and transient tics affect up to 20%. Prevalence rates in special education populations are higher.
The reported prevalence of TS varies "according to the source, age, and sex of the sample; the ascertainment procedures; and diagnostic system", with a range reported between .4% and 3.8% for children ages 5 to 18. Robertson (2011) says that 1% of school-age children have Tourette's. According to Lombroso and Scahill (2008), the emerging consensus is that .1 to 1% of children have Tourette's, with several studies supporting a tighter range of .6 to .8%. Bloch and Leckman (2009) and Swain (2007) report a range of prevalence in children of .4 to .6%, Knight et al. (2012) estimate .77% in children, and Du et al. (2010) report that 1 to 3% of Western school-age children have Tourette's.
Singer (2011) states the prevalence of TS in the overall population at any time is .1% for impairing cases and .6% for all cases, while Bloch and colleagues (2011) state the overall prevalence as between .3 and 1%. Robertson (2011) also suggests that the rate of Tourette's in the general population is 1%. Using year 2000 census data, a prevalence range of .1 to 1% yields an estimate of 53,000–530,000 school-age children with Tourette's in the US, and a prevalence estimate of .1% means that in 2001 about 553,000 people in the UK age 5 or older would have Tourette's.
Tourette syndrome was once thought to be rare: in 1972, the US National Institutes of Health (NIH) believed there were fewer than 100 cases in the United States, and a 1973 registry reported only 485 cases worldwide. However, multiple studies published since 2000 have consistently demonstrated that the prevalence is much higher than previously thought. Discrepancies across current and prior prevalence estimates come from several factors: ascertainment bias in earlier samples drawn from clinically referred cases, assessment methods that may fail to detect milder cases, and differences in diagnostic criteria and thresholds. There were few broad-based community studies published before 2000 and until the 1980s, most epidemiological studies of Tourette syndrome were based on individuals referred to tertiary care or specialty clinics. Individuals with mild symptoms may not seek treatment and physicians may not confer an official diagnosis of TS on children out of concern for stigmatization; children with milder symptoms are unlikely to be referred to specialty clinics, so prevalence studies have an inherent bias towards more severe cases. Studies of Tourette syndrome are vulnerable to error because tics vary in intensity and expression, are often intermittent, and are not always recognized by clinicians, patients, family members, friends or teachers; approximately 20% of persons with Tourette syndrome do not recognize that they have tics. Newer studies—recognizing that tics may often be undiagnosed and hard to detect—use direct classroom observation and multiple informants (parent, teacher, and trained observers), and therefore record more cases than older studies relying on referrals. As the diagnostic threshold and assessment methodology have moved towards recognition of milder cases, the result is an increase in estimated prevalence.
Tourette's is associated with several comorbid conditions, or co-occurring diagnoses, which are often the major source of impairment for an affected child. Most individuals with tics do not seek medical attention, so epidemiological studies of TS "reflect a strong ascertainment bias", but among those who do warrant medical attention, the majority have other conditions, and up to 50% have ADHD or OCD.
The first presentation of Tourette syndrome is thought to be in the book, Malleus Maleficarum ("Witch's hammer") by Jakob Sprenger and Heinrich Kraemer, published in the late 15th century and describing a priest whose tics were "believed to be related to possession by the devil". A French doctor, Jean Marc Gaspard Itard, reported the first case of Tourette syndrome in 1825, describing Marquise de Dampierre, an important woman of nobility in her time. Jean-Martin Charcot, an influential French physician, assigned his resident Georges Albert Édouard Brutus Gilles de la Tourette, a French physician and neurologist, to study patients at the Salpêtrière Hospital, with the goal of defining an illness distinct from hysteria and from chorea.
In 1885, Gilles de la Tourette published an account in Study of a Nervous Affliction describing nine persons with "convulsive tic disorder", concluding that a new clinical category should be defined. The eponym was later bestowed by Charcot after and on behalf of Gilles de la Tourette.
Little progress was made over the next century in explaining or treating tics, and a psychogenic view prevailed well into the 20th century. The possibility that movement disorders, including Tourette syndrome, might have an organic origin was raised when an encephalitis epidemic from 1918–1926 led to a subsequent epidemic of tic disorders.
During the 1960s and 1970s, as the beneficial effects of haloperidol (Haldol) on tics became known, the psychoanalytic approach to Tourette syndrome was questioned. The turning point came in 1965, when Arthur K. Shapiro—described as "the father of modern tic disorder research"—treated a Tourette’s patient with haloperidol, and published a paper criticizing the psychoanalytic approach.
Since the 1990s, a more neutral view of Tourette's has emerged, in which biological vulnerability and adverse environmental events are seen to interact. In 2000, the American Psychiatric Association published the DSM-IV-TR, revising the text of DSM-IV to no longer require that symptoms of tic disorders cause distress or impair functioning, recognizing that clinicians often see patients who meet all the other criteria for Tourette's, but do not have distress or impairment.
Findings since 1999 have advanced TS science in the areas of genetics, neuroimaging, neurophysiology, and neuropathology. Questions remain regarding how best to classify Tourette syndrome, and how closely Tourette's is related to other movement disorders or psychiatric disorders. Good epidemiologic data is still lacking, and available treatments are not risk free and not always well tolerated. High-profile media coverage focuses on treatments that do not have established safety or efficacy, such as deep brain stimulation, and alternative therapies involving unstudied efficacy and side effects are pursued by many parents.
Society and culture
Not everyone with Tourette's wants treatment or a "cure", especially if that means they may "lose" something else in the process. Researchers Leckman and Cohen, and former US Tourette Syndrome Association (TSA) national board member Kathryn Taubert, believe that there may be latent advantages associated with an individual's genetic vulnerability to developing Tourette syndrome, such as a heightened awareness and increased attention to detail and surroundings that may have adaptive value. There is evidence to support the clinical lore that children with "TS-only" (Tourette's in the absence of comorbid conditions) are unusually gifted: neuropsychological studies have identified advantages in children with TS-only. Children with TS-only are faster than the average for their age group on timed tests of motor coordination.
Notable individuals with Tourette syndrome are found in all walks of life, including musicians, athletes, media figures, teachers, physicians, and authors. The best-known example of a person who may have used obsessive–compulsive traits to advantage is Samuel Johnson, the 18th-century English man of letters, who likely had Tourette syndrome as evidenced by the writings of James Boswell. Johnson wrote A Dictionary of the English Language in 1747, and was a prolific writer, poet, and critic. Tim Howard, described by the Chicago Tribune as the "rarest of creatures – an American soccer hero" and by the TSA as the "most notable individual with Tourette Syndrome around the world" says that his neurological makeup gave him an enhanced perception and an ability to hyper-focus that contributed to his success on the field.
Although it has been speculated that Mozart had Tourette's, no Tourette's expert or organization has presented credible evidence to support such a conclusion, and there are problems with the arguments supporting the diagnosis: tics are not transferred to the written form, as is supposed with Mozart's scatological writings; the medical history in retrospect is not thorough; side effects due to other conditions may be misinterpreted; "it is not proven whether written documents can account for the existence of a vocal tic" and "the evidence of motor tics in Mozart's life is doubtful."
Pre-dating Gilles de la Tourette's 1885 publication, likely portrayals of TS or tic disorders in fictional literature are Mr. Pancks in Little Dorrit by Charles Dickens and Nikolai Levin in Anna Karenina by Leo Tolstoy. The entertainment industry has been criticized for depicting those with Tourette syndrome as social misfits whose only tic is coprolalia, which has furthered stigmatization and the public's misunderstanding of those with Tourette's. The coprolalic symptoms of Tourette's are also fodder for radio and television talk shows in the US and in the British media.
- "Tourette Syndrome Fact Sheet". NINDS. 16 April 2014. Archived from the original on March 23, 2005. Retrieved 18 October 2016.
- Singer HS. "Tourette syndrome and other tic disorders". Handb Clin Neurol. 2011;100:641–57. doi:10.1016/B978-0-444-52014-2.00046-X PMID 21496613. Also see Singer HS. "Tourette's syndrome: from behaviour to biology". Lancet Neurol. 2005 Mar;4(3):149–59. doi:10.1016/S1474-4422(05)01012-4 PMID 15721825.
- Robertson MM. "Gilles de la Tourette syndrome: the complexities of phenotype and treatment". Br J Hosp Med (Lond). 2011 Feb;72(2):100–7. PMID 21378617
- Jankovic J. Movement Disorders, An Issue of Neurologic Clinics. The Clinics: Radiology: Elsevier, 2014, p. viii
- Peterson BS, Cohen DJ. "The treatment of Tourette's Syndrome: multimodal, developmental intervention". J Clin Psychiatry. 1998;59 Suppl 1:62–72; discussion 73–74. PMID 9448671. Quote: "Because of the understanding and hope that it provides, education is also the single most important treatment modality that we have in TS." Also see Zinner 2000.
- Du JC, Chiu TF, Lee KM, et al. "Tourette syndrome in children: an updated review". Pediatr Neonatol. 2010 Oct;51(5):255–64. doi:10.1016/S1875-9572(10)60050-2 PMID 20951354
- Leckman JF, Bloch MH, King RA, Scahill L. "Phenomenology of tics and natural history of tic disorders". Adv Neurol. 2006;99:1–16. PMID 16536348
- "Tourette's Disorder, 307.23 (F95.2)". Diagnostic and Statistical Manual of Mental Disorders, 2013, Fifth edition. American Psychiatric Association, p. 81.
- Neurodevelopmental disorders. American Psychiatric Association. Retrieved on December 29, 2011.
- Moran, M. "DSM-5 provides new take on neurodevelopment disorders". Psychiatric News. 18 January 2013;48(2):6–23. doi:10.1176/appi.pn.2013.1b11
- "Highlights of changes from DSM-IV-TR to DSM-5" (PDF). American Psychiatric Association. 2013. Retrieved on June 5, 2013.
- Du, Chiu, Lee, et al. 2010. See also ICD version 2007. World Health Organization. Retrieved on December 29, 2011.
- Bagheri MM, Kerbeshian J, Burd L. "Recognition and management of Tourette's syndrome and tic disorders". Archived March 31, 2005, at the Wayback Machine American Family Physician. 1999; 59:2263–74. PMID 10221310 Retrieved on October 28, 2006.
- The Tourette Syndrome Classification Study Group. "Definitions and classification of tic disorders". Arch Neurol. 1993 Oct;50(10):1013–16. PMID 8215958 Archived April 26, 2006.
- Dure LS 4th, DeWolfe J. "Treatment of tics". Adv Neurol. 2006;99:191–96. PMID 16536366
- Malone DA Jr, Pandya MM. "Behavioral neurosurgery". Adv Neurol. 2006;99:241–47. PMID 16536372
- Jankovic J. "Differential diagnosis and etiology of tics". Adv Neurol. 2001;85:15–29. PMID 11530424
- Cohen AJ, Leckman JF. "Sensory phenomena associated with Gilles de la Tourette's syndrome". J Clin Psychiatry. 1992 Sep;53(9):319–23. PMID 1517194
- Prado HS, Rosário MC, Lee J, Hounie AG, Shavitt RG, Miguel EC. "Sensory phenomena in obsessive–compulsive disorder and tic disorders: a review of the literature". CNS Spectr. 2008;13(5):425–32. PMID 18496480.
- Bliss J. "Sensory experiences of Gilles de la Tourette syndrome". Arch Gen Psychiatry. 1980 Dec;37(12):1343–47. PMID 6934713
- Kwak C, Dat Vuong K, Jankovic J. "Premonitory sensory phenomenon in Tourette's syndrome". Mov Disord. 2003 Dec;18(12):1530–33. doi:10.1002/mds.10618 PMID 14673893
- Swain JE, Scahill L, Lombroso PJ, King RA, Leckman JF. "Tourette syndrome and tic disorders: a decade of progress". J Am Acad Child Adolesc Psychiatry. 2007 Aug;46(8):947–68 doi:10.1097/chi.0b013e318068fbcc PMID 17667475
- Scahill LD, Leckman JF, Marek KL. "Sensory phenomena in Tourette's syndrome". Adv Neurol. 1995;65:273–80. PMID 7872145
- Miguel EC, do Rosario-Campos MC, Prado HS, et al. "Sensory phenomena in obsessive–compulsive disorder and Tourette's disorder". J Clin Psychiatry. 2000 Feb;61(2):150–56. PMID 10732667
- Black, KJ. Tourette Syndrome and Other Tic Disorders. eMedicine (March 30, 2007). Retrieved on August 10, 2009.
- Zinner SH. "Tourette disorder". Pediatr Rev. 2000;21(11):372–83. PMID 11077021
- Leckman JF, Zhang H, Vitale A, et al. "Course of tic severity in Tourette syndrome: the first two decades. (PDF). Pediatrics. 1998;102 (1 Pt 1):14–19. PMID 9651407.
- Rapin I. "Autism spectrum disorders: relevance to Tourette syndrome". Adv Neurol. 2001;85:89–101. PMID 11530449
- Robertson MM. "The prevalence and epidemiology of Gilles de la Tourette syndrome. Part 1: the epidemiological and prevalence studies". J Psychosom Res. 2008 Nov;65(5):461–72. doi:10.1016/j.jpsychores.2008.03.006 PMID 18940377
- Robertson MM. "The prevalence and epidemiology of Gilles de la Tourette syndrome. Part 2: tentative explanations for differing prevalence figures in GTS, including the possible effects of psychopathology, aetiology, cultural differences, and differing phenotypes". J Psychosom Res. 2008 Nov;65(5):473–86. doi:10.1016/j.jpsychores.2008.03.007 PMID 18940378
- Hounie AG, do Rosario-Campos MC, Diniz JB, et al. "Obsessive-compulsive disorder in Tourette syndrome". Adv Neurol. 2006;99:22–38. PMID 16536350
- Spencer T, Biederman J, Harding M, et al. "Disentangling the overlap between Tourette's disorder and ADHD". J Child Psychol Psychiatry. 1998 Oct;39(7):1037–44. doi:10.1111/1469-7610.00406 PMID 9804036
- Denckla MB. "Attention-deficit hyperactivity disorder (ADHD) comorbidity: a case for "pure" Tourette syndrome?" J Child Neurol. 2006 Aug;21(8):701–3. PMID 16970871
- Denckla MB. "Attention deficit hyperactivity disorder: the childhood co-morbidity that most influences the disability burden in Tourette syndrome". Adv Neurol. 2006;99:17–21. PMID 16536349
- Walkup, JT, Mink, JW, Hollenback, PJ, (eds). Advances in Neurology, Tourette syndrome. Lippincott, Williams & Wilkins, Philadelphia, PA. 2006;99:xv. ISBN 0-7817-9970-8 Search this book on . Google books.
- Bloch M, State M, Pittenger C. "Recent advances in Tourette syndrome". Curr. Opin. Neurol. 2011 Apr;24(2):119–25. doi:10.1097/WCO.0b013e328344648c PMID 21386676
- O'Rourke JA, Scharf JM, Yu D, et al. "The genetics of Tourette syndrome: A review". J Psychosom Res. 2009 Dec;67(6):533–545. doi:10.1016/j.jpsychores.2009.06.006 PMID 19913658
- Mejia NI, Jankovic J. "Secondary tics and tourettism" (PDF). Rev Bras Psiquiatr. 2005;27(1):11–17. PMID 15867978
- van de Wetering BJ, Heutink P. "The genetics of the Gilles de la Tourette syndrome: a review". J Lab Clin Med. 1993 May;121(5):638–45. PMID 8478592
- Tourette Syndrome: Frequently Asked Questions. Tourette Syndrome Association. Retrieved on May 8, 2013.
- PANDAS. NIH. Retrieved on November 25, 2006.
- Swerdlow, NR. "Tourette Syndrome: Current Controversies and the Battlefield Landscape". Curr Neurol Neurosci Rep. 2005, 5:329–31. doi:10.1007/s11910-005-0054-8 PMID 16131414
- Pauls DL, Towbin KE, Leckman JF, et al. "Gilles de la Tourette's syndrome and obsessive–compulsive disorder. Evidence supporting a genetic relationship". Arch Gen Psychiatry. 1986 Dec;43(12):1180–82. PMID 3465280
- Miguel EC, do Rosario-Campos MC, Shavitt RG, et al. "The tic-related obsessive–compulsive disorder phenotype and treatment implications". Adv Neurol. 2001;85:43–55. PMID 11530446
- Rapanelli M, Pittenger C. “Histamine and Histamine Receptors in Tourette Syndrome and Other Neuropsychiatric Conditions”. Neuropharmacology, 2016 Jul;106:85–90. PMID 26282120 doi:10.1016/j.neuropharm.2015.08.019
- Rapanelli, Maximiliano. “The Magnificent Two: Histamine and the H3 Receptor as Key Modulators of Striatal Circuitry”. Progress in Neuro-Psychopharmacology and Biological Psychiatry, 2017 Feb 6;73:36–40. PMID 27773554 doi:10.1016/j.pnpbp.2016.10.002
- Bolam, J. Paul, and Tommas J. Ellender. “Histamine and the Striatum.” Neuropharmacology, 2016 Jul;106:74–84. PMID 26275849 doi:10.1016/j.neuropharm.2015.08.013
- Sadek B, Saad A, Sadeq A, Jalal F, Stark H. “Histamine H3 Receptor as a Potential Target for Cognitive Symptoms in Neuropsychiatric Diseases.” Behavioural Brain Research 2016 Oct 1;312:415–30. PMID 27363923 doi:10.1016/j.bbr.2016.06.051
- Walkup JT, Ferrão Y, Leckman JF, Stein DJ, Singer H. "Tic disorders: some key issues for DSM-V". Depress Anxiety. 2010 Jun;27(6):600–10. doi:10.1002/da.20711 PMID 20533370
- Summary of Practice: Relevant changes to DSM-IV-TR. American Psychiatric Association. Retrieved from May 11, 2008 archive.org version on December 29, 2011.
- What is DSM-IV-TR? Retrieved on October 28, 2006.
- Scahill L, Erenberg G, Berlin CM Jr, Budman C, Coffey BJ, Jankovic J, Kiessling L, King RA, Kurlan R, Lang A, Mink J, Murphy T, Zinner S, Walkup J; Tourette Syndrome Association Medical Advisory Board: Practice Committee. "Contemporary assessment and pharmacotherapy of Tourette syndrome" (PDF). NeuroRx. 2006 Apr;3(2):192–206. doi:10.1016/j.nurx.2006.01.009 PMID 16554257
- Ringman JM, Jankovic J. "Occurrence of tics in Asperger's syndrome and autistic disorder". J Child Neurol. 2000 Jun;15(6):394–400. PMID 10868783
- Jankovic J, Mejia NI. "Tics associated with other disorders". Adv Neurol. 2006;99:61–68. PMID 16536352
- Freeman, RD. Tourette's Syndrome: minimizing confusion. Roger Freeman, MD, blog. Retrieved on February 8, 2006.
- Scahill L, Williams S, Schwab-Stone M, Applegate J, Leckman JF. "Disruptive behavior problems in a community sample of children with tic disorders". Adv Neurol. 2006;99:184–90. PMID 16536365
- Robertson MM. "Tourette syndrome, associated conditions and the complexities of treatment" (PDF). Brain. 2000;123 Pt 3:425–62. doi:10.1093/brain/123.3.425 PMID 10686169
- Stern JS, Burza S, Robertson MM. "Gilles de la Tourette's syndrome and its impact in the UK". Postgraduate Medicine Journal. 2005 Jan;81(951):12–19. doi:10.1136/pgmj.2004.023614 PMID 15640424
- Medication trade names may differ between countries. In general, this article uses North American trade names.
- Bloch, State, Pittenger 2011. See also Schapiro NA. "Dude, you don't have Tourette's:" Tourette's syndrome, beyond the tics. Pediatr Nurs. 2002 May–Jun;28(3):243–46, 249–53. PMID 12087644 Full text (free registration required).
- Coffey BJ, Shechter RL. "Treatment of co-morbid obsessive compulsive disorder, mood, and anxiety disorders". Adv Neurol. 2006;99:208–21. PMID 16536368
- Hwang GC, Tillberg CS, Scahill L. Habit reversal training for children with tourette syndrome: update and review. J Child Adolesc Psychiatr Nurs. 2012 Nov;25(4):178–83. PMID 23121140 doi:10.1111/jcap.12002
- Dutta N, Cavanna AE. The effectiveness of habit reversal therapy in the treatment of Tourette syndrome and other chronic tic disorders: a systematic review. Funct Neurol. 2013 Jan–Mar;28(1):7–12. PMID 23731910
- Woods DW, Himle MB, Conelea CA. "Behavior therapy: other interventions for tic disorders". Adv Neurol. 2006;99:234–40. PMID 16536371
- Statement: Deep Brain Stimulation and Tourette Syndrome. Tourette Syndrome Association. Retrieved on February 26, 2005.
- Viswanathan A, Jimenez-Shahed J, Baizabal Carvallo JF, Jankovic J. Deep brain stimulation for Tourette syndrome: target selection. Stereotact Funct Neurosurg. 2012;90(4):213–24. PMID 22699684 doi:10.1159/000337776
- Kammer T. "Mozart in the neurological department—who has the tic?" (PDF). Front Neurol Neurosci. 2007;22:184–92. doi:10.1159/0000102880 PMID 17495512
- What is Tourette Syndrome? Tourette Syndrome Foundation of Canada. Retrieved on July 2, 2013.
- Todd, Olivier. Malraux: A Life. Knopf, 2005.
- Guidotti TL. André Malraux: a medical interpretation (PDF). J R Soc Med. 1985 May;78(5):401–6. PMID 3886907
- Liebmann, Lisa. Lisa Liebmann on the Mona Lisa. TATEetc. Issue 6 / Spring 2006. Retrieved on March 1, 2008.
- Pappert EJ, Goetz CG, Louis ED, et al. "Objective assessments of longitudinal outcome in Gilles de la Tourette's syndrome." Neurology. 2003 Oct 14;61(7):936–40. PMID 14557563
- Singer HS. "Tourette's syndrome: from behaviour to biology". Lancet Neurol. 2005 Mar;4(3):149–59. doi:10.1016/S1474-4422(05)01012-4 PMID 15721825
- Burd L, Kerbeshian PJ, Barth A, et al. "Long-term follow-up of an epidemiologically defined cohort of patients with Tourette syndrome". J Child Neurol. 2001;16(6):431–37. PMID 11417610
- Howard, Tim. Tim Howard: Growing up with Tourette syndrome and my love of football. The Guardian. December 6, 2014. Retrieved on March 21, 2015.
- Knight T, Steeves T, Day L, Lowerison M, Jette N, Pringsheim T. Prevalence of tic disorders: a systematic review and meta-analysis. Pediatr Neurol. 2012 Aug;47(2):77–90. PMID 22759682 doi:10.1016/j.pediatrneurol.2012.05.002
- Leckman JF, Cohen DJ. Tourette's Syndrome—Tics, Obsessions, Compulsions: Developmental Psychopathology and Clinical Care. John Wiley & Sons, Inc., New York. 1999:37. ISBN 0-471-16037-7 Search this book on . Google books. "For example, individuals who were misunderstood and punished at home and at school for their tics or who were teased mercilessly by peers and stigmatized by their communities will fare worse than a child whose interpersonal environment was more understanding and supportive."
- Cohen DJ, Leckman JF, Pauls D. "Neuropsychiatric disorders of childhood: Tourette’s syndrome as a model". Acta Paediatr Suppl 422; 106–11, Scandinavian University Press, 1997. "The individuals with TS who do the best, we believe, are: those who have been able to feel relatively good about themselves and remain close to their families; those who have the capacity for humor and for friendship; those who are less burdened by troubles with attention and behavior, particularly aggression; and those who have not had development derailed by medication."
- Bloch MH, Leckman JF. "Clinical course of Tourette syndrome". J Psychosom Res. 2009 Dec;67(6):497–501. doi:10.1016/j.jpsychores.2009.09.002 PMID 19913654
- Lombroso PJ, Scahill L. "Tourette syndrome and obsessive–compulsive disorder". Brain Dev. 2008 Apr;30(4):231–37. doi:10.1016/j.braindev.2007.09.001 PMID 17937978
- Cohen DJ, Jankovic J, Goetz CG, (eds). Advances in Neurology, Tourette syndrome. Lippincott, Williams & Wilkins, Philadelphia, PA. 2001;85:xviii. ISBN 0-7817-2405-8 Search this book on .
- Abuzzahab FE, Anderson FO. "Gilles de la Tourette's syndrome; international registry". Minnesota Medicine. 1973 Jun;56(6):492–96. PMID 4514275
- Scahill, L. "Epidemiology of Tic Disorders". Medical Letter: 2004 Retrospective Summary of TS Literature. Tourette Syndrome Association. The first page (PDF), is available at archive.org without subscription. Retrieved on June 11, 2007.
- Bloch, State, Pittenger 2011. See also Zohar AH, Apter A, King RA, et al. "Epidemiological studies". In Leckman JF, Cohen DJ. Tourette's Syndrome—Tics, Obsessions, Compulsions: Developmental Psychopathology and Clinical Care. John Wiley & Sons, Inc., New York. 1999:177–92. ISBN 0-471-16037-7 Search this book on .
- Bloch, State, Pittenger 2011. See also Schapiro 2002 and Coffey BJ, Park KS. "Behavioral and emotional aspects of Tourette syndrome". Neurol Clin. 1997 May;15(2):277–89. PMID 9115461
- Hawley, JS. Tourette Syndrome. eMedicine (June 23, 2008). Retrieved on August 10, 2009.
- Leckman JF. "Tourette's syndrome". Lancet. 2002 Nov 16;360(9345):1577–86. doi:10.1016/S0140-6736(02)11526-1 PMID 12443611
- Teive HA, Chien HF, Munhoz RP, Barbosa ER. "Charcot's contribution to the study of Tourette's syndrome". Arq Neuropsiquiatr. 2008 Dec;66(4):918–21. PMID 19099145 as reported in Finger S. "Some movement disorders." In Finger S (ed). Origins of neuroscience: the history of explorations into brain function. New York: Oxford University Press, 1994:220–239.
- Germiniani FM, Miranda AP, Ferenczy P, Munhoz RP, Teive HA. Tourette's syndrome: from demonic possession and psychoanalysis to the discovery of gene. Arq Neuropsiquiatr. 2012 Jul;70(7):547–9. PMID 22836463
- Itard JMG. "Mémoire sur quelques functions involontaires des appareils de la locomotion, de la préhension et de la voix". Arch Gen Med. 1825;8:385–407. From Newman, Sara. "Study of several involuntary functions of the apparatus of movement, gripping, and voice" by Jean-Marc Gaspard Itard (1825) History of Psychiatry. 2006;17:333–39. doi:10.1177/0957154X06067668
- What is Tourette syndrome? Tourette Syndrome Association. Retrieved on January 14, 2012.
- Gilles de la Tourette G, Goetz CG, Llawans HL, trans. "Étude sur une affection nerveuse caractérisée par de l'incoordination motrice accompagnée d'echolalie et de coprolalie". In: Friedhoff AJ, Chase TN, eds. Advances in Neurology: Volume 35. Gilles de la Tourette syndrome. New York: Raven Press; 1982;1–16. Discussed at Black, KJ. Tourette Syndrome and Other Tic Disorders. eMedicine (March 30, 2007). Retrieved on August 10, 2009. Original text (in French). Retrieved on August 10, 2009.
- Robertson MM, Reinstein DZ. "Convulsive tic disorder: Georges Gilles de la Tourette, Guinon and Grasset on the phenomenology and psychopathology of Gilles de la Tourette syndrome". Behavioural Neurology, 1991;4(1), 29–56.
- Enersen, Ole Daniel. Georges Albert Édouard Brutus Gilles de la Tourette. Archived March 9, 2005, at the Wayback Machine WhoNamedIt.com Retrieved on May 14, 2007.
- Blue, Tina. Tourette syndrome. Essortment 2002. Pagewise Inc. Retrieved on August 10, 2009.
- Rickards H, Hartley N, Robertson MM. "Seignot's paper on the treatment of Tourette's syndrome with haloperidol. Classic Text No. 31". Hist Psychiatry. 1997 Sep;8 (31 Pt 3):433–36. PMID 11619589
- Gadow KD, Sverd J. "Attention deficit hyperactivity disorder, chronic tic disorder, and methylphenidate". Adv Neurol. 2006;99:197–207. PMID 16536367
- Walkup, JT, Mink, JW, Hollenback, PJ, (eds). Advances in Neurology, Tourette syndrome. Lippincott, Williams & Wilkins, Philadelphia, PA. 2006;99:xvi–xviii. ISBN 0-7817-9970-8 Search this book on . Google books.
- Sacks, O. The man who mistook his wife for a hat: and other clinical tales. Harper and Row, New York. 1985:92–100. ISBN 0-684-85394-9 Search this book on .
- Leckman JF, Cohen DJ. Tourette's Syndrome—Tics, Obsessions, Compulsions: Developmental Psychopathology and Clinical Care. John Wiley & Sons, Inc., New York. 1999:408. ISBN 0-471-16037-7 Search this book on .
- Leckman JF, Cohen DJ. Tourette's Syndrome—Tics, Obsessions, Compulsions: Developmental Psychopathology and Clinical Care. John Wiley & Sons, Inc., New York. 1999:18–19, 148–151; 408. ISBN 0-471-16037-7 Search this book on .
- Schuerholz LJ, Baumgardner TL, Singer HS, et al. "Neuropsychological status of children with Tourette's syndrome with and without attention deficit hyperactivity disorder". Neurology. 1996 Apr;46(4):958–65. PMID 8780072
- Schuerholz LJ, Cutting L, Mazzocco MM, et al. "Neuromotor functioning in children with Tourette syndrome with and without attention deficit hyperactivity disorder". J Child Neurol. 1997 Oct;12(7):438–42. PMID 9373800
- Portraits of adults with TS. Tourette Syndrome Association. Retrieved from July 16, 2011 archive.org version on December 21, 2011.
- Samuel Johnson. Tourette Syndrome Association. Retrieved from April 7, 2005 archive.org version on December 30, 2011.
- Pearce JM. "Doctor Samuel Johnson: 'the great convulsionary' a victim of Gilles de la Tourette's syndrome" (PDF). Journal of the Royal Society of Medicine. 1994 Jul;87(7):396–9. PMID 8046726
- Keilman, John. Reviews: The Game of Our Lives by David Goldblatt, The Keeper by Tim Howard. Chicago Tribune. January 22, 2015. Retrieved on March 21, 2015.
- Tim Howard receives first-ever Champion of Hope Award from the National Tourette Syndrome Association. Archived March 30, 2015, at the Wayback Machine Tourette Syndrome Association. October 14, 2014. Retrieved on March 21, 2015.
- Simkin B. "Mozart's scatological disorder". BMJ. 1992 Dec 19–26;305(6868):1563–7. PMID 1286388 Also see: Simkin, Benjamin. Medical and Musical Byways of Mozartiana. Fithian Press. 2001. ISBN 1-56474-349-7 Search this book on . Review, Retrieved on May 14, 2007.
- Did Mozart really have TS? Tourette Syndrome Association. Retrieved from April 7, 2005 archive.org version on December 30, 2011.
- Kammer T. "Mozart in the neurological department—who has the tic?" (PDF). Front Neurol Neurosci. 2007;22:184–92. PMID 17495512 doi:10.1159/0000102880 Retrieved on February 7, 2012.
- Ashoori A, Jankovic J. "Mozart's movements and behaviour: a case of Tourette's syndrome?" J Neurol Neurosurg Psychiatry. 2007 Nov;78(11):1171–5 doi:10.1136/jnnp.2007.114520 PMID 17940168.
- Sacks O. "Tourette's syndrome and creativity". BMJ. 1992 Dec 19–26;305(6868):1515–6. doi:10.1136/bmj.305.6868.1515 PMID 1286364
- Voss H. The representation of movement disorders in fictional literature. J Neurol Neurosurg Psychiatry. 2012 Oct;83(10):994–9. PMID 22752692 doi:10.1136/jnnp-2012-302716
- Holtgren, Bruce. "Truth about Tourette's not what you think". Cincinnati Enquirer. January 11, 2006. "As medical problems go, Tourette's is, except in the most severe cases, about the most minor imaginable thing to have. ... the freak-show image, unfortunately, still prevails overwhelmingly. The blame for the warped perceptions lies overwhelmingly with the video media – the Internet, movies and TV. If you search for 'Tourette' on Google or YouTube, you'll get a gazillion hits that almost invariably show the most outrageously extreme examples of motor and vocal tics. Television, with notable exceptions such as Oprah, has sensationalized Tourette's so badly, for so long, that it seems beyond hope that most people will ever know the more prosaic truth."
- US media:
- Oprah and Dr. Laura – Conflicting Messages on Tourette Syndrome. Oprah Educates; Dr. Laura Fosters Myth of TS as "Cursing Disorder". Tourette Syndrome Association. May 31, 2001. Retrieved from October 6, 2001 archive.org version on December 21, 2011.
- Letter of response to Dr. Phil. Tourette Syndrome Association. Retrieved from August 31, 2008 archive.org version on December 21, 2011.
- Letter of response to Garrison Keillor radio show. Tourette Syndrome Association. Retrieved from February 7, 2009 archive.org version on December 21, 2011.
- UK media:
- Guldberg, Helene. Stop celebrating Tourette's. Spiked. May 26, 2006. Retrieved on December 26, 2006.
- Kushner, HI. A Cursing Brain?: The Histories of Tourette Syndrome. Harvard University Press. 2000. ISBN 0-674-00386-1 Search this book on ..
- Olson, S. "Making Sense of Tourette's" (PDF). Science. 2004 Sep 3;305(5689):1390–92. doi:10.1126/science.305.5689.1390 PMID 15353772
|Wikimedia Commons has media related to Tourette syndrome.|
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Coding for Burns
Approximately every minute, someone in the United States sustains a burn injury serious enough to require treatment. According to the American Burn Association, an estimated 486,000 hospital admissions and visits to hospital emergency departments occur annually for burn evaluation and treatment in the United States. The likelihood for a medical coder to have to code a burn case is extremely high. Here’s what you need to know.
A burn is tissue damage with partial or complete destruction of the skin caused by heat, chemicals, electricity, sunlight, or nuclear radiation. Proper selection of burn codes requires consideration of the location of the burn, severity, extent, and external cause in addition to laterality and encounter. ICD-10 makes a distinction between burns and corrosions:
- Burn codes apply to thermal burns (except sunburns) that come from a heat source, such as fire, hot appliance, electricity, and radiation.
- Corrosions are burns due to chemicals.
Burn severity is classified based on the depth of the burn. There are six degrees of burns:
- First-degree burns damage the outer layer (epidermis) of the skin; erythema
- Second-degree burns indicate blistering with damage extending beyond the epidermis partially into the layer beneath it (dermis)
- Third-degree burns indicate full-thickness tissue loss with damage or complete destruction of both layers of skin (including hair follicles, oil glands, & sweat glands)
ICD-10 Coding Using the “Rules of Nines”
You need at least three codes to properly report burn diagnoses:
First-listed code(s): S/S for site and severity (categories T20-T25)
- Your first-listed code will be a combination code that reports both the site and severity of the injury. The descriptions of codes in the T20-T28 range are first defined by an anatomical location of the body affected by burn or corrosion.
- The fourth character for each category identifies the severity (except categories T26-T28). Using the layers of the skin, the severity of a burn is identified by degree.
- The fifth character reports additional details regarding the anatomical site of the burn.
- The sixth character represents laterality.
Next listed code: E for extent (categories T31/32)
- Burns and corrosions are classified according to the extent, or percentage, of the total body surface area involved (TBSA).
- Code T31 to report a burn and T32 to report corrosion, based on the classic “rule of nines.”
- The rule of nines, for adult patients, assigns 1% of TBSA to the genitalia, and multiples of 9% to other body areas (9% head, 9% per arm, 18% per leg, etc.).
- A modified rule of nines is applied for infants, to account for their relatively larger head (18%) and smaller legs (14%, each).
- The required fourth character identifies the percentage of the patient’s entire body affected by burns. The fifth character identifies the percentage of the patient’s body that is suffering from third-degree burns or corrosions only.
Lastly, code(s): E for external cause code(s)
- External Cause – To identify the source, place, and intent of the burn.
- Agent – To identify the chemical substance of the corrosion.
ICD-10-CM guidelines recommend reporting appropriate external cause codes for burn patients. Not all payers accept these codes, however.
CPT Coding Using the Lund-Browder Classification
CPT codes to report local treatment of burns and many skin grafting procedure codes, specify the surface area (TBSA) treated. CPT® utilizes the more precise Lund-Browder classification method to calculate TBSA for burns and grafts. Lund-Browder divides the body into 19 distinct areas and specifies six different age groups to account for the changes in body composition during development into adulthood.
The CPT® code book contains a Lund-Browder classification method chart for easy TBSA calculation by body area and patient age. | <urn:uuid:a072bfe9-f101-42a3-af45-902693cbf7a3> | {
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Cysticercosis Classification and external resources
Magnetic resonance image of a patient with neurocysticercosis demonstrating multiple cysticerci within the brain.
ICD-10 B69 ICD-9 123.1 DiseasesDB 3341 MedlinePlus 000627 eMedicine emerg/119 med/494 ped/537 MeSH D003551
Cysticercosis refers to tissue infection after exposure to eggs of Taenia solium, the pork tapeworm. The disease is spread via the fecal-oral route through contaminated food and water, and is primarily a food borne disease. After ingestion the eggs pass through the lumen of the intestine into the tissues and migrate preferentially to the brain and muscles. There they form cysts that can persist for years. In some cases the cysts will eventually cause an inflammatory reaction presenting as painful nodules in the muscles and seizures when the cysts are located in the brain. Symptomatic disease from Taenia solium cysts in the brain is referred to as neurocysticercosis and is the most common helmenthic (tapeworm) infection of the brain worldwide. Cysticercosis should be differentiated from taeniasis: carriage of the adult tapeworm in the intestine (which is through ingestion of cysts in an intermediate host, not the ingestion of the eggs as in cysticerosis). These represent two different stages of the parasite’s life cycle. Though both forms of infection can potentially occur in the same individual at the same time, they are distinct disease entities and have different treatments and potential outcomes.
The cause of human cysticercosis is the larval form of Taenia solium (pork tapeworm). T. solium is a member of Phylum Platyhelminthes, class Cestoda, Order Cyclophyllidea and family Taeniidae. The common larval stage of T. solium was also known as Cysticercus cellulosae.
History of discovery
The earliest reference to tapeworms were found in the works of ancient Egyptians that date back to almost 2000 BC. The description of measled pork in the History of Animals written by Aristotle (384–322 BC) showed that the infection of pork with tapeworm was known to ancient Greeks at that time. It was also known to Jewish and later to early Muslim physicians and has been proposed as one of the reasons for pork being forbidden by Jewish and Islamic dietary laws. Recent examination of evolutionary histories of hosts and parasites and DNA evidence show that over 10,000 years ago, ancestors of modern humans in Africa became exposed to tapeworm when they scavenged for food or preyed on antelopes and bovids, and later passed the infection on to domestic animals such as pigs.
Cysticercosis was described by Johannes Udalric Rumler in 1555; however, the connection between tapeworms and cysticercosis had not been recognized at that time. Around 1850, Friedrich Küchenmeister fed pork containing cysticerci of T. solium to humans awaiting execution in a prison, and after they had been executed, he recovered the developing and adult tapeworms in their intestines. By the middle of the 19th century, it was established that cysticercosis was caused by the ingestion of the eggs of T. solium.
Humans are T. solium reservoirs. They are infected by eating undercooked pork that contains viable cysticerci. The cysticercus develops into an adult tape worm in the gut and produces large numbers of eggs which pass out in the feces. The presence of an adult tape worm in the gut is reasonably harmless. The condition known as cysticercosis in humans occurs due to the ingestion of tape worm eggs, either from external sources or from the person's own feces. The human has then become an accidental and "dead-end" intermediate host (that is, the infection can not progress any further). Pigs, which are the "normal" intermediate host for this parasite, get infected with cysticerci when they ingest human feces. The incubation period ranges from months to over ten years.
T. solium worms may reach a length of several meters. The scolex has four suckers, and a double crown of prominent hooks, which attach to the intestinal mucosa. T. solium eggs are spherical and 30 to 40 µm in diameter.
The cysticercus larva completes development in about 2 months. It is semitransparent, opalescent white, and elongate oval in shape and may reach a length of 0.6 to 1.8 cm.
The life cycle involves humans as a definite host and pigs as an intermediate host. Pigs ingest contaminated food or water that contains eggs or proglottids from human’s feces. The ova develop into cysticercus in pig muscles. Human becomes infected when they ingest raw or undercooked “measly pork” that contains viable cysticercus. Upon reaching the small intestine, the scolex attaches to the intestinal wall and a proglottid chain grows. T. solium releases three to six proglottids/day, bearing 30,000 to 70,000 eggs (ova) per proglottid into the intestine. Nearly 250,000 ova are passed daily into the human feces and to the environment, and the cycle continues. Infections with cysticercus occur after humans consume the ova from exogenous sources or through self-infection via the fecal-oral route. Humans, in this case, are intermediate hosts. Ova are digested in the stomach and release oncospheres which penetrate the intestinal wall and reach the bloodstream. These oncospheres develop into cysticerci in any organ but are common in brain, subcutaneous tissue, or eyes.
Clinical presentations in humans
Cysticercosis in muscles
Cysticerci can develop in any voluntary muscle in humans. Invasion of muscle by cysticerci can cause myositis, with fever, eosinophilia, and muscular pseudohypertrophy, which initiate with muscle swelling and later progress to atrophy and fibrosis. In most cases, it is asymptomatic since the cysticerci die and become calcified.
In some cases, cysticerci may be found in the globe, extraocular muscles, and subconjunctiva. Depending on the location, they may cause visual difficulties that fluctuate with eye position, retinal edema, hemorrhage, a decreased vision or even a visual loss.
Subcutaneous cysts are in the form of firm, mobile nodules, occurring mainly on the trunk and extremities. Subcutaneous nodules are sometimes painful.
The traditional method of demonstrating tapeworm eggs in stool samples diagnoses only taeniasis, carriage of the tapeworm stage of the life cycle. Only a small minority of patients with cysticercosis will harbor a tapeworm, rendering stool studies ineffective for diagnosis.
In CDC’s immunoblot assay, cysticercosis-specific antibodies can react with structural glycoprotein antigens from the larval cysts of T. solium. However this is mainly a research tool not widely available in clinical practice and nearly unobtainable in resource limited settings.
The diagnosis of neurocysticercosis is mainly clinical, based on a compatible presentation of symptoms and findings of imaging studies. Neuroimaging with CT or MRI is the most useful method of diagnosis. CT scan shows both calcified and uncalcified cysts, as well as distinguishing active and inactive cysts. MRI is more sensitive in detection of intraventricular cysts.
Management and therapy
Neurocysticercosis most often presents as headaches and acute onset seizures, thus the immediate mainstay of therapy is anticonvulsant medications. Once the seizures have been brought under control, antihelminthic treatments may be undertaken. The decision to treat with antiparasitic therapy is complex and based on the stage and number of cysts present, their location, and the patient's specific clinical presentation. Antiparasitic treatment should be given in combination with corticosteroids and anticonvulsants to reduce inflammation surrounding the cysts and lower the risk of seizures. Albendazole is generally preferable over praziquantel due to its lower cost and fewer drug interactions.
Asymptomatic cysts, such as those discovered incidentally on neuroimaging done for another reason, may never lead to symptomatic disease and in many cases do not require therapy.
Calcified cysts have already died and involuted. Further antiparasitic therapy will be of no benefit.
Surgical intervention is much more likely to be needed in cases of intraventricular, racemouse, or spinal neurocysticercosis. Treatments includes direct excision of ventricular cysts, shunting procedures, and removal of cysts via endoscopy.
In ophthalmic disease surgical removal is necessary for cysts within the eye itself, while antihelminth drug with steroids alone might be sufficient to treat cysts outside globe. Treatment recommendations for subcutaneous cysticercosis includes surgery, praziquantel and albendazole.
In general, subcutaneous disease does not need specific therapy. Painful or bothersome cysts can be surgically excised.
Public health and prevention strategies
Cysticercosis is considered as “tools-ready disease” according to WHO. International Task Force for Disease Eradication in 1992 reported that cysticercosis is potentially eradicable. It is feasible because there are no animal reservoirs besides humans and pigs. The only source of T. solium infection for pigs is from humans, a definite host. Theoretically, breaking the life cycle seems easy by doing intervention strategies from various stages in the life cycle.
- Massive chemotherapy of infected individuals, improving sanitation, and educating people are all major ways to discontinue the cycle at Step 1, in which eggs from human feces are transmitted to other humans and/or pigs.
- Cooking of pork or freezing it and inspecting meat are effective means to cease the life cycle at Step 3.
- The management of pigs by treating them or vaccinating them is another possibility to intervene Step 4 of the life cycle.
- The separation of pigs from human faeces by confining them in enclosed piggeries. In Western European countries post World War 2 the pig industry developed rapidly and most pigs were housed. This was the main reason for pig cysticercosis largely being eliminated from the region. This of course is not a quick answer to the problem in developing countries.
Intervention by concurrent treatment of humans and pigs
The intervention strategies to eradicate cysticercosis includes surveillance of pigs in foci of transmission and massive chemotherapy treatment of humans. In reality, control of T. solium by a single intervention, for instance, by treating only human population will not work because the existing infected pigs can still carry on the cycle. The proposed strategy for eradication is to do multilateral intervention by treating both human and porcine populations. It is feasible because treatment pigs with oxfendazole have been shown to be effective and once treated, they are protected from further infections for at least 3 months.
Even with the concurrent treatment of humans and pigs, complete elimination is hard to achieve. In one study conducted in 12 villages in Peru, both humans and porcine were treated with praziquantel and oxfendazole, with the coverage of more than 75% in humans and 90% in pigs The result shows a decreased in prevalence and incidence in the intervention area; however the effect did not completely eliminate T. solium. The possible reason includes the incomplete coverage and re-infection. Even though T. solium could be eliminated through mass treatment of human and porcine population, it is not sustainable. Moreover, both tapeworm carriers of humans and pigs tend to spread the disease from endemic to non-endemic areas resulting in periodic outbreaks of cysticercosis or outbreaks in new areas.
Vaccine against porcine cysticercosis
Given the fact that pigs are part of a life cycle, vaccination of pigs is another feasible intervention to eliminate cysticercosis. Research studies have been focusing on vaccine against cestode parasites, since many immune cell types are found to be capable of destroying cysticercus. Many vaccine candidates are extracted from antigens of different cestodes such as T. solium, T. crassiceps, T. saginata, T. ovis and target oncospheres and/or cysticerci. In 1983, Molinari et al. reported the first vaccine candidate against porcine cysticercosis using antigen from cysticercus cellulosae drawn out from naturally infected. Recently, vaccines extracted from genetically engineered 45W-4B antigens have been successfully tested to pigs in an experimental condition. This type of vaccine can protect against cysticercosis in both Chinese and Mexican type of T. solium. However, it has not been tested in endemic field conditions, which is important because the realistic condition in the field differ greatly from experimental condition, and this can result in a great difference in the chances of infection and immune reaction.
The S3PVAC vaccine
The vaccine constituted by 3 peptide synthetically produced (S3Pvac) has proven its efficacy in natural conditions of transmission. The S3PVAC vaccine so far, can be considered as the best vaccine candidate to be used in endemic areas such as Mexico (20). S3Pvac consists of three protective peptides: KETc12, KETc1 and GK1, whose sequences belong to native antigens that are present in the different developmental stages of T. solium and other cestode parasites.
Non-infected pigs from rural villages in Mexico were vaccinated with S3Pvac and the vaccine reduced 98% the number of cysticerci and 50% the number of prevalence. The diagnostic method involves necropsy and tongue inspection of pigs. The natural challenge conditions used in the study proved the efficacy of the S3Pvac vaccine in transmission control of T. solium in Mexico. The S3Pvac vaccine is owned by the National Autonomous University of Mexico and the method of high scale production of the vaccine has already been developed. The validation of the vaccine in agreement with the Secretary of Animal Health in Mexico is currently in the process of completion. It is also hoped that the vaccine will be well-accepted by pig owners because they also lose their income if pigs are infected cysticercosis. Vaccination of pigs against cysticercosis, if succeeded, can potentially have a great impact on transmission control since there is no chance of re-infection once pigs receive vaccination.
Limitations of vaccines
Even though vaccines have been successfully generated, the feasibility of its production and usage in rural free ranging pigs still remains a challenge. If a vaccine is to be injected, the burden of work and the cost of vaccine administration to pigs will remain high and unrealistic. The incentives of using vaccines by pig owners will decrease if the vaccine administration to pigs takes time by injecting every single pig in their livestock. An oral vaccine is proposed to be more effective in this case as it can be easily delivered to the pigs with the food, though no one has ever achieved it yet.
Other types of interventions and limitations
Cysticercosis can also be prevented by routine inspection of meat and condemnation of measly meat by the local government. However, in areas where food is scarce, cyst-infected meat might be considered as wasted since pork can provide high quality protein. At times, infected pigs are consumed within the locality or sold at low prices to traffickers who take the uninspected pigs at urban areas for sale.
Due to these limitations, cysticercosis has not been eliminated in any endemic areas.
The tapeworm that causes cysticercosis is endemic to many parts of the world including China, Southeast Asia, India, sub-Saharan Africa, and Latin America. Some studies suggest that the prevalence of cysticercosis in Mexico is between 3.1 and 3.9 percent. Other studies have found the seroprevalence in areas of Guatemala, Bolivia, and Peru as high as 20 percent in humans, and 37 percent in pigs. In Ethiopia, Kenya and the Democratic Republic of Congo around 10% of the population is infected, in Madagascar 16%. The frequency has decreased in developed countries owing to stricter meat inspection, better hygiene and better sanitary facilities. The distribution of cysticercosis coincides with the distribution of T. solium. Cysticercosis is the most common cause of symptomatic epilepsy worldwide.
In Latin America, an estimated 75 million persons live in endemic areas and 400,000 people have symptomatic disease. Cysticercosis is also found to be associated with Hispanic ethnicity, immigrant status, and exposure to areas of endemicity. In the US, the disease is found in immigrants from Mexico, Central and South America. Current livestock for pigs in the U.S do not play a role in the transmission of Taenia solium, and thus cysticercosis in the U.S is an imported disease.
In the USA during 1990–2002, 221 cysticercosis deaths were identified. Mortality rates were highest for Latinos and men. The mean age at death was 40.5 years (range 2–88). Most patients, 84.6%, were foreign born, and 62% had emigrated from Mexico. The 33 US-born persons who died of cysticercosis represented 15% of all cysticercosis-related deaths. The cysticercosis mortality rate was highest in California, which accounted for ˜60% of all deaths.
In popular culture
- The first patient on the television show House (in the pilot episode) suffered from cysticercosis.
- In the crossover of the series Grey's Anatomy (season 5, episode 15) and Private Practice (season 2), Archer Montgomery, brother of Addison Forbes Montgomery, suffered from neurocysticercosis. He was cured via the surgical removal of the cysts by his former brother-in-law Derek Shepherd.
- Neurocysticercosis MR and CT scans
- ^ García HH, Evans CA, Nash TE, et al. (October 2002). "Current consensus guidelines for treatment of neurocysticercosis". Clin. Microbiol. Rev. 15 (4): 747–56. doi:10.1128/CMR.15.4.747-756.2002. PMC 126865. PMID 12364377. http://cmr.asm.org/cgi/pmidlookup?view=long&pmid=12364377.
- ^ Mandell, Douglas, and Bennett (2010). Principles and Practice of Infectious Diseases, 7th ed.. Churchill Livingstone. ISBN 978-0-443-06839-3
- ^ a b c Wadia, NH, Singh, G. “Taenia Solium: A Historical Note” Taenia Solium Cysticercosis: From Basic to Clinical Science CABI Publishing, 2002. 157-168.
- ^ Ancient Hebrew Medicine <http://www.healthguidance.org/entry/6309/1/Ancient-Hebrew-Medicine.html>
- ^ Oscar H. del Brutto, Brutto Et Al, Julio Sotelo, Gustavo C. Román (1998). Neurocysticercosis. Taylor and Francis. p. 3. ISBN 9026515138
- ^ http://www.ars.usda.gov/is/AR/archive/may01/worms0501.htm
- ^ a b Cox, F.E.G. “History of Human Parasitology” Clinical Microbiology Reviews. October 2002. 15(4) 595-612.
- ^ Küchenmeister, F. The Cysticercus cellulosus transformed within the organism of man into Taenia solium. Lancet 1861 i:39.
- ^ a b c d e f g h i Markell EK, John DT, Krotoski WA. Medical Parasitology Eighth Edition. Pennsylvania: Saunders, 1999.
- ^ a b c d e f g Davis, LE. “Neurocysticercosis” Emerging Neurological Infections edited by Power, C and Johnson RT. Taylor & Francis Group, 2005. 261-287.
- ^ a b c http://www.cdc.gov/ncidod/dpd/parasites/cysticercosis/factsht_cysticercosis.htm.
- ^ Kerstein AH, Massey AD (2010). "Neurocysticercosis". Kansas Journal of Medicine 3 (4): 52–4. http://archie.kumc.edu/handle/2271/867.
- ^ Suri A, Goel RK, Ahmad FU, Vellimana AK, Sharma BS, Mahapatra AK (2008 Jan). "Transventricular, transaqueductal scope-in-scope endoscopic excision of fourth ventricular neurocysticercosis: a series of 13 cases and a review.". Emerg Radiol. 1 (1): 35–9.
- ^ Hauptman JS, Hinrichs C, Mele C, Lee HJ (2005 Apr). "Radiologic manifestations of intraventricular and subarachnoid racemose neurocysticercosis.". J Neurosurg Pediatr 11 (3): 153–7.
- ^ Jang JW, Lee JK, Lee JH, Seo BR, Kim SH. (2010 Mar). "Recurrent primary spinal subarachnoid neurocysticercosis.". Spine 35 (5): E172–5. doi:10.1097/BRS.0b013e3181b9d8b6. PMID 20118838.
- ^ a b Wortman PD. “Subcutaneous cysticercosis” J Am Acad Dermatol. 1991 (2 Pt 2): 409-14.
- ^ HH Garcia, R Araoz, RH Gilman, J Valdez, AE Gonzalez, C Gavidia, ML Bravo, and VC Tsang (1998). "Increased prevalence of cysticercosis and taeniasis among professional fried pork vendors and the general population of a village in the Peruvian highlands. Cysticercosis Working Group in Peru". Am. J. Trop. Med. Hyg. 59 (6): 902–905. PMID 9886197.
- ^ White, Jr., A. Clinton (2009). "New developments in the management of neurocysticercosis". The Journal of Infectious Diseases 199 (9): 1261. doi:10.1086/597758. PMID 19358667.
- ^ Dimitrios K. Matthaiou, Georgios Panos, Eleni S. Adamidi,Matthew E. Falagas “Albendazole versus Praziquantel in the Treatment of Neurocysticercosis: A Meta-analysis of Comparative Trials” PLoS Negl Trop Dis. 2008 March; 2(3): e194
- ^ WHO, “Global Plan to Combat Neglected Tropical Diseases 2008-2015. World Health Organization 2007
- ^ a b CDC, International Task Force for Disease Eradication, 1992. MMWR weekly. 1992. 41(37); 691, 697-698. http://www.cdc.gov/mmwr/preview/mmwrhtml/00017648.htm
- ^ a b Schantz, P. “Eradication of T. solium Cysticercosis” International Conference on Emerging Infectious Diseases 2002. CDC. ftp://ftp.cdc.gov/pub/infectious_diseases/iceid/2002/pdf/schantz.pdf
- ^ a b Gonzalez AE, García HH, Gilman RH, Tsang VCW, Cysticercosis Working Group in Peru. “Control of Taenia solium” Acta Tropica 2003 87(1): 103-109.
- ^ Gonzalez, A.E., Gavidia, C., Falcon, N., Bernal, T., Verastegui, M., Garcia, H.H., Gilman, R.H., Tsang, V.C., 2001.“Protection of pigs with cysticercosis from further infections after treatment with oxfendazole.” Am. J. Trop. Med. Hyg.65, 15-18.
- ^ Garcia, H.H., 2002. “Effectiveness of an interventional control program for human and porcine Taenia solium cysticercosis in field conditions.” In: International Health. Johns Hopkins University, Baltimore, p. 250.
- ^ Gilman, R.H., Garcia, H.H., Gonzalez, A.E., Dunleavy, M., Verastegui, M., Peru, T.C.W.G.I., 1999. Short cuts to development: methods to control the transmission of cysticercosis in developing countries. In: Garci´a, H.H., Marti´nez, M. (Eds.), Taenia solium taeniasis/cysticercosis. Editorial Universo, Lima,313-326.
- ^ Margono, S.S., Subahar, R., Hamid, A., Wandra, T., Sudewi, S.S., Sutisna, P., Ito, A., 2001. “Cysticercosis in Indonesia: epidemiological aspects.” Southeast Asian J. Trop. Med.Public Health 32 (Suppl. 2), 79-84.
- ^ Wandra, T., Subahar, R., Simanjuntak, G.M., Margono, S.S.,Suroso, T., Okamoto, M., Nakao, M., Sako, Y., Nakaya, K., Schantz, P.M., Ito, A., 2000. Resurgence of cases of epileptic seizures and burns associated with cysticercosis in Assologaima, Jayawijaya, Irian Jaya, Indonesia, 1991-1995. Trans. R. Soc. Trop. Med. Hyg. 94: 46-50.
- ^ a b c d e f g Sciutto E, Fragoso G. Aluja, A.S.de, Hernandez M, Rosas G. Larralde, C. 2008 “Vaccines Against Cisticercosis” Current Topics in Medicinal Chemistry. 8: 415-423.
- ^ Molinari J. L, Meza R, Suarez B, Palacios S, Tato P, Retana A. 1983 “Taenia solium : immunity in hogs to the Cysticercus.”Exp. Parasitol 55: 340-57.
- ^ Luo X, Zheng Y, Hou J, Zhang S, Cai X. 2009 “Protection against Asiatic Taenia solium Induced by a Recombinant 45W-4B Protein Clinical and Vaccine Immunology, 16 (2): 230-232.
- ^ a b Huerta M, De Aluja AS, Fragoso G, Toledo A, Villalobos N, Hernandez M, Gevorkian G, Acero G, Diaz A, Alvarez I, Avila R, Beltran C, Garcia G, Martinez J J, Larralde C, Sciutto E. (2001) Synthetic peptide vaccine against Taenia solium pig cysticercosis: successful vaccination in a controlled field trial in rural Mexico. Vaccine 20: 262-6.
- ^ http://www-lab.biomedicas.unam.mx/cistimex/s1.html#capitulo6
- ^ Sciutto E, Morales J, Martinez JJ, Toledo A, Villalobos MN, Cruz-Revilla C, Meneses G, Hernandez M, Diaz A, Rodarte LF, Acero G, Gevorkian G, Manoutcharian, K, Paniagua J, Fragoso G, Fleury A, Larralde R De, Aluja AS, Larralde C. (2007) “Further evaluation of the synthetic peptide vaccine S3Pvac against Taenia solium cysticercosis in pigs in an endemic town of Mexico.” Parasitology 134: 129-33.
- ^ a b E-mail interview with Edda Sciutto. Feb 26 2009.
- ^ http://www.cwgesa.org/CWGESA%20Action%20Plan/CWGESA%20Action%20Plan.aspx
- ^ CWGESA. 5th General Assembly of the Cysticercosis Working Group in Eastern and Southern Africa. 2007. CIRAD http://pigtrop.cirad.fr/sp/recursos/publications/procedimientos/5th_general_assembly_of_the_cysticercosis_working_group_in_eastern_and_southern_africa
- ^ Morales J, Martínez JJ, Garcia-Castella J,Peña N, Maza V, Villalobos N, Aluja AS, Fleury A, Fragoso G, Larralde C, Sciutto E. (2006) “Taenia solium: the complex interactions, of biological, social, geographical and commercial factors, involved in the transmission dynamics of pig cysticercosis in highly endemic areas” Annals of Tropical Medicine and Parasitology, 100(2) 123-135.
- ^ Garcia HH, Gonzalez AE, Evans CA, Gilman RH. Cysticercosis Working Group in Peru. Taenia solium cystericercosis. Lancet 2003;362:547-556.
- ^ http://virtualmentor.ama-assn.org/2008/04/cprl1-0804.html
- ^ http://www.who.int/zoonoses/diseases/taeniasis/en/index.html
- ^ International League Against Epilepsy. Relationship between epilepsy and tropical diseases. Epilepsia 1994;35:89-93.
- ^ Bern C, Garcia HH, Evans C, Gonzalez AE, Verastegui M, Tsang VC, Gilman RH. “Magnitude of the disease burden from neurocysticercosis in a developing country.” Clin Infect Dis 1999 Nov 29 (5): 1203-9.
- ^ http://www.cdc.gov/EID/content/13/2/230.htm
Infectious diseases · Parasitic disease: helminthiases (B65–B83, 120–129) Flatworm/
(Trematode infection)Blood flukeLung flukeIntestinal flukeFasciolopsis buski (Fasciolopsiasis)
(Filariasis)ThelazioideaSpiruroideaEnterobius vermicularis (Enterobiasis · Pinworm)
helm, arth (lice), zoon
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Cysticercosis — An infection caused by the pork tapeworm, Taenia solium. Infection occurs when the tapeworm larvae enter the body and form cysticerci (SIS tuh sir KEY) (cysts). When cysticerci are found in the brain, the condition is called neurocysticercosis… … Medical dictionary
cysticercosis — noun (plural cysticercoses) Etymology: New Latin Date: 1905 infestation with or disease caused by cysticerci … New Collegiate Dictionary
Cysticercosis — Klassifikation nach ICD 10 B69 Zystizerkose B69.0 Zystizerkose des Zentralnervensystems B69.1 Zystizerkose der Au … Deutsch Wikipedia
cysticercosis — n. [Gr. kystis, bladder; osis, suff. denoting disease] An infection with one or more cysticerci … Dictionary of invertebrate zoology
cysticercosis — /sis teuh seuhr koh sis/, n. Pathol. infestation with the larval form of beef or pork tapeworm, producing fever, malaise, muscle pain, and other symptoms depending on the area of the body affected. [1900 05; CYSTICERC(US) + OSIS] * * * … Universalium
cysticercosis — noun A common parasitic infestation of the central nervous system, caused by the ingestion of eggs or larvae of the tapeworm Taenia solium. Syn: neurocysticercosis … Wiktionary
cysticercosis — cys·ti·cer·co·sis … English syllables
cysticercosis — n. a disease caused by the presence of tapeworm larvae (see cysticercus) of the species Taenia solium in any of the body tissues. Humans become infected on ingesting tapeworm eggs in contaminated food or drink. The presence of cysticerci in the… … The new mediacal dictionary
cysticercosis — cys•ti•cer•co•sis [[t]ˌsɪs tə sərˈkoʊ sɪs[/t]] n. pat infestation with larvae of the pork or beef tapeworm that have migrated from the intestines to other body parts • Etymology: 1900–05 … From formal English to slang
cysticercosis — … Useful english dictionary | <urn:uuid:3932c2a4-45ef-4548-9252-f42ef91e50b2> | {
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Dysplastic nevus Classification and external resources ICD-10 D48.5 (ILDS D48.540) ICD-9 238.2 ICD-O: M8727/0 OMIM 155600 MeSH D004416
A dysplastic nevus (also known as a: Atypical mole, Atypical nevus, B-K mole, Clark's nevus, Dysplastic melanocytic nevus, Nevus with architectural disorder) is an atypical melanocytic nevus; a mole whose appearance is different from that of common moles. Dysplastic nevi are generally larger than ordinary moles and have irregular and indistinct borders. Their color frequently is not uniform and ranges from pink to dark brown; they usually are flat, but parts may be raised above the skin surface. Dysplastic nevi can be found anywhere, but are most common on the trunk in men, and on the calves in women. In 1992, the NIH recommended that the term "dysplastic nevus" be avoided in favor of the term "atypical mole."
According to the National Cancer Institute, researchers have shown that atypical moles are more likely than ordinary moles to develop into a type of skin cancer called melanoma. It is worth noting that the vast majority of atypical moles will never become malignant. However, numerous studies indicate that about half of melanomas arise from atypical moles. Evidence supporting this connection arises from clinical photodocumentation of evolving lesions, patient self-reports of changing lesions, pathology studies showing dysplastic nevi in histologic contiguity with melanoma, and epidemiology studies indicating that about half of individuals affected by melanoma also have atypical moles. Epidemiology studies have also shown that individuals with multiple dysplastic nevi are at much higher risk for developing melanomas. Because of this, moles should be checked regularly by a doctor or nurse specialist, especially if they look complex; grow larger; or change in color, or shape; or if any changes occur, such as itching, flaking or oozing.
Precaution for individuals with dysplastic nevi
Although there are limited data to support its efficacy, skin self-examination is frequently recommended for preventing melanoma (by identifying atypical moles that can be removed) or for early detection of existing tumors. Examination by a dermatologist has been shown to be beneficial for early melanoma detection. Some dermatologist recommend that an individual with either histologic diagnosis of dysplastic nevus, or clinically apparent atypical moles should be examined by an experienced dermatologist with dermatoscopy once a year (or more frequently). [[Image:WB032021.JPG|thumb|230px|
The acronym ABCDE has been useful for helping health care providers and laypersons remember the key characteristics of a melanoma (see "ABCDE" mnemonic below) moles Changes (in shape, size, color, itching or bleeding) should be brought to the attention of a dermatologist .
A popular method for remembering the signs and symptoms of melanoma is the mnemonic "ABCDE":
- Asymmetrical skin lesion.
- Border of the lesion is irregular.
- Color: melanomas usually have multiple colors.
- Diameter: moles greater than 6 mm are more likely to be melanomas than smaller moles.
- Evolution: The evolution (ie change) of a mole or lesion may be a hint that the lesion is becoming malignant.
The E is sometimes omitted, as in the ABCD guideline. A weakness in this system is the D. Many melanomas present themselves as lesions smaller than 6 mm in diameter. An astute physician will examine all abnormal moles, including ones less than 6 mm in diameter. Unfortunately for the average person, many seborrheic keratosis, some lentigo senilis, and even warts may have ABCD characteristics, and cannot be distinguished from a melanoma without a trained eye or dermatoscopy.
A recent and novel method of melanoma detection is the "Ugly Duckling Sign" It is simple, easy to teach, and highly effective in detecting melanoma. Simply, correlation of common characteristics of a person's skin lesion is made. Lesions which greatly deviate from the common characteristics are labeled as an "Ugly Duckling", and a dermatologist exam is required. The "Little Red Riding Hood" sign, suggests that individuals with fair skin and light colored hair might prove more challenging. These fair skinned individuals often have lightly pigmented or amelanotic melanomas which will not present with easy to observe color changes and variation in colors. The borders of these amelanotic melanomas are often indistinct, making visual identification without a dermatoscope (dermatoscopy) very difficult. A dermatoscope must be used to detect "ugly ducklings" among those with light skin or blonde/red hair.
People with a personal or family history of skin cancer or of dysplastic nevus syndrome (multiple atypical moles) should see a dermatologist at least once a year to be sure they are not developing melanoma.
When an atypical mole has been identified, a skin biopsy takes place in order to best diagnose it. Local anesthetic is used to numb the area, then the mole is biopsied. The biopsy material is then sent to a laboratory to be evaluated by a pathologist. A skin biopsy can be a punch, shave, or complete excision. The complete excision is the preferred method, but a punch biopsy can suffice if the patient has cosmetic concerns (i.e. the patient does not want a scar) and the lesion is small. A scoop or deep shave biopsy is often advocated, but should be avoided due to risk of a recurrent nevus, which can complicate future diagnosis of a melanoma, and the possibility that resulting scar tissue can obscure tumor depth if a melanoma is found to be present and re-excised.
Most dermatologists and dermatopathologists use a system devised by the NIH for classifying melanocytic lesions. In this classification, a nevus can be defined as benign, having atypia, or being a melanoma. A benign nevus is read as (or understood as) having no cytologic or architectural atypia. An atypical mole is read as having architectural atypia, and having (mild, moderate, or severe) cytologic (melanocytic) atypia. Usually, cytologic atypia is of more important clinical concern than architectural atypia. Usually, moderate to severe cytologic atypia will require further excision to make sure that the surgical margin is completely clear of the lesion.
The most important aspect of the biopsy report is that the pathologist indicates if the margin is clear (negative or free of melanocytic nevus), or if further tissue (a second surgery) is required. If this is not mentioned, usually a dermatologist or clinician will require further surgery if moderate to severe cytologic atypia is present - and if residual nevus is present at the surgical margin.
Dysplastic nevus syndrome
"Dysplastic nevus syndrome" refers to individuals who have high numbers of benign moles and also have dysplastic nevi. A small percent of these individuals are members of melanoma kindreds. Inherited dysplastic nevus syndrome is an autosomal dominant hereditary condition. Dysplastic nevi are more likely to undergo malignant transformation when they occur among members of melanoma families. At least one study indicates a cumulative lifetime risk of nearly 100% in individuals who have dysplastic nevi and are members of melanoma kindreds. (ref needed) Roughly half of melanomas arise "de novo" on clear skin growth, whereas the other half arise within atypical moles. Those with dysplastic nevi have an elevated risk of melanoma. Such persons need to be checked regularly for any changes in their moles and to note any new ones. In 40-50% of cases, the disorder has been linked with germline mutations in the CDKN2A gene, which codes for p16 (a regulator of cell division).
- ^ Rapini, Ronald P.; Bolognia, Jean L.; Jorizzo, Joseph L. (2007). Dermatology: 2-Volume Set. St. Louis: Mosby. pp. 1732. ISBN 1-4160-2999-0.
- ^ "dysplastic nevus" at Dorland's Medical Dictionary
- ^ , (Sep 1992). "NIH Consensus conference. Diagnosis and treatment of early melanoma". JAMA 268 (10): 1314–9. doi:10.1001/jama.268.10.1314. PMID 1507379.
- ^ Friedman R, Rigel D, Kopf A (1985). "Early detection of malignant melanoma: the role of physician examination and self-examination of the skin". CA Cancer J Clin 35 (3): 130–51. doi:10.3322/canjclin.35.3.130. PMID 3921200.
- ^ http://www.skincancer.org/melanoma/Warning-Signs.html
- ^ a b Mascaro JM Jr, Mascaro JM. The dermatologist's position concerning nevi: a vision ranging from 'the ugly duckling' to 'little red riding hood'. Arch Dermatol 1998; 134:1484–5.
- ^ http://www.labpath.com/new1.html
- ^ "dysplastic nevus syndrome" at Dorland's Medical Dictionary
- ^ Pope DJ, Sorahan T, Marsden JR, Ball PM, Grimley RP, Peck IM (Sep 1992). "Benign pigmented nevi in children. Prevalence and associated factors: the West Midlands, United Kingdom Mole Study". Arch Dermatol. 128 (9): 1201–6. doi:10.1001/archderm.128.9.1201. PMID 1519934.
- ^ Goldgar DE, Cannon-Albright LA, Meyer LJ, Piepkorn MW, Zone JJ, Skolnick MH (Dec 1991). "Inheritance of nevus number and size in melanoma and dysplastic nevus syndrome kindreds". J Natl Cancer Inst. 83 (23): 1726–33. doi:10.1093/jnci/83.23.1726. PMID 1770551. http://jnci.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=1770551.
Gonadal tumors, paraganglioma, and glomus (ICD-O 8590-8719) Gonadal/
sex cord-gonadal stromal (8590-8679)
Glomus tumors (8680-8719)
tumr, epon, para
Tumors: Skin neoplasm, Nevi and melanomas (C43/D22, 172/216, ICD-O 8720-8799) MelanomaMucosal melanoma · Superficial spreading melanoma · Nodular melanoma · lentigo (Lentigo maligna/Lentigo maligna melanoma, Acral lentiginous melanoma)Amelanotic melanoma · Desmoplastic melanoma · Melanoma with features of a Spitz nevus · Melanoma with small nevus-like cells · Polypoid melanoma · Soft-tissue melanoma Nevus/
Balloon cell nevus · Dysplastic nevus/Dysplastic nevus syndrome
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Look at other dictionaries:
dysplastic nevus — dysplastic melanocytic nevus a type of acquired, atypical melanocytic nevus with an irregular border, indistinct margin, and mixed coloring, characterized by dysplastic melanocytes in the epidermis. Particularly in patients with other family who… … Medical dictionary
dysplastic nevus — An atypical mole; a mole whose appearance is different from that of a common mole. A dysplastic nevus is generally larger than an ordinary mole and has irregular and indistinct borders. Its color frequently is not uniform and ranges from pink to… … English dictionary of cancer terms
dysplastic nevus syndrome — the occurrence of dysplastic nevi in persons having or at risk for having familial malignant melanoma. Called also atypical mole s., atypical nevus s., familial atypical mole–malignant melanoma s., and FAMMM s … Medical dictionary
Nevus of Ota — Classification and external resources ICD 10 D22.3 (ILDS D22.301) DiseasesDB … Wikipedia
Nevus — Not to be confused with Naevius, Nevis, or Nevius. Naevus and Nevi redirect here. For the British experimental rock group, see Naevus (band). For the Eritrean footballer, see Nevi Ghebremeskez. For the Norwegian bank, see Nevi (company). Nevus… … Wikipedia
nevus with architectural disorder — new name proposed for dysplastic nevus … Medical dictionary
Nevus — A pigmented spot on the skin, such as a mole. The plural of nevus is nevi. * * * 1. A circumscribed malformation of the skin, especially if colored by hyperpigmentation or increased vascularity; a n. may be predominantly epidermal, adnexal,… … Medical dictionary
Melanocytic nevus — Classification and external resources Mole, more specifically an intradermal nevus ICD 10 D22 … Wikipedia
Congenital melanocytic nevus — Classification and external resources Congenital nevus ICD 10 D22 (ILDS D22.L60) The congenital melanocytic nevus is a type of … Wikipedia
Blue nevus — Classification and external resources Micrograph of a blue nevus showing the characteristic pigmented melanocytes between bundles of collagen. H E stain … Wikipedia | <urn:uuid:7c3e3255-dabe-4920-8c04-dab81e5a971d> | {
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Types and Diagnosis of Cardiosclerosis
ICD-10( International Classification of Tenth Revision) includes all types of cardiosclerosis in the class of diseases of the heart and blood vessels( I20.0-I20.9).The terms used in Russia are adapted to ICD-10, but sometimes they do not coincide with it.
By the amount of damage to the heart muscle, 2 types are distinguished:
- focal cardiosclerosis - connective tissue appears in small patches, does not germinate the muscle through, is characteristic of acute myocarditis in children or adults, may not show any symptoms at all, is revealed during preventive examination;
- diffuse - the replacement of muscle tissue with scar tissue occurs intensively, captures large surfaces and the entire depth of the muscle. It often occurs against the background of coronary heart disease. Progression of the disease complicates the patient's condition.
In order to diagnose, the doctor should carefully read the history of the disease. The inquiry of the patient or parents of the child about the transferred diseases, allergic reactions, traumas and their treatment in this case is of great importance.
To establish the state of the heart muscle, such types of examinations as electrocardiography, echocardiography, ultrasound of the heart, radiographs help. These methods allow to evaluate the correctness and completeness of myocardial contractions, closure of the heart valves, to reveal the "working capacity" of individual muscle sites.
Clinical signs of cardiosclerosis
Cardiosclerosis manifests itself in three types of symptoms:
- heart rate abnormalities;
- appearance and increase of heart failure;
- myocardial ischemia.
Rhythm abnormalities in cardiosclerosis may occur suddenly or permanently due to physical exertion. The type of disorders depends on the location of the scar relative to the conduction system of the heart. The connective tissue "obstructs" the normal flow of the nerve impulse, forcing it to look for other ways. So there is an arrhythmia in the form of extrasystoles( extraordinary contractions), blockages of varying degrees, changes in rhythm in the form of frequent or rare pulse, atrial fibrillation.
Ventricular tachycardia and complete atrioventricular blockade are life-threatening.
If the rhythm of the patient is disturbed, palpitations, "irregularities" of the heart rhythm, dizziness, weakness, memory loss, loss of consciousness are possible.
Cardiac failure develops in the left or right ventricular type. The undisturbed part of the heart is forced to take on an increased load. The muscle thickens. But, despite this, oxygen in the tissues of the body is not enough. The first signs appear with little physical exertion or excitement. During a quiet walk disturb frequent heartbeats, shortness of breath. By the evening on the feet and legs, edema is noted. In the future, these symptoms occur without stress. At night, suffocation appears, a cough with pink phlegm. I have to sleep on high pillows. There are pressing pains in the right hypochondrium( due to the growth of stagnation in the liver).
Lung edema is dangerous for life, as an extreme degree of heart failure.
Symptoms of ischemia are associated with the increasing lack of nutrition of the heart muscle itself. Through the narrowed blood vessels there is little blood. The "starving" myocardium manifests itself as angina attacks with retrosternal pain during physical exertion and at rest. Pain is given to the left shoulder, arm, scapula. Sometimes they are "burning" in nature, accompanied by a feeling of pressure, lack of air. The lack of strength of the heartbeats reacts to the brain. There is dizziness, memory loss, loss of consciousness.
Prevention and treatment of cardiosclerosis
Prevention of cardiosclerosis is reduced to timely diagnosis and therapy of all diseases leading to scar replacement of muscle fibers. Particular attention should be paid to the prevention of infectious and allergic myocarditis. It is necessary to finish the sore throats, pass blood control tests, which allow to establish the activity of the inflammatory process. Electrocardiographic and ultrasound examination of children after a previous infectious disease will allow timely treatment of myocarditis and reduce the consequences to a minimum( there will be a small hem).Any suspicion of a pediatrician for listening to heart murmur should be confirmed by examination, consultation of a specialist, a pediatric cardiologist.
The intoxication of an adult organism with nicotine and alcohol minimizes immunity. Any infection in this case will lead to heart damage. Intensive development of atherosclerosis will further worsen the condition. Bad habits, malnutrition, stressful situations make the heart defenseless, contribute to the formation of cardiosclerosis.
Cigarette smoking causes great damage to the heart
Cardiosclerosis is incurable. It is impossible to replace scar tissue with a new one. Is that, heart transplant can solve all the problems completely. Studies on the use of stem cells for this purpose are still conducted only in the laboratory. It is necessary to remember that cardiosclerosis is superimposed on the underlying disease, which requires treatment.
In therapy, the doctor has only two options:
- to slow the process of sclerosing more normal muscle cells;
- help the heart to support activity in conditions of circulatory failure.
Importance is attached to adherence to a special diet.
To discharge the bloodstream, it is necessary to limit the consumption of liquid, salty and spicy foods. It is recommended to cook all food without salt. On the table for clarity, put a salt shaker with one teaspoon of salt( 5 g), this is the daily rate.
The products should include potassium-rich raisins, dried apricots, fruits and vegetables, boiled potatoes "in uniform", greens in the form of lettuce, dill, parsley, cabbage.
Compliance with the principles of an anti-cholesterol diet helps to slow the development of atherosclerotic cardiosclerosis. It is not recommended fried and fatty meat, butter, mayonnaise, confectionery, white bread, coffee and strong tea, sweet fizzy drinks. They need to be replaced with boiled poultry meat, fish, vegetable oil, honey, green tea, fruit drinks and fruit compotes and berries. It is recommended to refrain from everything that causes flatulence( bloating).
Drugs are prescribed only by a doctor, the dosage should be observed accurately and do not change independently.
- When establishing an infectious cause, antibiotics, antifungal, anti-inflammatory drugs are prescribed.
- Patients with cardiosclerosis should avoid stressful situations, take sedatives.
- Diuretics, cardiac glycosides, drugs that reduce oxygen consumption are prescribed to ease the load on the heart muscle.
- With a disturbed rhythm, you have to take constantly or from time to time antiarrhythmic drugs.
- Statins - prevent the deposition of cholesterol and the development of atherosclerosis of the heart vessels.
- Vasodilators help maintain blood supply to organs. Preparations containing nitrates are recommended only at high blood pressure.
Recommendations of traditional medicine
Folk recipes advise to use constantly instead of tea broth of dogrose, hawthorn, add cranberries to drinks. Tincture of clover and hawthorn in ready-made form is sold in a pharmacy. It has long been known the healing power of garlic, lemon and honey, twisted and mixed in approximately equal proportions.
The development of cardiosclerosis does not necessarily lead to a serious condition, if you take care of your heart in advance.
Causes of cardiosclerosis, and methods of its treatment
Cardiosclerosis is a violation of the tissue structure of the heart. It occurs in two forms: fine-focal cardiosclerosis and large-focal cardiosclerosis. What is it? As many remember from the course of school biology, our body consists of organs, and organs - from tissues. Fabric is a system of homogeneous cells that perform a single function. Each tissue in the body has its own purpose and takes its place in the "design" of the organs.
Epithelial tissue serves as an outer cover, both of the entire human body and of individual organs. The nerve tissue "works" as a conductor of signals between the brain and external "sensors" - receptors( actually the brain itself is a "clot" of nervous tissue).Muscle tissue has the property of contracting, obeying the signal-impulses coming from the brain and is the basis for the muscles of the body. The connective tissue serves as a support, the "skeleton" of the body, both internal( bone and cartilage) and external( dermis - the upper layer of the skin).
Transversely striated heart tissue
The basis for the structure of the heart is muscle tissue, but not ordinary. The cardiac muscle has a special fibrous structure and a characteristic structure, because of which the muscle tissue of the heart is called a striated muscle tissue. Transversely striated cardiac tissue, from which the myocardium is almost completely composed, the main part of the heart, is the most important property, without which the work of the heart would be impossible. The cardiac muscle can contract under the action of signals that originate in the cells of the heart tissue.
In addition to cardiac tissue, the heart has in its "design" the endocardial covering tissue, the inner surface of the heart wall, and the connective tissue - a thin film not more than half a millimeter in thickness, of which the epicardium consists. Everyone who has dealt with raw meat can imagine this film visually, a characteristic film covering individual muscles and veins of meat has a similar structure.
What is cardiosclerosis
With cardiosclerosis( from the Greek "cardia" - the heart and "scleras" - solid), the epicardium film connective tissue grows and thickens and gradually turns into a scar. The scar is a kind of connective tissue( some even call it - scar tissue) with an increased content of collagen, a protein that imparts tissue strength. The scar is formed where the tissue is regenerated, restored after damage. The scar can change over time with a normal cloth, and can remain for life, turning into a scar. Thus, cardiosclerosis is a scar on the heart.
Cardiosclerosis can be focal or diffuse. Diffuse cardiosclerosis( from the Latin diffusio - spread, spread) is a uniform thickening of the connective tissue throughout the entire area of the epicardium. May result without scar formation.
In focal( cicatricial) cardiosclerosis, the pathological proliferation of connective tissue is localized in the focal zones, where scars are formed. Most often, scar scarred cardiosclerosis is a consequence of myocardial infarction - necrosis( withering) of the site of the heart muscle.
How the disease develops
Thickened sclerotic connective tissue
Connective tissue, unlike muscle, can not shrink and produce useful work. If the epicardium of a healthy heart is a thin film and does not interfere with its work, the enlarged, pathologically thickened sclerotic connective tissue becomes a sensitive ballast for the heart. A hard, resilient scar prevents more cardiac contractions. The result is an increased stress on the heart, its early wear.
With the development of the disease in the absence of treatment, scar tissue begins to be more and more "implanted" into the muscle thickness of the heart wall, replacing the transverse striated cardiac tissue, gradually destroying the myocardium and deforming the heart valves.
Usually, cardiosclerosis is a so-called secondary disease. Depending on the causes of the occurrence of cardiosclerosis happens:
The cause of atherosclerotic cardiosclerosis
Occurs because of atherosclerosis, that is, clogging deposits, coronary vessels responsible for supplying oxygen and necessary substances of the myocardium and other parts of the heart. Lack of blood supply causes hypoxia( oxygen starvation) and metabolic disorders, which causes a complex of negative phenomena( including atrophy and death of individual myocardial fibers), one of which is cardiosclerosis.
Atherosclerotic cardiosclerosis has a chronic, diffuse character, manifests itself following symptoms:
- ischemic heart disease;
- angina - attacks of acute chest pain;
- arrhythmia - a violation of the rhythm of the heart.
Diagnosis of atherosclerotic cardiosclerosis includes an electrocardiogram, an echocardiogram and a blood test for the number of cholesterol and lipoproteins.
The result of atherosclerotic cardiosclerosis can be acquired heart disease, valve failure, aortic stenosis and bradycardia due to scarring of the heart valves and sinus node.
Myocarditis( myocarditis) cardiosclerosis
Heart affected by myocarditis
With this form of the disease, the scar is formed on the site of the cardiac muscle affected by myocarditis - zonal inflammatory myocardial lesion. Most often, myocarditis, and, consequently, myocarditis and cardiosclerosis are infectious, although they can sometimes be caused by allergic reactions, acute rheumatic fever( rheumatic carditis), and age-related changes.
Symptoms of myocarditis are:
- shortness of breath;
- pain and discomfort in the sternum;
- tachycardia - attacks of rapid heart rate;
However, it should be remembered that myocarditis cardiosclerosis in the initial stages can proceed without symptoms, which complicates the diagnosis and timely initiation of treatment.
Dead tissue of heart tissue
Postinfarction cardiosclerosis is the most dangerous form of the disease, requiring serious treatment. As the name suggests, the cause of cardiosclerosis in this case is myocardial necrosis of the myocardium due to impaired blood circulation. The dead tissue areas are replaced by scars, which further exacerbates the course of the disease. Symptoms of postinfarction cardiosclerosis include:
- shortness of breath;
- cardiac asthma - acute left ventricular failure;
- swelling of the legs and swelling of the veins on the neck due to cardiac asthma.
According to the degree of localization, postinfarction cardiosclerosis happens:
- fine-focal cardiosclerosis( disseminated cardiosclerosis)
- large-scleroid cardiosclerosis.
Diagnosis of the disease with the help of electrocardiography, echocardiography and fluoroscopy. Great importance for diagnosis, clarification of the picture and the choice of methods of treatment of the disease has a method of study, known as coronary angiography.
Coronary angiography is a fluoroscopic examination of coronary vessels. The heart, like other muscle tissues, is almost completely transparent to X-rays, so coronary vessels are specially "tinted" for research, launching into the blood a soluble, non-transparent material for X-rays( X-ray contrast).The introduction of "X-ray dye" is made by a catheter through the femoral artery. The "tinted" coronary system is clearly visible on the X-ray. Several pictures taken from different angles allow us to obtain a complete picture of the state of the coronary vessels.
Treatment of cardiosclerosis involves, firstly, the cure of a primary disease that caused the scarring of the heart tissue. Of course, this paragraph is applicable only in those cases when the disease did not lead to irreversible changes.
Medication for cardiosclerosis
Secondly, the growth processes of connective tissue and scar formation are slowing down. To this end, ACE inhibitors are used( substances that reduce blood pressure - enap, hood), nitrates( nitrosorbide, cardiac, isomonate, monomac), disaggregants( acetylsalicylic acid), diuretics, metabolism stimulating drugs( riboxin, panangin), b- adrenoblockers( propranolol, metoprolol).
Treatment is conducted in a hospital setting and is usually conservative( without surgery).An exception is the formation of an aneurysm - thinning and bloating of the vessel wall. In this case, urgent surgical treatment is indicated, in order to avoid internal hemorrhage.
Methods of cardiosclerosis prophylaxis and restorative procedures in the course of treatment are generally similar to the prevention of other cardiovascular diseases and include diet, exercise therapy, strict physical exertion, sanatorium therapy, etc.
Cardiosclerosis is a dangerous and serious disease, but with timely and competent treatment, the prognosis is usually positive. The main thing is not to run!
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Symptoms and Diagnosis of Cardiosclerosis of the Heart
Cardiosclerosis is characterized as a progressive pathology in which normal muscle tissue in the myocardium is replaced by an inelastic connective tissue. As a result of this process, the heart muscle loses its basic functions, that is, it ceases to carry out impulses and contract. Symptoms of cardiosclerosis depend not only on the form of the disease, but also on its localization. By the way, heart valves are subject to cardiosclerosis.
Cardiac sclerosis occurs in people of all ages. The causes of this pathological process differ and depend on many factors, including age.
The replacement of normal heart tissue in children, as a rule, is the outcome of inflammatory( dystrophic) processes in the myocardium. In adults, the cause of cardiosclerosis lies in the transferred heart diseases, metabolic disorders or, which is less common, as a result of changes that occur after inflammation in the myocardium.
So, the following factors lead to the development of the pathological process in the myocardium:
- First of all, this is the result of myocarditis, that is inflammation of the heart muscle;
- Another cause of cardiosclerosis is cardiomyopathy, that is, muscle damage as a result of a disturbance in its nutrition;
- Also the cause of this process may be ischemic heart disease;
- No less dangerous is the atherosclerosis of the coronary arteries, which arises due to a violation of blood supply and myocardial nutrition.
Dystrophic cardiosclerosis is likely with the following disorders and situations:
- dystrophic processes can be formed against a background of prolonged severe anemia;
- also with severe physical exertion( as a rule, in athletes);
- cardiosclerosis can result from any endocrine pathology - thyroid disease, obesity or diabetes;
- is no less dangerous and a violation of the exchange of vitamins, or rather their chronic deficiency;
- with intoxication;
- for amyloidosis, that is, a disease in which a special substance accumulates in the heart tissues;
- with hemosiderosis( impaired iron metabolism and its subsequent accumulation in tissues).
In atherosclerotic cardiosclerosis, the lumen of vessels with chronic shortage in the heart muscle of oxygen, as well as nutrients, is disturbed.
The development mechanism of
The reasons that we listed above lead to a shortage of oxygen in the tissues of the heart. Gradually, the normal muscles are replaced by a connective tissue that is incapable of carrying a functional load. Thus, the work of the heart begins to perform adjacent normal tissue sites.
As a result of this process, normal sections that perform double work are hypertrophied, that is, they increase due to their activity. However, such a heavy load the heart can not stand, so the "tired" muscles are replaced with a connective tissue. This tissue stretches, myocardial cavities widen, disrupting the circulation. All this leads to heart failure.
Varieties of cardiosclerosis
The degree of spread of the process implies two types of cardiosclerosis:
- focal cardiosclerosis( small patches have connective tissue, in fact, they are scars);
- diffuse cardiosclerosis( a situation where connective tissue actively replaces large areas of the myocardium).
Also cardiosclerosis is divided into certain forms, namely:
- primary cardiosclerosis( occurs against the background of systemic ailments of connective tissue);
- postinfarction( formed after myocardial infarction and forms a scar);
- myocarditis( develops against a background of severe inflammation of the muscle, while the vessels of the heart are not damaged);
- is a substitute cardiosclerosis, also called myofibrosis. With this form in place of "starving" muscle cells, scars form. Dying cells of the myocardium replace the connective tissue.
Large-scale cardiosclerosis, usually postnecrotic, characterized by the formation of large, large foci of scar tissue. While small-focal cardiosclerosis is characterized by small areas of scar tissue.
The severity of symptoms of large-focal and small-focal cardiosclerosis largely depends on the extent of damage to the heart muscles and the location of foci of connective tissue.
- pain in the chest during heavy loads;
- weakness and general impairment;
- pressure fluctuations.
A connective tissue site located in the area of the cardiac pathways can trigger the development of arrhythmia.
The most common diffuse form of cardiosclerosis. In this case, the patient feels the following symptoms of heart failure:
- swelling on the upper and lower extremities;
- shortness of breath;
- cough that occurs usually at night( due to congestion in the lungs);
- tachycardia and pressure reduction;
- in the abdominal and thoracic cavity accumulates fluid.
Complications of cardiosclerosis are dangerous and threaten:
- development of arrhythmia;
- aneurysm in localization sites. In this case, protrusion of the tissues is observed. The danger of a break is great;
- development of heart failure.
For diagnosis of pathology, a specialist should not only be aware of the patient's heart disease, but also carefully examine it and listen to complaints. To date, the main methods of diagnosing cardiosclerosis are:
- heart ultrasound, assessing contractility, structure, size and shape;
- vascular doplerography, assessing blood flow through coronary vessels, areas of myocardial ischemia and other indicators;
- ECG, showing the presence or absence of recent heart attacks, their localization;
- X-ray of the heart( for better visual assessment of its condition and size, it is better to do with several projections);
- MRI of the heart.
After diagnosing cardiosclerosis, do not ignore the recommendations of specialists, as it has already been said, the consequences can be severe and even lethal. Trust therapists and cardiologists who will help you stop the proliferation of connective tissue. If necessary, the help of cardiac surgeons will be needed, which will correct the changes in the heart surgically.
To my great regret, for today there are no methods or medicines that could cause the connective tissue to be transformed into a muscle tissue. Therefore, the whole emphasis in the treatment is on maintaining the remaining myocardium in an efficient state. It is also important to stop the proliferation of connective tissue.
In addition, in the treatment of cardiosclerosis, it is worth paying attention to the existing heart disorders, which were caused by a painful process:
- is used to treat myocardial dystrophy, and atherosclerosis;
- also needs treatment that will help to eliminate myocardial ischemia;
- it is necessary to take medications aimed at normalizing the heart rhythm. These drugs include cordarone, rhythm monm, amiodarone and others;
- is prescribed the administration of drugs aimed at activation and improvement of metabolic processes in the myocardium. These include dopamine, actovegin, simdaks, korglikon and others;
- an important role is played by diet. The patient should consume less salt and sugar, reduce the intake of foods containing cholesterol;
- loads should also be minimized;
- The last measure in the treatment of cardiosclerosis is surgical correction of aneurysms, implantation of pacemakers, etc.
The basis for the prevention of cardiosclerosis is to take care of it from a young age. It is important to monitor your diet and limit toxic effects. Timely treat a cold, sore throat and inflammation.
To all this, it is important to regularly monitor your blood pressure and vascular status, as well as overweight. | <urn:uuid:1b36c496-cdce-4a2c-9652-e8fe4b31d48b> | {
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Table of Contents
Dementia is defined as a decline in memory with the impairment of at least 1 other cognitive domain. Other cognitive functions that may be impaired include skilled movements, language, or executive functioning. To be classified as dementia, the impairment in memory and other cognitive functions must interfere with social and occupational functioning and cannot be accounted for by other psychiatric conditions or psychoses.
- Alzheimer’s disease is not synonymous with dementia but is the most common cause (75%).
- Dementia is not a feature of normal aging and is always indicative of pathology.
- Mild cognitive impairment (MCI) is a transition stage to Alzheimer’s disease; 10% of patients with MCI develop Alzheimer’s each year.
Dementia as a symptom complex
Dementia per se is not a diagnosis but a symptom complex that can occur as a consequence of different organic diseases. It is, therefore, a dementing syndrome, a state that is, according to the Tenth Revision of the International Statistical Classification of Diseases and Related Health Problems (ICD-10) criteria, characterized by:
- Impairment of memory
- Impairment of at least 1 other cognitive function such as thinking, orientation, perception, calculating ability, learning ability, language, and the ability to judge
- A change in emotional control, social behavior, and motivation, without impairment of consciousness, for a minimum of 6 months
The most common cause of dementia is Alzheimer’s disease (also known as Alzheimer’s dementia); this disease accounts for almost two-thirds of all dementia cases. This is followed by vascular dementia (15%) and combined forms of vascular and Alzheimer’s disease (15%). The remaining 10% of cases are caused by other neurological diseases or other disorders.
Dementia is age-related and has an estimated prevalence of 20% in those older than 85 years. Up to 11% of dementia cases are considered to be reversible. Early treatment in these cases can reverse the condition and restore normal functioning.
The first warning signs of dementia are often subtle and only apparent to close relatives, not to the affected person themselves. They include repetition of the same questions, a narration of an always identical story, and the misplacing of objects (often, others are accused of having misplaced the item). Secure handling of financial issues is lost, as well as the ability to properly care for oneself.
An extraordinary psychological strain arises for dementia patients, especially during the early phases of the disease. They suffer from apathy, aberrant motor behavior (wandering aimlessly), eating of non-edibles, irritability, aggression, sleep disturbances, and depression.
Insecure fine motor skills and decreased vocabulary accrue when the disease progresses. Inner self-reflection diminishes and unfounded outbursts of anger and violence occur. As the disease progresses, close relatives are no longer recognized and the ability to master everyday tasks is lost. Musculature shrinks and patients begin to suffer from urinary and fecal incontinence. Another characteristic is small, tripping steps.
The disease, in the end, leads to bedridden patients who are totally dependent on nursing care. Most patients only survive due to the implantation of a percutaneous endoscopic gastrostomy tube, as the ability to swallow is lost. Patients die due to pneumonia or heart failure.
Patients with Lewy body dementia suffer from hallucinations, which are mostly dominated by fear and feature topics such as kidnapping or similarly frightening scenarios.
Neuropsychological test devices for the diagnosis of dementia
The ICD-10 classification of mental and behavioral disorders criteria needs to be fulfilled in order to diagnose a dementing disorder. Neuropsychological test devices such as the Mini-Mental State Examination (MMSE), the clock-drawing test, and the DemTect test are used for diagnosis and quantify cognitive deficiencies.
The MMSE is a test for the detection of cognitive impairments. It includes questions and tasks in 10 categories:
- Orientation: 10 questions concerning temporal and spatial orientation (maximum 10 points)
- Retention: repeating 3 words, up to 3 repetitions (maximum 3 points)
- Attention and calculation: progressive subtraction by 7, starting at 100 (maximum 5 points with 5 correct calculation steps)
- Memory: remembering 3 words from the beginning (maximum 3 points)
- Naming: correct naming of 2 shown items (e.g., a watch, pencil; maximum 2 points)
- Repetition: e.g., “without fuss or quibble” (maximum 1 point)
- Active part and speech comprehension: e.g., “Take this piece of paper in your hands, fold it in the middle, and put it on the ground” (1 point for every correctly performed action; maximum 3 points)
- Reading: reading and performing an instruction (e.g., “close your eyes”; maximum 1 point)
- Writing: writing any sentence (maximum 1 point)
- Drawing: copying a given geometric figure (e.g., 2 interlocked pentagons; maximum 1 point)
The maximum obtainable score in the MMSE is 30 points. A score lower than 26 may indicate mild dementia.
|< 9||Severe dementia|
The clock test examines spatial imagination and visual thinking. The patient is asked to draw the dial of a clock including a time set by the examiner (e.g., 10 to 12). The presentation of the dial (recognizability of the clock, correct filling in of the digits), the position of the clock’s hands (correct presentation of the set time), and the size of the hands in relation to each other are evaluated using a grading system.
Understanding the possible reasons for cognitive decline is a key part of diagnosing either a potentially reversible or irreversible dementing disorder.
Potentially reversible dementing syndromes
Potentially reversible dementing disorders can arise within the scope of different diseases and disorders; this should be clarified as a possible reason before other investigations begin. They include the following:
- Psychiatric diseases (pseudodementia or depression-related cognitive dysfunction)
- Electrolyte imbalances
- Renal or liver dysfunction
- Endocrinological impairments (hyper- or hypothyreosis, diabetes mellitus (hypoglycemia))
- Malnutrition and hypovitaminosis (vitamin B12, B6, B3, or folic acid deficiency)
- Infectious diseases (syphilis, borreliosis, HIV)
- Overdose (e.g., from alcohol or digitalis glycosides)
- Metabolic diseases (e.g., Wilson’s disease)
- Autoimmune diseases (SLE, vascular inflammations, multiple sclerosis)
- Cerebral lesions (meningioma, metastasis)
- Traumatic brain injury
Irreversible dementing syndromes
Irreversible dementing disorders include different diseases that are characterized by structural brain damage. These include:
- Alzheimer dementia and vascular dementia, the main forms of dementia
- Frontotemporal dementia
- Lewy body dementia
- Dementia due to Parkinson’s disease
- Dementia due to Creutzfeldt-Jakob disease
- Dementia due to Huntington’s disease
Anamnesis, or a patient’s medical history, is also an essential part of diagnosing dementia. Subjective descriptions given by the patient (personal anamnesis), as well as descriptions from close relatives such as a spouse or children can give important clues to the underlying disease. A patient’s medical history should include the following:
- Primary diseases (exclusion of a reversible dementing syndrome)
- Development (subtle or acute beginning) and symptom expression (e.g., are there impairments in daily living?)
- Family anamnesis (Huntington’s disease, Parkinson’s disease)
- Cardiovascular risk factors/previous cardiovascular events (vascular dementia)
- Prior trauma
- Attendant symptoms such as a change in personality (frontotemporal dementia), gait disorder, or extrapyramidal movement disorders (Parkinson’s dementia, Lewy body dementia, subcortical dementia), visual hallucinations (Lewy body dementia), or urinary incontinence (normal pressure hydrocephalus)
Regular medication (e.g., drug-induced reversible dementing syndrome due to digitalis or benzodiazepine overdose)
Physical examination includes a thorough internal and neurological examination with a special focus on:
- Possible reasons for a reversible dementing syndrome
- Neurological disorders (reflex status, an examination of brain nerves and motor skills)
- Extrapyramidal movement disorders
- Gait disorders
- Signs of increased intracranial pressure (funduscopy)
Laboratory diagnostics and further instrument examinations
The following examinations should be part of the standard repertoire of every dementia diagnosis:
- Lab tests: blood count, electrolytes, transaminases, bilirubin, gamma-GT, AP, creatinine clearance, urea, vitamin B12, folic acid, glucose, TSH
- Imaging: computed tomography (CT) or magnetic resonance imaging (MRI) (to uncover possible cerebral tumor, bleeding, atrophy or infracted areas)
- ECG (electroencephalogram, for atrial fibrillation)
Optional examinations should also be carried out depending on the suspected diagnosis. These include:
- Laboratory examinations (e.g., syphilis and borreliosis serology, HIV test, CDT (for suspected alcohol abuse), copper (for Wilson’s disease) and B-vitamin test)
- Diagnosis of cerebrospinal fluid (especially in cases of suspected normal pressure hydrocephalus or Creutzfeldt-Jakob disease)
- EEG (repetitive triphasic waves with Creutzfeldt-Jakob disease)
Approach to the evaluation of patients with cognitive dysfunction
The assessment of cognitive function and dementia is often perceived as subjective. Accordingly, a stepwise approach that can help confirm the diagnosis of dementia and exclude the possible causes of potentially reversible dementia is recommended.
A detailed history should be taken. The main cognitive domain that is affected must be clearly defined from the history. It is important to document the onset and progression of cognitive decline since dementia is a progressive disease. The severity of functional impairment is also assessed in this step. A history of stroke, malignancy, metabolic derangements, or endocrinopathies needs to be explored. The patient’s medication list should also be noted.
A complete physical examination needs to be performed. A neurological examination is also a must for the evaluation of any patient with cognitive dysfunction.
Formal cognitive testing should be attempted. This can be done using an MMSE, the Blessed dementia scale, Alzheimer’s disease assessment, or a national adult reading test.
All patients presenting with new-onset dementia need to have a complete blood cell count, electrolytes, renal, liver, and thyroid function tests taken, as well as tests for vitamin B12 levels and routine relative peak ratio. These tests can help exclude some common potential causes of reversible dementia such as anemia.
Some patients, such as those with alcohol-use disorders, should also undergo thiamine testing. Patients who partake in high-risk sexual behavior should be given an HIV test. Rheumatologic screening is indicated in patients who have symptoms and signs suggestive of rheumatologic disease.
Routine brain imaging is indicated in all patients and should include a noncontrast CT scan or MRI. Vascular dementia can be diagnosed with routine brain imaging.
The final step is to refer the patient to a dementia specialist, who will assess the patient again, order a neuropsychological evaluation, arrange an appointment and/or intervention by a social worker, and refer the patient to a geriatric psychiatrist if needed. | <urn:uuid:d3d754d1-095e-4d65-87d4-b34cbeb43894> | {
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Pasteurella multocida is a bacterial microorganism primarily found in cats and dogs. Human disease, most commonly in the form of localized skin and soft tissue infection, occurs after close contact with animal hosts. Respiratory tract infections and bacteremia, particularly in immunocompromised individuals, may also occur. The diagnosis mandates a thorough clinical workup and isolation of the organism from adequate patients samples through microbiological methods.
Pasteurella multocida belongs to the normal microbial flora of the oral cavity of various animals, but is most abundant in cats and dogs, as studies estimate that up to 90% of cats and 50% of dogs harbor this pathogen in their mouths . Hence, this gram-negative anaerobic coccobacillus is principally encountered in general practice as a causative agent of cellulitis and soft-tissue infections developing as a result of close animal contact (a scratch or a bite) . Signs and symptoms - erythema, hyperemia, and discharge (often purulent) from the wound being typical findings, appear shortly after contact . Proximal lymphadenitis is a frequent finding, while fever is reported in about 20% of cases . Main complications include the formation of abscesses and dissemination of the infection into the skeletal system (septic arthritis and osteomyelitis) . In addition to skin infections, Pasteurella multocida is also able to colonize the human respiratory tract, presumably after being in contact with carrier animals as well . Several reports have described the wide range of respiratory infections (from rhinosinusitis to pneumonia and abscess formation) that are seen in elderly patients suffering from chronic lung disorders or immunosuppression . Furthermore, bacteremia and systemic infections may ensue as a complication of pneumonia and respiratory spread, particularly in patients with hepatic disease (cirrhosis), diabetes mellitus, chronic kidney disease and malignant diseases . Rare reports have documented endocarditis, central nervous system (CNS) infection, and intraabdominal infections by P. multocida .
We report a case in which hemoptysis was the sole manifestation of Pasteurella infection. The patient was a middle-aged man with severe obstructive lung disease and exposure to cats. [ncbi.nlm.nih.gov]
Pasteurella multocida Background: —————————————————————————— Gram-Negative Cocci & Coccobacilli —————————————————————————— Aggregatibacter aphrophilus (formally known as Haemophilus aphrophilus) Bordetella pertussis (Causative agent of pertussis or whooping [globalrph.com]
Depending on the site, appropriate patients samples (sputum, exudate from the skin, synovial fluid, or blood) should be obtained. [symptoma.com]
This case report suggests that P. multocida infection can be potentially caused from saliva of cows as well as dogs or cats. [ncbi.nlm.nih.gov]
Ampicillin-sulbactam (Unasyn) 1.5 – 3.0 grams IV q6h Piperacillin-tazobactam (Zosyn ) 3.375 grams IV q6h Imipenem 500mg IV every 6 hours [Range: 250-1000 mg q6-8h] Disclaimer The authors make no claims of the accuracy of the information contained herein; and these suggested [globalrph.com]
In vivo studies suggest that concentration in phagocytes may contribute to drug distribution to inflamed tissues. Treats mild-to-moderate microbial infections. [emedicine.medscape.com]
A case of neonatal sepsis and meningitis resulting from horizontal transmission of P. multocida is described. [ncbi.nlm.nih.gov]
[…] multocida A28.0 ICD-10-CM Codes Adjacent To A28.0 A26.7 Erysipelothrix sepsis A26.8 Other forms of erysipeloid A26.9 Erysipeloid, unspecified A27 Leptospirosis A27.0 Leptospirosis icterohemorrhagica A27.8 Other forms of leptospirosis A27.81 Aseptic meningitis [icd10data.com]
The diagnosis of P. multocida infection should be made early on, as this bacterial pathogen is highly susceptible to antimicrobial therapy, but also because more severe forms may be life-threatening . One of the most important parts of the workup is a thoroughly obtained patient history that will confirm recent or previous close animal contact . Additionally, physicians must inquire about the presence of underlying diseases and comorbidities that could serve as risk factors for respiratory and systemic infections by P. multocida, whereas a complete physical examination is also important in identifying the site of infection. Once a presumptive diagnosis of a bacterial etiology is made, microbiological studies are necessary to determine the exact pathogen. Depending on the site, appropriate patients samples (sputum, exudate from the skin, synovial fluid, or blood) should be obtained. Cultivation of P. multocida on standard media is a convenient method for its detection, but it is frequently masked by other structurally similar pathogens that could be present in nonsterile specimens (for example, haemophilus influenzae and francisella tularensis, the causative agents of whooping cough and tularemia, respectively) . Furthermore, skin and soft-tissue infections are often polymicrobial . Still, the presence of large buttery colonies on blood agars consisting of gram-negative coccobacilli, developing after only one night of incubation, should be sufficient to make the diagnosis . Molecular methods, such as polymerase chain reaction (PCR), can be used for more detailed analysis of P. multocida .
- Giordano A, Dincman T, Clyburn BE, Steed LL, Rockey DC. Clinical Features and Outcomes of Pasteurella multocida Infection. Barbara A, ed. Medicine (Baltimore). 2015;94(36):e1285.
- Wilson BA, Ho M. Pasteurella multocida: from Zoonosis to Cellular Microbiology. Clin Microbiol Rev. 2013;26(3):631-655.
- Orsini J, Perez R, Llosa A, Araguez N. Non-zoonotic Pasteurella multocida Infection as a Cause of Septic Shock in a Patient with Liver Cirrhosis: A Case Report and Review of the Literature. Journal of Global Infectious Diseases. 2013;5(4):176-178.
- Weber DJ, Wolfson JS, Swartz MN, Hooper DC. Pasteurella multocida infections. Report of 34 cases and review of the literature. Medicine (Baltimore) 1984;63:133–154
- Mandell GL, Bennett JE, Dolin R. Mandel, Douglas and Bennett's Principles and Practice of Infectious Diseases. 8th ed. Philadelphia, Pennsylvania: Churchill Livingstone; 2015
- Murray PR, Rosenthal KS, Pfaller MA. Medical Microbiology. Seventh edition. Philadelphia: Elsevier/Saunders; 2013.
- Kofteridis DP, Christofaki M, Mantadakis E, et al. Bacteremic community-acquired pneumonia due to Pasteurella multocida. Int J Infect Dis. 2009;13(3):e81-83. | <urn:uuid:adae2826-c967-4202-88d5-2d18deb83b90> | {
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oPatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.
Synonym: autistic spectrum disorder (ASD)
Autism is characterised by a 'triad of impairments' in social interaction, imaginative thought and communication.
There is a spectrum of disability from severely affected individuals, who produce no meaningful verbal or non-verbal communication, to high-functioning individuals, who are articulate but socially awkward and viewed as "eccentric" at the other extreme. The overarching term used by the International Statistical Classification of Diseases and Related Health Problems (ICD-10) and the Diagnostic and Statistical Manual of Mental Disorders Fourth Edition (DSM-IV) is pervasive developmental disorder. The diagnoses of autism and Asperger's syndrome fall within this spectrum.
The Autism Act was passed in 2009 and the Department of Health has followed this with "Fulfilling and rewarding lives: the strategy for adults with autism in England", which has fundamental strategies for increasing awareness in the public and diagnosis within professionals.
The National Institute for Health and Clinical Excellence (NICE) has also published guidance on recognising and diagnosing autism in children and young people.
Autism is a complex disorder with an established genetic basis.
- Chromosome 7q is particularly important, although others are also thought to be involved.
- There is 88% concordance in identical twins. Siblings are more likely to be diagnosed. Twins may be differently affected within the spectrum of disability.
- Environmental factors have been implicated, although there is little conclusive evidence:
- Toxins like lead, antimony and mercury have been found in high levels in the hair and blood samples of affected children. It may be that ASD children are unable to detoxify as efficiently as other children.
- This hypothesis is similar to the premise behind the gluten- and casein-free diet. Peptides produced by gluten and casein act as morphine-like substances to ASD children and exaggerate their behaviours. Currently, however, there is insufficient evidence for improved behaviour with the exclusion diet.
- Measles, mumps and rubella (MMR) vaccine and autism:
- This has been heavily covered in the media. The position of the Medical Research Council is that, "there are no epidemiological studies that provide reliable evidence to support the hypothesis that there might be an association between MMR and ASD". The majority of the original researchers who claimed a link have retracted their interpretations. Wakefield has been widely discredited.
- In the USA, several claims for vaccine injury are currently progressing through the courts.
- Prevalence is rising. In 1979 the National Autistic Society (NAS) estimated that there were 39 cases per 10,000.
- Current incidence figures are approximately 1%.
- It is thought that the rise is due to a combination of increased and earlier, more specific diagnosis with possibly environmental factors added on. This is also supported by similar autism prevalence rates in adults (compared to children now being diagnosed) when non-selected communities are sampled and examined.
- Consistent male:female ratio 4:1
50% of parents (and more) have cause for concern by 12-18 months of age. Speech delay is a common first concern. Other common concerns include:
- Lack of, or inconsistent use of eye contact.
- Lack of social smile, imitation, response to name.
- Lack of interest in others.
- Lack of emotional expression.
- Few directed vocalisations.
- Absence of joint attention skills (pointing to "show," following a point, monitoring others' gaze, and referencing objects or events).
- Few requesting behaviours.
- Few social gestures (such as waving, clapping, nodding, and shaking head).
- Pretend play is also reduced in many children.
Regression (losing skills that have been acquired) is seen in approximately 25% of children. The skills may be in language, play or social skills.
Associated medical problems
- 25-30% of children on the autistic spectrum may have seizures. This usually appears in puberty. These are more common in children who have significant cognitive problems or dysmorphic features.
- Visual impairment.
- Hearing impairment.
- Approximately 70% also meet diagnostic criteria for at least one other (often unrecognised) psychiatric disorder, such as depression or attention deficit hyperactivity disorder (ADHD). This may also be impairing their social functioning.
- Intellectual disability (IQ below 70) occurs in approximately 50%.
- Underlying medical conditions, such as untreated phenylketonuria, congenital rubella, cytomegalovirus or toxoplasmosis, fragile X syndrome or tuberous sclerosis.
- Pica (or mouthing) is also commonly seen.
- Sleep disorders (of onset, maintenance and duration) are also common.
There is currently no policy for routine screening in the UK (unlike in the USA). These tools may help with a decision to refer for specialist assessment after a parent has raised concerns about their child. There are several screening questionnaires in use including:
- The CHAT (= CH ecklist for A utism in T oddlers) and its modifications CHAT 23 and M-CHAT.
- Pervasive developmental disorder screening test (PDDST).
- Screening tool for autism in two-year-olds (STAT).
- Social communication questionnaire (SCQ) is used in school-aged children.
All focus on assessing key characteristics, such as joint attention, social communication and play. A negative result from screening does not rule out the diagnosis. If parental concerns continue, a referral is advisable.
The assessment of children and young people with developmental delay, emotional and behavioural problems, or genetic syndromes should include surveillance for ASD as part of routine practice.
- Asperger's syndrome.
- Communication disorder.
- Learning disability.
- Childhood disintegrative disorders arising after 30 months of age (Heller's disease).
- Rett's disorder.
Making the diagnosis
The condition can be reliably diagnosed between 2-3 years of age. NICE has published guidance for assessment and referral of children with suspected autism:
- Specialist diagnosis is required. This is probably best done by paediatric neurologists, developmental and behavioural paediatricians, child psychiatrists or psychologists. Ideally there should be a multidisciplinary team ('the autism team'), with specific training and experience in evaluating children with autism. Involvement of speech and language and occupational therapists, special educators, and social workers may provide a more detailed assessment of specific domains.
- Other conditions need to be excluded and investigations for chromosome analysis, hearing and sight tests are usually taken prior to reaching the diagnosis. Where clinically relevant, the following should be considered for all children and young people with ASD:
- Examination of physical status, with particular attention to neurological and dysmorphic features.
- Karyotyping and fragile X DNA analysis.
- Hearing examination.
- Investigations to rule out recognised causes of ASD, eg tuberous sclerosis.
- Assessments of children and young people for ASD cannot be rushed. It may not be possible to obtain sufficient evidence in one session and the child/young person may require observation in different settings, eg at school (especially in unstructured activity such as break-time) as well as clinic.
- Autistic disorder is diagnosed when an individual exhibits six or more symptoms across the three core areas.
- All children and young people with ASD should have a comprehensive assessment of their speech, language and communication skills. This will help to decide which interventions are best suited for that child.
When to refer
- Children whose language or social skills have regressed.
- If you are concerned about possible autism on the basis of reported or observed signs and symptoms. Even if a screening tool is negative, consider referral if concerns persist.
- If there are risk factors which make autism more likely:
- Factors associated with birth; gestational age ≤35 weeks; birth defects associated with central nervous system malformation, eg cerebral palsy.
- Family; a sibling with autism.
- Parental ill health consequences; schizophrenia-like psychosis; sodium valproate use during pregnancy
- A child's own health problems; intellectual disability; neonatal encephalopathy; chromosomal disorders, eg trisomy; genetic disorders, eg fragile X, muscular dystrophy, neurofibromatosis, tuberous sclerosis.
Management is usually undertaken in educational settings. Local support networks may be in place for educational support in mainstream school if appropriate and will feed down from paediatrician or educational psychologist. Occupational therapy, speech therapy and physiotherapy may help specific problems.
Many educational approaches are commonly used:
- Applied behavioural analysis - Lovaas pioneered a system for teaching skills in bite-sized pieces by using motivators (specific to the child) to reward achievement. It is taught intensively (40 hours per week) in a one-to-one situation. It should be started as early as possible. There are some specialised schools which use this method extensively. They tend to be independent and expensive. Tutors can be contacted to come to the home. See the PEACH website under 'Internet and further resources', below. There is some evidence in support of this approach, particularly for >30 hours per week. However, the Lovaas programme should not be presented as an intervention that will lead to normal functioning.
- Early start Denver model - this combines applied behavioural analysis with developmental and relationship based approaches. It is aimed at toddlers and uses a developmental curriculum. The principles include bringing the child into interactive social relationships, using positive emotional exchanges, and developing joint play activities to target deficits. It has been shown to improve cognitive performance, language skills and adaptive behaviour skills in some young children with autism. Unfortunately, the research methods are not robust.
- TEACCH method (= T reatment and E ducation of A utistic and C ommunication related handicapped CH ildren) - this approach emphasises the organisation of the child's physical learning environment. Teachers use predictable sequences of activities. The child is reassured by visual schedules and visually structured activities. There is flexibility built into routines.
Other supportive interventions include:
- Interventions supporting communication, such as the use of visual augmentation, eg pictures of objects. The picture exchange communication system (PECS) is a system of easily recognisable pictures which the child uses to communicate. This may help to reduce frustration and anxiety.
- Speech and language therapy; this is most effective when they train and work with teachers, families and peers promoting functional communication in normal environments.
- Social skills (in joint attention, interactive play, responding to social overtures, and initiating and maintaining social behaviour) can be taught explicitly. When children are school-aged, social skills groups can be useful. Using videos and social stories can help to teach specific skills.
- Occupational therapy focuses on development and maintenance of fine motor and adaptive skills. It can also look at problems of processing and integrating sensory input.
No matter which approach is used, it is recommended that the intervention should be systematically planned and delivered for at least 25 hours a week, consistently. It is also recommended that classrooms should have a high degree of structure and a low student-to-teacher ratio. The child's developmental level should dictate their curriculum.
Behavioural management for parents
Advise parents to join a self-help group. The NAS or parent-school partnerships often run local groups. The NAS run 'Early Bird' courses for parents. This a 12-week programme to help parents try to understand their child's behaviour and begin to cope. Contact: Early Bird Centre 01226 779218 or via email.
The behaviours that the children display can be upsetting, and misunderstood by the general public, who may stare at a "naughty child". Insight into why the child is doing these things can be helpful in helping to moderate behaviour and manage it:
- It may be useful to try to think of the child's senses as underactive or overactive:
- For example, if the child is under-sensitive in respect of sight, he or she may seek visual stimulation by flicking lights on and off, lining things up and holding them at the corners of his or her eyes.
- If the child is over-sensitive, he or she may prefer the dark, blink a lot and avoid being in the sun.
- In respect of touch, if over-sensitive, the child may find the touch of clothes (or their labels) intolerable and constantly undress. He or she may dislike hair cutting and washing and may avoid certain foods.
- If under-sensitive, the child may bump into people for stimulation, (or have poor proprioception), want long crushing hugs, grind teeth and rarely cry when hurt.
- Poor communication can lead to intense frustration and tantrums. Anxiety (which also leads to tantrums) can be managed with use of visual timetabling.
- A particular problem can be fluorescent lighting, which some sufferers are able to see flickering quite clearly. This can cause bad behaviour because of sensory overload.
There are many strategies available to help parents. All claim good success, although the efficacy is not well-established for any. The major ones will be outlined and there are links if further information is required. Very few are available on the NHS and costs are generally borne by the parents:
- Sensory integration therapy has been used when there are marked sensory perception issues, eg over-sensitivity to touch. Occupational therapists desensitise the child gently over time. Auditory Integration Therapy (AIT) is offered to children on the autistic spectrum because they appear to experience pain when listening to certain sounds. In AIT the child listens to modulated music tapes through headphones for a certain period of time. However, 50% of the studies show no benefit. Therefore AIT is not recommended.
- Evidence from trials is lacking for a gluten-/casein-free diet, although many parents claim excellent results. Luke Jackson wrote an excellent "user's guide" whilst he was a teenager.
- Risperidone is useful for short-term treatment of significant aggression, tantrums or self-injury in children with autism. There is some evidence of benefits in irritability, repetition and social withdrawal.
- Methylphenidate may be considered for treatment of attention difficulties/hyperactivity in children or young people with ASD, although it tends to be less well tolerated.
- Melatonin may be considered for treatment of sleep problems which have persisted despite behavioural interventions. Meta-analysis has showed significant improvement with minimal side-effects.
- Some children may improve at 4-6 years of age when they may be able to model normal behaviour from school peers. There is currently a policy of inclusion within the education system which will attempt to support the majority of autistic spectrum disorder (ASD) sufferers within mainstream schools.
- Articulate people with ASD are writing about their experiences (Temple Grandin, Donna Williams), and the public is more knowledgeable and sometimes sympathetic. Adults are living full lives; however, the NAS published a report in 2001 called "Ignored or ineligible? The reality for adults living with Autistic Spectrum Disorders". The results were not positive and showed 49% of adults still living with parents. 12% at the higher-functioning end were in full-time employment.
- Some will need external support and this can be accessed through a community care assessment.
- The NAS publish good practice guidelines for services dealing with adults with ASD.
- "Prospects" is an NAS-supported employment service.
The term autism was first used by psychiatrist Eugen Bleuler in 1911, to describe a schizophrenic patient who had withdrawn into his own world. Hans Asperger and Leo Kanner both used the term in the 1940s, working separately. Asperger described very able children. Kanner described children who were severely affected. His description, and the downbeat prognosis, persisted for the next 30 years.
Further reading & references
- Autism - The management and support of children and young people on the autism spectrum, NICE Guideline (Aug 2013)
- Autism, NICE Quality Standards (Jan 2014)
- National Autistic Society
- PEACH, Parents for the Early Intervention of Autism in CHildren (Peach), UK parent-led charity established to promote early behavioural intervention for young children with autism, Applied Behavioural Analysis (ABA)
- Humphreys JS, Gringras P, Blair PS, et al; Sleep patterns in children with autistic spectrum disorders: a prospective cohort study. Arch Dis Child. 2014 Feb;99(2):114-8. doi: 10.1136/archdischild-2013-304083. Epub 2013 Sep 23.
- The Extreme Male Brain Theory of Autism. Simon Baron-Cohen. Trends in Cognitive Sciences.6:248-254
- Picture Exchange Communication System
- Wing L; The spectrum of autistic disorders. Hosp Med. 2004 Sep;65(9):542-5.
- Fulfilling and rewarding lives: the strategy for adults with autism in England, Dept of Health, March 2010
- Autism spectrum disorders in children and young people, NICE Clinical Guideline (September 2011)
- Bonora E, Lamb JA, Barnby G, et al; Mutation screening and association analysis of six candidate genes for autism on chromosome 7q. Eur J Hum Genet. 2005 Feb;13(2):198-207.
- Blenner S, Reddy A, Augustyn M; Diagnosis and management of autism in childhood. BMJ. 2011 Oct 21;343:d6238. doi: 10.1136/bmj.d6238.
- Millward C, Ferriter M, Calver S, et al; Gluten- and casein-free diets for autistic spectrum disorder. Cochrane Database Syst Rev. 2008 Apr 16;(2):CD003498.
- Doja A, Roberts W; Immunizations and autism: a review of the literature. Can J Neurol Sci. 2006 Nov;33(4):341-6.
- Fitzpatrick M; The end of the road for the campaign against MMR. Br J Gen Pract. 2007 Aug;57(541):679.
- Review of Autism and Research: Epidemiology and Causes, London Medical Research Council (MRC), December 2001; review of the MMR debate
- Murch SH, Anthony A, Casson DH, et al; Retraction of an interpretation. Lancet. 2004 Mar 6;363(9411):750.
- Dyer C; Wakefield was dishonest and irresponsible over MMR research, says GMC. BMJ. 2010 Jan 29;340:c593. doi: 10.1136/bmj.c593.
- Stewart AM; When vaccine injury claims go to court. N Engl J Med. 2009 Jun 11;360(24):2498-500.
- No authors listed; Prevalence of autism spectrum disorders - Autism and Developmental Disabilities MMWR Surveill Summ. 2009 Dec 18;58(10):1-20.
- Brugha TS, McManus S, Bankart J, et al; Epidemiology of autism spectrum disorders in adults in the community in England. Arch Gen Psychiatry. 2011 May;68(5):459-65.
- Pickett J, Xiu E, Tuchman R, et al; Mortality in Individuals With Autism, With and Without Epilepsy. J Child Neurol. 2011 Apr 6.
- Tuchman R, Cuccaro M, Alessandri M; Autism and epilepsy: historical perspective. Brain Dev. 2010 Oct;32(9):709-18. Epub 2010 May 26.
- Lugnegard T, Hallerback MU, Gillberg C; Psychiatric comorbidity in young adults with a clinical diagnosis of Asperger Res Dev Disabil. 2011 Apr 23.
- Murray MJ; Attention-deficit/Hyperactivity Disorder in the context of Autism spectrum Curr Psychiatry Rep. 2010 Oct;12(5):382-8.
- Assessment, diagnosis and clinical interventions for children and young people with autism spectrum disorders; Scottish Intercollegiate Guidelines Network - SIGN (2007)
- Lovaas OI; Behavioral treatment and normal educational and intellectual functioning in young autistic children. J Consult Clin Psychol. 1987 Feb;55(1):3-9.
- Virues-Ortega J; Applied behavior analytic intervention for autism in early childhood: Clin Psychol Rev. 2010 Jun;30(4):387-99. Epub 2010 Feb 11.
- Sinha Y, Silove N, Wheeler D, et al; Auditory integration training and other sound therapies for autism spectrum Arch Dis Child. 2006 Dec;91(12):1018-22. Epub 2006 Aug 3.
- The Gluten Free/Casein Free Diet: a User's guide by Luke Jackson. London. Jessica Kingsley Publishers. ISBN 1-84310-055-x
- Hazell P; Drug therapy for attention-deficit/hyperactivity disorder-like symptoms in autistic disorder. J Paediatr Child Health. 2007 Jan;43(1-2):19-24.
- Jesner OS, Aref, Coren E; Risperidone for autism spectrum disorder. Cochrane Database Syst Rev. 2007 Jan 24;(1):CD005040.
- Rossignol DA, Frye RE; Melatonin in autism spectrum disorders: a systematic review and meta-analysis. Dev Med Child Neurol. 2011 Apr 19. doi: 10.1111/j.1469-8749.2011.03980.x.
- Thinking In Pictures and Other Reports from My Life with Autism by Temple Grandin. New York. Bantam Doubleday Dell Publishing
- Autism: An Inside-out Approach by Donna Williams. London. Jessica Kingsley Publishers. First hand account of what it's like to live with ASD
- Ignored or ineligible? The reality for adults with autism spectrum disorders, The National Autistic Society, 2001
- Supporting adults with autism: a good practice guide for NHS and local authorities, The National Autistic Society, 2009
- Good practice in supporting adults with autism, The National Autistic Society, 2009
- Prospects, The National Autistic Society
Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.
Dr Hayley Willacy
Dr Hayley Willacy
Dr Helen Huins | <urn:uuid:e54b7ade-b9e1-4eac-9d1a-b837f8c5e10e> | {
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|Classification and external resources|
Post-concussion syndrome, also known as postconcussive syndrome or PCS, is a set of symptoms that may continue for weeks, months, or a year or more after a concussion – a minor form of traumatic brain injury (TBI). The rates of PCS vary, but most studies report that about 15% of individuals with a history of a single concussion develop persistent symptoms associated with the injury. A diagnosis may be made when symptoms resulting from concussion last for more than three months after the injury. Loss of consciousness is not required for a diagnosis of concussion or post-concussion syndrome.
The condition is associated with a wide range of symptoms: physical, such as headache; cognitive, such as difficulty concentrating; and emotional and behavioral, such as irritability. Many of the symptoms associated with PCS are common or may be exacerbated by other disorders, so there is considerable risk of misdiagnosis. Headaches that occur after a concussion may feel like Migraine headaches or tension-type headaches. Most headaches are tension-type headaches, which may be associated with a neck injury that occurred at the same time of the head injury.
Though there is no treatment for PCS, symptoms can be treated; medications and physical and behavioral therapy may be used, and individuals can be educated about symptoms and provided with the expectation of recovery. The majority of PCS cases resolve after a period of time.
It is not known what causes PCS to occur and persist, or why some people who suffer a minor traumatic brain injury later develop PCS while others do not. The nature of the syndrome and the diagnosis itself have been the subject of intense debate since the 19th century. However, certain risk factors have been identified; for example, preexisting medical or psychological conditions, expectations of disability, being female, and older age all increase the chances that someone will suffer PCS. Physiological and psychological factors present before, during, and after the injury are all thought to be involved in the development of PCS.
Some experts believe post-concussion symptoms are caused by structural damage to the brain or disruption of neurotransmitter systems, resulting from the impact that caused the concussion. Others believe that post-concussion symptoms are related to common psychological factors. Most common symptoms like headache, dizziness, and sleep problems are similar to those often experienced by individuals diagnosed with depression, anxiety, or post traumatic stress disorder. In many cases, both physiological effects of brain trauma and emotional reactions to these events play a role in the development of symptoms.
- 1 Signs and symptoms
- 2 Causes
- 3 Diagnosis
- 4 Treatment
- 5 Prognosis
- 6 Epidemiology
- 7 History
- 8 Controversy
- 9 See also
- 10 References
Signs and symptoms
In the past, the term PCS was also used to refer to immediate physical symptoms or post-concussive symptoms following a minor TBI or concussion. The severity of these symptoms typically decreases rapidly. In addition, the nature of the symptoms may change over time: acute symptoms are most commonly of a physical nature, while persisting symptoms tend to be predominantly psychological. Symptoms such as noise sensitivity, problems with concentration and memory, irritability, depression, and anxiety may be called 'late symptoms' because they generally do not occur immediately after the injury, but rather in the days or weeks after the injury. Nausea and drowsiness commonly occur acutely following concussion. Headache and dizziness occur immediately after the injury, but also can be long lasting.
A common condition associated with PCS is headache. While most people have headaches of the same type they experienced before the injury, people diagnosed with PCS often report more frequent or longer-lasting headaches. Between 30% and 90% of people treated for PCS report having more frequent headaches and between 8% and 32% still report them a year after the injury.
Dizziness is another common symptom reported in about half of people diagnosed with PCS and is still present in up to a quarter of them a year after the injury. Older people are at especially high risk for dizziness, which can contribute to subsequent injuries and higher rates of mortality due to falls.
About 10% of people with PCS develop sensitivity to light or noise, about 5% experience a decreased sense of taste or smell, and about 14% report blurred vision. People may also have double vision or ringing in the ears, also called tinnitus. PCS may cause insomnia, fatigue, or other problems with sleep.
Psychological and behavioral
Psychological conditions, which are present in about half of people with PCS, may include irritability, anxiety, depression, and a change in personality. Other emotional and behavioral symptoms include restlessness, aggression, and mood swings. Some common symptoms, such as apathy, insomnia, irritability, or lack of motivation, may result from other co-occurring conditions, such as depression.
Higher mental functions
Common symptoms associated with a diagnosis of PCS are related to cognition, attention, and memory, especially short-term memory, which can also worsen other problems such as forgetting appointments or difficulties at work. In one study, one in four people diagnosed with PCS continued to report memory problems a year after the injury, but most experts agree that cognitive symptoms clear within six months to a year after injury in the vast majority of individuals.
The question of the cause or causes of PCS has been heavily debated for many years and remain controversial. It is not known to exactly what degree the symptoms are due to physiological changes or to other factors, such as pre-existing psychiatric disorders or factors related to secondary gain or disability compensation. The subjectivity of the complaints complicates assessment and makes it difficult to determine whether symptoms are being exaggerated or feigned.
While the causes of symptoms occurring immediately after a concussion are likely to be physiological, it is less evident that persistent post-concussive symptoms have an entirely organic basis, and nonorganic factors are likely to be involved in symptoms that last longer than three months. PCS may also be exacerbated by psychosocial factors, chronic pain, or an interaction of some or all of these. The majority of experts believe that PCS results from a mix of factors, including preexisting psychological factors and those directly relating to the physical injury.
Conventional neuroimaging studies of the brain following a concussion are typically normal. However, studies have found some subtle physiological changes associated with PCS using more novel imaging modalities. Studies using positron emission tomography have linked PCS to a reduction in glucose use by the brain. Changes in cerebral blood flow have also been observed as long as three years after a concussion in studies using single photon emission computed tomography (SPECT). At least one study with functional magnetic resonance imaging (fMRI) has shown differences in brain function during tasks involving memory after MTBI although they were not examining PCS specifically. Not all people with PCS have abnormalities on imaging, however, and abnormalities found in studies such as fMRI, PET, and SPECT could result from other comorbid conditions such as depression, chronic pain, or post-traumatic stress disorder (PTSD). Proponents of the view that PCS has a concussion. A few studies have shown that people with PCS score lower than controls on neuropsychological tests that measure attention, verbal learning, reasoning, and information processing, but issues related to effort and secondary gain can not be ruled out as contributing to these differences. Recovery as measured by scores on cognitive tests frequently do not correlate with resolution of symptoms; individuals diagnosed with PCS may still report subjective symptoms after their performance on tests of cognitive functioning have returned to normal. Another study found that although children with PCS had poorer scores on tests of cognitive functioning after the injury, they also had poorer behavioral adjustment before the injury than children with no persistent symptoms; these findings support the idea that PCS may result from a combination of factors such as brain dysfunction resulting from head injury and preexisting psychological or social problems. Different symptoms may be predicted by different factors; for example, one study found that cognitive and physical symptoms were not predicted by the manner in which parents and family members coped with the injury and adjusted to its effects, but psychological and behavioral symptoms were.
It has been argued that psychological factors play an important role in the presence of post-concussion symptoms. The development of PCS may be due to a combination of factors such as adjustment to effects of the injury, preexisting vulnerabilities, and brain dysfunction. Setbacks related to the injury, for example problems at work or with physical or social functioning, may act as stressors that interact with preexisting factors such as personality and mental conditions to cause and perpetuate PCS. In one study, levels of daily stress were found to be correlated to PCS symptoms in both concussed subjects and controls, but in another, stress was not significantly related to symptoms.
Iatrogenic effects (those caused by the medical intervention) may also occur when individuals are provided with misleading or incorrect information related to recovery of symptoms. This information may cause people to focus and dwell on the idea that their brains are permanently damaged,. It appears that even the expectation of symptoms may contribute to the development of PCS by causing individuals with MTBI to focus on symptoms and therefore perceive them to be more intense, to attribute symptoms that occur for other reasons to the injury, and to underestimate the rate of symptoms before the injury.
anxiety, or depression
The International Statistical Classification of Diseases and Related Health Problems (ICD-10) and the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders have set out criteria for PCS and postconcussional disorder (PCD), respectively.
The ICD-10 established a set of diagnostic criteria for PCS in 1992. In order to meet these criteria, a patient has had a head injury "usually sufficiently severe to result in loss of consciousness" and then develop at least three of the eight symptoms marked with a check mark in the table at right under "ICD-10" within four weeks. About 38% of people who suffer a head injury with symptoms of concussion and no radiological evidence of brain lesions meet these criteria. In addition to these symptoms, people that meet the ICD-10 criteria for PCS may fear that they will have permanent brain damage, which may worsen the original symptoms. Preoccupation with the injury may be accompanied by the assumption of a "sick role" and hypochondriasis. The criteria focus on subjective symptoms and mention that neuropsychological evidence of significant impairment is not present. With their focus on psychological factors, the ICD-10 criteria support the idea that the cause of PCS is functional. Like the ICD-10, the ICD-9-CM defines PCS in terms of subjective symptoms and discusses the greater frequency of PCS in people with histories of mental disorders or a financial incentive for a diagnosis.
The DSM-IV lists criteria for diagnosis of PCD in people who have suffered a head trauma with persistent post-traumatic amnesia, loss of consciousness, or post-traumatic seizures. In addition, for a diagnosis of PCD, patients must have neuropsychological impairment as well as at least three of the symptoms marked with a check mark in the table at right under "DSM-IV". These symptoms must be present for three months after the injury and must have been absent or less severe before the injury. In addition, the patient must experience social problems as a result, and must not meet criteria for another disorder that explains the symptoms better.
Neuropsychological tests exist to measure deficits in cognitive functioning that can result from PCS. The Stroop Color Test and the 2&7 Processing Speed Test (which both detect deficits in speed of mental processing) can predict the development of cognitive problems from PCS. A test called the Rivermead Postconcussion Symptoms Questionnaire, a set of questions that measure the severity of 16 different post-concussion symptoms, can be self-administered or administered by an interviewer. Other tests that can predict the development of PCS include the Hopkins Verbal Learning A test (HVLA) and the Digit Span Forward examination. The HVLA tests verbal learning and memory by presenting a series of words and assigning points based on the number recalled, and digit span measures attention efficiency by asking the examinee to repeat back digits spoken by the tester in the same order as they are presented. In addition, neuropsychological tests may be performed to detect malingering.
PCS, which shares symptoms with a variety of other conditions, is highly likely to be misdiagnosed in people with these conditions. Cognitive and affective symptoms that occur following a traumatic injury may be attributed to MTBI, but in fact be due to another factor such as post-traumatic stress disorder, which is easily misdiagnosed as PCS and vice versa. Affective disorders such as depression have some symptoms that can mimic those of PCS and lead to a wrongful diagnosis of the latter; these include problems with concentration, emotional lability, anxiety, and sleep problems. Depression, which is highly common in persistent PCS, can worsen other PCS symptoms, such as headaches and problems with concentration, memory, and sleep. PCS also shares symptoms with chronic fatigue syndrome, fibromyalgia, and exposure to certain toxins. Traumatic brain injury may cause damage to the hypothalamus or the pituitary gland, and deficiencies of pituitary hormones (hypopituitarism) can cause similar symptoms to post-concussion syndrome; in these cases, symptoms can be treated by replacing any hormones that are deficient.
Management of post-concussion syndrome typically involves treatments addressing specific symptoms; for example, people can take pain relievers for headaches and medicine to relieve depression or insomnia,. Rest is advised, but is only somewhat effective. Physical and behavioral therapy may also be prescribed for problems such as loss of balance and difficulties with attention, respectively.
Though no pharmacological treatments exist for PCS, doctors may prescribe medications used for symptoms that also occur in other conditions; for example, antidepressants are used for the depression that frequently follows MTBI. Side effects of medications may affect people suffering the consequences of MTBI more severely than they do others, and thus it is recommended that medications be avoided if possible; there may be a benefit to avoiding narcotic medications. In addition, some pain medications prescribed for headaches can cause rebound headaches when they are discontinued.
Psychological treatment, to which about 40% of PCS patients are referred for consultation, has been shown to reduce problems. Ongoing disabilities may be treated with therapy to improve function at work, or in social or other contexts. Therapy aims to aid in the gradual return to work and other preinjury activities, as symptoms permit. A protocol for PCS treatment has been designed based on the principles behind Cognitive behavioral therapy (CBT), a psychotherapy aimed at influencing disturbed emotions by improving thoughts and behaviors. CBT may help prevent persistence of iatrogenic symptoms – those that occur because health care providers create the expectation that they will. A risk exists that the "power of suggestion" may worsen symptoms and cause long-term disabilities; therefore, when counseling is indicated, the therapist must take a psychological origin of symptoms into account and not assume that all symptoms are a direct result of neurological damage from the injury.
In situations such as motor vehicle accidents or following a violent attack, the post-concussion syndrome may be accompanied by post-traumatic stress disorder, which is important to recognize and treat in its own right. People with PTSD, depression, and anxiety can be treated with medication and psychotherapy.
Education about symptoms and their usual time course is a part of psychological therapy, and is most effective when provided soon after the injury. Since stress exacerbates post-concussion symptoms, and vice versa, an important part of treatment is reassurance that PCS symptoms are normal, and education about how to deal with impairments. One study found that PCS patients who were coached to return to activities gradually, told what symptoms to expect, and trained how to manage them had a reduction in symptoms compared to a control group of uninjured people. Early education has been found to reduce symptoms in children as well.
Neurotherapy is an operant conditioning test where patients are given conditional audio/visual rewards after producing particular types of brainwave activity. Recent neurotherapy improvements in QEEG can identify the specific brainwave patterns that need to be corrected. Studies have shown that neurotherapy is effective in the treatment of post-concussion syndrome and other disorders with similar symptoms.
The prognosis for PCS is generally considered positive, with total resolution of symptoms in many, but not all, cases. For 50% of people, post-concussion symptoms go away within a few days to several weeks after the original injury occurs. In others, symptoms may remain for three to six months, but evidence indicates that many cases are completely resolved within 6 months. The majority of symptoms are largely gone in about half of people with concussion one month after the injury, and about two thirds of people with minor head trauma are nearly symptom-free within three months. Persistent, often severe headaches are the longest lingering symptom in most cases and are the most likely symptom to never fully resolve. It is frequently stated in the literature and considered to be common knowledge that 15–30% of people with PCS have not recovered by a year after the injury, but this estimate is imprecise because it is based on studies of people admitted to a hospital, the methodologies of which have been criticized. In approximately 15% of people, symptoms may persist for years or be permanent. If symptoms are not resolved by one year, they are likely to be permanent, though improvements may occur after even two or three years, or may suddenly occur after a long time without much improvement. Older people and those who have previously suffered another head injury are likely to take longer to recover.
The way in which children cope with the injury after it occurs may have more of an impact than factors that existed prior to the injury. Children's mechanisms for dealing with their injuries may have an effect on the duration of symptoms, and parents who do not deal effectively with anxiety about children's post-injury functioning may be less able to help their children recover.
If another blow to the head occurs after a concussion but before its symptoms have gone away, there is a slight risk of developing the serious second-impact syndrome (SIS). In SIS, the brain rapidly swells, greatly increasing intracranial pressure. People who have repeated mild head injuries over a prolonged period, such as boxers and Gridiron football players, are at risk for chronic traumatic encephalopathy (or the related variant dementia pugilistica), a severe, chronic disorder involving a decline in mental and physical abilities.
It is not known exactly how common PCS is. Estimates of the prevalence at 3 months post-injury are between 24 and 84%, a variation possibly caused by different populations or study methodologies. The estimated incidence of PPCS is around 10% of MTBI cases. Since PCS by definition only exists in people who have suffered a head injury, demographics and risk factors are similar to those for head injury; for example, young adults are at higher risk than others for receiving head injury, and, consequently, of developing PCS.
The existence of PCS in children is controversial. It is possible that children's brains have enough plasticity that they are not affected by long-term consequences of concussion (though such consequences are known to result from moderate and severe head trauma). On the other hand, children's brains may be more vulnerable to the injury, since they are still developing and have fewer skills that can compensate for deficits. Clinical research has found higher rates of post-concussion symptoms in children with TBI than in those with injuries to other parts of the body, and that the symptoms are more common in anxious children. Symptoms in children are similar to those in adults, but children exhibit fewer of them. Evidence from clinical studies found that high school-aged athletes had slower recoveries from concussion as measured by neuropsychological tests than college-aged ones and adults. PCS is rare in young children.
A wide range of factors have been identified as being predictive of PCS, including low socioeconomic status, previous MTBI, a serious associated injury, headaches, an ongoing court case, and female gender. Being older than 40 and being female have also been identified as being predictive of a diagnosis of PCS, and women tend to experience more severe symptoms. In addition, the development of PCS can be predicted by having a history of alcohol abuse, low cognitive abilities before the injury, a personality disorder, or a medical illness not related to the injury. PCS is also more prevalent in people with a history of psychiatric conditions such as clinical depression or anxiety before the injury.
Mild brain injury-related factors that increase the risk for persisting post-concussion symptoms include an injury associated with acute headache, dizziness, or nausea; an acute Glasgow Coma Score of 13 or 14; and suffering another head injury before recovering from the first. The risk for developing PCS also appears to be increased in people who have traumatic memories of the injury or expect to be disabled by the injury.
The symptoms that occur after a concussion have been described in various reports and writings for hundreds of years. The idea that this set of symptoms forms a distinct entity began to attain greater recognition in the latter part of the 19th century. John Erichsen, a surgeon from London, played an important role in developing the study of PCS. The controversy surrounding the cause of PCS began in 1866 when Erichsen published a paper about persisting symptoms after sustaining mild head trauma. He suggested that the condition was due to "molecular disarrangement" to the spine. The condition was originally called "railroad spine" because most of the injuries studied had happened to railroad workers. While some of his contemporaries agreed that the syndrome had an organic basis, others attributed the symptoms to psychological factors or to outright feigning. In 1879, the idea that a physical problem was responsible for the symptoms was challenged by Rigler, who suggested that the cause of the persisting symptoms was actually "compensation neurosis": the railroad's practice of compensating workers who had been injured was bringing about the complaints. Later, the idea that hysteria was responsible for the symptoms after a mild head injury was suggested by Charcot. Controversy about the syndrome continued through the 20th century. During World War I many soldiers suffered from puzzling symptoms after being close to a detonation but without any evidence of a head wound. The illness was called shell shock, and a psychological explanation was eventually favoured. By 1934 the current concept of PCS had replaced ideas of hysteria as the cause of post-concussion symptoms. British authorities banned the term shell shock during World War II to avoid an epidemic of cases, and the term posttrauma concussion state was coined in 1939 to describe "disturbance of consciousness with no immediate or obvious pathologic change in the brain". The term postconcussion syndrome was in use by 1941.
In 1961, H. Miller first used the term "accident neurosis" to refer to the syndrome which is now called PCS and asserted that the condition only occurs in situations where people stand to be compensated for the injury. The real causes of the condition remain unclear.
Though no universally accepted definition of postconcussive syndrome exists, most of the literature defines the syndrome as the development of at least 3 of the following symptoms: headache, dizziness, fatigue, irritability, impaired memory and concentration, insomnia, and lowered tolerance for noise and light., One complication in diagnosis is that symptoms of PCS also occur in people who have no history of head injury, but who have other medical and psychological complaints. In one study, 80% of healthy, uninjured people reported having three or more symptoms similar to those found after concussion. In another study, 64% of people with TBI met the criteria set out by the ICD-10 for post-concussion syndrome, but so did 40% of people that had injuries not to the head; 11% of those with brain injuries and 7% of those with other injuries met the DSM-IV criteria for post-concussion syndrome (see diagnosis, below).
Headache is one of the criteria for PCS, but it is notably undetermined where the headache comes from. Couch, Lipton, Stewart and Scher (2007) argue that headaches, one of the hallmarks of PCS, occur in a variety of injuries to the head and neck. Further, Lew et al. (2006) reviewed ample studies comparing headaches to post-traumatic headaches and found that there is wide heterogeneity in the source and causes of headaches. They point out that the International Headache Society lists 14 known causes of headaches, as well. Furthermore, the headaches may be better accounted for by mechanical causes, such as whiplash, which is often mistaken for PCS. An additional possibility is that Post-traumatic Stress Disorder can account for some cases diagnosed as PCS, but for emotional regulation as well.
Depression, post-traumatic stress disorder, and chronic pain share symptoms resembling those of PCS. One study found that while people with chronic pain without TBI do report many symptoms similar to those of post-concussion syndrome, they report fewer symptoms related to memory, slowed thinking, and sensitivity to noise and light than people with MTBI do. Additionally, it has been found that neuroendocrinology may account for depressive symptoms and stress management due to irregularities in cortisol regulation, and thyroid hormone regulation. Lastly, there is evidence that major depression following TBI is quite common, but may be better accounted for with a diagnosis of dysexecutive syndrome
In a syndrome, a set of symptoms is consistently present, and symptoms are linked such that the presence of one symptom suggests that of others. Because PCS symptoms are so varied and many can be associated with a large number of other conditions, doubt exists about whether the term "syndrome" is appropriate for the constellation of symptoms found after concussion. The fact that the persistence of one symptom is not necessarily linked to that of another has similarly led to doubt about whether "syndrome" is the appropriate term.
A longstanding controversy surrounding PCS concerns the nature of its etiology – that is, the cause behind it – and the degree to which psychological factors and organic factors involving brain dysfunction are responsible. The debate has been referred to as 'psychogenesis versus physiogenesis' (psychogenesis referring to a psychological origin for the condition, physiogenesis to a physical one).
- Daniel Amen, post-concussion expert for the National Football League
- Rao V, Lyketsos C (2000). "Neuropsychiatric sequelae of traumatic brain injury". Psychosomatics 41 (2): 95–103. doi:10.1176/appi.psy.41.2.95. PMID 10749946.
- Mittenberg W, Strauman S (2000). "Diagnosis of mild head injury and the postconcussion syndrome". Journal of Head Trauma Rehabilitation 15 (2): 783–791. doi:10.1097/00001199-200004000-00003. PMID 10739967.
- McHugh T, Laforce R, Gallagher P, Quinn S, Diggle P, Buchanan L (2006). "Natural history of the long-term cognitive, affective, and physical sequelae of a minor traumatic brain injury". Brain and Cognition 60 (2): 209–11. PMID 16646125.
- Bigler ED (2008). "Neuropsychology and clinical neuroscience of persistent post-concussive syndrome". Journal of the International Neuropsychological Society 14 (1): 1–22. doi:10.1017/S135561770808017X. PMID 18078527.
- Iverson GL, Lange RT (2003). "Examination of "postconcussion-like" symptoms in a healthy sample". Applied Neuropsychology 10 (3): 137–144. doi:10.1207/S15324826AN1003_02. PMID 12890639.
- King NS (1996). "Emotional, neuropsychological, and organic factors: Their use in the prediction of persisting postconcussion symptoms after moderate and mild head injuries". Journal of Neurology, Neurosurgery, and Psychiatry 61 (1): 75–81. doi:10.1136/jnnp.61.1.75. PMC 486463. PMID 8676166.
- Ryan LM, Warden DL (2003). "Post concussion syndrome". International Review of Psychiatry 15 (4): 310–6. doi:10.1080/09540260310001606692. PMID 15276952.
- Kushner D (1998). "Mild traumatic brain injury: Toward understanding manifestations and treatment". Archives of Internal Medicine 158 (15): 1617–24. doi:10.1001/archinte.158.15.1617. PMID 9701095.
- Weight DG (1998). "Minor head trauma". Psychiatric Clinics of North America 21 (3): 609–624. doi:10.1016/S0193-953X(05)70026-5. PMID 9774799.
- Anderson T, Heitger M, Macleod AD (2006). "Concussion and mild head injury". Practical Neurology 6 (6): 342–357. doi:10.1136/jnnp.2006.106583.
- Hall RC, Hall RC, Chapman MJ (2005). "Definition, diagnosis, and forensic implications of postconcussional syndrome". Psychosomatics 46 (3): 195–202. doi:10.1176/appi.psy.46.3.195. PMID 15883140.
- Maskell F, Chiarelli P, Isles R (2006). "Brain Injury". pp. 293–305.
- Barth JT, Ruff R, Espe-Pfeifer P (2006). "Mild traumatic brain injury: Definitions". In Nicholson, Keith; Young, Gerald; Andrew K. Kane. Psychological Knowledge in Court: PTSD, Pain and TBI. Berlin: Springer. pp. 271–7. ISBN 0-387-25609-1.
- Margulies S (September 2000). "The postconcussion syndrome after mild head trauma: Is brain damage overdiagnosed? Part 1". Journal of Clinical Neuroscience 7 (5): 400–8. doi:10.1054/jocn.1999.0681. PMID 10942660.
- King NS. 2003. Post-concussion syndrome: clarity amid the controversy?. Accessed January 1, 2007.
- Shaw NA (2002). "The neurophysiology of concussion". Progress in Neurobiology 67 (4): 281–344. doi:10.1016/S0301-0082(02)00018-7. PMID 12207973.
- Jagoda A, Riggio S (2000). "Mild traumatic brain injury and the postconcussive syndrome". Emergency Medicine Clinics of North America 18 (2): 355–363. doi:10.1016/S0733-8627(05)70130-9. PMID 10798893.
- Evans RW (1992). "The postconcussion syndrome and the sequelae of mild head injury". Neurologic Clinics 10 (4): 815–47. PMID 1435659.
- Cobb S, Battin B (2004). "Second-impact syndrome". The Journal of School Nursing 20 (5): 262–7. doi:10.1177/10598405040200050401. PMID 15469376.
- Olver J (2005). "Traumatic brain injury—the need for support and follow up". Australian Family Physician 34 (4): 269–71. PMID 15861750.
- Merck manuals online medical library. 2003. Concussion. Accessed May 11, 2008.
- Goodyear B, Umetsu D (2002). "Selected issues in forensic neuropsychology". In Van Dorsten B. Forensic Psychology: From Classroom to Courtroom. New York: Kluwer Academic/Plenum. pp. 289–290. ISBN 0-306-47270-8.
- Jacobson RR (August 1995). "The post-concussional syndrome: physiogenesis, psychogenesis and malingering. An integrative model". Journal of Psychosomatic Research 39 (6): 675–693. doi:10.1016/0022-3999(95)00006-5. PMID 8568727.
- Iverson GL (2005). "Outcome from mild traumatic brain injury". Current Opinion in Psychiatry 18 (3): 301–317. doi:10.1097/01.yco.0000165601.29047.ae. PMID 16639155.
- Jorge RE (2005). "Neuropsychiatric consequences of traumatic brain injury: A review of recent findings". Current Opinion in Psychiatry 18 (3): 289–299. doi:10.1097/01.yco.0000165600.90928.92. PMID 16639154.
- Yeates KO, Taylor HG (2005). "Neurobehavioural outcomes of mild head injury in children and adolescents". Pediatric Rehabilitation 8 (1): 5–16. doi:10.1080/13638490400011199. PMID 15799131.
- Bryant RA (2008). "Disentangling mild traumatic brain injury and stress reactions". New England Journal of Medicine 358 (5): 525–7. doi:10.1056/NEJMe078235. PMID 18234757.
- Lee LK (2007). "Controversies in the sequelae of pediatric mild traumatic brain injury". Pediatric Emergency Care 23 (8): 580–3. doi:10.1097/PEC.0b013e31813444ea. PMID 17726422.
- Boake C; McCauley SR; Levin HS; Pedroza C; Contant CF; Song JX et al. (2005). "Diagnostic criteria for postconcussional syndrome after mild to moderate traumatic brain injury". Journal of Neuropsychiatry and Clinical Neurosciences 17 (3): 350–6. doi:10.1176/appi.neuropsych.17.3.350. PMID 16179657.
- ICD-10, International Statistical Classification of Diseases and Related Health Problems 10th Revision (ICD-10) Version for 2010, F07.2 Postconcussional syndrome, World Health Organization.
- Sivák S, Kurca E, Jancovic D, Petriscák S, Kucera P (2005). "[Contemporary view on mild brain injuries in adult population]" (PDF). Cas. Lek. Cesk. (in Slovak) 144 (7): 445–50; discussion 451–4. PMID 16161536.
- Mittenberg W, Canyock EM, Condit D, Patton C (2001). "Treatment of post-concussion syndrome following mild head injury". Journal of Clinical and Experimental Neuropsychology 23 (6): 829–836. doi:10.1076/jcen.23.6.829.1022. PMID 11910547.
- Legome E. 2006. Postconcussive syndrome. eMedicine.com. Accessed January 1, 2007.
- Bazarian JJ, Atabaki S (August 2001). "Predicting postconcussion syndrome after minor traumatic brain injury". Academic Emergency Medicine 8 (8): 788–795. doi:10.1111/j.1553-2712.2001.tb00208.x. PMID 11483453.
- Hulshoff Pol HE, Hijman R, Baaré WF, van Eekelen S, van Ree JM (August 2000). "Odor discrimination and task duration in young and older adults". Chemical Senses 25 (4): 461–464. doi:10.1093/chemse/25.4.461. PMID 10944510.
- Iverson GL, Zasler ND, Lange RT (2006). "Post-concussive disorder". In Zasler ND, Katz DI, Zafonte RD. Brain Injury Medicine: Principles and Practice. Demos Medical Publishing. pp. 374–385. ISBN 1-888799-93-5. Retrieved 2008-06-05.
- Rees PM (2003). "Contemporary issues in mild traumatic brain injury". Archives of Physical Medicine and Rehabilitation 84 (12): 1885–94. doi:10.1016/j.apmr.2003.03.001. PMID 14669199.
- Schapiro S, Mandel S, Sataloff RT (1993). Minor Head Trauma: Assessment, Management, and Rehabilitation. Berlin: Springer-Verlag. p. 152. ISBN 0-387-97943-3.
- Willer B, Leddy JJ (September 2006). "Management of concussion and post-concussion syndrome". Current Treatment Options in Neurology 8 (5): 415–426. doi:10.1007/s11940-006-0031-9. PMID 16901381.
- Schnadower D, Vazquez H, Lee J, Dayan P, Roskind CG (2007). "Controversies in the evaluation and management of minor blunt head trauma in children". Current Opinion in Pediatrics 19 (3): 258–264. doi:10.1097/MOP.0b013e3281084e85. PMID 17505183.
- McAllister TW, Arciniegas D (2002). "Evaluation and treatment of postconcussive symptoms". NeuroRehabilitation 17 (4): 265–83. PMID 12547976.
- Ropper AH, Gorson KC (2007). "Clinical practice. Concussion". New England Journal of Medicine 356 (2): 166–172. doi:10.1056/NEJMcp064645. PMID 17215534.
- Gualtieri CT (1999). "The pharmacologic treatment of mild brain injury". In Varney NR, Roberts RJ. The Evaluation and Treatment of Mild Traumatic Brain Injury. Hillsdale, N.J.: Lawrence Erlbaum Associates. pp. 411–2. ISBN 0-8058-2394-8.
- Alexander MP (1995). "Mild traumatic brain injury: Pathophysiology, natural history, and clinical management". Neurology 45 (7): 1253–60. doi:10.1212/WNL.45.7.1253. PMID 7617178.
- Duff J (2004). "The Usefulness of Quantitative EEG(QEEG) and Neurotherapy in the Assessment and Treatment of Post-concussion Syndrome". Clinical EEG and Neuroscience 35 (4).
- McCrea 2008, pp. 163–4
- Komaroff A, Harvard University Harvard Business School (1999). The Harvard Medical School Family Health Guide. New York: Simon & Schuster. p. 359. ISBN 0-684-84703-5.
- Signoretti, S; Lazzarino, G; Tavazzi, B; Vagnozzi, R (October 2011). "The pathophysiology of concussion". PM & R : the journal of injury, function, and rehabilitation 3 (10 Suppl 2): S359–68. doi:10.1016/j.pmrj.2011.07.018. PMID 22035678.
- Wetjen, NM; Pichelmann, MA; Atkinson, JL (October 2010). "Second impact syndrome: concussion and second injury brain complications". Journal of the American College of Surgeons 211 (4): 553–7. doi:10.1016/j.jamcollsurg.2010.05.020. PMID 20822744.
although the syndrome might be uncommon
- Saulle M, Greenwald BD (2012). "Chronic traumatic encephalopathy: a review". Rehabil Res Pract 2012: 816069. doi:10.1155/2012/816069. PMC 3337491. PMID 22567320.
- Necajauskaite O, Endziniene M, Jureniene K (2005). "The prevalence, course and clinical features of post-concussion syndrome in children". Medicina (Kaunas) 41 (6): 457–64. PMID 15998982.
- Lovell MR, Fazio V; Fazio (February 2008). "Concussion management in the child and adolescent athlete". Current Sports Medicine Reports 7 (1): 12–5. doi:10.1097/01.CSMR.0000308671.45558.e2. PMID 18296938.
- Traumatic Brain Injury: Hope Through Research. NINDS. Publication date February 2002. NIH Publication No. 02-2478. Prepared by: Office of Communications and Public Liaison, National Institute of Neurological Disorders and Stroke, National Institutes of Health
- Benton AL, Levin HS, Eisenberg HM (1989). "Historical notes on the postconcussion syndrome". Mild Head Injury. Oxford [Oxfordshire]: Oxford University Press. pp. 3–5. ISBN 0-19-505301-X.
- Evans RW (2004). "Post-traumatic headaches". Neurological Clinics 22 (1): 237–249. doi:10.1016/S0733-8619(03)00097-5. PMID 15062537.
- Jones E, Fear NT, Wessely S; Fear; Wessely (November 2007). "Shell shock and mild traumatic brain injury: A historical review". The American Journal of Psychiatry 164 (11): 1641–5. doi:10.1176/appi.ajp.2007.07071180. PMID 17974926.
- McCrea, MA (2008). Mild Traumatic Brain Injury and Postconcussion Syndrome: The New Evidence Base for Diagnosis and Treatment. Oxford [Oxfordshire]: Oxford University Press. p. 157. ISBN 0-19-532829-9.
- Couch JR, Lipton RB, Stewart WF, Scher AI; Lipton; Stewart; Scher (September 2007). "Head or neck injury increases the risk of chronic daily headache: a population-based study". Neurology 69 (11): 1169–77. doi:10.1212/01.wnl.0000276985.07981.0a. PMID 17846416.
- Lew HL, Lin PH, Fuh JL, Wang SJ, Clark DJ, Walker WC; Lin; Fuh; Wang; Clark; Walker (July 2006). "Characteristics and treatment of headache after traumatic brain injury: a focused review". Am J Phys Med Rehabil 85 (7): 619–27. doi:10.1097/01.phm.0000223235.09931.c0. PMID 16788394.
- Kasch H, Bach FW, Jensen TS; Bach; Jensen (June 2001). "Handicap after acute whiplash injury: a 1-year prospective study of risk factors". Neurology 56 (12): 1637–43. doi:10.1212/WNL.56.12.1637. PMID 11425927.
- Hickling EJ, Blanchard EB, Silverman DJ, Schwarz SP; Blanchard; Silverman; Schwarz (March 1992). "Motor vehicle accidents, headaches and post-traumatic stress disorder: assessment findings in a consecutive series". Headache 32 (3): 147–51. doi:10.1111/j.1526-4610.1992.hed3203147.x. PMID 1563947.
- Jorge R, Robinson RG; Robinson (November 2003). "Mood disorders following traumatic brain injury". Int Rev Psychiatry 15 (4): 317–27. doi:10.1080/09540260310001606700. PMID 15276953.
- Abreu, B.C.; Zgaljardic, D.; Borod, J.C.; Seale, G.; Temple, R.O.; Ostir, G.V.; Ottenbacher, K.J. (2009). "Emotional Regulation, Processing, and Recovery After Acquired Brain Injury". In Matuska, K.; Christiansen, C.H.; Polatajko, H.; Davis, J.A. Life Balance: Multidisciplinary Theories and Research. Thorofare NJ: SLACK/AOTA Press. pp. 223–240. ISBN 1556429061.
- Jorge RE, Robinson RG, Moser D, Tateno A, Crespo-Facorro B, Arndt S; Robinson; Moser; Tateno; Crespo-Facorro; Arndt (January 2004). "Major depression following traumatic brain injury". Arch. Gen. Psychiatry 61 (1): 42–50. doi:10.1001/archpsyc.61.1.42. PMID 14706943.
- Smith DH (2006). "Postconcussional symptoms not a syndrome". Psychosomatics 47 (3): 271–2. doi:10.1176/appi.psy.47.3.271. PMID 16684949. | <urn:uuid:6c7fb128-2fb8-45e6-9cd2-3cb82137199c> | {
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Family and community are important aspects of society, but the way in which they contribute to progress is difficult to define and measure. The quality and strength of people’s relationships and bonds with others - their family, friends and the wider community - are important ingredients of the level of social cohesion. And a more cohesive society is one in which communities are strong and inclusive, and where fewer people fall through the cracks.
Rather than present a single indicator, this commentary presents some measures which illustrate aspects of family and community life in Australia, particularly those that are important to social cohesion.
People are social beings. They require love, companionship and agreeable engagements with others (including those that involve the formal exchange of goods and services) to flourish. The absence of family, friendship or other caring or cooperative social relationships at any stage of life, but particularly when people are least able to care for themselves, can have a serious impact on personal wellbeing. And there are often high costs to the wider community associated with assisting people with poor or broken social relationships.
People's relationships and bonds with one
another - be it their family, friends or the wider community - together with their shared values contribute to social cohesion. The family unit takes on a large part of the burden of caring for people in need of support, and the vast range of services provided within communities by groups, clubs and charitable organisations are a crucial adjunct to the institutionalised care provided by governments. Families are responsible for providing guidance on social values which helps to form the basis of a civil society. Day to day interactions between people in a community build trust and reciprocity.
The discussion here focuses on the contribution that family and community functioning makes to social cohesion. There is no conceivable single indicator that captures all that might be important. Therefore a selection of indicators is presented that paint a picture of the way our families and communities function, and the cohesiveness of Australian society.
Families and family functioning
The family can be seen as the wellspring from which some of the dimensions crucial to social cohesion develop, such as trust, social support and the extension of social networks. It is also the place where, through the everyday performance of family life, people make an enormous contribution to those who require special assistance. Most of the care provided to children, and to people with a disability is provided by immediate and extended family members.
|Social cohesion and related concepts|
Social cohesion refers to the social ties and community commitments that bind people together.1 Closely related to the concept of social cohesion are the notions of 'social capital' and ‘social exclusion’.
Social capital consists of networks, together with shared norms, values and understandings which facilitate cooperation within and among groups. It is a contributor to community strength, and can be accumulated when people interact with one another formally and informally, for example informal interaction with family and friends and formal interaction in groups and organisations in the wider community.2
Social exclusion is a form of social disadvantage encompassing economic and non-economic factors. Excluded individuals and groups are separated from
institutions and wider society, and consequently from both rights and duties.3
Desired directions of change
Families have long been viewed as the core social unit that serves to maintain people's welfare. Over recent decades, the emphasis of debate has shifted from the maintenance of the ideal family form (earlier viewed as the so-called traditional family involving a married couple and their children), to one in which the quality of relationships between family members, irrespective of form, is viewed as being more important. Yet, to members of the community who hold on to traditional
values, the decline of traditional family structures may be viewed as regress.
Well established research suggests that there are positive health outcomes, such as greater longevity, from having high quality relationships with close family members and friends. It also suggests that other aspects of life (such as employment outcomes) are better for people with wide social networks.2
While views about ideal levels of social cohesion vary, for some aspects of social cohesion there is likely to be general agreement that change in a particular direction is good or bad. For instance, most would agree that decreases in the suicide rate, in the incidence of drug-induced deaths, or in the level of omelessness, represent improvements. But for many other aspects of social cohesion, the choice and interpretation of indicators may be problematic.
Changing nature of the family
Over recent decades there have been extensive change in the way families are structured and function. These trends have a range of social implications. Later partnering, later child bearing and smaller family size have implications for the size and age profile of the population. The increasing propensity to live alone has implications for housing and support.
There is considerable interest in determining whether families are undergoing more transitions than in the past and what the implications of this might be. The impact of divorce and family breakup on families is of concern, as is the quality of relationships between children and parents, and children and step-parents.4
Types of families in Australia
According to the 2001 Census of Population and Housing, 83% of people lived in a family, 3% lived in group households, 9% lived alone, less than 1% were boarders living in a family home, and 4% were residing in institutions such as prisons, nursing homes, and hostels.
In 2003, there were over five million families in Australia. The most common type of family was a couple family with children (45%), followed by a couple family without children (38%). There were 821,800 one parent families which represented 15% of all families. In the years from 1993 to 2003, the proportion of one parent families increased from 14% to 15%. However, there has been a more marked increase in the proportion of children under 15 living in one parent families, which rose from 15% to 20% over ten years.
Largely due to the ageing of the population creating 'empty nesters', but also including trends towards childlessness, over the past decade the proportion of families with children has declined from 65% of families to 60%. The decline has been driven by couple families with children, which fell from 52% of families to 45% in this period.
Assuming these trends continue, by 2021 the most common family type is projected to change from couples with children to couples without children. Lone person households will also become more common. The number of lone person households is projected to increase from 1.6 million households in 1996 to between 2.4 million and 3.4 million households in 2021, increasing from 9% of the population to between 11% and 15% of the population.5
Family formation and dissolution
Ideally we would like to measure all family formation and dissolution, whether formed through registered or de facto marriages, and dissolved through divorces or separations. As such detailed family history data is not available we use registered marriage and divorce statistics.
Marriage and divorce
The commitment to a formal marriage (in a religious ceremony or by a civil celebrant) has become less popular. In 1970, the crude marriage rate stood at 9.3 marriages per 1,000 people. Between 1992 and 2002 the crude marriage rate declined from 6.6 to 5.4 marriages per 1,000 people, a continuation of a longer term trend.
The trend away from marriage is partly explained by a growth in the proportion of people who form de facto marriage relationships and a growth in people living without partners. Comparisons from the 1986 and 2001 Censuses of Population and Housing show that de facto couples as a proportion of all couples has doubled over the period, from 6% to 12%. Further comparisons from 1986 to 2001 show that the proportion of adults who did not have a partner (in either a legal marriage or a de facto marriage relationship) increased from 33% to 38%. The change was greater for younger people (those in the 18-34 year age range), but the proportion of people who were not living with a partner increased for each age group under 65.6
The dissolution of legal marriages through divorce has contributed to the increase in the proportion of people not living with a partner. However, while divorce rates increased over the decade up to 1996, the data indicate a decline in divorce rates from then until 2001, when they increased again. The decline in the latter half of the 1990s needs to be viewed in the context of the decline in the number of registered marriages.
In 2001, the crude divorce rate (2.9 divorces per 1,000 people) was higher than that in the preceding year (2.6 divorces per 1,000 people) and had returned to the longer term peak of 2.9 recorded in 1996.
Children and divorce
Impact of divorce and separation
An increase in the number of divorces may reflect a greater prevalence of unhappy marriages, or greater acceptance of dissolving unhappy marriages.
Divorce and separation of couples is a disruption to family life. Some families manage the transition well; others find it stressful. The process of adjusting to the new family circumstances can take differing lengths of time with some people feeling stressed by the divorce or separation years after it occured.
As the rate of divorces increases so too does the number of children experiencing parental divorce. Over the 10-year period from 1991-2001, there has been a steady increase in the number of children under 18 experiencing divorce. In 2001, approximately 53,400 children under 18 experienced divorce. In 1991, it was 46,700.
One of the impacts of divorce and separation on family structure is to create fewer families where children live with both natural parents. The proportion of families with children under 18 which were intact was 76% in 1992 and declined to 72% in 1997.7 Over the same period, while the proportion of step families and blended families with children under 18 stayed fairly similar in size (step families 4% and blended families 3%), the proportion of one parent families grew, as noted in the commentary on types of families in Australia.
One parent families are also more prone to disadvantage in a number of areas, and this is discussed in the article Multiple disadvantage.
Caring role of families
The care and support a family provides is a foundation for people's health and social functioning. Care and guidance take place within the family across the life cycle, beginning with parents (and sometimes grandparents) caring for children, and often ending with children caring for parents.
Raising children is a time consuming job. Figures from the 1997 Time Use Survey indicate that parents spend on average six and a half hours a day caring for children; for mothers this is over eight and a half hours a day while for fathers it is four hours a day. The largest component (65%) is low intensity, child minding activities.
|Stress to families|
Families and communities play a key role in raising capable and functioning people. When considering the relationship of the family to progress it might be ideal to find indicators which measure how effectively families undertake this role. Such data are not available, although some key outcomes of family life, such as whether people behave well in society, achieve good educational and work outcomes are measured by other indicators in this publication (Crime, Work and Education). Instead we discuss some of the stresses which can threaten the optimal functioning of the family unit. Families can experience a range of pressures: the dissolution through relationship breakdown has already been discussed. Other factors widely regarded as key include: the quality of parent-child relationships (both resident and non-resident), financial stress, conflict between parent figures, parental mental health and substance use, and abuse or neglect of children.8
Feeling pressed for time is one important stressor for which we have data. Parents with small children feel the greatest amount of time pressure. Over 60% of mothers living in couple relationships, with a youngest child aged 0-4 years old, always feel pressed for time. For fathers in the same family type, it is 52%. The reporting of always feeling time stressed decreases as children age, with 48% of mothers and 34% of fathers in couple families, whose youngest child is aged 15-24 years old reporting always feeling pressed for time. By the time the children are over 25 years of age, 35% of mothers and 23% of fathers report always feeling time stressed. For fathers this is in line with the experience of adults who live in households with no children present.
The job of raising children is complex. And if one or both parents suffers from illness or psychological distress this may result in poor outcomes for children.9 In the 2001 National Health Survey, 13% of mothers and 9% of fathers in couple families reported high or very high psychological distress. For lone mothers the proportion expressing high or very high psychological distress was almost double that of mothers in couple families (23%). While some mothers with very young children suffer from post-natal depression, the proportion of mothers with children younger than five reporting high or very high psychological distress was much the same as that for mothers with children aged 10-14 (14% and 13% respectively).
Young adults (18-24) living in one parent families report higher distress than young adults living in couple families. This is particularly true for young men in one parent families who were twice as likely to report high psychological distress (18% compared with 9%).
Developmental activities such as playing with children take, on average, an hour of a parent's day, with mothers and fathers spending proportionally the same amount of their child care time playing with their children (15%). On the other hand mothers spend 15% of their child care time providing such physical care as feeding, bathing, and dressing children, compared with 8% for fathers.
Primary carers of the elderly and disabled, 1998
When mothers work outside the house, in paid employment, the contact time between them and children reduces. Recent research indicates that, on the whole, mothers choose to maintain the time spent on developmental activities while substantially reducing low intensity, child minding activities. As mother's hours of paid work increase, fathers increase slightly the time they spend with children in developmental activities and in low intensity care.10
|Relationship to recipient||Recipient of care||no.|
|Daughter||Does not live with|
|Son||Does not live with|
|Other female||Does not live with|
|Female friend/neighbour||Does not live with|
|(a) Total Includes other relationships not defined in list above.|
Source: Data available on request, Survey of Disability, Ageing and Carers 1998.
Families also often care for elderly and disabled relatives. In 1998, the Survey of Disability, Ageing and Carers identified that there were over 450,000 people who were primary carers. A primary carer is a person of any age who provides the most informal assistance, in terms of help or supervision, to a person with one or more disabilities. Most of these carers (79%) lived with the person requiring care. And it is a role that most often falls to the immediate family: 89% of primary carers were either a partner, parent or offspring. While many husbands, fathers and sons do provide care, 70% of primary carers were women.
Given some of the trends outlined in this chapter and in the Population and Work chapters (ageing of the population, declining fertility rate, increased female labour force participation and relationship breakdown) there are some concerns about the future availability of carers.11
|NOTE: In Measures of Australia's Progress, the graph and some of the commentary relating to 'Children without an employed parent' incorrectly included information relating to children in jobless households. Other commentary incorrectly referred to numbers of parents.|
Children living without an employed parent
The number of children living without an employed parent is related in part to the structure of the labour market, and in part to the changing structure of Australian families. Children living without an employed parent are a source of particular concern, both because the joblessness is an indicator that the children are at greater risk of experiencing financial hardship and because the joblessness may also have impacts on their psychological wellbeing and long-run personal development.
While studies have shown that there are correlations between someone's childhood circumstances and adult outcomes, there is ongoing debate about the causal relationships involved. It is difficult to obtain all the data needed to fully examine the impacts of and inter- relationships between inherited capabilities, parental and other care, role-models (both parental and other), education, childhood health, income levels, etc. It is also important to note that while studies point to a higher incidence of poor outcomes the results do not suggest simple deterministic patterns — that is while there may be higher risks, such childhood experiences do not necessarily result in adverse outcomes.12
The accompanying chart shows that, since the mid 1990s, the proportion of children living without an employed parent in the same household has been relatively steady at between 16% and 19%. Over half these children lived in one parent families (even though one parent families only accounted for 20% of all children in 2000–01), and about one-third lived in one parent families in which the youngest child was under 5.
In 2000-01, in sole parent families where the youngest child was under 5, 79% of children were living with a jobless parent. This compares to 46% of children in sole parent families where the youngest child was between 5 and 14. In contrast, 55% of children living in couple families had both parents employed.
The longer term effects on children are likely to be greater if the period of joblessness is extended, and may differ depending on the circumstances of the joblessness. For example, if a parent undertakes study, the economic wellbeing of the household may be improved later on. Also, the impact of parental joblessness may be offset if other household members are employed.
People's contact with family and friends
Relationships with family and friends are the basis of the informal networks operating in society. Interaction is key to the maintenance of these networks and provides the opportunity to generate trust. Strong networks in turn act as a reservoir for support.
In the 2002 General Social Survey, most people (95%) reported having contact in the previous week (either in person or via telephone, mail or email) with family or friends outside their household. There was little variation across age groups or between men and women. Less than 1% of people had had no contact with family or friends outside the home, in the previous month.
More people are living alone and time spent alone is also increasing. Adults, of all ages, are increasingly more likely to live alone. Between 1992 and 2002, the proportion of people aged 15-64 years who lived alone increased from 6% to 9%. Among those aged 65 years and over it increased from 29% to 30%.13
Partly associated with more people living alone, people are also spending more of their time alone. Between 1992 and 1997, the average waking time per week spent alone among people aged 15 years and over increased from a little under 18½ to a little over 21 hours. The increases occurred in most age groups, but were typically greater among men than women, and greatest among people who lived alone.14
Most people participate in social activities of one kind or another. In 2002, most Australians living in private dwellings (92%) participated in at least one of a nominated set of social activities in the three months prior to being surveyed. Popular activities were going out to restaurants (80% of people), attending movies (60%), attending or participating in sporting events (57%), visiting parks, zoos and theme parks (51%). Not surprisingly, as people age they are less likely to participate in such social activities. By 75 years and over, 21% of people did not participate in any of the nominated social activities in the previous three months.
Involvement in paid employment provides an important means of meeting, and developing relationships with, a more diverse range of people. As noted in the commentary Work, there have been changes in the levels of labour force participation of both men and women (decreasing for men and increasing for women) which suggests that women have more work-related social contacts than in the past. In 2002, 8% of unemployed people had had no contact with friends and family outside the household in the previous week. Only 4% of employed people and 6% of people not in the labour force had had no contact. Unemployed people were also much more likely to feel they did not have the ability to ask for small favours from persons outside the household (12% compared with 5% for employed people).
Social participation by adults in 2002(a)
No participation in selected social activities(a)(b), 2002
Undertaking voluntary work is another way in which people meet and interact with one another, and this is discussed in the next section.
Levels of participation in organised, non-organised and social sport or physical activities grew during the 1990s. In 2002, 65% of men and 60% of women had participated in sport or physical activities at some time during the previous 12 months.
According to the 2002 General Social Survey (GSS), 23% of Australian adults participated in church or religious activities during the three months prior to interviewing. Women (26%) were more likely than men (20%) to have participated in church or religious activities. Female participation was higher than male participation among all age groups but for both, participation increased with age.
Participation in religious activities, 2002
In 2002, adults who had participated in church or religious activities within the three months prior to the survey were much more likely to have undertaken voluntary work than those who did not participate (52% to 29%). In particular, they were twice as likely to have volunteered for a welfare or community organisation than those who had not participated in religious activities (18% compared with 9%), and were also more likely to volunteer for an organisation providing education, training or youth development (12% compared with 7%).15
Trust and trustworthiness are two sides of the same coin, acting to lubricate social interaction and the smooth functioning of society. Trust refers to confidence in the reliability of a person or a system. It is based on the expectation that people or organisations will act in ways that are expected or promised, and will take into account the interest of others. Trustworthiness involves honesty, accountability, fair dealing and a level of competence.17
Trust is widely regarded as an important element of social capital, and, therefore, an important part of social cohesion. The ABS does not collect data about trust, per se, although the 2002 GSS collected information on people’s feelings of safety at home, which sheds some light on trust in Australia. About 82% of people reported feeling very safe or safe at home alone after dark, with the rate higher for men (91%) than women (72%).
Reciprocity can be defined as any relationship between two people (or groups of people) where there is a giving and taking. It can be regarded as the general expectation that assistance or support may be returned at some undefined time in the future. Examples of reciprocal actions include contributing time or money to the community, making charitable donations, and sharing support among friends and family. One important and widespread expression of reciprocity is that which occurs over time in families, with reciprocal provision of support that occurs between different family members. Reciprocity is important to social cohesion: a society in which reciprocity is strong may also encourage the sharing of support, knowledge, and ideas between individuals, groups and communities. In a community where reciprocity is strong, people care for each other's interests. The expectation of reciprocity may make people more willing to behave cooperatively or altruistically.17
In 2002, most people (93%) felt they could ask people outside their household for small favours, such as looking after pets, collecting mail, watering gardens, minding a child for a brief period, or borrowing equipment. Overall, there were no significant differences between men and women in being able to ask for small favours.
The picture is much the same for people’s ability to access support from outside the household in times of crisis, with 94% of people reporting they would have support. The greatest source of potential support is family members (82% of people thought their family would help), friends (66%) followed by neighbours (34%) and work colleagues (21%).
Some groups in Australia do report lower levels of ability to access support in times of crisis. People who were born overseas and not proficient in English were more likely to report an inability to access support than people born in Australia (14% felt they could not access support compared with 5%). Some 11% of people aged under 65 with a disability resulting in a core activity restriction felt they could not access support in times of crisis.
Strong community bonds can be formed through things like volunteering and donating money to groups and organisations in the community. Such networks may involve people who do not normally associate with one another, and in this way help to form bridging relationships between these community members. When the support offered by people's families and communities declines or is absent, it can contribute to serious social exclusion and problems such as homelessness, suicide and deaths from drug taking.
Building social support
The likelihood that people will voluntarily give their time to do some work for an organisation or group might be regarded as one of the stronger expressions of social capital, as it involves providing assistance, fulfilling needs and providing opportunities in the community. Participation in voluntary work also reinforces networks and adds to the richness of community life. Between 1995 and 2002, the proportion of people aged 18 years and over who reported that they did some voluntary work during the previous 12 months increased from 24% to 34%. The increases occurred for both sexes and across all age groups, but were proportionately greater for those in the age groups 18-24 (17% to 28%) and 55-64 (24% to 38%).16
Proportions of people volunteering by age
Another indicator of community support is the willingness to donate money or goods to community groups or charities. The Business Generosity Survey showed that in 2002, some 36% of operating businesses made donations, 4% participated in supporting community projects, and 11% sponsored individuals or charities. Some businesses did all three.
Making donations of money to disaster relief funds, charities or groups or organisations in the community is common. In 2000, 74% of adults donated money to an organisation. Women were more likely than men to donate (77% compared with 72%) and 80% of people aged between 35-54 donate. Those most likely to donate money were people already donating their time, with 84% of volunteers donating money.18
Breaking the bonds of social support
When the bonds between people are sufficiently weakened by stresses such as mental illness, abuse, destructive and self-destructive behaviours, individuals may permanently or temporarily become alienated or marginalised from families and social support networks. Deaths as a result of suicide or drug taking and homelessness provide pointers to a disintegration of social support, and hence social cohesion.
Homelessness might be seen as an indicator of poor social cohesion. Homeless people are without settled accommodation and do not have access to the economic and social support that a home normally affords. Of course, there are many, often interrelated, personal and situational factors that may cause people to become or remain homeless. These include family breakdown, drug abuse, gambling, mental health problems, domestic violence and poverty.
People experiencing homelessness can stay in any number of places, including sleeping rough, staying in stop gap accommodation (with friends or in community refuges for those in crisis situations) or in other low cost accommodation (such as rooms in boarding houses). As a result it is very difficult to measure the numbers of people involved. Nevertheless, there have been some attempts to provide authoritative estimates. Those prepared by Chamberlain, MacKenzie and the ABS, based on the 2001 Census of Population, estimated almost 100,000 homeless people in Australia on Census night 2001. Of these, approximately 14,000 were sleeping rough and nearly half (48,600) were staying with friends and relatives.20 The estimate of homeless people, using the 1996 Census of Population was 105,000 people. As an indicator of the difficulty experienced in counting the homeless, in 1997 researchers of the Consilium group, using different methodologies to those used in the Chamberlain/ABS study produced a smaller estimate of 53,000 people.21
Information obtained from community organisations providing crisis accommodation and support services (compiled by the Australian Institute of Health and Welfare) indicate that greater numbers of clients received daily support in 2002-03 (about 21,100 to 22,500 per day) than in 1996-97 (about 13,000 to 14,000 per day).22 But these numbers are understood to represent only a fraction of homeless people in Australia on any one day, and may be influenced by an increased willingness to use such services. They cannot by themselves be taken as reliable evidence of deteriorating levels of social attachment.
The suicide rate is one widely used indicator of social cohesion.23 While many complex factors might influence a person's decision to take his or her own life, suicide points to a loss of will to live as part of society and an inability of others to ensure that the person's sense of wellbeing was maintained. The prevalence of drug-induced deaths is used as another indicator of social cohesion for similar reasons. While such deaths can occur for many reasons, their occurrences point to individuals who may not be well integrated into a supportive community.
The annual, age standardised, suicide rate has fluctuated substantially over the last century, with the long term ups and downs being more the result of changes in the male suicide rate, which has been more volatile and consistently higher than the female rate. Despite a recent fall in the male suicide rate to 18.8 suicide deaths per 100,000 men in 2002, the general shift from the relatively low rates recorded through the 1970s to higher rates in the late 1980s and 1990s stands in contrast to the downward shift in female rates since the 1970s.
Youth suicide deaths(a)
For young people aged 15-24, the suicide rate showed a period of steady increases in the late 1980s through to the peak of 19.3 suicides per 100,000 people in 1997. Since then it has declined sharply to the current rate in 2002 of 11.8 suicides per 100,000 people. A rate last experienced in 1984.
Drug-induced death rates are mostly due to the use of opiates such as heroin.24 Like suicide, the drug-induced death rate for women has been relatively low and stable over the last two decades, but for men the trend has been quite different. Starting at similar levels as for women in 1982 (about four deaths per 100,000 people), by 1990 the male rate had grown close to seven deaths per 100,000. After remaining stable at about the 1990 level for several years, it rapidly doubled to 14 deaths per 100,000 men in 1999, falling to 6 deaths per 100,000 men in 2002.
For women, on the other hand, the drug-induced death rate at the end of the 20-year period was the same as the beginning (4 and 3.6 per 100,000 women in 1982 and 2002, respectively). The fluctuations over time for women show periods of relative stability with a peak in 1999 of 5 deaths per 100,000 women, and some decline in recent years.
Links to other dimensions of progress
See also the commentaries Crime, Health, Work, Financial hardship, Multiple disadvantage, Culture and leisure, and Democracy, governance and citizenship.
Endnotes suicide by drugs (X60-X64)
1. Berger-Schmitt, R. and Noll, H. 2000, Conceptual Frameworks and Structure of a European System of Social Indicators, EU Reporting Working Paper
No. 9, Centre for Social Research and Methodology, Mannheim.
2. Organisation for Economic Co-operation and Development (OECD) 2001, The Wellbeing of Nations: The Role of Human and Social Capital, Education and Skills, OECD Centre for Educational Research and Innovation, Paris, France.
3. Jary, D. and Jary, J. 2000, Collins Dictionary of Sociology, Harper Collins Publishers, Glasgow.
4. Rodgers, B. 1996, 'Social and psychological wellbeing of children from divorced families: Australian research findings', Australian Psychologist 31, pp. 174-182.
5. Australian Bureau of Statistics 1999, Household and Family Projections 1996 to 2021, cat. no. 3236.0, ABS, Canberra.
6. Australian Bureau of Statistics 2000, 'People without partners', pp. 43-46 in Australian Social Trends, 2000, cat. no. 4102.0, ABS, Canberra.
7. Data on intact families is only available from the Characteristics of Families Survey 1992 & 1997. The next Characteristics of Families Survey, which was undertaken in 2003, is due for publication in 2004.
8. Pryor, J. and Rodgers, B. 2001, Children in Changing Families: Life after Separation, Blackwell Publishers, Great Britain.
9. Silburn, S., Zubrick, S., Garton, A., Gurrin, L., Burton, P., Dalby, R. et al, 1996, Western Australia Child Health Survey: Family and Community Health, ABS and TVW Telethon Institute for Child Health Research, Perth.
10. Bittman, M., Craig, L. and Folbre, N. 2003 'What happens when children receive non-parental care?', pp. 133-151, in Bittman, M., Craig, L. and Folbre, N. (eds) Family Time: Social Organisation of Care, Routledge, New York.
11. Australian Institute of Health and Welfare, 2003, Australia's Welfare 2003, pp. 106-113, AIHW cat. no. AUS 41, AIHW, Canberra.
12. See, for example: Dawkins, P., Gregg, P, and Scutella, R. 2002, 'The growth of jobless households in Australia', Australian Economic Review, vol. 35(2), pp. 133-154; and Gregory, R. 1999 Children and the Changing Labour Market: Joblessness in Families with Dependent Children, Discussion Paper No. 406, Centre for Economic Policy Research, Australian National University.
13. Statistics on proportions of people living alone are published in Family and community: national summary, pp. 28-29, in Australian Social Trends 2003, cat. no. 4102.0, ABS, Canberra.
14. Australian Bureau of Statistics 1999, 'Spending time alone', pp. 35-38 in Australian Social Trends, 1999, cat. no. 4102.0, ABS, Canberra.
15. Australian Bureau of Statistics 2004, 'Religious affiliation and activity', in Australian Social Trends, 2004, cat. no. 4102.0, ABS, Canberra. Due for publication mid-2004.
16. Australian Bureau of Statistics 2001, Voluntary Work, 2000, cat. no. 4441.0, ABS, Canberra. Also, Australian Bureau of Statistics 2003, General Social Survey,
cat. no. 4159.0, ABS, Canberra.
17. Australian Bureau of Statistics 2004, Information Paper: Measuring Social Capital: An Australian Framework and Indicators, cat. no. 1378.0, ABS, Canberra.
18. Australian Bureau of Statistics 2001, Voluntary Work, 2000, cat. no. 4441.0, ABS, Canberra.
19. Standardised death rates enable comparisons of death rates between populations of different age structures by relating them to a standard population. Death rates have been standardised to the 2001 total population.
20. Chamberlain, C. and MacKenzie, D. 2003, Australian Census Analytic Program: Counting the homeless, 2001, cat. no. 2050.0, ABS, Canberra.
21. Consilium Group 1998, Estimating the Number of Homeless People in Australia, FaCS, Canberra.
22. Australian Institute of Health and Welfare (AIHW) 2003, Homeless People in SAAP, SAAP National Data Collection Annual Report 2002-03 Australia. AIHW
cat. no. HOU 91, AIHW, Canberra.
23. Organisation for Economic Co-operation and Development (OECD) 2001, Society at a Glance: OECD Social Indicators, OECD, Paris.
24. For further analysis, see ABS 2001, 'Drug-induced deaths', pp. 71-74 in Australian Social Trends, 2001, cat. no. 4102.0, ABS, Canberra.
25. Drug-induced deaths are those caused directly or indirectly by drug abuse, including deaths from organ damage caused by drugs. They include deaths from illegal drugs as well as the misuse of legal drugs.
Excluded from the death rates presented in this commentary are: deaths directly attributable to alcohol and tobacco use; deaths from poisoning or exposure to volatile organic compounds (such as petrol); and murder where drugs were the weapon. Also excluded are deaths such as some road traffic accidents or AIDS deaths where drug use partly contributed to the death.
Deaths from 1980 to 1998 were classified according to the International Statistical Classification of Diseases Ninth Edition (ICD-9), while deaths from 1999 were classified according to the Tenth Edition (ICD-10). The drug-induced deaths from these different classifications have been matched to facilitate comparisons over time.
In this article, drug-induced deaths include the following categories from the ICD-10:
accidental drug-induced deaths, which include two components: accidental poisoning by drugs (X40-X44) and mental and behavioral disorders due to drug use (F11-F16, F19 & F55)
drug deaths where the intent of the poisoning was undetermined (Y10-Y14).
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Methods | Statistics | Clinical | Educational | Industrial | Professional items | World psychology |
|ICD-10||A83-A86, B941, G05|
Encephalitis is a brain disorder due to an acute inflammation of the brain. It can be caused by a bacterial infection such as bacterial meningitis spreading directly to the brain (primary encephalitis), or may be a complication of a current infectious disease like rabies or syphilis (secondary encephalitis). Certain parasitic or protozoal infestations, such as toxoplasmosis, malaria, or primary amoebic meningoencephalitis, can also cause encephalitis in people with compromised immune systems. Lyme disease may also cause encephalitis. Bartonella henselae can also lead to this. Brain damage occurs as the inflamed brain pushes against the skull, and can lead to death.
Patients with encephalitis suffer from fever, headache and photophobia with weakness and seizures also common. Less commonly, stiffness of the neck can occur with rare cases of patients also suffering from stiffness of the limbs, slowness in movement and clumsiness depending on which specific part of the brain is involved. The symptoms of encephalitis are caused by the brain's defense mechanisms activating to get rid of the infection. Other symptoms can include drowsiness and coughing.
Encephalitis may be caused by a variety of afflictions. One such affliction is rabies. Encephalitis may also be caused by HIV. The major causes of encephalitis outbreaks all over the world are viruses like Japanese Encephalitis, West Nile virus, Chandipura virus, St. Louis Encephalitis, Equine Encephalitis, La Crosse encephalitis, Murray Valley encephalitis virus, California encephalitis virus, Tick-borne meningoencephalitis, Herpes simplex, Influenza A virus. Less common are e.g. RSSE (Russian spring-summer encephalitis) viruses. In addition, consuming excess amounts of brain and nerve tonic may put one at risk for encephalitis, accompanied by Gigantism.[How to reference and link to summary or text]
Adult patients with encephalitis present with acute onset of fever, headache, confusion, and sometimes seizures. Younger children or infants may present irritability, anorexia and fever.
Neurological examinations usually reveal a drowsy or confused patient. Stiff neck, due to the irritation of the meninges covering the brain, indicates that the patient has either meningitis or meningeoncephalitis. Examination of the cerebrospinal fluid obtained by a lumbar puncture procedure usually reveals increased amounts of protein and white blood cells with normal glucose, though in a significant percentage of patients, the cerebrospinal fluid may be normal. CT scan often is not helpful, as cerebral abscess is uncommon. Cerebral abscess is more common in patients with meningitis than encephalitis. Bleeding is also uncommon except in patients with herpes simplex type 1 encephalitis. Magnetic resonance imaging offers better resolution. In patients with herpes simplex encephalitis, electroencephalograph may show sharp waves in one or both of the temporal lobes. Lumbar puncture procedure is performed only after the possibility of prominent brain swelling is excluded by a CT scan examination. Diagnosis is often made with detection of antibodies in the cerebrospinal fluid against a specific viral agent (such as herpes simplex virus) or by polymerase chain reaction that amplifies the RNA or DNA of the virus responsible (such as varicella zoster virus).
Treatment is usually symptomatic. Reliably tested specific antiviral agents are available only for a few viral agents (e.g. acyclovir for herpes simplex virus) and are used with limited success for most infection except herpes simplex encephalitis. In patients who are very sick, supportive treatment, such as mechanical ventilation, is equally important.
- Main article: Encephalitis lethargica
Encephalitis lethargica is an atypical form of encephalitis which caused an epidemic from 1917 to 1928, resulting in millions of deaths worldwide. Those who survived sank into a semi-conscious state that lasted for decades until the Parkinsons drug L-dopa was used to revive those still alive in the late 1960s by Oliver Sacks.
There have been only a small number of isolated cases in the years since, though in recent years a few patients have shown very similar symptoms. The cause is now thought to be either a bacterial agent or an autoimmune response following infection.
Herpes simplex encephalitis
- Main article: Herpes simplex encephalitis
Herpes simplex encephalitis is caused by the herpes simplex virus that manifests in oral cold sores or genital sores. When this triggers brain inflammation, which occurs in 10% of cases of encephalitis (2 cases per million people), half of all untreated patients die (1 case per million people). Brain damage, partial paralysis, seizures, hallucinations and an altered state of consciousness are all common symptoms. HSE can be passed from mother to child during birth in rare cases, where symptoms include lethargy, tremors, irritability, seizures and poor feeding in the first two weeks after birth.
Limbic system encephalitis
In a small number of cases, called limbic encephalitis, the pathogens responsible for encephalitis attack primarily the limbic system (a collection of structures at the base of the brain responsible for basic autonomic functions).
- Awakenings Movie (1990)
- California encephalitis virus
- Equine Encephalitis
- Granulomatous amoebic encephalitis
- Herpes simplex
- Herpes zoster
- Infectious disorders
- La Crosse encephalitis
- Limbic encephalitis
- Japanese Encephalitis
- Murray Valley encephalitis virus
- Powassan encephalitis
- Rasmussen's encephalitis
- St. Louis Encephalitis
- Tick-borne meningoencephalitis
- http://www.encephalitis.info resource providing evidence based support to people affected and professionals
- WHO: Encephalitis
- eMedicine-1 and eMedicine-2 Information on the causes, symptoms, and treatment options for Encephalitis.
- Encephalitis Global, Inc. Website offering information and support to encephalitis survivors, caregivers and loved ones. Encephalitis Global Inc. is a USA 501(c)(3) public charity; annual FACES Encephalitis Conference information available at the website.
- A case study of a Limbic Encephalitis patient
- A website about Garrett Taylor a 2 year old who lost his life after a battle with encephalitis
- Meningitis and Encephalitis Information Page at NINDS
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|ICD-10||J00, J30, J31.0|
|eMedicine||ent/194 med/104, ped/2560|
Rhinitis // or coryza is irritation and inflammation of the mucous membrane inside the nose. Common symptoms of rhinitis are a stuffy nose, runny nose, and post-nasal drip. The most common kind of rhinitis is allergic rhinitis, which is usually triggered by airborne allergens such as pollen and dander. Allergic rhinitis may cause additional symptoms, such as sneezing and nasal itching, coughing, headache, fatigue, malaise, and cognitive impairment. The allergens may also affect the eyes, causing watery, reddened, or itchy eyes and puffiness around the eyes.
In rhinitis, the inflammation of the mucous membrane is caused by viruses, bacteria, irritants or allergens. The inflammation results in the generation of large amounts of mucus, commonly producing a runny nose, as well as a stuffy nose and post-nasal drip. In the case of allergic rhinitis, the inflammation is caused by the degranulation of mast cells in the nose. When mast cells degranulate, they release histamine and other chemicals, starting an inflammatory process that can cause symptoms outside the nose, such as fatigue and malaise. In the case of infectious rhinitis, it may occasionally lead to pneumonia, either viral pneumonia or bacterial pneumonia. Sneezing also occurs in infectious rhinitis to expel bacteria and viruses from respiratory system.
Rhinitis is categorized into three types: (i) infective rhinitis includes acute and chronic bacterial infections; (ii) nonallergic (vasomotor) rhinitis includes autonomic, hormonal, drug-induced, atrophic, and gustatory rhinitis, as well as rhinitis medicamentosa; (iii) allergic rhinitis, triggered by pollen, mold, animal dander, dust, Balsam of Peru, and other similar inhaled allergens.
Rhinitis is commonly caused by a viral or bacterial infection, including the common cold, which is caused by Rhinoviruses, Coronaviruses, and influenza viruses, others caused by adenoviruses, human parainfluenza viruses, human respiratory syncytial virus, enteroviruses other than rhinoviruses, metapneumovirus, and measles virus, or bacterial sinusitis, which is commonly caused by Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis. Symptoms of the common cold include rhinorrhea, sneezing, sore throat (pharyngitis), cough, congestion, and slight headache.
Non-allergic rhinitis refers to runny nose that is not due to allergy. Non-allergic rhinitis can be classified as either non-inflammatory or inflammatory rhinitis.
One very common type of non-inflammatory, non-allergic rhinitis that is sometimes confused with allergy is called vasomotor rhinitis, in which certain nonspecific stimuli, including changes in environment (temperature, humidity, barometric pressure, or weather), airborne irritants (odors, fumes), dietary factors (spicy food, alcohol), sexual arousal, exercise, and emotional factors trigger rhinitis. There is still much to be learned about this, but it is thought that these non-allergic triggers cause dilation of the blood vessels in the lining of the nose, which results in swelling and drainage.
Vasomotor rhinitis can coexist with allergic rhinitis, and this is called "mixed rhinitis." The pathology of vasomotor rhinitis appears to involve neurogenic inflammation and is as yet not very well understood. Vasomotor rhinitis appears to be significantly more common in women than men, leading some researchers to believe that hormones play a role. In general, age of onset occurs after 20 years of age, in contrast to allergic rhinitis which can be developed at any age. Individuals with vasomotor rhinitis typically experience symptoms year-round, though symptoms may be exacerbated in the spring and autumn when rapid weather changes are more common. An estimated 17 million United States citizens have vasomotor rhinitis.
The antihistamine azelastine, applied as a nasal spray, may be effective for vasomotor rhinitis. Fluticasone propionate or budesonide (both are steroids) in nostril spray form may also be used for symptomatic treatment.
Allergic rhinitis or hay fever may follow when an allergen such as pollen, dust, or Balsam of Peru is inhaled by an individual with a sensitized immune system, triggering antibody production. These antibodies mostly bind to mast cells, which contain histamine. When the mast cells are stimulated by an allergen, histamine (and other chemicals) are released. This causes itching, swelling, and mucus production.
Symptoms vary in severity between individuals. Very sensitive individuals can experience hives or other rashes. Particulate matter in polluted air and chemicals such as chlorine and detergents, which can normally be tolerated, can greatly aggravate the condition.
Characteristic physical findings in individuals who have allergic rhinitis include conjunctival swelling and erythema, eyelid swelling, lower eyelid venous stasis, lateral crease on the nose, swollen nasal turbinates, and middle ear effusion.
Even if a person has negative skin-prick, intradermal and blood tests for allergies, they may still have allergic rhinitis, from a local allergy in the nose. This is called local allergic rhinitis. Many people who were previously diagnosed with nonallergic rhinitis may actually have local allergic rhinitis.
A patch test may be used to determine if a particular substance is causing the rhinitis.
It is a condition of rebound nasal congestion brought on by extended use of topical decongestants (e.g., oxymetazoline, phenylephrine, xylometazoline, and naphazoline nasal sprays) that work by constricting blood vessels in the lining of the nose.
Chronic atrophic rhinitis
Chronic rhinitis in form of atrophy of the mucous membrane and glands.
Chronic form of dryness of the mucous membranes.
Chronic rhinitis associated with polyps in the nasal cavity.
The management of rhinitis depends on the underlying cause. High-dose administration of Vitamin B12 has been additionally validated to stimulate the activity of the body's TH1 suppressor T-Cells, which then down-regulates the over-production of the allergen antibody IgE in allergic individuals, which could decrease both near- and long-term manifestations of rhinitis symptomology.
In the case of infectious rhinitis, vaccination against influenza viruses, adenoviruses, measles, rubella, Streptococcus pneumoniae, Haemophilus influenzae, diphtheria, Bacillus anthracis, and Bordetella pertussis may even help prevent it.
Coryza may have its roots in the Greek Koryza, which is likely to be compounded from "kara" and "zeein", which are the noun for head and the verb, to boil. Coryza would therefore be a boiling over of the head. According to another source, coryza was an ancient Greek word denoting a fool. According to physician Andrew Wylie, "we use the term for a cold in the head, but the two are really synonymous. The ancient Romans advised their patients to clean their nostrils and thereby sharpen their wits."
- Pfaltz, founding authors, Walter Becker, Hans Heinz Naumann, Carl Rudolf (2009). Ear, nose, and throat diseases : with head and neck surgery (3rd ed ed.). Stuttgart: Thieme. p. 150. ISBN 9783136712030.
- "Nonallergic rhinitis".
- "Allergic rhinitis".
- Sullivan, Jr., John B.; Krieger, Gary R. (2001). Clinical environmental health and toxic exposures. p. 341.
- "Allergic rhinitis".
- Quillen, DM; Feller, DB (2006). "Diagnosing rhinitis: Allergic vs. Nonallergic". American family physician 73 (9): 1583–90. PMID 16719251.
- Wilken, Jeffrey A.; Berkowitz, Robert; Kane, Robert (2002). "Decrements in vigilance and cognitive functioning associated with ragweed-induced allergic rhinitis". Annals of Allergy, Asthma & Immunology 89 (4): 372. doi:10.1016/S1081-1206(10)62038-8.
- Marshall, Paul S.; O'Hara, Christine; Steinberg, Paul (2000). "Effects of seasonal allergic rhinitis on selected cognitive abilities". Annals of Allergy, Asthma & Immunology 84 (4): 403. doi:10.1016/S1081-1206(10)62273-9.
- "Economic Impact and Quality-of-Life Burden of Allergic Rhinitis: Prevalence".
- "Inflammatory Nature of Allergic Rhinitis: Pathophysiology".
- "Immunopathogenesis of allergic rhinitis".
- "Vasomotor rhinitis ''Medline Plus". Nlm.nih.gov. Retrieved 2014-04-23.
- Silvers, WS; Poole, JA (February 2006). "Exercise-induced rhinitis: a common disorder that adversely affects allergic and nonallergic athletes.". Annals of Allergy, Asthma & Immunology 96 (2): 334–40. PMID 16498856.
- Adelman, Daniel (2002). Manual of Allergy and Immunology: Diagnosis and Therapy. Lippincott Williams & Wilkins. p. 66. ISBN 9780781730525.
- (Middleton's Allergy Principles and Practice, seventh edition.)
- Knipping, S; Holzhausen, HJ; Riederer, A; Schrom, T (2008). "Ultrastructural changes in allergic rhinitis vs. Idiopathic rhinitis". HNO 56 (8): 799–807. doi:10.1007/s00106-008-1764-4. PMID 18651116.
- Wheeler, PW; Wheeler, SF (2005). "Vasomotor rhinitis". American family physician 72 (6): 1057–62. PMID 16190503.
- Bernstein, Jonathan A. (2007). "Azelastine hydrochloride:a review of pharmacology, pharmacokinetics, clinical efficacy and tolerability". Current Medical Research and Opinion 23 (10): 2441–52. doi:10.1185/030079907X226302. PMID 17723160.
- Pamela Brooks (2012-10-25). The Daily Telegraph: Complete Guide to Allergies. Retrieved 2014-04-23.
- Valet RS, Fahrenholz JM. Allergic rhinitis: update on diagnosis. Consultant. 2009;49:610–613
- Rondón, Carmen; Canto, Gabriela; Blanca, Miguel (2010). "Local allergic rhinitis: A new entity, characterization and further studies". Current Opinion in Allergy and Clinical Immunology 10 (1): 1–7. doi:10.1097/ACI.0b013e328334f5fb. PMID 20010094.
- Rondón, C; Fernandez, J; Canto, G; Blanca, M (2010). "Local allergic rhinitis: Concept, clinical manifestations, and diagnostic approach". Journal of investigational allergology & clinical immunology 20 (5): 364–71; quiz 2 p following 371. PMID 20945601.
- O'Conner, Richard D. M.D. (1990). "FDA Investigative New Drug IND No. 30,488".[verification needed]
- Mansfield, Lyndon E. M.D. (1992). (paper under peer review for publication). Missing or empty
- Wylie, A, (1927). "Rhinology and laryngology in literature and Folk-Lore.". The Journal of Laryngology & Otology 42 (2): 81–87. doi:10.1017/S0022215100029959.
- Sinus Infection And Allergic Rhinitis
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Specific developmental disorder
|Specific developmental disorder|
|Classification and external resources|
Specific developmental disorders are disorders in which development is delayed in one specific area or areas, and in which basically all other areas of development are not affected. Specific developmental disorders are as opposed to pervasive developmental disorders that are characterized by delays in the development of multiple basic functions including socialization and communication.
The tenth revision of the International Statistical Classification of Diseases and Related Health Problems (ICD-10) has four categories of specific developmental disorder: specific developmental disorders of speech and language, specific developmental disorders of scholastic skills, specific developmental disorder of motor function, and mixed specific developmental disorder.
In the third edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-III), SDD was opposed to the pervasive developmental disorders (PDD). There were two factors that were considered:
- The specificity of the impairment: in SDD there is one single domain that is affected, whereas in PDD multiple areas of functioning are affected.
- The nature of the impairment: development in SDD is delayed but not otherwise abnormal, whereas in PDD there are behavioral deviations that are not typical for any developmental stage.
In the fourth edition of the DSM specific developmental disorders are no longer grouped together. Instead they are reclassified as communication disorders, learning disorders, and motor skills disorders.
Comparison and conditions
Specific developmental disorders of speech and language (F80):
Specific developmental disorders of scholastic skills (F81):
- Ahuja Vyas: Textbook of Postgraduate Psychiatry (2 Vols.), 2nd ed. 1999
- Dennis Cantwell & Lorian Baker: Developmental Speech and Language Disorders, 1987, page 4
- Sir Michael Rutter, Eric A. Taylor: Child and Adolescent Psychiatry, 4th ed. 2005
- Robert Jean Campbell, III: Campbell's Psychiatric Dictionary, 2003, page 184
- http://apps.who.int/classifications/icd10/browse/2010/en#/F80 Reference for all ICD-10 disorders mentioned in the table.
- http://behavenet.com/apa-diagnostic-classification-dsm-iv-tr#301 Reference for all DSM-IV-TR disorders mentioned in the table. | <urn:uuid:09a009d2-96b5-4fbb-9d10-a41b50325560> | {
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There are a number of differing definitions for the disease of addiction. Currently the most relevant ones in North America are those of the American Society for Addiction Medicine and the Canadian Society of Addiction Medicine who share a common agreed upon definition.
The only other definition is that of the World Health Organization (WHO). For legal purposes, the most widely recognized definitions are those of the DSM 4. The DSM does not contain a definition of Addiction per se, but rather gives definitions of Substance Abuse and Substance Dependence. The latter being the closest to a definition of Addiction.
CSAM and ASAM Definition of Addiction
A primary, chronic disease, characterized by impaired control over the use of a psychoactive substance and/or behaviour. Clinically, the manifestations occur along biological, psychological, sociological and spiritual dimensions.
Common features are change in mood, relief from negative emotions, provision of pleasure, pre-occupation with the use of substance(s) or ritualistic behaviour(s); and continued use of the substance(s) and/or engagement in behaviour(s) despite adverse physical, psychological and/or social consequences. Like other chronic diseases, it can be progressive, relapsing and fatal.
World Health Organization Definition of Addiction - Drug or Alcohol
Repeated use of a psychoactive substance or substances, to the extent that the user (referred to as an addict):
- is periodically or chronically intoxicated
- shows a compulsion to take the preferred substance (or substances)
- has great difficulty in voluntarily ceasing or modifying substance use
- exhibits determination to obtain psychoactive substances by almost any means.
Typically, tolerance is prominent and a withdrawal syndrome frequently occurs when substance use is interrupted. The life of the addict may be dominated by substance use to the virtual exclusion of all other activities and responsibilities. The term addiction also conveys the sense that such substance use has a detrimental effect on society, as well as on the individual; when applied to the use of alcohol, it is equivalent to alcoholism.
Addiction is a term of long-standing and variable usage. It is regarded by many as a discrete disease entity, a debilitating disorder rooted in the pharmacological effects of the drug, which is remorselessly progressive.
From the 1920s to the 1960s attempts were made to differentiate between addiction ; and "habituation", a less severe form of psychological adaptation. In the 1960s the World Health Organization recommended that both terms be abandoned in favour of dependence, which can exist in various degrees of severity. Addiction is not a diagnostic term in ICD-10, but continues to be very widely employed by professionals and the general public alike. See also: dependence; dependence syndrome
DSM definitions of Abuse and Dependence - Substance Abuse - a medical diagnosis, as specified in the Diagnostic and Statistical Manual of Mental Disorders - Fourth Edition (DSM IV).
A maladaptive pattern of substance use leading to clinically significant impairment or distress, as manifested by one (or more) of the following, occurring within a 12-month period:
- recurrent substance use resulting in a failure to fulfill major role obligations at work, school, or home (e.g., repeated absences or poor work performance related to substance use; substance-related absences, suspensions, or expulsions from school; neglect of children or household)
- recurrent substance use in situations in which it is physically hazardous (e.g., driving an automobile or operating a machine when impaired by substance use)
- recurrent substance-related legal problems (e.g., arrests for substance-related disorderly conduct)
- continued substance use despite having persistent or recurrent social or interpersonal problems caused by or exacerbated by the effects of the substance (e.g., arguments with spouse about consequences of intoxication, physical fights)
The symptoms have never met the criteria for Substance Dependence for this class of substance.
Substance Dependence - a medical diagnosis as specified the Diagnostic and Statistical Manual of Mental Disorders - Fourth Edition (DSM IV)
A maladaptive pattern of substance use, leading to clinically significant impairment or distress, as manifested by three (or more) of the following, occurring at any time in the same 12-month period:
- tolerance, as defined by either of the following:
- a need for markedly increased amounts of the substance to achieve intoxication or desired effect
- markedly diminished effect with continued use of the same amount of the substance
- withdrawal, as manifested by either of the following:
- the characteristic withdrawal syndrome for the substance (refer to Criteria A and B of the criteria sets for Withdrawal from the specific substances)
- the same (or closely related0 substance is taken to relieve or avoid withdrawal symptoms
- the substance is often taken in larger amounts or over a longer period of time than was intended
- there is persistent desire or unsuccessful efforts to cut down or control substance use
- a great deal of time is spent in activities necessary to obtain the substance (e.g., visiting multiple doctors or driving long distances), use the substance (e.g., chain-smoking), or recovering from its effects
- important social, occupational, or recreational activities are given up or reduced because of substance use
- the substance use is continued despite knowledge of having a persistent of recurrent physical or psychological problem that is likely to have been caused or exacerbated by the substance (e.g., current cocaine use despite recognition of cocaine-induce depression, or continued drinking despite recognition that an ulcer was made worse by alcohol consumption)
The policy of the College of Physicians and Surgeons of Alberta will be to adhere to the DSM definition of Substance Dependence in mandating treatment to addicted physicians. This diagnosis should be included in any assessments performed for the CPSA. It is upon the diagnostic criteria of the DSM 4 that the diagnosis will be made and treatment and maintenance and monitoring programs mandated. | <urn:uuid:bbf7e859-7f37-4524-8de8-e46d34e71201> | {
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Tissue damage caused by exposure to ionizing radiation. Structures with rapid cell turnover (e.g., skin, stomach or intestinal lining, and bone marrow) are most susceptible. High-dose irradiation of the last two causes radiation sickness. Nausea and vomiting subside in a few hours. They are followed in intestinal cases by abdominal pain, fever, and diarrhea leading to dehydration and a fatal shocklike state, and in bone-marrow cases (two to three weeks later) by fever, weakness, hair loss, infection, and hemorrhage. In severe cases, death occurs from infection and uncontrollable bleeding. Lower radiation doses can cause cancer (notably leukemia and breast cancer), sometimes years later. Radiation exposure in early pregnancy can produce abnormalities in the embryo, whose cells are multiplying rapidly.
Learn more about radiation injury with a free trial on Britannica.com.
Break in any body tissue due to external action (including surgery). It may be closed (blunt trauma) or open (penetrating trauma). Blood vessels, nerves, muscles, bones, joints, and internal organs may be damaged. A closed wound can be caused by impact, twisting, bending, or deceleration (as in a car crash). It can range from a minor bruise or sprain to a skull fracture with brain damage or a spinal-cord injury with paralysis. In an open wound, foreign matter such as bacteria, dirt, and clothing fragments entering through broken skin or mucous membrane may result in infection. Other factors affecting severity include depth, surface area, degree of tearing, and structures damaged. Minor wounds need only first aid. For others, after examination and perhaps diagnostic imaging and exploratory surgery, treatment may include fluid replacement or drainage, sterilization and antibiotics, tetanus antitoxin, and repair of damaged structures. A closed wound may need to be opened or an open one sutured closed. Seealso burn, coagulation, crush injury, dislocation, scar.
Learn more about wound with a free trial on Britannica.com.
Self-injury (SI) or self-harm (SH) is deliberate injury inflicted by a person upon their own body without suicidal intent. Some scholars use more technical definitions related to specific aspects of this behaviour. These acts may be aimed at relieving otherwise unbearable emotions, sensations of unreality and numbness. The illness is listed in the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR) as a symptom of borderline personality disorder and depressive disorders. It is sometimes associated with mental illness, a history of trauma and abuse including emotional abuse, sexual abuse, eating disorders, or mental traits such as low self-esteem or perfectionism, but a statistical analysis is difficult, as many self-injurers conceal their injuries.
Self harmers are often mistaken as suicidal, but in the majority of cases this is inaccurate. Non-fatal self-harm is common in young people worldwide and due to this prevalence the term self-harm is increasingly used to denote any non-fatal acts of deliberate self-harm, irrespective of the intention.
There are a number of different treatments available for self-injurers which concentrate on either treating the underlying causes or on treating the behaviour itself. When self-injury is associated with depression, antidepressant drugs and treatments may be effective. Alternative approaches involve avoidance techniques, which focus on keeping the self-injurer occupied with other activities, or replacing the act of self-harm with safer methods that do not lead to permanent damage.
A common belief regarding self-injury is that it is an attention-seeking behaviour; however, in most cases, this is inaccurate. Many self-injurers are very self-conscious of their wounds and scars and feel guilty about their behaviour leading them to go to great lengths to conceal their behaviour from others. They may offer alternative explanations for their injuries, or conceal their scars with clothing. Self-injury in such individuals is not associated with suicidal or para-suicidal behaviour. The person who self-injures is not usually seeking to end his or her own life; it has been suggested instead that he or she is using self-injury as a coping mechanism to relieve emotional pain or discomfort. Studies of individuals with developmental disabilities (such as mental retardation) have shown self-injury being dependent on environmental factors such as obtaining attention or escape from demands. Though this is not always the case, some individuals suffer from disassociation and they harbor a desire to feel real and/or to fit in to society's rules. A common form of self-injury involves making cuts in the skin of the arms, legs, abdomen, inner thighs, etc. However, the number of self-injury methods are only limited by an individual's creativity and include, but are not limited to, compulsive skin picking (dermatillomania), hair pulling (trichotillomania), burning, stabbing, poisoning, alcohol abuse and forms of self harm related to anorexia and bulimia. The locations of self-injury are often areas of the body that are easily hidden and concealed from the detection of others. As well as defining self-harm in terms of the act of damaging one's own body, it may be more accurate to define self-harm in terms of the intent, and the emotional distress that the person is attempting to deal with. Neither the DSM-IV-TR nor the ICD-10 provide diagnostic criteria for self-injury. It is often seen as only a symptom of an underlying disorder, though many people who self-injure would like this to be addressed.
This gender discrepancy is often distorted in specific populations where rates of self-injury are inordinately high, which may have implications on the significance and interpretation of psychosocial factors other than gender. A study in 2003 found an extremely high prevalence of self-injury among 428 homeless and runaway youth (age 16 to 19) with 72% of males and 66% of females reporting a past history of self-mutilation.
There does not appear to be a difference in motivation for self-harm in adolescent males and females. For example, for both genders there is an incremental increase in deliberate self-harm associated with an increase in consumption of cigarettes, drugs and alcohol. Triggering factors such as low self-esteem and having friends and family members who self-harm are also common between both males and females. One limited study found that, among those young individuals who do self-harm, both genders are just as equally likely to use the method of skin-cutting. However, females who self-cut are more likely than males to explain their self-harm episode by saying that they had wanted to punish themselves. In New Zealand, more females are hospitalised for intentional self-harm than males. Females more commonly choose methods such as self-poisoning that generally are not fatal, but still serious enough to require hospitalisation.
Some of the causes of deliberate self-poisoning in Sri Lankan adolescents included bereavement and harsh discipline by parents. The coping mechanisms are being spread in local communities as people are surrounded by others who have previously deliberately harmed themselves or attempted suicide. One way of reducing self-harm would be to limit access to poisons; however many cases involve pesticides or yellow oleander seeds, and the reduction of access to these agents would be difficult. Great potential for the reduction of self-harm lies in education and prevention, but limited resources in the developing world make these methods challenging.
Attempts to understand self-injury fall broadly into either attempts to interpret motives, or application of psychological models.
Motives for self-injury are often personal, often do not fit into medicalised models of behaviour and may seem incomprehensible to others, as demonstrated by this example:
My motivations for self-harming were diverse, but included examining the interior of my arms for hydraulic lines. This may sound strange.
Motives for self-injury can be different. Some feel as if they are not good enough and they might not want to take it out on the person who harmed them. It's often difficult for them to open up and tell about their "secret shame". Often when the sufferer does tell somebody there is a lack of understanding or knowledge of how to help.
Assessment of motives in a medical setting is usually based on precursors to the incident, circumstances and information from the patient however the limited studies comparing professional and personal assessments show that these differ with professionals suggesting more manipulative or punitive motives.
The UK ONS study reported only two motives: "to draw attention" and "because of anger". Many people who self-injure state that it allows them to "go away" or dissociate, separating the mind from feelings that are causing anguish. This may be achieved by tricking the mind into believing the suffering felt at the time is caused by self-injury instead of the issues they were facing before: the physical pain therefore acts as a distraction from emotional pain. To complement this theory, one can consider the need to 'stop' feeling emotional pain and mental agitation. "A person may be hyper-sensitive and overwhelmed; a great many thoughts may be revolving within their mind, and they may either become triggered or could make a decision to stop the overwhelming feelings." The sexual organs may be deliberately hurt as a way to deal with unwanted feelings of sexuality, or as a means of punishing sexual organs that may be perceived as having responded in contravention to the person's wellbeing. (e.g., responses to childhood sexual abuse).
Alternatively self-injury may be a means of feeling something, even if the sensation is unpleasant and painful. Those who self-injure sometimes describe feelings of emptiness or numbness (anhedonia), and physical pain may be a relief from these feelings. "A person may be detached from himself or herself, detached from life, numb and unfeeling. They may then recognise the need to function more, or have a desire to feel real again, and a decision is made to create sensation and 'wake up'."
It is also important to note that many self-injurers report feeling very little to no pain while self-harming. Those who engage in self-injury face the contradictory reality of harming themselves whilst at the same time obtaining relief from this act. It may even be hard for some to actually initiate cutting, but they often do because they know the relief that will follow. For some self-injurers this relief is primarily psychological whilst for others this feeling of relief comes from the beta endorphins released in the brain (the same chemicals that are thought to be responsible for the "runner's high" and are similar to morphine). Endorphins are endogenous opioids that are released in response to physical injury, act as natural painkillers, and induce pleasant feelings and would act to reduce tension and emotional distress.
As a coping mechanism, self-injury can become psychologically addictive because, to the self-injurer, it works; it enables him/her to deal with intense stress in the current moment. The patterns sometimes created by it, such as specific time intervals between acts of self-injury, can also create a behavioural pattern that can result in a wanting or craving to fulfill thoughts of self-injury.
Self-injury is known to have been a regular ritual practice by cultures such as the ancient Maya civilization, in which the Maya priesthood performed auto-sacrifice by cutting and piercing their bodies in order to draw blood. It is also practiced by the sadhu or Hindu ascetic and in Christian mortification of the flesh.
In individuals with developmental disabilities, occurrence of self-injury is often demonstrated to be related to its effects on the environment, such as obtaining attention or desired materials or escaping demands. As developmentally disabled individuals often have communication or social deficits, self-injury may be their way of obtaining these things which they are otherwise unable to obtain in a socially appropriate way (such as by asking). One approach for treating self-injury thus is to teach an alternative, appropriate response which obtains the same result as the self-injury.
Generating alternative behaviours that the sufferer can engage in instead of self-injury, and shaping the use of such behaviours, is one successful behavioural method that is employed to avoid self-harm. Techniques, aimed at keeping busy, may include journaling, taking a walk, participating in sports or exercise or being around friends when the sufferer has the urge to harm themselves. The removal of objects used for self-injury from easy reach is also helpful for resisting self-injurious urges. The provision of a card that allows sufferers to make emergency contact with counselling services should the urge to self-harm arise may also help prevent the act of self-injury. Alternative and safer methods of self-harm that do not lead to permanent damage, for example the snapping of a rubber band on the wrist, may also help calm the urge to self-harm. | <urn:uuid:7b054a9e-4ba0-4707-aa34-5b4e00d51d7f> | {
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The autism spectrum, also called autism spectrum disorders (ASD) or autism spectrum conditions (ASC), with the adjective autistic sometimes replacing the noun autism, is a spectrum of psychological conditions characterized by widespread abnormalities of social interactions and communication as well as restricted interests and repetitive behaviour.
The three forms of ASD are:
- Classic autism
- Asperger syndrome
- Pervasive Developmental Disorder Not Otherwise Specified (PDD-NOS), sometimes called atypical autism.
Autism forms the core of the autism spectrum disorders. Asperger syndrome is closest to autism in signs and likely causes; unlike autism, people with Asperger syndrome have no significant delay in language development. PDD-NOS is diagnosed when the criteria are not met for a more specific disorder. Some sources also include Rett syndrome and childhood disintegrative disorder, which share several signs with autism but may have unrelated causes; other sources combine ASD with these two conditions into the pervasive developmental disorders. According to the National Autistic Society of the United Kingdom, pathological demand avoidance syndrome belongs and is increasingly being recognised as belonging to the autistic spectrum.
The terminology of autism can be bewildering. Autism, Asperger syndrome, and PDD-NOS are sometimes called the autistic disorders instead of ASD, whereas autism itself is often called autistic disorder, childhood autism, or infantile autism. Although the older term pervasive developmental disorder and the newer term autism spectrum disorder largely or entirely overlap, the former was intended to describe a specific set of diagnostic labels, whereas the latter refers to a postulated spectrum disorder linking various conditions. ASD, in turn, is a subset of the broader autism phenotype (BAP), which describes individuals who may not have ASD but do have autistic-like traits, such as avoiding eye contact. Some autism are severe or moderate or light.
The defining characteristics of autism spectrum disorders are qualitative impairments of social communication and interaction, along with restricted and repetitive activities and interests. Individual symptoms occur in the general population and appear not to associate highly, without a sharp line separating pathological severity from common traits. Other aspects of ASD, such as atypical eating, are also common but are not essential for diagnosis; they can affect the individual or the family.
An estimated 0.5% to 10% of individuals with ASD show unusual abilities, ranging from splinter skills such as the memorization of trivia to the extraordinarily rare talents found in autistic savants.
Making and maintaining friendships often proves to be difficult for children with autism. For them, the quality of friendships, not the number of friends, predicts how lonely they are, despite the common belief that they prefer to be alone. Being on the autism spectrum does not keep children from understanding race and gender stereotypes in a society; like normal children they can learn aspects of stereotypical behaviour by observing their parents' actions.
The main goals of treatment are to lessen associated deficits and family distress, and to increase quality of life and functional independence. No single treatment is best and treatment is typically tailored to the child's needs. Intensive, sustained special education programmes and behaviour therapy early in life can help children acquire self-care, social, and job skills. Available approaches include applied behaviour analysis (ABA), developmental models, structured teaching, speech and language therapy, social skills therapy, and occupational therapy. ABA therapy has a strong research base but it maybe limited by diagnostic severity and IQ.
Many popular therapies including auditory integration therapy, GFCF diets, and chelation have repeatedly been shown to be ineffective and are not considered evidence-based practices.
Most recent reviews tend to estimate a prevalence of 1–2 per 1,000 for autism and close to 6 per 1,000 for ASD; because of inadequate data, these numbers may underestimate ASD's true prevalence. PDD-NOS's prevalence has been estimated at 3.7 per 1,000, Asperger syndrome at roughly 0.6 per 1,000, and childhood disintegrative disorder at 0.02 per 1,000. The number of reported cases of autism increased dramatically in the 1990s and early 2000s. This increase is largely attributable to changes in diagnostic practices, referral patterns, availability of services, age at diagnosis, and public awareness, though as-yet-unidentified environmental risk factors cannot be ruled out, and the available evidence does not rule out the possibility that autism's true prevalence has increased.
- World Health Organization. International Statistical Classification of Diseases and Related Health Problems. 10th ed. (ICD-10). 2006 [cited 2007-06-25]. F84. Pervasive developmental disorders.
- Lord C, Cook EH, Leventhal BL, Amaral DG. Autism spectrum disorders. Neuron. 2000;28(2):355–63. doi:10.1016/S0896-6273(00)00115-X. PMID 11144346.
- American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 4th ed., text revision (DSM-IV-TR). 2000. ISBN 0-89042-025-4. Diagnostic criteria for 299.80 Asperger's Disorder (AD).
- National Institute of Mental Health. Autism spectrum disorders (pervasive developmental disorders); 2009 [cited 2009-04-23].
- Freitag CM. The genetics of autistic disorders and its clinical relevance: a review of the literature. Mol Psychiatry. 2007;12(1):2–22. doi:10.1038/sj.mp.4001896. PMID 17033636.
- Piven J, Palmer P, Jacobi D, Childress D, Arndt S. Broader autism phenotype: evidence from a family history study of multiple-incidence autism families [PDF]. Am J Psychiatry. 1997;154(2):185–90. PMID 9016266.
- Klin A. Autism and Asperger syndrome: an overview. Rev Bras Psiquiatr. 2006;28(suppl 1):S3–S11. doi:10.1590/S1516-44462006000500002. PMID 16791390.
- Frith U, Happé F. Autism spectrum disorder. Curr Biol. 2005;15(19):R786–90. doi:10.1016/j.cub.2005.09.033. PMID 16213805.
- London E. The role of the neurobiologist in redefining the diagnosis of autism. Brain Pathol. 2007;17(4):408–11. doi:10.1111/j.1750-3639.2007.00103.x. PMID 17919126.
- Filipek PA, Accardo PJ, Baranek GT et al. The screening and diagnosis of autistic spectrum disorders. J Autism Dev Disord. 1999;29(6):439–84. doi:10.1023/A:1021943802493. PMID 10638459.
- Treffert DA. Wisconsin Medical Society. Savant syndrome: an extraordinary condition—a synopsis: past, present, future; 2006 [cited 2008-03-24].
- Burgess AF, Gutstein SE. Quality of life for people with autism: raising the standard for evaluating successful outcomes. Child Adolesc Ment Health. 2007;12(2):80–6. doi:10.1111/j.1475-3588.2006.00432.x.
- Hirschfeld L, Bartmess E, White S, Frith U. Can autistic children predict behavior by social stereotypes? Curr Biol. 2007;17(12):R451–2. doi:10.1016/j.cub.2007.04.051. PMID 17580071. Lay summary: ScienceDaily, 2007-06-19.
- Myers SM, Johnson CP, Council on Children with Disabilities. Management of children with autism spectrum disorders. Pediatrics. 2007;120(5):1162–82. doi:10.1542/peds.2007-2362. PMID 17967921. Lay summary: AAP, 2007-10-29.
- Shreck, K. A., Metz, B., Mulick, J.A. & Smith, A. (2000) Making it fit: A Provocative Look at Models of Early Intensive Behavioral Intervention for Children with Autism. The Behavior Analyst Today, 1(3), 27-32.
- Mary Jane Weiss and Lara Delmolino (2006): The Relationship Between Early Learning Rates and Treatment Outcome For Children With Autism Receiving Intensive Home-Based Applied Behavior Analysis. The Behavior Analyst Today, 7(1), 96 - 105
- Newschaffer CJ, Croen LA, Daniels J et al. The epidemiology of autism spectrum disorders [PDF]. Annu Rev Public Health. 2007 [cited 2009-10-10];28:235–58. doi:10.1146/annurev.publhealth.28.021406.144007. PMID 17367287.
- Caronna EB, Milunsky JM, Tager-Flusberg H. Autism spectrum disorders: clinical and research frontiers. Arch Dis Child. 2008;93(6):518–23. doi:10.1136/adc.2006.115337. PMID 18305076.
- Fombonne E. Epidemiology of pervasive developmental disorders. Pediatr Res. 2009;65(6):591–8. doi:10.1203/PDR.0b013e31819e7203. PMID 19218885.
- Wing L, Potter D. The epidemiology of autistic spectrum disorders: is the prevalence rising? Ment Retard Dev Disabil Res Rev. 2002;8(3):151–61. doi:10.1002/mrdd.10029. PMID 12216059.
- Rutter M. Incidence of autism spectrum disorders: changes over time and their meaning. Acta Paediatr. 2005;94(1):2–15. doi:10.1111/j.1651-2227.2005.tb01779.x. PMID 15858952.
- Baron IS. Autism Spectrum Disorder: complex, controversial, and confounding. Neuropsychol Rev. 2008;18(4):271–2. doi:10.1007/s11065-008-9070-1. PMID 18846426.
- For more information about Sensory Integration please visit www.sensoryintegration.org.uk
- For a short documentary about autism see BBC Four's 1992 Video here http://www.youtube.com/thefamilarity#p/u/2/PrViCkYF-lY | <urn:uuid:ec24c4e6-99df-4ec2-b7b4-f1ceed2af4f9> | {
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Focus: School Years
National Institute for Blind and Partially Sighted Children and Youth
+45 5957 0100
In the following I am going to talk about blindness, mental retardation and autism in children in order to elucidate some connections between the three impairments. By focusing especially on similarities I want to describe why blind children are at risk of developing autism related behaviours, and why they sometimes do so to a degree that an individual child may be diagnosed as an “autistic child”. Autism related symptoms of blind children range from the blind autistic child at one end to the well functioning blind child at the other. Between these extremities blind children with autism related symptoms in varying degrees are to be found.
The assumptions, descriptions and conclusions of this paper are based partly on research made in the separate fields concerning autism, blindness and mental retardation, partly on personal experience from my own work with blind children and partly from retrospective studies of Danish case records of blind children and youths.
The children I shall be talking about are, first of all, blind with or without light perception and, second, they are quite often mentally retarded to some degree. Thus, these children may be moderately mentally retarded, having an IQ between 35-50, or mildly retarded with an IQ between 50 and 70, or they may be normally functioning with an IQ above 70. I am not talking about the severely mentally retarded children with an IQ below 35, because this is not meaningful in connection with autism.
They all have the fundamental capacity to develop concepts and to categorise objects. Their capacity to acquire concepts therefore also enables them to learn to understand and use symbols..
In the moderately retarded group, the children’s way of thinking is very concrete. One will often find that they have difficulties in imagining changes based only on thinking. This means that they have difficulties in handling situations that demand new and alternative ways of action, and the children in this group have difficulties in learning to read and to learn arithmetic.
The mildly retarded children are able to develop most of the skills required for daily living and are thus able to learn to read and to do arithmetic. While they are also able to use symbols they have difficulties in using a symbol representing another symbol. In addition, compared with children of normal intelligence the mildly retarded children show a lower capacity for using abstract thinking in problem solving.
Mental retardation is not an uncommon impairment. For example, a study in the United States has shown that approximately 3% of the U.S. population are properly classified as mentally retarded. Children in the mild range of impairment make up the vast majority of those classified as retarded, 86% of the retarded population belonging to this group, while about 10% are classified as moderately retarded.
Why talk about mental retardation or autism in connection with blind children? In Denmark about 55% of all visually impaired children have other impairments as well, but we have no statistical record of the number of children with the combination of mental retardation and blindness. However, I know from my own experience with blind children that it is not unusual to meet this combination.
What, then, about the combination of autism and blindness? For many years, we have been focusing mainly on autism related symptoms in blind children when discussing the consequences of being blind. So, blind children’s risk of developing inappropriate social or emotional behaviour has often been stressed in the context of early intervention.
We have all been impressed with the descriptions made by authors such as Fraiberg of the development of blind children with autism related behaviour. It has made us curious to find out why blind children so often develop behaviour traits known from descriptions of children with autism. Other descriptions made on the basis of intensive studies of relatively small groups of blind children have further sharpened our curiosity.
These studies, combined with descriptive accounts of the development of individual blind children, have left us with a strong and emotional charged impression of a difficult social development in blind children. Descriptions of a normal functioning blind child do not leave us with the same emotional impressions. Are these emotional impressions the reason why we often stress the risk of a blind child at developing in an inappropriate social or emotional way and the reason why we talk about autism related traits in blind children? Based on my experience with blind children in Denmark I cannot help asking myself whether it really is true that blind children are relatively more at risk than normally sighted children of developing autism or autistic traits? Or is it a myth? Is it possible, by looking at similarities in the development of blind children and children with autism, respectively, to find a connection between blindness and autism?
Autism covers a number of key features, which together make up a syndrome. It is a rather newly discovered disorder first described by Kanner in 1943. Since then research has tried to reach an understanding of this special disorder and to find the causes of the syndrome.
Today there is general agreement about how autism is identified and diagnosed. For instance, in the ICD-10 the condition of childhood autism is defined as follows: Impaired or abnormal development must be present before 3 years of age, manifesting the full triad of impairments:
1. in reciprocal social interaction
2. in communication, and
3. in restricted, stereotyped, repetitive behaviour
The prevalence of autism has increased since Kanner described the first cases. Today the Medical Council of Research has mentioned that autism is to be found in about 0.6% of all children from 6 years and upwards. If we include children in the preschool years the figure will be approximately 0.9%. It means that the prevalence is 9:1000. This is a larger number than earlier mentioned, where the prevalence was estimated to be between 4 to 11 of every 10.000 child. Also, in studies of autism, it has been shown that mental retardation normally is an additional impairment in 3 out of 4 children with autism.
In Denmark we have about 1700 visually impaired children below 18 years of age. Therefore we may expect to have about 1 to 2 children with a diagnose of autism – independently of the visual impairment. But we have more children than that diagnosed as children with autism. Also, we have visually impaired children with all degrees of autism related symptoms without the diagnose autism. Often, these children are mentally retarded too.
Let me now turn to the possible similarities in behaviours of children with autism and blind children.
Because of the time limit here it is not possible to describe all the behaviour symptoms in details. I have chosen to list them on overheads and in the following I will briefly stress the most common behaviour symptoms that are related to deviant behaviour in blind children.
First about reciprocal social interaction:
The area of social impairment is often seen as the core deficit in autism.
For blind youths the social isolation in daily life is often mentioned as a problem. In early social development the blind child has to learn to solve a variety of problems. This may in general give a delayed development of social behaviour, which is often observed in blind children in their interaction with peers in nurseries and in schools. Some of these early problems are possibly not solved at all in some children and may be the cause of some abnormal social behaviour – also later in life. These problems all relate to the missing visual capacity and – to in some extent - to the mental retardation often found in the deviant blind children.
Below, all subjects marked with a star are problematic both for children with autism and for blind children.
* Deficits in joint attention
* Deficits in imitation
- Especially motor imitation
- In play and activities
Difficulties in perceiving emotional expressions of other people
In autistic children the abnormal behaviour symptoms in the area of social interaction are considered to be caused by a deficit concerning social understanding. In the blind children the abnormal behaviour is obviously caused by the blindness. Still they have overwhelming effects on the social development of blind children. The difficulty in perceiving emotional cues from people in the surroundings makes it more complicated for the child to get social references and the like. This, in combination with difficulties in perceiving non-verbal emotional signals that are often expressed in facial expressions and in body language, may create communicative difficulties in social interaction and conversations. Delayed use or problems in use of proto-declarative acts and joint attention may have consequences for, for instance, the development of theory of mind. Problems of imitative and imaginative play in general, especially in connection with pretend and symbolic play, create problems in play interaction with peers etc.
All these problems can be seen in normally functioning blind children. Often, however, they overcome some of the difficulties in time, resulting only in a delayed social development. But in some area there will remain a qualitative difference compared with the development of normally sighted children. The severity of these qualitative differences, especially in connection with reciprocal interaction, is extremely important when you evaluate the social development in a blind child suspected of having an autistic disorder in addition to blindness.
The next diagnostic criteria concern communication. Again I list the symptoms found in children with autism and compare them with behaviour known in blind children.
(*) Non verbal language
Difficulties in development and understanding of the use of dialogues
(*) Use of communication as a means of self-stimulation
Missing system of turn-taking
Missing initiative from the child in establishing communicative interaction
Approximately half of the children with autistic disorders do not develop meaningful speech, and in those who do, a variety of communication abnormalities have been identified. When blind children do not develop a verbal language some other impairment has to be present in addition to blindness. This may be mental retardation, specific language disorders, autism etc.
Two of the behaviour symptoms listed are commonly observed in the communicative development of blind children. These include as the most important element the phenomenon of echolalia.
In autistic children approximately 85% of those who develop speech display “echolalia” early in their language development.
Most of the blind children are exhibiting echolalia in their development of communication and language. Both autistic children and blind children use echolalia for a variety of reasons, for instance, to attract the attention of a partner, to mark joint attention, to show a lack of understanding, to indicate a question or an answer, to return greeting, to issue a communicative check or as part of normal language learning and development.
Also, the reversals of pronouns have often been mentioned in connection with blind children. It mirrors the difficult task of developing a sense of self, but this task is often accomplished around the age of 4 to 5 years if not before.
It is common to blind children that they generally exhibit a good capacity for developing communicative and language skills; hence, their most severe problems are rarely seen in this area, except for the echolalia and reversals of pronouns. Normally, problems in communication or language development, e.g. a failure to master the system of turn-taking or an abnormal resistance to quit echolalia, therefore have to be considered seriously.
The third diagnostic criteria of autism include
Resistance to changes, dependence on structures
Some of these symptoms can be seen in a variety of degrees in blind children. But most of them are seen in blind children who also are mentally retarded. Some of the symptoms may be suspected to have roots in more general or specific brain damages. The stereotyped behaviour is an exception. This behaviour is also seen in many normally functioning blind children without additional impairments. In these cases the stereotyped behaviour has a special connection to blindness and deserves to be referred to as “blindism”.
Similarities between blind children and children with autism.
According to the list of similarities mentioned above of traits of behaviour in blind children and children with autism I am now able to say that blind children are at risk of developing autistic traits. The consequences of blindness in themselves have an overwhelming impact on the social development of blind children resulting in some of the same difficulties in understanding social interaction as found in autistic children. Both the autistic and the blind child have to learn - by help of cognitive ways of thinking - what normal children without any impairment normally intuitively know. This natural “knowledge” stems from an innate capacity, which the autistic child is presumed to lack and from visual cues of emotional and communicative signals from people around the child. The problem of the blind children is especially the missing information from this visual capacity.
It is interesting that different causes may create similarities in the behaviour of blind and of autistic children. Both autistic and blind children need to use their cognitive capacities to develop social skills in interaction with other people. Therefore the broadness of the cognitive capacity is of extreme importance to the blind child as well as to an autistic child.
Blind children and children with autism have been observed to have similar problems in establishing joint attention, in developing a theory of mind, in experiencing and perceiving things as unified wholes, in separating and selecting essential information from the overwhelming input from their surroundings, in their lack of abilities to catch social signals from emotional expressions of other people, in imitating behaviours (except for language-imitation) and in not being able to signal emotions to other people, in missing ability to symbolise, in reduced ability of thinking in terms of unified wholes, in experiencing and bringing experience of sequences into a context, in imagination and in performing symbolic play or at a more or less abstract level. All these difficulties are mostly dependable of the function of the social as well as the cognitive capacities in the individual child.
Therefore we also have to look at a possible mental retardation. It applies to both children with autism and blind children that the higher or the more normal that the child’s functioning is, the fewer and the less pronounced are the deviancies and the eccentricities of the behaviour of the child. Conversely, the more mental retardation that the child has, the greater are deviancies of the child from normal behaviour and development. .
This applies to all areas mentioned above. A connection between abnormal behaviour and mental retardation in addition to blindness or autism is obvious. But one may also suspect that mental retardation in itself does cause some of the difficulties the children have and that these difficulties, combined with the specific difficulties based on being blind, may contribute further to the development of behaviour resembling that of autistic children.
The difficulties mentioned above are essential for the educational treatment and for the educational conditions we offer to blind children. It is important to find out how we create optimal development in the individual child considering their individual difficulties stemming from blindness, mental retardation and possibly autism. The BMA model tries to meet some of the fundamental needs in children with this combination of impairments (this model will be described in a paper on this conference too by Kirsten Larsen). The needs of these children and youths are met in an individualised education in natural settings in interaction with other people.
The teaching programme and other programmes made for autistic children have used principles from the education of blind children. But I want to suggest that the time is ripe for us to exploit (a) results from research and studies made of autistic children, (b) our increased knowledge of how cognitive capacity is used to establish social competencies, and (c) the experience gained in education of autistic children.
The blind children, especially the mentally retarded, may benefit from principle founded on knowledge concerning both blindness, autism and mental retardation. The need for stable surroundings, sameness, repetition, time to process the impressions, to build sequential experiences into wholes in context and to learn from experiences in social interaction are among other things basically to have in an educational setting in order to help the individual blind child to learn about social interaction by help of cognitive aids.
Please send comments or questions to firstname.lastname@example.org. | <urn:uuid:8afc048a-b2a3-4272-b7c6-49938023785b> | {
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|Classification and external resources|
|ICD-10||M62.8, T79.5, T79.6|
Rhabdomyolysis // is a condition in which damaged skeletal muscle tissue (Greek: ραβδω rhabdo- striped μυς myo- muscle) breaks down (Greek: λύσις –lysis) rapidly. Breakdown products of damaged muscle cells are released into the bloodstream; some of these, such as the protein myoglobin, are harmful to the kidneys and may lead to kidney failure. The severity of the symptoms, which may include muscle pains, vomiting, and confusion, depends on the extent of muscle damage and whether kidney failure develops. The muscle damage may be caused by physical factors (e.g., crush injury, strenuous exercise, medications, drug abuse, and infections). Some people have a hereditary muscle condition that increases the risk of rhabdomyolysis. The diagnosis is usually made with blood tests and urinalysis. The mainstay of treatment is generous quantities of intravenous fluids, but may include dialysis or hemofiltration in more severe cases.
Rhabdomyolysis and its complications are significant problems for those injured in disasters such as earthquakes and bombings. Relief efforts in areas struck by earthquakes often include medical teams with the skills and equipment to treat survivors with rhabdomyolysis. The disease was first described in the 20th century, and important discoveries as to its mechanism were made during the Blitz of London in 1941. Horses may also suffer from rhabdomyolysis from a variety of causes.
- 1 Signs and symptoms
- 2 Causes
- 3 Mechanism
- 4 Diagnosis
- 5 Treatment
- 6 Prognosis
- 7 Epidemiology
- 8 History
- 9 Other animals
- 10 References
Signs and symptoms
The symptoms of rhabdomyolysis depend on its severity and whether kidney failure develops. Milder forms may not cause any muscle symptoms, and the diagnosis is based on abnormal blood tests in the context of other problems. More severe rhabdomyolysis is characterized by muscle pain, tenderness, weakness and swelling of the affected muscles. If the swelling is very rapid, as may happen after someone is released from under a collapsed building, the movement of fluid from the bloodstream into damaged muscle may cause low blood pressure and shock. Other symptoms are nonspecific and result either from the consequences of muscle tissue breakdown or from the condition that originally led to the muscle breakdown. Release of the components of muscle tissue into the bloodstream causes electrolyte disturbances, which can lead to nausea, vomiting, confusion, coma or abnormal heart rate and rhythm. The urine may be dark, often described as "tea-colored", due to the presence of myoglobin. Damage to the kidneys may give rise to decreased or absent urine production, usually 12 to 24 hours after the initial muscle damage.
Swelling of damaged muscle occasionally leads to compartment syndrome—compression of surrounding tissues, such as nerves and blood vessels, in the same fascial compartment—leading to the loss of blood supply and damage or loss of function in the part(s) of the body supplied by these structures. Symptoms of this complication include pain or reduced sensation in the affected limb. A second recognized complication is disseminated intravascular coagulation (DIC), a severe disruption in blood clotting that may lead to uncontrollable bleeding.
Any form of muscle damage of sufficient severity can cause rhabdomyolysis. Multiple causes can be present simultaneously in one person. Some have an underlying muscle condition, usually hereditary in nature, that makes them more prone to rhabdomyolysis.
Common and important causes
|Exertional rhabdomyolysis||Extreme physical exercise (particularly when poorly hydrated), delirium tremens (alcohol withdrawal), tetanus, prolonged seizures or status epilepticus|
|Crush||Crush syndrome, blast injury, car accident, physical torture or abuse, or confinement in a fixed position such as after a stroke, due to alcohol intoxication or in prolonged surgery|
|Blood supply||Arterial thrombosis (blood clots forming locally) or embolism (clots or other debris from elsewhere in the body), clamping of an artery during surgery|
|Metabolism||Hyperglycemic hyperosmolar state, hyper- and hyponatremia (elevated or reduced blood sodium levels), hypokalemia (low potassium levels), hypocalcemia (low calcium levels), hypophosphatemia (low phosphate levels), ketoacidosis (e.g., in diabetic ketoacidosis) or hypothyroidism (abnormally low thyroid function)|
|Body temperature||Hyperthermia (high body temperature) and heat illness, hypothermia (very low body temperature)|
|Drugs and toxins||Many medications increase the risk of rhabdomyolysis. The most important ones are:
Poisons linked to rhabdomyolysis are heavy metals and venom from insects or snakes. Hemlock may cause rhabdomyolysis, either directly or after consuming quail that have fed on it. Haff disease is rhabdomyolysis after consuming fish; a toxic cause is suspected but has not been proven.
|Infection||Coxsackie virus, influenza A virus and influenza B virus, Epstein-Barr virus, primary HIV infection, Plasmodium falciparum (malaria), herpes viruses, Legionella pneumophila and salmonella|
|Inflammation||Autoimmune muscle damage: polymyositis, dermatomyositis|
Recurrent rhabdomyolysis may result from intrinsic muscle enzyme deficiencies, which are usually inherited and often appear during childhood. Many structural muscle diseases feature episodes of rhabdomyolysis that are triggered by exercise, general anesthesia or any of the other causes of rhabdomyolysis listed above. Inherited muscle disorders and infections together cause the majority of rhabdomyolysis in children.
- Glycolysis and glycogenolysis defects: McArdle's disease, phosphofructokinase deficiency, glycogen storage diseases VIII, IX, X and XI
- Lipid metabolism defects: carnitine palmitoyltransferase I and II deficiency, deficiency of subtypes of acyl CoA dehydrogenase (LCAD, SCAD, MCAD, VLCAD, 3-hydroxyacyl-coenzyme A dehydrogenase deficiency), thiolase deficiency
- Mitochondrial myopathies: deficiency of succinate dehydrogenase, cytochrome c oxidase and coenzyme Q10
- Others: glucose-6-phosphate dehydrogenase deficiency, myoadenylate deaminase deficiency and muscular dystrophies
Damage to skeletal muscle may take various forms. Crush and other physical injuries cause damage to muscle cells directly or interfere with blood supply, while non-physical causes interfere with muscle cell metabolism. When damaged, muscle tissue rapidly fills with fluid from the bloodstream, including sodium ions. The swelling itself may lead to destruction of muscle cells, but those cells that survive are subject to various disruptions that lead to rise in intracellular calcium ions; the accumulation of calcium outside the sarcoplasmic reticulum leads to continuous muscle contraction and depletion of ATP, the main carrier of energy in the cell. ATP depletion can itself lead to uncontrolled calcium influx. The persistent contraction of the muscle cell leads to breakdown of intracellular proteins and disintegration of the cell.
Neutrophil granulocytes—the most abundant type of white blood cell—enter the muscle tissue, producing an inflammatory reaction and releasing reactive oxygen species, particularly after crush injury. Crush syndrome may also cause reperfusion injury when blood flow to decompressed muscle is suddenly restored.
The swollen, inflamed muscle may directly compress structures in the same fascial compartment, causing compartment syndrome. The swelling may also further compromise blood supply into the area. Finally, destroyed muscle cells release potassium ions, phosphate ions, the heme-containing protein myoglobin, the enzyme creatine kinase and uric acid (a breakdown product of purines from DNA) into the blood. Activation of the coagulation system may precipitate disseminated intravascular coagulation. High potassium levels may lead to potentially fatal disruptions in heart rhythm. Phosphate binds to calcium from the circulation, leading to low calcium levels in the blood.
Rhabdomyolysis may cause kidney failure by several mechanisms. The most important is the accumulation of myoglobin in the kidney tubules. Normally, the blood protein haptoglobin binds circulating myoglobin and other heme-containing substances, but in rhabdomyolysis the quantity of myoglobin exceeds the binding capacity of haptoglobin. Myoglobinuria, the presence of myoglobin in the urine, occurs when the level in plasma exceeds 0.5–1.5 mg/dl; once plasma levels reach 100 mg/dl, the concentration in the urine becomes sufficient for it to be visibly discolored and corresponds with the destruction of about 200 grams of muscle. As the kidneys reabsorb more water from the filtrate, myoglobin interacts with Tamm–Horsfall protein in the nephron to form casts (solid aggregates) that obstruct the normal flow of fluid; the condition is worsened further by high levels of uric acid and acidification of the filtrate, which increase cast formation. Iron released from the heme generates reactive oxygen species, damaging the kidney cells. In addition to the myoglobinuria, two other mechanisms contribute to kidney impairment: low blood pressure leads to constriction of the blood vessels and therefore a relative lack of blood flow to the kidney, and finally uric acid may form crystals in the tubules of the kidneys, causing obstruction. Together, these processes lead to acute tubular necrosis, the destruction of the cells of tubules. Glomerular filtration rate falls and the kidney is unable to perform its normal excretory functions. This causes disruption of electrolyte regulation, leading to a further rise in potassium levels, and interferes with vitamin D processing, further worsening the low calcium levels.
A diagnosis of rhabdomyolysis may be suspected in anyone who has suffered trauma, crush injury or prolonged immobilization, but it may also be identified at a later stage due to deteriorating kidney function (abnormally raised or increasing creatinine and urea levels, falling urine output) or reddish-brown discoloration of the urine.
The most reliable test in the diagnosis of rhabdomyolysis is the level of creatine kinase (CK) in the blood. This enzyme is released by damaged muscle, and levels above 5 times the upper limit of normal (ULN) indicate rhabdomyolysis. Depending on the extent of the rhabdomyolysis, concentrations up to 100,000 U/l are not unusual. CK concentrations rise steadily for 12 hours after the original muscle injury, remain elevated for 1–3 days and then fall gradually. Initial and peak CK levels have a linear relationship with the risk of acute kidney failure: the higher the CK, the more likely it is that kidney damage will occur. There is no specific concentration of CK above which renal impairment definitely occurs; concentrations below 20,000 U/l are unlikely to be associated with a risk of renal impairment, unless there are other contributing risk factors. Mild rises without renal impairment are referred to as "hyperCKemia". Myoglobin has a short half-life, and is therefore less useful as a diagnostic test in the later stages. Its detection in blood or urine is associated with a higher risk of renal impairment. Despite this, use of urine myoglobin measurement is not supported by evidence as it lacks specificity and the research studying its utility is of poor quality.
Elevated concentrations of the enzyme lactate dehydrogenase (LDH) may be detected. Other markers of muscle damage, such as aldolase, troponin, carbonic anhydrase type 3 and fatty acid-binding protein (FABP), are mainly used in chronic muscle diseases. The transaminases, enzymes abundant in both liver and muscle tissue, are also usually increased; this can lead to the condition being confused with acute liver injury, at least in the early stages. The incidence of actual acute liver injury is 25% in people with non-traumatic rhabdomyolysis; the mechanism for this is uncertain.
High potassium levels tend to be a feature of severe rhabdomyolysis. Electrocardiography (ECG) may show whether the elevated potassium levels are affecting the conduction system of the heart, as suggested by the presence of T wave changes or broadening of the QRS complex. Low calcium levels may be present in the initial stage due to binding of free calcium to damaged muscle cells.
Urinalysis by urine test strip may reveal a positive result for "blood", even though no red blood cells can be identified on microscopy of the urine; this occurs because the reagent on the test strip reacts with myoglobin. The same phenomenon may happen in conditions that lead to hemolysis, the destruction of red blood cells; in hemolysis the blood serum is also visibly discolored, while in rhabdomyolysis it is normal. If kidney damage has occurred, microscopy of the urine also reveals urinary casts that appear pigmented and granular.
Compartment syndrome is a clinical diagnosis, i.e., no diagnostic test conclusively proves its presence or absence, but direct measurement of the pressure in a fascial compartment, and the difference between this pressure and the blood pressure, may be used to assess its severity. High pressures in the compartment and a small difference between compartment pressure and blood pressure indicate that the blood supply is likely to be insufficient, and that surgical intervention may be needed.
Disseminated intravascular coagulation, another complication of rhabdomyolysis and other forms of critical illness, may be suspected on the basis of unexpected bleeding or abnormalities in hematological tests, such as a decreasing platelet count or prolongation of the prothrombin time. The diagnosis can be confirmed with standard blood tests for DIC, such as D-dimer.
If an underlying muscle disease is suspected, for instance if there is no obvious explanation or there have been multiple episodes, it may be necessary to perform further investigations. During an attack, low levels of carnitine in the blood and high levels of acylcarnitine in blood and urine may indicate a lipid metabolism defect, but these abnormalities revert to normal during convalescence. Other tests may be used at that stage to demonstrate these disorders. Disorders of glycolysis can be detected by various means, including the measurement of lactate after exercise; a failure of the lactate to rise may be indicative of a disorder in glycolysis, while an exaggerated response is typical of mitochondrial diseases. Electromyography (EMG) may show particular patterns in specific muscle diseases; for instance, McArdle's disease and phosphofructokinase deficiency show a phenomenon called cramp-like contracture. There are genetic tests available for many of the hereditary muscle conditions that predispose to myoglobinuria and rhabdomyolysis.
Muscle biopsy can be useful if an episode of rhabdomyolysis is thought to be the result of an underlying muscle disorder. A biopsy sample taken during an episode is often uninformative, as it will show only evidence of cell death or may appear normal. Taking the sample is therefore delayed for several weeks or months. The histopathological appearance on the biopsy indicates the nature of the underlying disorder. For instance, mitochondrial diseases are characterised by ragged red fibers. Biopsy sites may be identified by medical imaging, such as magnetic resonance imaging, as the muscles may not be uniformly affected.
The main goal of treatment is to treat shock and preserve kidney function. Initially this is done through the administration of generous amounts of intravenous fluids, usually isotonic saline (0.9% weight per volume sodium chloride solution). In victims of crush syndrome, it is recommended to administer intravenous fluids even before they are extracted from collapsed structures. This will ensure sufficient circulating volume to deal with the muscle cell swelling (which typically commences when blood supply is restored), and to prevent the deposition of myoglobin in the kidneys. Amounts of 6 to 12 liters over 24 hours are recommended. The rate of fluid administration may be altered to achieve a high urine output (200–300 ml/h in adults), unless there are other reasons why this might lead to complications, such as a history of heart failure.
While many sources recommend additional intravenous agents to reduce damage to the kidney, most of the evidence supporting this practice comes from animal studies, and is inconsistent and conflicting. Mannitol acts by osmosis to enhance urine production and is thought to prevent myoglobin deposition in the kidney, but its efficacy has not been shown in studies and there is a risk of worsening renal function. The addition of bicarbonate to the intravenous fluids may alleviate acidosis (high acid level of the blood) and make the urine more alkaline to prevent cast formation in the kidneys, but there is limited evidence that it has benefits above saline alone, and it can worsen hypocalcemia by enhancing calcium and phosphate deposition in the tissues. If urine alkalinization is used, the pH of the urine is kept at 6.5 or above. Furosemide, a loop diuretic, is often used to ensure sufficient urine production, but evidence that this prevents renal failure is lacking.
In the initial stages, electrolyte levels are often abnormal and require correction. High potassium levels can be life-threatening, and respond to increased urine production and renal replacement therapy (see below). Temporary measures include the administration of calcium to protect against cardiac complications, insulin or salbutamol to redistribute potassium into cells, and infusions of bicarbonate solution.
Calcium levels initially tend to be low, but as the situation improves calcium is released from where it has precipitated with phosphate, and vitamin D production resumes, leading to hypercalcemia (abnormally high calcium levels). This "overshoot" occurs in 20–30% of those people who have developed kidney failure.
Acute renal impairment
Kidney dysfunction typically develops 1–2 days after the initial muscle damage. If supportive treatment is inadequate to manage this, renal replacement therapy (RRT) may be required. RRT removes excess potassium, acid and phosphate that accumulate when the kidneys are unable to function normally and is required until kidney function is regained.
Three main modalities of RRT are available: hemodialysis, continuous hemofiltration and peritoneal dialysis. The former two require access to the bloodstream (a dialysis catheter), while peritoneal dialysis is achieved by instilling fluid into the abdominal cavity and later draining it. Hemodialysis, which is normally done several times a week in chronic kidney disease, is often required on a daily basis in rhabdomyolysis. Its advantage over continuous hemofiltration is that one machine can be used multiple times a day, and that continuous administration of anticoagulant drugs is not necessary. Hemofiltration is more effective at removing large molecules from the bloodstream, such as myoglobin, but this does not seem to confer any particular benefit. Peritoneal dialysis may be difficult to administer in someone with severe abdominal injury, and it may be less effective than the other modalities.
Compartment syndrome is treated with surgery to relieve the pressure inside the muscle compartment and reduce the risk of compression on blood vessels and nerves in that area. Fasciotomy is the incision of the affected compartment. Often, multiple incisions are made and left open until the swelling has reduced. At that point, the incisions are closed, often requiring debridement (removal of non-viable tissue) and skin grafting in the process. The need for fasciotomy may be decreased if mannitol is used, as it can relieve muscle swelling directly.
Disseminated intravascular coagulation generally resolves when the underlying causes are treated, but supportive measures are often required. For instance, if the platelet count drops significantly and there is resultant bleeding, platelets may be administered.
The prognosis depends on the underlying cause and whether any complications occur. Rhabdomyolysis complicated by acute kidney impairment in patients with traumatic injury may have a mortality rate of 20%. Admission to the intensive care unit is associated with a mortality of 22% in the absence of acute kidney injury, and 59% if renal impairment occurs. Most people who have sustained renal impairment due to rhabdomyolysis fully recover their renal function.
The exact incidence of rhabdomyolysis is difficult to establish, because different definitions have been used. In 1995, hospitals in the U.S. reported 26,000 cases of rhabdomyolysis. Up to 85% of people with major traumatic injuries will experience some degree of rhabdomyolysis. Of those with rhabdomyolysis, 10–50% develop acute kidney injury. The risk is higher in people with a history of illicit drug use, alcohol misuse or trauma when compared to muscle diseases, and it is particularly high if multiple contributing factors occur together. Rhabdomyolysis accounts for 7–10% of all cases of acute kidney injury in the U.S.
Crush injuries are common in major disasters, but especially so in earthquakes. The aftermath of the 1988 Spitak earthquake prompted the establishment, in 1995, of the Renal Disaster Relief Task Force, a working group of the International Society of Nephrology (a worldwide body of kidney experts). Its volunteer doctors and nurses assisted for the first time in the 1999 İzmit earthquake in Turkey, where 462 people received dialysis, with positive results. Treatment units are generally established outside the immediate disaster area, as aftershocks could potentially injure or kill staff and make equipment unusable.
The Bible may contain an early account of rhabdomyolysis. In Numbers 11:4–6,31–33, the Pentateuch says that the Jews demanded meat while traveling in the desert; God sent quail in response to the complaints, and people ate large quantities of quail meat. A plague then broke out, killing numerous people. Rhabdomyolysis after consuming quail was described in more recent times and called coturnism (after Coturnix, the main quail genus). Migrating quail consume large amounts of hemlock, a known cause of rhabdomyolysis.
In modern times, early reports from the 1908 Messina earthquake and World War I on renal failure after injury were followed by studies by London physicians Eric Bywaters and Desmond Beall, working at the Royal Postgraduate Medical School and the National Institute for Medical Research, on four victims of The Blitz in 1941. Myoglobin was demonstrated in the urine of victims by spectroscopy, and it was noted that the kidneys of victims resembled those of patients who had hemoglobinuria (hemoglobin rather than myoglobin being the cause of the kidney damage). In 1944 Bywaters demonstrated experimentally that the renal failure was mainly caused by myoglobin. Already during the war, teams of doctors traveled to bombed areas to provide medical support, chiefly with intravenous fluids, as dialysis was not yet available. The prognosis of acute renal failure improved markedly when dialysis was added to supportive treatment, which first happened during the 1950–1953 Korean War.
Rhabdomyolysis is recognized in horses. Horses can develop a number of muscle disorders, many of which may progress to rhabdomyolysis. Of these, some cause isolated attacks of rhabdomyolysis (e.g., dietary deficiency in vitamin E and selenium, poisoning associated with pasture or agricultural poisons such as organophosphates), while others predispose to exertional rhabdomyolysis (e.g., the hereditary condition equine polysaccharide storage myopathy). 5–10% of thoroughbred horses and some standardbred horses suffer from the condition equine exertional rhabdomyolysis; no specific cause has been identified, but an underlying muscle calcium regulation disorder is suspected.
Rhabdomyolysis affecting horses may also occur in outbreaks; these have been reported in many European countries, and later in Canada, Australia, and the United States. It has been referred to as "atypical myopathy" or "myoglobinuria of unknown etiology". No single cause has yet been found, but various mechanisms have been proposed, and a seasonal pattern has been observed. Very high creatine kinase levels are detected, and mortality from this condition is 89%.
- Huerta-Alardín AL; Varon J; Marik PE (2005). "Bench-to-bedside review: rhabdomyolysis – an overview for clinicians". Critical Care 9 (2): 158–69. doi:10.1186/cc2978. PMC 1175909. PMID 15774072.
- Bosch X; Poch E; Grau JM (2009). "Rhabdomyolysis and acute kidney injury". New England Journal of Medicine 361 (1): 62–72. doi:10.1056/NEJMra0801327. PMID 19571284.
- Vanholder R; Sever MS; Erek E; Lameire N (1 August 2000). "Rhabdomyolysis". Journal of the American Society of Nephrology 11 (8): 1553–61. PMID 10906171.
- Aleman M (April 2008). "A review of equine muscle disorders". Neuromuscular Disorders 18 (4): 277–87. doi:10.1016/j.nmd.2008.01.001. PMID 18395447.
- Sauret JM; Marinides G; Wang GK (2002). "Rhabdomyolysis". American Family Physician 65 (5): 907–12. PMID 11898964.
- Warren JD; Blumbergs PC; Thompson PD (March 2002). "Rhabdomyolysis: a review". Muscle & Nerve 25 (3): 332–47. doi:10.1002/mus.10053. PMID 11870710.
- Elsayed EF; Reilly RF (2010). "Rhabdomyolysis: a review, with emphasis on the pediatric population". Pediatric Nephrology 25 (1): 7–18. doi:10.1007/s00467-009-1223-9. PMID 19529963.
- Armitage J (November 2007). "The safety of statins in clinical practice". The Lancet 370 (9601): 1781–90. doi:10.1016/S0140-6736(07)60716-8. PMID 17559928.
- Sathasivam S,; Lecky B (2008). "Statin induced myopathy". BMJ 337: a2286. doi:10.1136/bmj.a2286. PMID 18988647.
- Buchholz U; Mouzin E; Dickey R; Moolenaar R; Sass N; Mascola L (2000). "Haff disease: from the Baltic Sea to the U.S. shore". Emerging Infectious Diseases 6 (2): 192–5. doi:10.3201/eid0602.000215. PMC 2640861. PMID 10756156.
- Guis S; Mattei JP; Cozzone PJ; Bendahan D (2005). "Pathophysiology and clinical presentations of rhabdomyolysis". Joint Bone Spine 72 (5): 382–91. doi:10.1016/j.jbspin.2004.04.010. PMID 16214072.
- Ropper AH, Brown RH (2005). "45: Electrophysiologic and laboratory aids in the diagnosis of neuromuscular disease". In Ropper AH, Brown RH. Adams and Victor's Principles of Neurology (8th ed.). New York: McGraw-Hill Professional. pp. 1092–1109. doi:10.1036/0071469710. ISBN 0-07-141620-X.
- Brancaccio P; Lippi G; Maffulli N (June 2010). "Biochemical markers of muscular damage". Clinical Chemistry and Laboratory Medicine 48 (6): 757–67. doi:10.1515/CCLM.2010.179. PMID 20518645.
- Rodríguez-Capote K; Balion CM; Hill SA; Cleve R; Yang L; El Sharif A (December 2009). "Utility of urine myoglobin for the prediction of acute renal failure in patients with suspected rhabdomyolysis: a systematic review". Clinical Chemistry 55 (12): 2190–7. doi:10.1373/clinchem.2009.128546. PMID 19797717.
- Weisberg LS (December 2008). "Management of severe hyperkalemia". Critical Care Medicine 36 (12): 3246–51. doi:10.1097/CCM.0b013e31818f222b. PMID 18936701.
- Shadgan B; Menon M; O'Brien PJ; Reid WD (September 2008). "Diagnostic techniques in acute compartment syndrome of the leg". Journal of Orthopedic Trauma 22 (8): 581–7. doi:10.1097/BOT.0b013e318183136d. PMID 18758292.
- Shadgan B; Menon M; Sanders D et al. (October 2010). "Current thinking about acute compartment syndrome of the lower extremity". Canadian Journal of Surgery 53 (5): 329–34. PMC 2947124. PMID 20858378.
- Favaloro EJ (June 2010). "Laboratory testing in disseminated intravascular coagulation". Seminars in Thrombosis and Hemostasis 36 (4): 458–67. doi:10.1055/s-0030-1254055. PMID 20614398.
- Sever MS; Vanholder R; Lameire M (2006). "Management of crush-related injuries after disasters". New England Journal of Medicine 354 (10): 1052–63. doi:10.1056/NEJMra054329. PMID 16525142.
- Greaves I; Porter K; Smith JE (2003). "Consensus statement on the early management of crush injury and prevention of crush syndrome" (PDF). Journal of the Royal Army Medical Corps 149 (4): 255–9. doi:10.1136/jramc-149-04-02. PMID 15015795.
- Ho KM; Sheridan DJ (2006). "Meta-analysis of frusemide to prevent or treat acute renal failure". BMJ 333 (7565): 420–25. doi:10.1136/bmj.38902.605347.7C. PMC 1553510. PMID 16861256.
- Levi M (September 2007). "Disseminated intravascular coagulation". Critical Care Medicine 35 (9): 2191–5. doi:10.1097/01.CCM.0000281468.94108.4B. PMID 17855836.
- Ouzounellis T (16 February 1970). "Some notes on quail poisoning". JAMA 211 (7): 1186–7. doi:10.1001/jama.1970.03170070056017. PMID 4904256.
- Bywaters EG; Beall D (1941). "Crush injuries with impairment of renal function". British Medical Journal 1 (4185): 427–32. doi:10.1136/bmj.1.4185.427. PMC 2161734. PMID 20783577. Reprinted in Bywaters EG; Beall D (1 February 1998). "Crush injuries with impairment of renal function" (PDF). Journal of the American Society of Nephrology 9 (2): 322–32. PMID 9527411.
- Bywaters EG (1990). "50 years on: the crush syndrome". BMJ 301 (6766): 1412–5. doi:10.1136/bmj.301.6766.1412. PMC 1679829. PMID 2279155.
- Schrier RW; Wang W; Poole B; Mitra A (July 2004). "Acute renal failure: definitions, diagnosis, pathogenesis, and therapy". Journal of Clinical Investigation 114 (1): 5–14. doi:10.1172/JCI22353. PMC 437979. PMID 15232604.
- "Overview of Myopathies in Horses". Merck Veterinary Manual, 10th edition (online version). 2012. Retrieved 25 December 2013.
- Votion DM; Serteyn D (November 2008). "Equine atypical myopathy: a review". Veterinary Journal 178 (2): 185–190. doi:10.1016/j.tvjl.2008.02.004. PMID 18375157. | <urn:uuid:1c163af5-1ad9-4441-a663-b6e1fa7fc64e> | {
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Textbook of Psychiatry/Self-harm and suicide
Self harm is commonly used by psychiatrists and mental health professionals to describe a wide variety of behaviors that may or may not be related to suicide. Both self harming behaviors and suicide permeate society around the world and across demographics. Suicide is defined as self inflicted death with evidence that the person intended to die according to APA practice guidelines. Self harm is more difficult to define because its causes are poorly understood and the spectrum of behaviors can vary widely between individuals and between cultures. Behaviors commonly included in the self harm spectrum include overdoses, self battery, cutting, burning, poisoning, hanging and jumping from high places that do not result in death (Skegg, 2005). Suicide ultimately results in intentional self-inflicted death and self harm may lead to suicide.
The APA practice guidelines define terms related to self harm and suicide as the following:
Suicide self inflicted death with evidence that the person intended to die
Suicide attempt self injurious behavior with a nonfatal outcome and evidence that the person intended to die Aborted suicide attempt-potentially self injurious behavior with evidence that the person intended to die but stopped before physical damage occurred
Suicide ideation thoughts of serving as the agent of one’s own death
Suicidal intent subjective expectation and desire for self-destructive act to end in death
Lethality objective danger to life associated with suicide action or method
Deliberate self harm willful self-infliction of painful, destructive or injurious acts without intent to die
Both of these phenomenons are important to clinicians to understand and be aware of because of their prevalence in the mental health patient population. An estimated 4.3 to 17% of the psychiatric patient population will engage in deliberate self-harm, with higher rates in some subgroups (Fliege, 2006). Self-harm and suicidal behaviors pose a significant public health burden and utilize a tremendous amount of hospital resources (Sinclar, 2006). Up to 40% of people who deliberately harm themselves will go on to become repeat offenders (Zahl, 2004). Treatment of chronic self-harmers can be frustrating to the treatment team due to the poorly understood nature of the behavior and high rates of repeat admissions. Many patients are managed in emergency departments or do not seek treatment after performing these behaviors. Management depends largely on the underlying pathology and controlled trials of therapies are limited (Skegg, 2005).
- 1 Phenomenology
- 2 Epidemiology
- 3 Clinical Symptoms and Classification
- 3.1 Assessment
- 3.2 Pathogenesis
- 3.2.1 Biological Factors
- 3.2.2 Psychological Factors
- 3.2.3 Social/Cultural Factors
- 4 Treatment
- 5 References
Naming and classifying self-harm has been a topic of debate since the early 1900’s (Skegg, 2005; Mcalister, 2003). Different terms that have historically been used to delineate self-harm behaviors include attempted suicide, parasuicide, deliberate self injury and deliberate self poisoning. Terminology can vary in different parts of the world and imply intent. Recent literature suggests that many who self-harm do so without suicidal intent (Skegg, 2005).
Skegg describes self-harming behaviors in a 2005 review on a spectrum from self-harmful behaviors without visible injury to highly lethal traditional methods of suicide. Excessive exercise, denying oneself as punishment, stopping medication or deliberate recklessness fall on the end of this spectrum without visible injury. Self battery behaviors include head banging, self-hitting or hair-pulling. Self-injury with tissue damaging behaviors include self-biting, scratching, gouging, carving words or symbols into skin, sticking needles or pins into skin and interfering with wound healing. At the other extreme less lethal traditional methods of non-intentional suicide include overdose, recreational drug ingestion as self-harm, cutting and burning. Traditional highly lethal methods of suicide include hanging, shooting, jumping from a high place, poisoning, stabbing, electrocution and drowning.
When considering these behaviors on a spectrum, it is important to consider intent. Traditional risk assessments correlate lethality with suicidal intent, however in a sample of survivors of near-fatal self harm, only two-thirds of patients experienced suicidal thoughts prior to the event (Douglas, 2004). The current consensus view is that those who self harm, despite how seriously, believe that they will survive (Mcallister, 2003). It is important to consider, however, that patients who harm themselves are more likely to go on to commit suicide than those who do not.
Rates of self-harm and suicide vary widely around the world and have historically been difficult to quantify because many people do not seek medical attention after attempts and discussion of such behaviors is sometimes considered socially taboo. Birth cohort studies show higher odds for self harm in people born in recent years. The WHO/EURO study of parasuicide showed lower rates in southern European areas compared to northern areas (Skegg, 2005). In the United States, African Americans are at lower risk for self harm than other ethnic groups. Self-harming behaviors are common in adolescents and an estimated 5-9% of Australian, US and English adolescents reported self-harm over a one year period (Skegg, 2005). Lifetime self-harm ranged from 13-30% in these samples of adolescents (Skegg, 2005).
Skegg (2005) correlated demographic variables with risk of self-harm behaviors. It is rare before pubery and becomes common through adolescence. Older people are at much lower risk for self harm. More women than men present to mental health facilities with complaints of self-harm. Separated and divorced people appear to have higher rates of self-harm than other populations. Low socioeconomic status, less education and living in poverty are also risk factors for self harm (Skegg, 2005).
Further studies investigating suicidal behaviors are necessary to better understand the phenomenon and to create prevention strategies. Using three national medical databases, the annual rate of nonfatal emergency department treated intentional self-harm events in 2002-3 was between 127.2 and 164.7 per 100,000 US population (Classen, 2006). However, these rates do not include behavior of individuals not seeking treatment or seeking treatment in other medical facilities.
Clinical Symptoms and Classification
Sue was a 25 year old female who presented to the emergency room with a 3cm laceration on her left wrist. The laceration was superficial but deep enough that it required sutures. There were multiple other superficial lacerations that did not require sutures as well as multiple healed scars from previous lacerations all up and down her forearm.
After Sue’s wrist was sutured, she was evaluated by a psychiatrist for a possible suicide attempt. Sue revealed that she had been having a fight on the phone with her boyfriend and they had broken up. She denied any thoughts of suicide but rather said she was trying to reduce the tension and anger she felt about the situation. When asked about whether the self harm helped, she said it did release tension and therefore makes her feel more normal. She described it as a coping skill and did not see it as a problem behavior. She was discussing plans for going out with friends and maybe getting together with a boy who might want to be her new boyfriend.
Sue’s past history is significant for sexual abuse at age 5 years by a cousin who was living with the family for the summer. Sue said she had always been sad and depressed but she did not endorse enough symptoms to qualify for a major depressive disorder. She said that she has a history of getting more depressed whenever someone left her or told her she was not making them happy. That was when she would cut on herself. She was very clear that she did not intend to kill herself during those times although she endorsed the idea that she might be better off dead than alive.
Sue was deemed to be safe to go home. She was referred to therapy to work on the issues that caused her to use self harming behaviors for comfort.
Assessment of suicide and self harming behaviors takes place in a variety of treatment situations. It is often evaluated during an initial meeting with a patient in the emergency setting or at an outpatient intake. On an inpatient ward, assessment of suicide and self harm should be completed prior to advancement in privilege level, passes and discharge. If changes in the patient’s presentation occur or if the patient begins to display evidence of suicidal or self harming thoughts, an assessment should be completed. The APA practice guidelines describe a thorough assessment of the suicidal patient.
During the interview, the psychiatrist obtains information about the patient’s psychiatric history, medical history and current psychologic state through direct question and collateral information. This enables the psychiatrist to make a risk assessment, determine the patient’s current level of safety, choose an appropriate treatment setting and develop a treatment strategy. Suicide scales can be used to supplement the interview, but should not be used as a substitute because they lack the predictive validity to take the place of a thorough interview (APA practice guidelines).
A suicide assessment should include evaluation of current suicidal state, consisting of thoughts and plans regarding suicide. Specific methods should be elicited, including perceived lethality and access to firearms. The presence of hopelessness, guilt and anhedonia should be determined as well as reasons that prevent the patient from carrying out suicide plans. It should also include current and previous psychiatric illnesses including mood disorders, psychotic disorders, substance use disorders and anxiety disorders. Personal and family history of suicide and self harm behaviors should be noted, as well as outcomes. An individual’s psychosocial state should be assessed to evaluate current stressors that could exacerbate suicidal behaviors, as well as cultural or religious beliefs that could be protective (APA practice guidelines).
It is important for the psychiatrist to collect as much information as possible regarding current suicidal or self harming behaviors. These include frequency and duration of thoughts, specific plans and preparation made to complete plans. Attention should also be given to prior attempts, including timing, intent, relation to substance use and outcome. If a specific method is identified as a current suicidal ideation, perceived lethality should be determined. Highly lethal and irreversible means with advance planning place an individual at increased risk. If firearms are involved, the psychiatrist should contact a friend or relative and have them removed from the patient’s home before release (APA practice guidelines).
The pathogenesis of self harm and suicidal behavior is complicated and multifactorial. Sourander et al. (2006) attempted to identify early factors correlating with self-harm behaviors in childhood and adolescents. In this longitudinal study, parents rated children on Childhood Behavior Checklist and adolescents and their parents rated psychopathology at ages 12 and 15. Psychopathology in the child, poor parental well-being and living in a broken home at age 12 correlated with deliberate self harm at age 15. School and problems with peer groups at age 12 correlated with ideations of self harm at age 15. Acts of deliberate self harm in pre-adolescences led to higher rates of future behaviors.
Studies have found that up to 90% of individuals who present with self harm meet diagnostic criteria for psychiatric disorders. The most common is depression, followed by substance use disorders and anxiety disorders (Skegg, 2005). General population studies have indicated that individuals with psychopathology are at increased risk of self harm and suicide. Individuals with antisocial and borderline personality disorders exhibit high rates of self harming behaviors. Eating disorders, schizophrenia and post traumatic stress disorder have also been found in study samples of self harmers (Skegg, 2005). Treating underlying psychopathology may reduce risk in affected individuals.
Table 1: Selected Risk Factors for Self Harm
|1. Between puberty and old age|
|3. Separated or divorced|
|4. Low socioeconomic status|
|5. Less education|
Deliberate Self-Harm (DSH) and Depression
While DSH is almost always associated with dysphoria, it is not always associated with the syndrome of depression. DSH can occur in the setting of depression associated with both bipolar disorder and unipolar major depressive disorder. Haw et al. (2001) when he looked at a cohort of 106 patients who presented to a hospital following an episode of DSH found that 92% of these patients had a psychiatric diagnosis and that the most common diagnosis was affective disorder (72% using ICD-10 criteria).
Early adverse life events have a major impact on subsequent mood states. Similarly, early adversity is a major correlate of subsequent DSH behaviors (Gladstone et al. 2004; Parker et al. 2005). Gladstone et al. (2004) examined DSH behaviors, personality characteristics, and childhood variables, including parental styles and childhood sexual/physical abuse, among 125 women with depressive disorders. Findings indicated that participants who were victims of childhood sexual assaults were more likely to engage in DSH as adults (Gladstone et al. 2004). In addition, respondents who were victims of childhood sexual abuse became depressed earlier in life than non-abused controls (Gladstone et al. 2004).
Adolescents with DSH generally have less severe depressive symptoms than individuals with suicidal ideation, but more severe symptoms than those without any history of self-injurious ideation. In a community sample, adolescents who have a history of self-harm reported more depressive symptoms than those without a self-harm history (Muehlenkamp et al. 2004). In a study of 218 adolescents, ages 13-19, who were receiving outpatient treatment for a depressive mood disorder, adolescents who had DSH behavior had less severe depressive symptoms than those with suicidal ideation or suicide attempts (Tuisku et al. 2006). Similarly, among adults the degree of seriousness of a self injurious act was associated with depression and with intent. In a study of 49 prisoners in Germany, measures of depression and hopelessness were both highly correlated with suicidal intent and lethality; less lethal methods were not correlated with depression (Lohner et al. 2006). Impulsive acts of self-harm were rarely associated with depression (Lohner et al. 2006).
DSH behaviors are not fixed over the life time. For example, 70% of 132 adolescents who had deliberately poisoned themselves and who were followed for 6 years stopped the self-harm behaviors within 3 years of the index event (Harrington et al. 2006). DSH continued into adulthood mainly among those with psychiatric disorders. Only 56% of these study participants had a psychiatric disorder, and the most common psychiatric diagnosis was depression (Harrington et al. 2006). DSH behaviors may appear de novo in the elderly. Lamprecht et al. (2005) looked at older people presenting to an acute hospital with an episode of DSH. Sexual distribution among males and females was equal. Only 37% had a major depressive illness at the time of the DSH assessment, but 21% of the males had no psychiatric diagnoses at the time of the DSH (Lamprecht et al. 2005).
In young adults, the lack of depression in subjects with DSH has also been noted. Among 1,986 high-functioning military recruits (62% male), only 10% of those with a history of DSH reported depressive symptoms on the Beck’s Depression Inventory (Klonsky et al. 2003). Peers viewed self-harmers as having strange and intense emotions and a heightened sensitivity to interpersonal rejection (Klonsky et al. 2003). Given that DSH may not necessarily be associated with depression, why does it occur? Tzemoz and Birchwood (2006) examined dysfunctional thinking patterns and intrusive memories in patients diagnosed with both unipolar depressive and bipolar mood disorders. They recruited 49 participants diagnosed with major depression, manic, or hypomanic episodes. Twenty healthy controls were also recruited from the same areas in Central England. Compared to the healthy controls, dysfunctional attitudes were abnormal in the mood disordered groups when ill (Tzemoz and Birchwood, 2006). Interestingly, whereas dysfunctional attitudes resolved in bipolar subjects as they became euthymic, they persisted into euthymia for those diagnosed with unipolar major depression (Tzemoz and Birchwood, 2006).
Deliberate Self Harm and Bipolar Illness
Intentional self harm in mania is rare and is probably related to the depressed mood that can occur during manic episodes (Ostacher and Eidelman, 2006). However, DSH during bipolar depressions is more common than DSH in unipolar depressive illness (Parker et al. 2005). Parker et al. (2005) reported that across samples of depressed individuals, more individuals with bipolar disorder tended to report DSH behaviors compared to those with unipolar depression. Smith et al. (2005) examined the prevalence rates of bipolar disorders and major depression among 87 young adults with recurrent depression; 83.9% of study respondents met criteria for major depressive disorder, 16.1% met criteria for a DSM-IV-defined bipolar disorder. The authors reported that among the respondents diagnosed with major depression, 45.7% had a history of DSH, and 13.0% had a history of a previous suicide attempt. Of the 14 respondents diagnosed with BP disorder, 71.4% had DSH and 28.6% had a history of deliberate self-harm.
One of the best known occurrences of DSH was performed by Vincent van Gogh (1853-1890), a Dutch Impressionist artist who had bipolar disorder (Jamison, 1993). On Christmas Eve in 1888, Van Gogh cut off his own earlobe with a razor blade as he was apparently attempting to attack an acquaintance. Following this episode of self-harm, van Gogh exhibited alternating states of "madness and lucidity," and received treatment in an asylum in Saint-Remy. Two months after his discharge from the asylum, he committed suicide by shooting himself "for the good of all" (Anonymous, 2007).
Mood Disorders and Suicide
Suicide, the act of ending one’s life, is the most dramatic form of self-harm. Epidemiologic research indicates that in 2004, 31,484 individuals in the US died from suicide or self-inflicted injury (10.8 per 100,000 population) (Center for Disease Control, 2006). Extensive research has examined risk factors for suicide, and several studies have identified a history of prior suicide attempts as a very strong predictor of suicide risk (American Psychiatric Association, 2003; Borges et al. 2006; Gaynes et al. 2004). Certain sociodemographic characteristics have also been associated with high suicide risk. These include male gender, European-American ethnicity, and advanced age. However, the National Comorbidity Survey Replication Study, found that low income, "non-Hispanic Black" (p. 1750) ethnicity, and age less than 45 were significant correlates of suicide ideation (Borges et al. 2006). Additional risk factors include the presence of a psychiatric disorder, particularly depression, alcohol abuse, physical and sexual abuse, and a family history of suicide (Gaynes et al. 2004). Psychiatric disorders may be present in up to 90% of those who commit suicide (American Psychiatric Association, 2003). Divorced, separated, or widowed individuals have a higher risk of suicide (American Psychiatric Association, 2003). Conversley, high-conflict or violent marriages may increase the risk for suicide among married individuals (American Psychiatric Association, 2003).
Unipolar Depression and Suicide
Numerous studies have identified depression as a significant risk factor for suicide. This contributes to mortality rates associated with depression that are approximately 20 times higher than the general population (American Psychiatric Association, 2003). The fraction of people who have committed suicide that were depressed at the time of their death has been estimated to range from 15% (Rich et al. 1986) to 97.5% (Sinclair et al. 2005). However, most studies, including those that are based on psychological autopsies, estimate a rate of 30-34% (Arato et al. 1988; Henriksson et al. 1993; Foster et al. 1999). The fraction of adolescent suicides that involve depression may be slightly higher at 43% (Brent et al. 1999).
Co-morbid psychiatric conditions may additionally increase the risk for suicide. Paramount among these is co-occurring substance use which accounts for some 45% of completed suicides (Rich et al. 1986). Additionally, aggression (Dervic et al. 2006; Keilp et al. 2006) and cluster B personality disorders (Dervic et al. 2006) are associated with suicide attempts in depressed individuals with a history of childhood sexual abuse.
A decline in depression and hopelessness was associated with a decline in suicidal ideation in 198 people diagnosed with major depression (Sokero et al. 2006). There is a close correlation between the increased use of antidepressants and an observed decline in overall suicide rate (Korkeila et al. 2007; Gibbons et al. 2006), but this trend may have begun prior to the introduction of antidepressants (Safer and Zito, 2007). Antidepressants may have no effect on suicide ideation (Hammad et al. 2006) or may actually increase the risk of suicide attempt among depressed adults (Tiihonen et al. 2006) and suicide ideation among adolescents (Bridge et al. 2007; Dubicka et al. 2006), but may reduce completed suicides (Tiihonen et al. 2006). The United States Food and Drug Administration (FDA) has placed a warning on all antidepressants, that they may increase suicidal ideation in adolescents (Kuehn, 2007). While lithium is rarely used in major depressive disorder, it appears to have an anti-suicide effect, similar to that seen in bipolar illness (Guzzetta et al. 2007).
John was a 61 year old male who presented to the emergency room with a 7cm laceration on his left inner forearm. The laceration was moderately deep and required multiple sutures. There were no other signs of current or former abuse on his arms or the rest of his body. After John’s arm was sutured, he was evaluated by a psychiatrist for a possible suicide attempt. John revealed that he was in a marriage that had not been healthy for quite some time and that his wife had called to say she was not coming home and that she wanted a divorce. John decided he could not face life without his wife and saw no way to call for help so cut himself. He denied suicidal intention at the time of the injury and denied it again at the time of the interview. John could not identify any social support persons and did not have any plans for the future. He kept insisting that he needed to go home but would not say what he needed to do there. John’s past history was significant for physical abuse by his father when he was a child. His father then left when he was 11 years old. His mother was not emotionally available and was overwhelmed at being left with 4 children to care for when she only had a minimum wage job. John was on his own for most of his teen age life. As the oldest child, he was responsible for helping with the other 3 children when his mother was not around. John related that he had always thought the marriage to his husband was going to be different from his mother’s and was not going to end in divorce. He said he felt like it was all his fault and he would never find another person to love him. John’s psychiatrist felt that he was a risk for attempting suicide when he returned home and placed him in a psychiatric hospital for safety and stabilization.
Bipolar Disorder and Suicide
Lifetime prevalence of all bipolar disorders is approximately 2%; bipolar I disorder has a incidence rate of 0.8%, compared to 1.2% for bipolar II disorder. Suicide risk is high in bipolar disorder. Angst et al. (1995) followed 406 patients for 36 years; findings indicated that 11% committed suicide, regardless of whether patients were diagnosed with type I or II disorder. Other estimates approach 19% (Ostacher and Eidelman, 2006). The risk appears higher than in unipolar major depression. Chen et al. (1996) examined data from the Epidemiologic Catchment Area Study (ECA) to estimate lifetime rates of suicide attempts in mood disorders; findings indicated that 29.2% of respondents with bipolar disorder attempted suicide, compared to 15.9% among those with unipolar depressive disorder. Additionally, when subjects with bipolar disorder attempt suicide, the lethality of that attempt may be greater. Among 2,395 hospital admissions of patients with unipolar depression and bipolar disorder subjects with bipolar disorder had a higher incidence of more lethal suicide attempts (Raja et al. 2004). The odds of completed suicide in those with bipolar disorder is 2.0 times higher compared to those with unipolar depression (Raja et al. 2004). However, prevalence rates of suicide may be inflated, since researchers typically focus on hospitalized patients and those who have received treatment from a mental health provider. This self-selected population may be more ill compared to those who receive treatment from primary care providers, or those who do not receive any psychiatric treatment. Risk for suicide is highest during a depressive episode of bipolar disorder. Isometsa et al. (1994) found that among patients diagnosed with bipolar disorder, 80% of completed suicides occur during a depressive episode. Mortality from suicide in bipolar depression may be 30 times that of normal controls (Ostacher and Eidelman. 2006). However suicidal ideation and suicide completions may occur during the mixed (Dilsaver et al. 1994) or even manic phase (Cassidy et al. 2001). Rapid cycling also carries a higher likelihood for more serious suicide attempts but not an increase in completed suicides compared to other types of episodes (42 vs 27%) (MacKinnon et al. 2003). Suicide risk is highest in newly diagnosed bipolar patient. Fagiolini et al. (2004) found that among 104 patients with bipolar disorder, 50% attempted suicide within 7.5 years of the initial onset of the illness (either mania or depression). In these young bipolar patients, suicide rarely occurs during episodes of mania. Lithium appears to have a clear effect on reducing completed suicide in bipolar patients with a five fold reduction in relative risk (Baldessarini et al. 2006; Tondo et al. 2001). More impressively, lithium reduces non-suicidal DSH and non-psychiatric mortality in bipolar patients (Cipriani et al. 2005).
Dick was a 24 year old young man in law school when he had his first manic episode. He had a history of a depressive episode that had been difficult to treat when he was 18 but had not had any problems since that time and was not on any medications at the time of this manic episode. During the episode, he lost his job, his relationship with his girlfriend and he spent thousands more dollars than he could afford to spend in cars, jewelry, vacations and gifts to his girlfriend. He was hospitalized and stabilized on appropriate anti-manic medications. Approximately 4 months later, Dick began another depressive episode. This time he was thinking of all the things he had lost. He felt like his life as a lawyer was over and that he was destined to be a disabled person with no job, no family and no friends for the rest of his life. He did continue to take his medicines and see his psychiatrist but did not discuss any of these thoughts with any of his support persons. 2 months after the depressive episode began, Dick was found in his home, having hung himself from a rafter in the garage.
Serotonin System and Suicide
On a molecular level, the serotonin system has been implicated in self harm population studies. Low levels of 5 HIAA have been found in cerebrospinal fluid in self-harmers (Skegg, 2005). There are many biological associations between mood symptoms and aggression or violence. These include increased aggression with increased cytokine activity (Zalcman and Siegel, 2006), catecholamine metabolism (Volavka et al. 2004), testosterone (Pope et al. 2000), and hypothalamic-pituitary-adrenal axis dysfunction (Shea et al. 2005; Malkesman et al. 2005). However, the most consistent findings are with the serotonergic system.
Among the many findings associated with serotonergic dysfunction in aggression, platelet serotonin 2A receptor (5-HT2A) binding was increased in subjects with trait aggression (Lauterbach et al. 2006). Prefrontal cortical 5-HT2A binding was also increased in aggressive suicidal patients (Oquendo et al. 2006). Similarly, relative increases in plasma tryptophan levels (a precursor to serotonin) are associated with increased aggression and hostility (Lauterbach et al. 2006; Suarez and Krishnan. 2006) Lower CSF 5-HIAA concentration was independently associated with severity of lifetime aggressivity and a history of a higher lethality suicide attempt and may be part of the diathesis for these behaviors. The dopamine and norepinephrine systems do not appear to be as significantly involved in suicidal acts, aggression, or depression (Placidi et al. 2002). However, the most compelling findings regarding the involvement of serotonin in both mood disturbance and violence is found in the serotonin transporter polymorphisms.
Several recent studies have investigated the role of polymorphisms in the serotonin reuptake pump or the serotonin transporter gene (5HTTLPR). A common polymorphism of this gene is a deletion in the area of the gene that regulates its transcription into messenger RNA, and ultimately translation into expressed protein, the promoter region. Individuals with this deletion, called the short or "s" allele, express fewer serotonin transporters. Individuals who are homozygous for the "s" allele (ss), are more likely to develop depression (OR 1.5-179) (Cervilla et al. 2006) and depression after a traumatic event (Kaufman et al. 2004; Caspi et al. 2003). Thus, the observed link between early life adversity, or later life trauma, and subsequent depression, is related, at least in part, to having the ss genotype (Kaufman et al. 2004; Caspi et al. 2000). While stressful life events or extreme adversity are clearly associated with subsequent depression, adversity is quite potent in inducing depression in subjects with the ss genotype; so that the dosage of adversity required to produce depression is much lower in individuals homozygous for the short form of the 5HTTLPR (Cervilla et al. 2007). Several studies have also found that the ss genotype is also associated with subclinical depressive symptoms in individuals without depression (Gonda et al. 2005, 2006; Gonda and Bagdy, 2006).
The ss genotype of the 5HTTLPR is also associated with aggression. In a case control study of conduct disorder with or without aggression, it was found that the ss genotype was strongly associated with aggression but not conduct disorder without aggression (Sakai et al. 2006). A positron emission tomography (PET) study of 5HRRLPR density found that reduced transporter density is associated with impulsive aggression (Frankle et al. 2005). While this study did not examine the genotype of the study subjects, it found that the phenotype that is expected with the ss genotype is associated with aggression (Frankle et al. 2005). Among schizophrenic patients who attempted suicide, the ss genotype of the 5HTTLPR was associated with violent suicide attempts but not with non-violent attempts nor with non-attempters (Bayle et al. 2003).
Many psychological factors may also contribute to self harm and suicidal behaviors. It has been suggested that rage towards others, feelings of abandonment, guilt or desperation may play a role in these behaviors at a subconscious level (Skegg, 2005). Poor problem solving skills, impaired decision making skills and factors that contribute to the former have been studied and indicated as risk factors in those who harm themselves (Skegg, 2005). Neuroticism, dissociation and novelty-seeking personality traits are associated with suicide and self harm (Skegg, 2005).
Direct Abuse or Neglect
Childhood abuse and neglect are clearly associated with a substantial increase in the risk for subsequent depression and maladaptive behaviors (Cukor and McGinn, 2006; Reigstad et al. 2006; Widom et al. 2007). This is true in all cultures in which it has been studied (Afifi, 2006).
Verbal and Emotional Abuse
The experience of verbal abuse during childhood (e.g., "you are stupid") increases depression, anger and hostility in young adults (Teicher et al. 2006; Sachs-Ericsson et al. 2006). Verbal and emotional abuse influence the development of self-concept, and lead to a self-critical style of cognitive processing that contributes to low self esteem (Cukor and McGinn, 2006; Sachs-Ericsson et al. 2006). This impaired self-image may be one of the underlying phenomena that increase the risk of subsequent sexual victimization as a young adult (Rich et al. 2005).
Physical abuse may be a major contributing factor in the development of violence in later life (Huizinga et al. 2006). Physical abuse is also pivotal in the development of depression in youths and on into adulthood (Widon et al. 2007; Cukor and McGinn, 2006; Reigstad et al. 2006; Wright et al. 2004). Physical abuse may occur in either the home environment or in school. Bullying is a form of verbal and physical violence that can have major impact on development. The odds of experiencing social problems, depression with suicidal ideation and attempts are 3.9 times higher among victims of bullying compared to non-victims (Brunstein Klomek et al. 2007; Kim et al. 2006). Furthermore, bullying behaviors have been linked to mood disturbances. The odds of bullies developing social problems, depression, and suicidality are 1.8 times higher compared to people who are not bullies, and bullies who are also targets of other bullies are 4.9 times as likely to develop social problems (Brustein Klomek et al. 2007; Kim et al. 2006). High profile school shooters, such as Columbine High School or Virginia Tech University, have been bullied by class mates.
Sexual abuse of children is associated with a wide variety of physical and psychological sequelae, many of which are life-long. Early sexual abuse is associated with a significant increase in depression in both males and females (Peleikis et al. 2005; Conway et al. 2004; Gladstone et al. 2004; Martin et al. 2004). The risk of subsequent suicide attempts is 15 times higher in boys who experience early sexual abuse compared to non-abused boys (Martin et al. 2004); among women suicide ideation is 4.5 times higher (Masho et al. 2005). The consequences of childhood sexual abuse includes greater severity of depressive illness in adult patients over age 50 (Gamble et al. 2006; McGuigan and Middlemiss, 2005). Adult women who have experienced childhood sexual abuse are more likely to be victims of violence (Gladstone et al. 2004) and other forms of trauma, including sexual assault (Rich et al. 2005; Banyard et al. 2002). Sexual abuse perpetrated by adult women can be just as harmful as sexual abuse perpetrated by men (Denov, 2004).
Experiences early in life may be an important risk factor for later self harm. Children of divorced parents, women of low education or socioeconomic status and children of parents with psychopathology are at higher risk of deliberate self harm (Skegg, 2005). Trauma early in life such as physical, sexual or emotional abuse and exposure to household violence has been identified as risk factors (Skegg, 2005). It has been difficult to determine if these experiences are independent risk factors, or if they lead to impairment in relationships that may also be a risk factor for self harm (Skegg, 2005).
Social support appears to play a key protective role in self harming behaviors as evidenced by groups of people who have been found to be a higher risk. Divorced and separated individuals are at a higher risk, as are unemployed individuals. It has been found that social support reduces self harming behaviors and moderate stress (Skegg, 2005). Multiple studies have also found moral obligations and religious beliefs to be protective against suicide (Skegg, 2005).
Risk assessment and the patient’s ability to follow through with treatment are key factors in determining treatment modality in the suicidal patient. Depending on the circumstances, treatment can range from involuntary hospitalization on secure psychiatric wards to outpatient clinic follow-up. Treatment should be carried out in the environment that is least restrictive, but includes adequate measures for safety. Goals of management include establishing a therapeutic alliance, establishing safety and determining the patient’s needs. Incorporating the patient’s individual needs into the treatment plan is important to promote adherence (APA practice guidelines).
When establishing the therapeutic alliance, it is important for the psychiatrist to be aware of countertransferance and transference reactions between themselves and the suicidal patient. Dealing with suicidal individuals can uncover the psychiatrist’s own feelings about death and suicide and may provoke anger in some. On the other hand, some patients with a strong desire to die may become angry at the treating physician, and others may have a desire to be saved instead of taking responsibility for their own actions (APA practice guidelines).
Attending to the patient’s immediate safety is a priority in the treatment setting, especially in the acute phase. In the emergency setting, it is imperative to remove personal objects that the patient could use to harm themselves. Removing personal items such as purses and shoestrings that the patient could use to harm themselves may be necessary on inpatient units. Close surveillance via frequent safety checks or surveillance cameras may be necessary in acutely suicidal individuals (APA practice guidelines).
A balance between suicide risk and risk associated with hospitalization must be accomplished to determine the most appropriate setting. While establishing safety is a priority, there are also effects of hospitalization that may have negative effects on a patient’s life situation. These include financial risks including hospital bills and lost time from work, social stigmatization and psychosocial stressors. Generally, hospitalization is indicated when patients are at high risk of self harm, have new onset of suicidal behaviors, require treatments that can only be performed in the hospital setting, or are unable to comply with less restrictive treatment options (APA practice guidelines).
Evidence clearly indicates that underlying mood disorders must be treated to optimize treatment in the suicidal or self-harming patient as discussed above in the pathogenesis discussion. A brief summary of findings regarding specific classes of drugs as related to self-harming behaviors is included below.
According to the American Psychiatric Association practice guidelines, pharmacotherapy is commonly used in suicidal patients suffering from depression and anxiety disorders. They have also been used to treat suicidal patients with comorbid substance disorders. However, limited evidence based studies exist to support that this treatment modality reduces rates of suicide. Studies using FDA databases do not show differences in rates of suicide with the use of antidepressants (APA practice guidelines).
Conflicting evidence exists regarding the increased incidence of suicide following SSRI treatment. Several case reports were published, however, and patients should be educated regarding these findings. However, clinicians must be careful to not neglect treatment of real mood pathology due to fear.
The APA practice guidelines identify treatment with lithium salts as an evidenced based treatment to reduce suicide risk in patients with bipolar disorder and major depressive disorder. They report that this treatment has been shown to decrease suicidal acts by 14-fold. Practitioners should be aware of the high lethality of overdose on lithium when prescribing quantities to potentially suicidal patients.
Other Mood Stablilzers
Anti-convulsant agents are frequently used as mood stabilizer therapy. They may reduce suicidal behaviors, however, are not as evidenced supportive as Lithium (APA practice guidelines).
Atypical antipsychotics are commonly used to reduce hallucinations, delusions, agitation, aggression and contusion, which may reduce self-harm and suicidal behaviors. These agents are indicated for use in patients with schizophrenia, schizoaffective disorder, and mood disorders with psychotic features. These include aripiprazone, clozapine, olanzapine, quitiapine, risperidone and ziprasidone. Clozapine is typically reserved for patients who do not respond to other agents due to side effects. For the same reason, typical antipsychotics are usually reserved for people not responding to newer agents (APA practice guidelines).
Theroetically, antianxiety agents would have the potential to reduce suicide and self-harm risk since anxiety is a risk factor. However, studies are limited. Agents commonly used are benzodiazepines and buspirone.
Since suicide is relatively rare in the general population, it is difficult to conduct studies with enough events to reach statistical significance. A meta-analysis of psychosocial interventions by Crawford et al. (2007) suggests that specific psychosocial interventions following acts of self-harm do little more than standard care to prevent subsequent suicide. Of the interventions studied, Cognitive Behavioral therapy appeared to have a trend towards reducing risk of suicide. Overall mortality in the intense intervention group was lower, however. Interventions that improve existing mood symptoms will ultimate reduce self destructive behaviors as discussed above.
Afifi M. Depression in adolescents: gender differences in Oman and Egypt. East Mediterr Health J 2006; 12:61-71.
American Psychiatric Association. Practice Guideline for the Assessment and Treatment of Patients With Suicidal Behaviors. Acessed at http://archive.psych.org/cme/apacme/courses/sections.cfm?apacme=00160008 on 11/1/08.
Angst J, Preisig M. Outcome of a clinical cohort of unipolar, bipolar and schizoaffective patients. Results of a prospective study from 1959 to 1985. Schweiz Archiv Neurol Psychiatry 1995; 146: 17-23.
Arato M, Demeter E, Rihmer Z, Somogyi E. Retrospective psychiatric assessment of 200 suicides in Budapest. Acta Psychiatr Scand 1988; 77:454-456.
Baldessarini RJ, Tondo L, Davis P, Pompili M, Goodwin FK, Hennen J. Decreased risk of suicides and attempts during long-term lithium treatment: a meta-analytic review. Bipolar Disord. 2006; 8:625-39.
Banyard VL, Williams LM, Siegel JA. Re-trumatization among adult women sexually abuse in childhood: exploratory analyses in a prospective study. J Child Sex Abus 2002; 11:19-48.
Bayle FJ, Leroy S, Gourion D, Millet B, Olie JO, Poirier MF, Krebs MO. 5HTTLPR polymorphism in schizophrenic patients: further support for association with violent suicide attempts. Am J Med Genet B Neuropsychiatr Genet 2003; 119:12-17.
Bogat GA, DeJonghe E, Levendosky AA, Davidson WS, von Eye A. Trauma symptoms among infants exposed to intimate partner violence. Child Abuse Negl 2006; 30:109-125.
Brent DA, Perper JA., Moritz G, Allman C, Friend A, Roth C, Schweers J, Balach L, Baugher M. Psychiatric risk factors for adolescent suicide: A case-control study. J Am Acad Child Adoles Psychiatry 1993; 32:521-529.
Bridge JA, Iyengar S, Salary CB, Barbe RP, Birmaher B, Pincus HA, Ren L, Brent DA. Clinical response and risk of reported suicidal ideation and suicide attempts in pediatric antidepressant treatment: a meta-analysis of randomized controlled trials. JAMA 2007; 297:1683-1696
Brunstein Klomek A, Marrocco F, Kleinman M, Schonfeld IS, Gould MS. Bullying, depression, and suicidality in adolescents. J Am Acad Child Adolesc Psychiatry 2007; 46:40-49.
Caspi A, Sugden K, Moffitt TE, Taylor A, Craig IW, Harrington H, McClay J, Mill J, Martin J, Braithwaite A, Poulton R. Influence of life stress on depression: moderation by a polymorphism in the 5-HTT gene. Science 2003; 301:291-293.
Cassidy F, Carroll BJ. Frequencies of signs and symptoms in mixed and pure episodes of mania: implications for the study of manic episodes. Prog Neuropsychopharmacol Biol Psychiatry 2001; 25: 659-665.
Cervilla JA, Rivera M, Molina E, Torres-Gonzalez F, Bellon JA, Moreno B, de Dios Luna J, de Diego-Otero Y, King M, Nazareth I, Gutierrez B, PRECiCT Study Core Group. The 5-HTTTLPR s/s genotype at the serotonin trasporter gene (SLC6A4) increases the risk for depression in a large cohort of primary care attendees: the PREDICT-gene study. Am J Med Genet B Neuropsychiatr Genet 2006;141:912-917 Cipriani A, Pretty H, Hawton K, Geddes JR. Lithium in the prevention of suicidal behavior and all cause mortality in patients with mood disorders: a systematic review of randomized trials. Am J Psychiatry 2005; 162:1805-1819.
Chen YW, Dilsaver SC. Lifetime rates of suicide attempts among subjects with bipolar and unipolar disorders relative to subjects with other Axis I disorders. Biol Psychiatry 1996; 39: 896-899.
Classen C et al. Epidemiology of nonfatal deliberate self-harm in the United States as described in three medical databases. Suicide and Life Threatening Behavior 2006; 36:192-211. Conway M, Mendelson M, Glannopoulos C, Czank PA, Holm SL. Childhood and adult sexual abuse, rumination on sadness, and dysphoria. Child Abuse Negl 2004; 28:393-410
Cukor D, McGinn LK. History of child abuse and severity of adult depression: the mediating role of cognitive schema. J Child Sex Abus 2006; 15:19-34.
Denov MS. The-long term effects of child sexual abuse by female perpetrators: a qualitative study of male and female victims. J Interpers Violence 2004; 19:1137-1156. Dilsaver SC, Chen YW, Swann AC, Shoaib AM, Tsai-Dilsaver Y, Krajewski KJ. Suicidality in patients with pure and depressive mania. American Journal of Psychiatry 1994; 151: 1312-1315.
Dubicka B, Hadley S, Roberts C. Suicidal behaviour in youths with depression treated with new generation antidepressants: meta analysis. Br J Psychiatry 2006; 189:393-398.
Fagiolini A, Kupfer DJ, Rucci P, Scott JA, Novick DM, Frank E. Suicide attempts and ideation in patients with bipolar I disorder. J Clin Psychiatry 2004; 65: 509-514.
Fliege H et al. Three assessment tools for deliberate self-harm and suicide behavior: evaluation and psychopathological correlates. Journal of Psychosomatic Research 2006; 61: 113-21.
Foster T, Gillespie K, McClelland R, Patterson C. Risk factors for suicide independent of DSM-III-R Axis I disorder. Br J Psychiatry 1999; 175:175-179.
Frankle WG, Lombardo I, New AS, Goodman M, Talbot PS, Huang Y, Hwang DR, Slifstein M, Curry S, Abi-Dargham A, Laruelle M, Siever LJ. Brain serotonin transporter distribution in subjects with impulsive aggressivity: a positron emission study with [11C]McN 5652. Am J Psychiatry 2005; 162:915-923.
Gamble SA, Talbot NL, Duberstein PR, Conner KR, Franus N, Beckman AM, Conwell Y. Childhood sexual abuse and depressive symptom severity: the role of neuroticism. J Nerv Ment Dis 2006; 194:382-385.
Gibbons RD, Hur K, Bhaumik DK, Mann JJ. The relationship between antidepressant prescription rates and rate of early adolescent suicide. Am J Psychiatry 2006; 163:1898-1904
Gladstone GL, Parker GB, Mitchell PB, Malhi GS, Wilhelm K, Austin MP. Implications of childhood trauma for depressed women: an analysis of pathways from childhood sexual abuse to deliberate self-harm and revictimization. Am J Psychiatry 2004; 161:1417-1425.
Gonda X, Bagdy G. [Relationship between serotonin transporter gene 5HTTLPR polymorphism and the symptoms of neuroticism in healthy population]. (Article in Hungarian) Psychiatr Hung 2006;21(5):379-85.
Gonda X, Juhasz G, Laszik A, Rihmer Z, Bagdy G. Subthreshold depression is linked to the functional polymorphism of the 5HT transporter gene. J Affect Disord 2005; 87:291-297.
Gonda X, Rihmer Z, Zsombok T, Bagdy G, Akiskal KK, Akiskal HS. The 5HTTLPR polymorphism of the serotonin transporter gene is associated with affective temperaments as measured by TEMPS-A. J Affect Disord 2006;91:125-131.
Guzzetta F, Tondo L, Centorrino F, Baldessarini RJ. Lithium treatment reduces suicide risk in recurrent major depressive disorder. J Clin sychiatry 2007; 68:380-383.
Hammad TA, Laughren TP, Racoosin JA. Suicide rates in short-term randomized controlled trials of newer antidepressants. J Clin Psychopharmacol 2006; 26:203-207.
Haw C, Hawton K, Houston K, Townsend E. Psychiatric and personality disorders in deliberate self-harm patients. Br J Psychiatry 2001; 178:48-54.
Harrington R, Pickles A, Aglan A, Harrington V, Burroughs H, Kerfoot M. Early adult outcomes of adolescents who deliberately poisoned themselves. J Am Acad Child Adoles Psychiatry 2006; 45:337-345.
Henriksson MM, Aro HM, Marttunen MJ, Heikkinen ME, Isometa ET, Kuoppasalmi KI, Lonqvist JK. Mental disorders and comorbidity in suicide. Am J Psychiatry 1993; 150:935-940.
Huizinga D, Haberstick BC, Smolen A, Menard S, Young SE, Corley RP, Stallings MC, Grotpeter J, Hewitt JK. Childhood maltreatment, subsequent antisocial behavior, and the role of monoamine oxidase A genotypes. Biol Psychiatry 2006; 60:677-683.
Isometsa ET, Henriksson MM, Aro HM, Lonnqvist JK. Suicide in bipolar disorder in Finland. Am J Psychiatry 1994; 151: 1020-1024.
Jamison KR. Touched with Fire: Manic-Depressive Illness and the Artistic Temperament. Ontario: Free Press, 1993
Kaufman J, Yang BZ, Douglas-Palumberi H, Houshvar S, Lipschitz D. Social supports and serotonin transporter gene moderate depression in maltreated children. Proc Natl Acad Sci U S A 2004; 101:17316-17321
Kim YS, Leventhal BL, Koh YJ, Hubbard A, Boyce WT. School bullying and youth violence: causes or consequences of psychopathologic behavior? Arch Gen Psychiatry 2006; 63:1035-1041.
Klonsky ED, Oltmanns TF, Turkheimer E. Deliberate self-harm in a nonclinical population: prevalence and psychological correlates. Am J Psychiatry 2003; 160:1501-1508.
Korkeila J, Salminen JK,Hiekkanen H, Salokangas RKR. Use of antidepressants and suicide rate in Finland: An ecological study. J Clin Psychiatry 2007; 68:505-511.
Kuehn BM. FDA panel seeks to balance risks in warnings for antidepressants. JAMA 2007; 297:573-574
Lamprecht HC, Pakrasi S, Gash A, Swann AG. Deliberate self-harm in older people revisited. Int J Geriat Psychiatry 2005; 20:1090-1096.
Lauterbach E, Brunner J, Hawelleck B, lewitzka U, Ising M, Bondy B, Rao ML, Frahnert C, Rujescu D, Muller-Oerlinghausen B, Schley J, Heuser I, Maier W, Hohagen F, Felber W, Bronisch T. Platelet 5-HT2A receptor binding and tryptophan availability are not associated with recent history of suicide attempts but with personality traits characteristic for suicidal behavior. J Affect Disord 2006; 91:57-62.
Lohner J, Konrad N. Deliberate self-harm and suicide attempt in custody: Distinguishing features in male inmates’ self-injurious behavior. Int J Law Psychiatry 2006; 29:370-385.
MacKinnon DF, Zandi PP, Gershon E, Nurnberger JI Jr, Reich T, DePaulo JR. Rapid switching of mood in families with multiple cases of bipolar disorder. Arch Gen Psychiatry 2003; 60:921-928.
Malkesman O, Maayan R, Weizman A, Weller A. Aggressive behavior and HPA axis hormones after social isolation in adult rats of two different genetic animal models for depression. Behav Brain Res 2006;175:408-414
Martin J, Langley J, Millchamp J. Domestic violence as witnessed by New Zealand children. N Z Med J 2006; 119:U1817.
Masho SW, Odor RK, Adera T. Sexual assault in Virginia: A population-based study. Womens Health Issues 2005; 15:157-166.
McGuigan WM, Middlemiss W. Sexual abuse in childhood and interpersonal violence in adulthood: a cumulative impact on depressive symptoms in women. J Interpers Violence 2005; 20:1271-1287.
Muehlenkamp JJ, Gutierrez PM. An investigation of differences between self-injurious behavior and suicide attempts in a sample of adolescents. Suicide Life Threat Behav 2004; 34:12-23.
Oquendo MA, Russo SA, Underwood MD, Kassir SA, Ellis SP, Mann JJ, Arango V. Higher postmortem prefrontal 5-HT2A receptor binding correlates with lifetime aggression in suicide. Biol Psychiatry 2006; 59:235-243.
Ostacher MJ, Eidelman P. Suicide in Bipolar Depression. In: El-Mallakh RS, Ghaemi SN (Eds.) Bipolar “Depression a comprehensive guide. Washington, DC: American Psychiatric Publishing Inc. 2006; Chapter 5, 117-144.
Parker G, Malhi G, Mitchell P, Kotze B, Wilhelm K, Parker K. Self-harming in depressed patients: pattern analysis. Aust N Z J Psychiatry 2005; 39: 899-906.
Peleikis DE, Mykletun A, Dahl AA. Long-term social status and intimate relationship in women with childhood sexual abuse who got outpatient psychotherapy for anxiety disorder and depression. Nord J Psychiatry 2005; 59:31-38.
Placidi GP, Oquendo MA, Malone KM, Huang YY, Ellis SP, Mann JJ. Aggressivity, suicide attempts, and depression: relationship to cerebrospinal fluid monoamine metabolite levels. Biol Psychiatry 2002; 52:375-376.
Pope HG Jr, Kouri EM, Hudson JI. Effects of supraphysiologic doses of testosterone on mood and aggression in normal men: a randomized
Raja M, Azzoni A. Suicide attempts: differences between unipolar and bipolar patients and among groups with different lethality risk. J Affect Disord 2004; 82:437-442.
Rich CL, Gidycz CA, Warkentin JB, Loh C, Weiland P. Child and adolescent abuse and subsequent victimization: a prospective study. Child Abuse Negl 2005; 29:1373-1394.
Rich CL, Young D, Fowler RC. San Diego suicide study: Young vs old subjects. Arch Gen Psychiatry 1986; 43:577-582.
Sachs-Ericsson N, Verona E, Joiner T, Preacher KJ. Parental verbal abuse and the mediating role of self-criticism in adult internalizing disorders. J Affect Disord 2006; 93:71-78.
Safer DJ, Zito JM. Do antidepressants reduce suicide rates? Public Health 2007; 121:274-277.
Sakai JT, Young SE, Stallings MC, Tiberlake D, Smolen A, Stetler GL, Crowley TJ. Case control and within-family tests for an association between conduct disorder and 5HTTLPR. Am J Med Genet B Neuropscyhiatr Genet 2006; 141:825-832.
Shea A, Walsh C, Macmillan H, Steiner M. Child maltreatment and HPA axis dysregulation: relationship to major depressive disorder and post traumatic stress disorder in females.
Sinclair J et al. Systematic review of resource utilization in the hospital management of deliberate self-harm. Psychological Medicine 2006; 36:1682-1693.
Skegg K. Self-harm. The Lancet 2005; 366:1471-83.
Smith DJ, Harrison N, Muir W, Blackwood DHR. The high prevalence of bipolar spectrum disorders in young adults with recurrent depression: toward an innovative diagnostic framework. J Affect Disord 2005; 84:167-178.
Sourander et al. Early predictors of deliberate self harm among adolescents . A prospective followup study from age 3 to age 15. Journal of Affective Disorders 2006; 93:87-96.
Suarez EC, Krishnan KR. The relation of free plasma tryptophan to anger, hostility, and aggression in a nonpatient sample of adult men and women. Ann Behav med 2006; 31:254-260.
Teicher MH, Samson JA, Polcari A, MaGreenery CE. Sticks, stones, and hurtful words: relative effects of various forms of childhood maltreatment. Am J Psychiatry 2006; 163:993-1000.
Tiihonen J, Lonnqvist J, Wahlbeck K, Klaukka T, Tanskanen A, Haukka J. Antidepressants and the risk of suicide, attempted suicide, and overall mortality in a nationwide cohort. Arch Gen Psychiatry 2006; 63:1358-1367.
Tondo L, Hennen J, Baldessarini RJ. Lower suicide risk with long-term lithium treatment in major affective illness: a meta-analysis. Acta Psychiatr Scand 2001; 104:163-72.
Tuisku V, Pelkonen M, Karlsson L, Kiviruusu O, Holi M, Ruuttu T, Punamaki R, Marttunen M. Suicidal ideation, deliberate self-harm behavior and suicide attempts among adolescent outpatients with depressive mood disorders and comorbid axis I disorders. Eur Child Adolesc Psychiatry 2006; 15:199-206.
Tzemou E, Birchwood M. A prospective study of dysfunctional thinki8ng and the regulation of negative intrusive memories in bipolar 1 disorder: implications for affect regulation theory. Psychol Med 2007; 37:689-698.
Volavka J, Bilder R, Nolan K. Catecholamines and aggression: The role of COMT and MAO polymorphisms. Ann NY Acad Sci 2004; 1036:393-398.
Widom CS, DuMont K, Czaja SJ. A prospective investigation of major depressive disorder and comorbidity in abused and neglected children grown up. Arch Gen Psychiatry 2007; 64:49-56.
Wright J, Friedrich W, Cinq-Mars C, Cyr M, McDuff P. Self-destructive and delinquent behaviors of adolescent female victims of child sexual abuse: rates and covariates in clinical and nonclinical samples. Violence Vict 2004; 19:627-643.
Zalcman SS, Siegel A. The neurobiology of aggression and rage: role of cytokines. Brain Behav Immun 2006; 20:507-514. | <urn:uuid:cd09056e-7dd1-4ca3-a246-003148527eae> | {
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|Classification and external resources|
|ICD-10||C62.9 (ILDS C62.930)|
|DiseasesDB||3604 12952 12966|
A teratoma is a tumor with tissue or organ components resembling normal derivatives of more than one germ layer. Although the teratoma may be monodermal or polydermal (originating from one or more germ layers), its cells may differentiate in ways suggesting other germ layers. The tissues of a teratoma, although normal in themselves, may be quite different from surrounding tissues and may be highly disparate; teratomas have been reported to contain hair, teeth, bone and, very rarely, more complex organs or processes such as eyes, torso, and hands, feet, or other limbs.
Usually, however, a teratoma will contain no organs but rather one or more tissues normally found in organs such as the brain, thyroid, liver, and lung. Sometimes, the teratoma has within its capsule one or more fluid-filled cysts; when a large cyst occurs, there is a potential for the teratoma to produce a structure within the cyst that resembles a fetus. Because they are encapsulated, teratomas are usually benign, although several forms of malignant teratoma are known and some of these are common forms of teratoma. A mature teratoma is typically benign and found more commonly in women, while an immature teratoma is typically malignant and is more often found in men.
Teratomas are thought to be present at birth (congenital), but small ones are often not discovered until much later in life.
- 1 Terminology
- 2 Pathophysiology
- 3 Classification
- 4 Diagnosis
- 5 Time of presentation
- 6 Complications
- 7 Treatment
- 8 Epidemiology
- 9 Research
- 10 In other animals
- 11 See also
- 12 References
- 13 External links
As is true throughout oncology (the study of tumors, malignant and benign), the nomenclature for these tumors continually evolves on the basis of threads of consensus in the scientific literature regarding the tumors' classification (which is based on shared embryologic origins, clinicopathologic characteristics, and so on). As science advances, more is understood about how one can differentiate tumors that formerly seemed alike. For example, the scientific knowledge of tumor markers, genomics, and proteomics regularly advances. In this environment, tumor names may slip over the years between synonymity, hyponymy and hypernymy, and deprecation. Some terms that have been synonymous with teratoma include dysembryoma, teratoblastoma, organoid tumor, and teratoid tumor.
The words "teratoma" and "mature teratoma" both have been used to refer to a benign growth, while the word "teratoma" may also refer to "immature teratoma", a cancerous growth. Avoiding misunderstanding due to such polysemy is part of why tumor nomenclature changes over decades. The nomenclatural changes are voluntary, based on scientists agreeing or debating in the literature regarding what to call particular neoplastic entities (types of tumors).
Teratomas belong to a class of tumors known as nonseminomatous germ cell tumor (N.S.G.C.T.). All tumors of this class are the result of abnormal development of pluripotent cells: germ cells and embryonal cells. Teratomas of embryonic origin are congenital; teratomas of germ cell origin may or may not be congenital (this is not known). The kind of pluripotent cell appears to be unimportant, apart from constraining the location of the teratoma in the body.
Teratomas derived from germ cells occur in the testes in men and ovaries in women. Teratomas derived from embryonic cells usually occur on the subject's midline: in the brain, elsewhere in the skull, in the nose, in the tongue, under the tongue, and in the neck (cervical teratoma), mediastinum, retroperitoneum, and attached to the coccyx. However, teratomas may also occur elsewhere: very rarely in solid organs (most notably the heart and liver) and hollow organs (such as the stomach and bladder), and more commonly on the skull sutures.
Hypotheses of origin
Concerning the origin of teratomas, there exist numerous hypotheses. These hypotheses are not to be confused with the unrelated hypothesis that fetus in fetu (see below) is not a teratoma at all but rather a parasitic twin.
A mature teratoma is a grade 0 teratoma. Mature teratomas are highly variable in form and histology, and may be solid, cystic, or a combination of solid and cystic. A mature teratoma often contains several different types of tissue such as skin, muscle, and bone. Skin may surround a cyst and grow abundant hair (see Dermoid cyst). Mature teratomas generally are benign; malignant mature teratomas are of several distinct types.
A dermoid cyst is a mature cystic teratoma containing hair (sometimes very abundant) and other structures characteristic of normal skin and other tissues derived from the ectoderm. The term is most often applied to teratoma on the skull sutures and in the ovaries of females.
Fetus in fetu and fetiform teratoma
Fetus in fetu and fetiform teratoma are rare forms of mature teratoma that include one or more components resembling a malformed fetus. Both forms may contain or appear to contain complete organ systems, even major body parts such as torso or limbs. Fetus in fetu differs from fetiform teratoma in having an apparent spine and bilateral symmetry.
Most authorities agree that fetiform teratomas are highly developed mature teratomas; the natural history of fetus in fetu, however, is controversial. There also may be a cultural difference, with fetiform teratoma being reported more often in ovarian teratomas (by gynecologists) and fetus in fetu being reported more often in retroperitoneal teratomas (by general surgeons). Fetus in fetu has often been interpreted as a fetus growing within its twin. As such, this interpretation assumes a special complication of twinning, one of several grouped under the term parasitic twin. In this regard, it is noteworthy that in many cases the fetus in fetu is reported to occupy a fluid-filled cyst within a mature teratoma. Cysts within mature teratoma may have partially developed organ systems; reports include cases of partial cranial bones, long bones and a rudimentary beating heart.
Regardless of whether fetus in fetu and fetiform teratoma are one entity or two, they are distinct from and not to be confused with ectopic pregnancy.
Regardless of location in the body, a teratoma is classified according to a cancer staging system. This indicates whether chemotherapy or radiation therapy may be needed in addition to surgery. Teratomas commonly are classified using the Gonzalez-Crussi grading system: 0 or mature (benign); 1 or immature, probably benign; 2 or immature, possibly malignant (cancerous); and 3 or frankly malignant. If frankly malignant, the tumor is a cancer for which additional cancer staging applies.
Teratomas are also classified by their content: a solid teratoma contains only tissues (perhaps including more complex structures); a cystic teratoma contains only pockets of fluid or semi-fluid such as cerebrospinal fluid, sebum, or fat; a mixed teratoma contains both solid and cystic parts. Cystic teratomas usually are grade 0 and, conversely, grade 0 teratomas usually are cystic.
Grade 0, 1 and 2 pure teratomas have the potential to become malignant (grade 3), and malignant pure teratomas have the potential to metastasize. These rare forms of teratoma with malignant transformation may contain elements of somatic (non germ cell) malignancy such as leukemia, carcinoma or sarcoma. A teratoma may contain elements of other germ cell tumors, in which case it is not a pure teratoma but rather is a mixed germ cell tumor and is malignant. In infants and young children, these elements usually are endodermal sinus tumor, followed by choriocarcinoma. Finally, a teratoma can be pure and not malignant yet highly aggressive: this is exemplified by growing teratoma syndrome, in which chemotherapy eliminates the malignant elements of a mixed tumor, leaving pure teratoma which paradoxically begins to grow very rapidly.
A "benign" grade 0 (mature) teratoma nonetheless has a risk of malignancy. Recurrence with malignant endodermal sinus tumor has been reported in cases of formerly benign mature teratoma, even in fetiform teratoma and fetus in fetu. Squamous cell carcinoma has been found in a mature cystic teratoma at the time of initial surgery.
A grade 1 immature teratoma that appears to be benign (e.g., because AFP is not elevated) has a much higher risk of malignancy, and requires adequate follow-up. This grade of teratoma also may be difficult to diagnose correctly. It can be confused with other small round cell neoplasms such as neuroblastoma, small cell carcinoma of hypercalcemic type, primitive neuroectodermal tumor, Wilm's tumor, desmoplastic small round cell tumor, and non-Hodgkin lymphoma.
A teratoma with malignant transformation (TMT) is a very rare form of teratoma that may contain elements of somatic (non germ cell) malignant tumors such as leukemia, carcinoma or sarcoma. Of 641 children with pure teratoma, nine developed TMT: five carcinoma, two glioma, and two embryonal carcinoma (here, these last are classified among germ cell tumors).
Teratomas are thought to be present since birth, or even before birth, and therefore can be considered congenital tumors. However, many teratomas are not diagnosed until much later in childhood or in adulthood. Large tumors are more likely to be diagnosed early on. Sacrococcygeal and cervical teratomas are often detected by prenatal ultrasound. Additional diagnostic methods may include prenatal MRI. In rare circumstances, the tumor is so large that the fetus may be damaged or die. In the case of large sacrococcygeal teratomas, a significant portion of the fetus' blood flow is redirected toward the teratoma (a phenomenon called steal syndrome), causing heart failure, or hydrops, of the fetus. In certain cases, fetal surgery may be indicated.
Beyond the newborn period, symptoms of a teratoma depend on its location and organ of origin. Ovarian teratomas often present with abdominal or pelvic pain, caused by torsion of the ovary or irritation of its ligaments. A recently discovered condition where ovarian teratomas cause encephalitis associated with antibodies against the N-methyl-D-aspartate receptor (NMDAR) - often simply referred to as "Anti-NMDA receptor encephalitis", was identified as a serious complication. Patients develop a multistage illness that progresses from psychosis, memory deficits, seizures, and language disintegration into a state of unresponsiveness with catatonic features often associated with abnormal movements, and autonomic and breathing instability. Testicular teratomas present as a palpable mass in the testis; mediastinal teratomas often cause compression of the lungs or the airways and may present with chest pain and/or respiratory symptoms.
Some teratomas contain yolk sac elements, which secrete alpha-fetoprotein (AFP). Detection of AFP may help to confirm the diagnosis and is often used as a marker for recurrence or treatment efficacy, but is rarely the method of initial diagnosis. (Maternal serum alpha-fetoprotein, or MSAFP, is a useful screening test for other fetal conditions, including Down syndrome, spina bifida and abdominal wall defects such as gastroschisis).
Time of presentation
Teratomas of germ cell origin usually are found (i.e., present) in adult men and women, but they may also be found in children and infants. Teratomas of embryonal origin are most often found in babies at birth, in young children, and, since the advent of ultrasound imaging, in fetuses.
The most commonly diagnosed fetal teratomas are sacrococcygeal teratoma (Altman types I, II, and III) and cervical (neck) teratoma. Because these teratomas project from the fetal body into the surrounding amniotic fluid, they can be seen during routine prenatal ultrasound exams. Teratomas within the fetal body are less easily seen with ultrasound; for these, MRI of the pregnant uterus is more informative.
Teratomas are not dangerous for the fetus unless there is either a mass effect or a large amount of blood flow through the tumor (known as vascular steal). The mass effect frequently consists of obstruction of normal passage of fluids from surrounding organs. The vascular steal can place a strain on the growing heart of the fetus, even resulting in heart failure, and thus must be monitored by fetal echocardiography.
After surgery, there is a risk of regrowth in place, or in nearby organs.
The treatment of choice is complete surgical removal (i.e., complete resection). Teratomas normally are well encapsulated and non-invasive of surrounding tissues, hence they are relatively easy to resect from surrounding tissues. Exceptions include teratomas in the brain, and very large, complex teratomas that have pushed into and become interlaced with adjacent muscles and other structures.
Prevention of recurrence does not require en bloc resection of surrounding tissues.
For malignant teratomas, usually, surgery is followed by chemotherapy.
Teratomas that are in surgically inaccessible locations, or are very complex, or are likely to be malignant (due to late discovery and/or treatment) sometimes are treated first with chemotherapy.
Although often described as benign, a teratoma does have malignant potential. In a UK study of 351 infants and children diagnosed with "benign" teratoma reported 227 with MT, 124 with IT. Five years after surgery, event-free survival was 92.2% and 85.9%, respectively, and overall survival was 99% and 95.1%. A similar study in Italy reported on 183 infants and children diagnosed with teratoma. At 10 years after surgery, event free and overall survival were 90.4% and 98%, respectively.
Depending on which tissue(s) it contains, a teratoma may secrete a variety of chemicals with systemic effects. Some teratomas secrete the "pregnancy hormone" human chorionic gonadotropin (βhCG), which can be used in clinical practice to monitor the successful treatment or relapse in patients with a known HCG-secreting teratoma. This hormone is not recommended as a diagnostic marker, because most teratomas do not secrete it. Some teratomas secrete thyroxine, in some cases to such a degree that it can lead to clinical hyperthyroidism in the patient. Of special concern is the secretion of alpha-fetoprotein (AFP); under some circumstances AFP can be used as a diagnostic marker specific for the presence of yolk sac cells within the teratoma. These cells can develop into a frankly malignant tumor known as yolk sac tumor or endodermal sinus tumor.
Embryonal teratomas most commonly occur in the sacrococcygeal region: sacrococcygeal teratoma is the single most common tumor found in newly born humans.
Teratoma qualifies as a rare disease, but is not extremely rare. Sacrococcygeal teratoma alone is diagnosed at birth in one out of 40,000 humans. Given the current human population and birth-rate, this equals five per day or 1800 per year. Add to that number sacrococcygeal teratomas diagnosed later in life, and teratomas in other locales, and the incidence approaches ten thousand new diagnoses of teratoma per year.
Teratomas also occur, rarely, in other species.
In light of the ethical issues surrounding the source of human stem cells, teratomas are being looked at as an alternative source for research because they lack the potential to grow into functional human beings.
In other animals
- Chi JG, Lee YS, Park YS, Chang KY (July 1984). "Fetus-in-fetu: report of a case". American Journal of Clinical Pathology 82 (1): 115–9. PMID 6540049.
- Sergi C, Ehemann V, Beedgen B, Linderkamp O, Otto HF (1999). "Huge fetal sacrococcygeal teratoma with a completely formed eye and intratumoral DNA ploidy heterogeneity". Pediatric and Developmental Pathology : the Official Journal of the Society for Pediatric Pathology and the Paediatric Pathology Society 2 (1): 50–7. doi:10.1007/s100249900089. PMID 9841706.
- Kuno N, Kadomatsu K, Nakamura M, Miwa-Fukuchi T, Hirabayashi N, Ishizuka T (January 2004). "Mature ovarian cystic teratoma with a highly differentiated homunculus: a case report". Birth Defects Research. Part a, Clinical and Molecular Teratology 70 (1): 40–6. doi:10.1002/bdra.10133. PMID 14745894.
- Arlikar JD, Mane SB, Dhende NP, Sanghavi Y, Valand AG, Butale PR (March 2009). "Fetus in fetu: two case reports and review of literature". Pediatric Surgery International 25 (3): 289–92. doi:10.1007/s00383-009-2328-8. PMID 19184054.
- "Tumor in baby’s brain contained tiny foot". msnbc.msn.com. December 18, 2008. Retrieved 2008-12-19.
- Elsevier, Dorland's Illustrated Medical Dictionary, Elsevier.
- Harding MJ, Paul J, Gillis CR, Kaye SB (April 1993). "Management of malignant teratoma: does referral to a specialist unit matter?". Lancet 341 (8851): 999–1002. doi:10.1016/0140-6736(93)91082-W. PMID 8096954.
- Gonzalez-Crussi, F. (1982) Extragonadal Teratomas. Atlas of Tumor Pathology, Second Series, Fascicle 18. Armed Forces Institute of Pathology, Washington D.C.
- Abbott TM, Hermann WJ, Scully RE (1984). "Ovarian fetiform teratoma (homunculus) in a 9-year-old girl". International Journal of Gynecological Pathology : Official Journal of the International Society of Gynecological Pathologists 2 (4): 392–402. doi:10.1097/00004347-198404000-00007. PMID 6724790.
- Saito K, Katsumata Y, Hirabuki T, Kato K, Yamanaka M (2007). "Fetus-in-fetu: parasite or neoplasm? A study of two cases". Fetal. Diagn. Ther. 22 (5): 383–8. doi:10.1159/000103301. PMID 17556829.
- Kajbafzadeh AM, Baharnoori M (2006). "Fetus in fetu". Can J Urol 13 (5): 3277–8. PMID 17076951.
- Chua JH, Chui CH, Sai Prasad TR, Jabcobsen AS, Meenakshi A, Hwang WS (2005). "Fetus-in-fetu in the pelvis: report of a case and literature review". Ann. Acad. Med. Singap. 34 (10): 646–9. PMID 16382253.
- Lee, Y. H.; Kim, S. G.; Choi, S. H.; Kim, I. S.; Kim, S. H. (December 2003). "Ovarian mature cystic teratoma containing homunculus: A case report". Journal of Korean Medical Science 18 (6): 905–907. PMC 3055135. PMID 14676454.
- Kazez A, Ozercan IH, Erol FS, Faik Ozveren M, Parmaksiz E (2002). "Sacrococcygeal heart: a very rare differentiation in teratoma". European Journal of Pediatric Surgery 12 (4): 278–80. doi:10.1055/s-2002-34483. PMID 12369008.
- Harms D, Zahn S, Göbel U, Schneider DT (2006). "Pathology and molecular biology of teratomas in childhood and adolescence". Klinische Pädiatrie 218 (6): 296–302. doi:10.1055/s-2006-942271. PMID 17080330.
- Ohno Y, Kanematsu T (1998). "An endodermal sinus tumor arising from a mature cystic teratoma in the retroperitoneum in a child: is a mature teratoma a premalignant condition?". Hum. Pathol. 29 (10): 1167–9. doi:10.1016/S0046-8177(98)90432-4. PMID 9781660.
- Utsuki S, Oka H, Sagiuchi T, Shimizu S, Suzuki S, Fujii K (Jun 2007). "Malignant transformation of intracranial mature teratoma to yolk sac tumor after late relapse. Case report". J. Neurosurg. 106 (6): 1067–9. doi:10.3171/jns.2007.106.6.1067. PMID 17564180.
- Chen YH, Chang CH, Chen KC, Diau GY, Loh IW, Chu CC (2007). "Malignant transformation of a well-organized sacrococcygeal fetiform teratoma in a newborn male". J. Formos. Med. Assoc. 106 (5): 400–2. doi:10.1016/S0929-6646(09)60326-0. PMID 17561476.
- Hopkins KL, Dickson PK, Ball TI, Ricketts RR, O'Shea PA, Abramowsky CR (1997). "Fetus-in-fetu with malignant recurrence". J. Pediatr. Surg. 32 (10): 1476–9. doi:10.1016/S0022-3468(97)90567-4. PMID 9349774.
- Arioz DT, Tokyol C, Sahin FK, et al. (2008). "Squamous cell carcinoma arising in a mature cystic teratoma of the ovary in young patient with elevated carbohydrate antigen 19-9". Eur. J. Gynaecol. Oncol. 29 (3): 282–4. PMID 18592797.
- Muscatello L, Giudice M, Feltri M (2005). "Malignant cervical teratoma: report of a case in a newborn". European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery 262 (11): 899–904. doi:10.1007/s00405-005-0917-2. PMID 15895292.
- Ukiyama E, Endo M, Yoshida F, Tezuka T, Kudo K, Sato S, Akatsuka S, Hata J (2005). "Recurrent yolk sac tumor following resection of a neonatal immature gastric teratoma". Pediatr. Surg. Int. 21 (7): 585–8. doi:10.1007/s00383-005-1404-y. PMID 15928937.
- Bilik R, Shandling B, Pope M, Thorner P, Weitzman S, Ein SH (1993). "Malignant benign neonatal sacrococcygeal teratoma". J. Pediatr. Surg. 28 (9): 1158–60. doi:10.1016/0022-3468(93)90154-D. PMID 7508500.
- Hawkins E, Issacs H, Cushing B, Rogers P (1993). "Occult malignancy in neonatal sacrococcygeal teratomas. A report from a Combined Pediatric Oncology Group and Children's Cancer Group study". The American journal of pediatric hematology/oncology 15 (4): 406–9. PMID 7692755.
- Ramalingam P, Teague D, Reid-Nicholson M (Jul 2008). "Imprint cytology of high-grade immature ovarian teratoma: A case report, literature review, and distinction from other ovarian small round cell tumors". Diagn. Cytopathol. 36 (8): 595–9. doi:10.1002/dc.20849. PMID 18618728.
- Biskup W, Calaminus G, Schneider DT, Leuschner I, Göbel U (2006). "Teratoma with malignant transformation: experiences of the cooperative GPOH protocols MAKEI 83/86/89/96". Klinische Pädiatrie 218 (6): 303–8. doi:10.1055/s-2006-942272. PMID 17080331.
- Aktuğ T, Hakgüder G, Sarioğlu S, Akgür FM, Olguner M, Pabuçcuoğlu U (2000). "Sacrococcygeal extraspinal ependymomas: the role of coccygectomy". J. Pediatr. Surg. 35 (3): 515–8. doi:10.1016/S0022-3468(00)90228-8. PMID 10726703.
- Dalmau J, Lancaster E, Martinez-Hernandez E, Rosenfeld MR, Balice-Gordon R (January 2011). "Clinical experience and laboratory investigations in patients with anti-NMDAR encephalitis". Lancet Neurol 10 (1): 63–74. doi:10.1016/S1474-4422(10)70253-2. PMC 3158385. PMID 21163445.
- Danzer E, Hubbard AM, Hedrick HL, et al. (2006). "Diagnosis and characterization of fetal sacrococcygeal teratoma with prenatal MRI". AJR Am J Roentgenol 187 (4): W350–6. doi:10.2214/AJR.05.0152. PMID 16985105.
- Kocaoglu M, Frush DP (2006). "Pediatric presacral masses". Radiographics 26 (3): 833–57. doi:10.1148/rg.263055102. PMID 16702458.
- Choi, K. W.; Jeon, W. J.; Chae, H. B.; Park, S. M.; Youn, S. J.; Shin, H. M.; Sung, R. H.; Lee, S. J. (September 2003). "A recurred case of a mature ovarian teratoma presenting as a rectal mass". The Korean Journal of Gastroenterology (in Korean) 42 (3): 242–245. PMID 14532748.
- Tapper D, Lack EE (1983). "Teratomas in infancy and childhood. A 54-year experience at the Children's Hospital Medical Center". Ann. Surg. 198 (3): 398–410. doi:10.1097/00000658-198309000-00016. PMC 1353316. PMID 6684416.
- Göbel, U.; Schneider, D. T.; Calaminus, G.; Haas, R. J.; Schmidt, P.; Harms, D. (March 2000). "Germ-cell tumors in childhood and adolescence.". Annals of Oncology 11 (3): 263–271. doi:10.1023/a:1008360523160. PMID 10811491.
- Mann JR, Gray ES, Thornton C, Raafat F, Robinson K, Collins GS, Gornall P, Huddart SN, Hale JP, Oakhill A (July 2008). "Mature and immature extracranial teratomas in children: the UK Children's Cancer Study Group Experience". Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology 26 (21): 3590–7. doi:10.1200/JCO.2008.16.0622. PMID 18541896.
- Lo Curto M, D'Angelo P, Cecchetto G, Klersy C, Dall'Igna P, Federico A, Siracusa F, Alaggio R, Bernini G, Conte M, De Laurentis T, Di Cataldo A, Inserra A, Santoro N, Tamaro P, Indolfi P (April 2007). "Mature and immature teratomas: results of the first paediatric Italian study". Pediatric Surgery International 23 (4): 315–22. doi:10.1007/s00383-007-1890-1. PMID 17333214.
- Marina NM, Cushing B, Giller R, Cohen L, Lauer SJ, Ablin A, Weetman R, Cullen J, Rogers P, Vinocur C, Stolar C, Rescorla F, Hawkins E, Heifetz S, Rao PV, Krailo M, Castleberry RP (1999). "Complete surgical excision is effective treatment for children with immature teratomas with or without malignant elements: A Pediatric Oncology Group/Children's Cancer Group Intergroup Study". J. Clin. Oncol. 17 (7): 2137–43. PMID 10561269.
- Cushing B, Giller R, Ablin A, Cohen L, Cullen J, Hawkins E, Heifetz SA, Krailo M, Lauer SJ, Marina N, Rao PV, Rescorla F, Vinocur CD, Weetman RM, Castleberry RP (1999). "Surgical resection alone is effective treatment for ovarian immature teratoma in children and adolescents: a report of the pediatric oncology group and the children's cancer group". Am. J. Obstet. Gynecol. 181 (2): 353–8. doi:10.1016/S0002-9378(99)70561-2. PMID 10454682.
- Orbital dermoid cyst at eMedicine
- López RM, Múrcia DB (Aug 2008). "First description of malignant retrobulbar and intracranial teratoma in a lesser kestrel (Falco naumanni)". Avian Pathol. 37 (4): 413–4. doi:10.1080/03079450802216660. PMID 18622858.
- Catone G, Marino G, Mancuso R, Zanghì A (April 2004). "Clinicopathological features of an equine ovarian teratoma". Reprod. Domest. Anim. 39 (2): 65–9. doi:10.1111/j.1439-0531.2003.00476.x. PMID 15065985.
- Lefebvre R, Theoret C, Doré M, Girard C, Laverty S, Vaillancourt D (November 2005). "Ovarian teratoma and endometritis in a mare". Can. Vet. J. 46 (11): 1029–33. PMC 1259148. PMID 16363331.
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- humpath pathology images #2657 (Teratomas), #4541 (Mature teratoma), #5350 (Immature teratoma)
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- Monster Tumors Show Scientific Potential in War Against Cancer article in the NYTimes
- Mature teratoma entry in the public domain NCI Dictionary of Cancer Terms
- Mystery illness - ovarian teratoma associated encephalitis (audio report) | <urn:uuid:98bd411e-ad37-448b-8f51-14f5f5910724> | {
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From Wikipedia, the free encyclopedia - View original article
People with Asperger syndrome often display intense interests, such as this boy's fascination with molecular structure.
|Classification and external resources|
|Patient UK||Asperger syndrome|
People with Asperger syndrome often display intense interests, such as this boy's fascination with molecular structure.
|Classification and external resources|
|Patient UK||Asperger syndrome|
Asperger syndrome (AS), also known as Asperger's syndrome, Asperger disorder (AD) or simply Asperger's, is an autism spectrum disorder (ASD) that is characterized by significant difficulties in social interaction and nonverbal communication, alongside restricted and repetitive patterns of behavior and interests. It differs from other autism spectrum disorders by its relative preservation of linguistic and cognitive development. Although not required for diagnosis, physical clumsiness and atypical (peculiar or odd) use of language are frequently reported. The diagnosis of Asperger's was eliminated in the 2013 fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) and replaced by a diagnosis of autism spectrum disorder on a severity scale.
The syndrome is named after the Austrian pediatrician Hans Asperger who, in 1944, studied and described children in his practice who lacked nonverbal communication skills, demonstrated limited empathy with their peers, and were physically clumsy. The modern conception of Asperger syndrome came into existence in 1981 and went through a period of popularization, becoming standardized as a diagnosis in the early 1990s. Many questions and controversies remain about aspects of the disorder. There is doubt about whether it is distinct from high-functioning autism (HFA); partly because of this, its prevalence is not firmly established.
The exact cause of Asperger's is unknown. Although research suggests the likelihood of a genetic basis, there is no known genetic cause and brain imaging techniques have not identified a clear common pathology. There is no single treatment, and the effectiveness of particular interventions is supported by only limited data. Intervention is aimed at improving symptoms and function. The mainstay of management is behavioral therapy, focusing on specific deficits to address poor communication skills, obsessive or repetitive routines, and physical clumsiness. Most children improve as they mature to adulthood, but social and communication difficulties may persist. Some researchers and people with Asperger's have advocated a shift in attitudes toward the view that it is a difference, rather than a disability that must be treated or cured.
The extent of the overlap between AS and high-functioning autism (HFA—autism unaccompanied by intellectual disability) is unclear. The ASD classification is to some extent an artifact of how autism was discovered, and may not reflect the true nature of the spectrum; methodological problems have beset Asperger syndrome as a valid diagnosis from the outset. In the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5), published in May 2013, AS, as a separate diagnosis, was eliminated and folded into autism spectrum disorder. Like the diagnosis of Asperger syndrome, the change was controversial and AS was not removed from the WHO's ICD-10.
The World Health Organization (WHO) defines Asperger syndrome (AS) as one of the autism spectrum disorders (ASD) or pervasive developmental disorders (PDD), which are a spectrum of psychological conditions that are characterized by abnormalities of social interaction and communication that pervade the individual's functioning, and by restricted and repetitive interests and behavior. Like other psychological development disorders, ASD begins in infancy or childhood, has a steady course without remission or relapse, and has impairments that result from maturation-related changes in various systems of the brain. ASD, in turn, is a subset of the broader autism phenotype, which describes individuals who may not have ASD but do have autistic-like traits, such as social deficits. Of the other four ASD forms, autism is the most similar to AS in signs and likely causes, but its diagnosis requires impaired communication and allows delay in cognitive development; Rett syndrome and childhood disintegrative disorder share several signs with autism but may have unrelated causes; and pervasive developmental disorder not otherwise specified (PDD-NOS) is diagnosed when the criteria for a more specific disorder are unmet.
As a pervasive developmental disorder, Asperger syndrome is distinguished by a pattern of symptoms rather than a single symptom. It is characterized by qualitative impairment in social interaction, by stereotyped and restricted patterns of behavior, activities and interests, and by no clinically significant delay in cognitive development or general delay in language. Intense preoccupation with a narrow subject, one-sided verbosity, restricted prosody, and physical clumsiness are typical of the condition, but are not required for diagnosis.
A lack of demonstrated empathy has a significant impact on aspects of communal living for persons with Asperger syndrome. Individuals with AS experience difficulties in basic elements of social interaction, which may include a failure to develop friendships or to seek shared enjoyments or achievements with others (for example, showing others objects of interest), a lack of social or emotional reciprocity (social "games" give-and-take mechanic), and impaired nonverbal behaviors in areas such as eye contact, facial expression, posture, and gesture.
People with AS may not be as withdrawn around others compared to those with other, more debilitating forms of autism; they approach others, even if awkwardly. For example, a person with AS may engage in a one-sided, long-winded speech about a favorite topic, while misunderstanding or not recognizing the listener's feelings or reactions, such as a wish to change the topic of talk or end the interaction. This social awkwardness has been called "active but odd". This failure to react appropriately to social interaction may appear as disregard for other people's feelings, and may come across as insensitive. However, not all individuals with AS will approach others. Some of them may even display selective mutism, speaking not at all to most people and excessively to specific people. Some may choose only to talk to people they like.
The cognitive ability of children with AS often allows them to articulate social norms in a laboratory context, where they may be able to show a theoretical understanding of other people's emotions; however, they typically have difficulty acting on this knowledge in fluid, real-life situations. People with AS may analyze and distill their observations of social interaction into rigid behavioral guidelines, and apply these rules in awkward ways, such as forced eye contact, resulting in a demeanor that appears rigid or socially naive. Childhood desire for companionship can become numbed through a history of failed social encounters.
The hypothesis that individuals with AS are predisposed to violent or criminal behavior has been investigated, but is not supported by data. More evidence suggests children with AS are victims rather than victimizers. A 2008 review found that an overwhelming number of reported violent criminals with AS had coexisting psychiatric disorders such as schizoaffective disorder.
People with Asperger syndrome display behavior, interests, and activities that are restricted and repetitive and are sometimes abnormally intense or focused. They may stick to inflexible routines, move in stereotyped and repetitive ways, or preoccupy themselves with parts of objects.
Pursuit of specific and narrow areas of interest is one of the most striking features of AS. Individuals with AS may collect volumes of detailed information on a relatively narrow topic such as weather data or star names, without necessarily having a genuine understanding of the broader topic. For example, a child might memorize camera model numbers while caring little about photography. This behavior is usually apparent by age 5 or 6. Although these special interests may change from time to time, they typically become more unusual and narrowly focused, and often dominate social interaction so much that the entire family may become immersed. Because narrow topics often capture the interest of children, this symptom may go unrecognized.
Stereotyped and repetitive motor behaviors are a core part of the diagnosis of AS and other ASDs. They include hand movements such as flapping or twisting, and complex whole-body movements. These are typically repeated in longer bursts and look more voluntary or ritualistic than tics, which are usually faster, less rhythmical and less often symmetrical.
According to the Adult Asperger Assessment (AAA) diagnostic test, a lack of interest in fiction and a positive preference towards non-fiction is common among adults with AS.
Although individuals with Asperger syndrome acquire language skills without significant general delay and their speech typically lacks significant abnormalities, language acquisition and use is often atypical. Abnormalities include verbosity, abrupt transitions, literal interpretations and miscomprehension of nuance, use of metaphor meaningful only to the speaker, auditory perception deficits, unusually pedantic, formal or idiosyncratic speech, and oddities in loudness, pitch, intonation, prosody, and rhythm. Echolalia has also been observed in individuals with AS.
Three aspects of communication patterns are of clinical interest: poor prosody, tangential and circumstantial speech, and marked verbosity. Although inflection and intonation may be less rigid or monotonic than in classic autism, people with AS often have a limited range of intonation: speech may be unusually fast, jerky or loud. Speech may convey a sense of incoherence; the conversational style often includes monologues about topics that bore the listener, fails to provide context for comments, or fails to suppress internal thoughts. Individuals with AS may fail to detect whether the listener is interested or engaged in the conversation. The speaker's conclusion or point may never be made, and attempts by the listener to elaborate on the speech's content or logic, or to shift to related topics, are often unsuccessful.
Children with AS may have an unusually sophisticated vocabulary at a young age and have been colloquially called "little professors", but have difficulty understanding figurative language and tend to use language literally. Children with AS appear to have particular weaknesses in areas of nonliteral language that include humor, irony, teasing, and sarcasm. Although individuals with AS usually understand the cognitive basis of humor, they seem to lack understanding of the intent of humor to share enjoyment with others. Despite strong evidence of impaired humor appreciation, anecdotal reports of humor in individuals with AS seem to challenge some psychological theories of AS and autism.
Individuals with Asperger syndrome may have signs or symptoms that are independent of the diagnosis, but can affect the individual or the family. These include differences in perception and problems with motor skills, sleep, and emotions.
Individuals with AS often have excellent auditory and visual perception. Children with ASD often demonstrate enhanced perception of small changes in patterns such as arrangements of objects or well-known images; typically this is domain-specific and involves processing of fine-grained features. Conversely, compared to individuals with high-functioning autism, individuals with AS have deficits in some tasks involving visual-spatial perception, auditory perception, or visual memory. Many accounts of individuals with AS and ASD report other unusual sensory and perceptual skills and experiences. They may be unusually sensitive or insensitive to sound, light, and other stimuli; these sensory responses are found in other developmental disorders and are not specific to AS or to ASD. There is little support for increased fight-or-flight response or failure of habituation in autism; there is more evidence of decreased responsiveness to sensory stimuli, although several studies show no differences.
Hans Asperger's initial accounts and other diagnostic schemes include descriptions of physical clumsiness. Children with AS may be delayed in acquiring skills requiring motor dexterity, such as riding a bicycle or opening a jar, and may seem to move awkwardly or feel "uncomfortable in their own skin". They may be poorly coordinated, or have an odd or bouncy gait or posture, poor handwriting, or problems with visual-motor integration. They may show problems with proprioception (sensation of body position) on measures of developmental coordination disorder (motor planning disorder), balance, tandem gait, and finger-thumb apposition. There is no evidence that these motor skills problems differentiate AS from other high-functioning ASDs.
Children with AS are more likely to have sleep problems, including difficulty in falling asleep, frequent nocturnal awakenings, and early morning awakenings. AS is also associated with high levels of alexithymia, which is difficulty in identifying and describing one's emotions. Although AS, lower sleep quality, and alexithymia are associated, their causal relationship is unclear.
Hans Asperger described common symptoms among his patients' family members, especially fathers, and research supports this observation and suggests a genetic contribution to Asperger syndrome. Although no specific gene has yet been identified, multiple factors are believed to play a role in the expression of autism, given the phenotypic variability seen in children with AS. Evidence for a genetic link is the tendency for AS to run in families and an observed higher incidence of family members who have behavioral symptoms similar to AS but in a more limited form (for example, slight difficulties with social interaction, language, or reading). Most research suggests that all autism spectrum disorders have shared genetic mechanisms, but AS may have a stronger genetic component than autism. There is probably a common group of genes where particular alleles render an individual vulnerable to developing AS; if this is the case, the particular combination of alleles would determine the severity and symptoms for each individual with AS.
A few ASD cases have been linked to exposure to teratogens (agents that cause birth defects) during the first eight weeks from conception. Although this does not exclude the possibility that ASD can be initiated or affected later, it is strong evidence that it arises very early in development. Many environmental factors have been hypothesized to act after birth, but none has been confirmed by scientific investigation.
Asperger syndrome appears to result from developmental factors that affect many or all functional brain systems, as opposed to localized effects. Although the specific underpinnings of AS or factors that distinguish it from other ASDs are unknown, and no clear pathology common to individuals with AS has emerged, it is still possible that AS's mechanism is separate from other ASDs. Neuroanatomical studies and the associations with teratogens strongly suggest that the mechanism includes alteration of brain development soon after conception. Abnormal migration of embryonic cells during fetal development may affect the final structure and connectivity of the brain, resulting in alterations in the neural circuits that control thought and behavior. Several theories of mechanism are available; none are likely to provide a complete explanation.
The underconnectivity theory hypothesizes underfunctioning high-level neural connections and synchronization, along with an excess of low-level processes. It maps well to general-processing theories such as weak central coherence theory, which hypothesizes that a limited ability to see the big picture underlies the central disturbance in ASD. A related theory—enhanced perceptual functioning—focuses more on the superiority of locally oriented and perceptual operations in autistic individuals.
The mirror neuron system (MNS) theory hypothesizes that alterations to the development of the MNS interfere with imitation and lead to Asperger's core feature of social impairment. For example, one study found that activation is delayed in the core circuit for imitation in individuals with AS. This theory maps well to social cognition theories like the theory of mind, which hypothesizes that autistic behavior arises from impairments in ascribing mental states to oneself and others, or hyper-systemizing, which hypothesizes that autistic individuals can systematize internal operation to handle internal events but are less effective at empathizing by handling events generated by other agents.
Standard diagnostic criteria require impairment in social interaction and repetitive and stereotyped patterns of behavior, activities and interests, without significant delay in language or cognitive development. Unlike the international standard, the DSM-IV-TR criteria also required significant impairment in day-to-day functioning; DSM-5 eliminated AS as a separate diagnosis in 2013, and folded it into the umbrella of autism spectrum disorders. Other sets of diagnostic criteria have been proposed by Szatmari et al. and by Gillberg and Gillberg.
Diagnosis is most commonly made between the ages of four and eleven. A comprehensive assessment involves a multidisciplinary team that observes across multiple settings, and includes neurological and genetic assessment as well as tests for cognition, psychomotor function, verbal and nonverbal strengths and weaknesses, style of learning, and skills for independent living. The "gold standard" in diagnosing ASDs combines clinical judgment with the Autism Diagnostic Interview-Revised (ADI-R)—a semistructured parent interview—and the Autism Diagnostic Observation Schedule (ADOS)—a conversation and play-based interview with the child. Delayed or mistaken diagnosis can be traumatic for individuals and families; for example, misdiagnosis can lead to medications that worsen behavior. Many children with AS are initially misdiagnosed with attention deficit hyperactivity disorder (ADHD). Diagnosing adults is more challenging, as standard diagnostic criteria are designed for children and the expression of AS changes with age; adult diagnosis requires painstaking clinical examination and thorough medical history gained from both the individual and other people who know the person, focusing on childhood behavior. Conditions that must be considered in a differential diagnosis include other ASDs, the schizophrenia spectrum, ADHD, obsessive–compulsive disorder, major depressive disorder, semantic pragmatic disorder, nonverbal learning disorder, Tourette syndrome, stereotypic movement disorder, bipolar disorder, and social-cognitive deficits due to brain damage from alcohol abuse.
Underdiagnosis and overdiagnosis are problems in marginal cases. The cost and difficulty of screening and assessment can delay diagnosis. Conversely, the increasing popularity of drug treatment options and the expansion of benefits has motivated providers to overdiagnose ASD. There are indications AS has been diagnosed more frequently in recent years, partly as a residual diagnosis for children of normal intelligence who are not autistic but have social difficulties.
There are questions about the external validity of the AS diagnosis. That is, it is unclear whether there is a practical benefit in distinguishing AS from HFA and from PDD-NOS; the same child can receive different diagnoses depending on the screening tool. The debate about distinguishing AS from HFA is partly due to a tautological dilemma where disorders are defined based on severity of impairment, so that studies that appear to confirm differences based on severity are to be expected.
Parents of children with Asperger syndrome can typically trace differences in their children's development to as early as 30 months of age. Developmental screening during a routine check-up by a general practitioner or pediatrician may identify signs that warrant further investigation. The diagnosis of AS is complicated by the use of several different screening instruments, including the Asperger Syndrome Diagnostic Scale (ASDS), Autism Spectrum Screening Questionnaire (ASSQ), Childhood Autism Spectrum Test (CAST) (previously called the Childhood Asperger Syndrome Test), Gilliam Asperger's disorder scale (GADS), Krug Asperger's Disorder Index (KADI), and the Autism-spectrum quotient (AQ; with versions for children, adolescents and adults). None have been shown to reliably differentiate between AS and other ASDs.
Asperger syndrome treatment attempts to manage distressing symptoms and to teach age-appropriate social, communication and vocational skills that are not naturally acquired during development, with intervention tailored to the needs of the individual based on multidisciplinary assessment. Although progress has been made, data supporting the efficacy of particular interventions are limited.
The ideal treatment for AS coordinates therapies that address core symptoms of the disorder, including poor communication skills and obsessive or repetitive routines. While most professionals agree that the earlier the intervention, the better, there is no single best treatment package. AS treatment resembles that of other high-functioning ASDs, except that it takes into account the linguistic capabilities, verbal strengths, and nonverbal vulnerabilities of individuals with AS. A typical program generally includes:
Of the many studies on behavior-based early intervention programs, most are case reports of up to five participants and typically examine a few problem behaviors such as self-injury, aggression, noncompliance, stereotypies, or spontaneous language; unintended side effects are largely ignored. Despite the popularity of social skills training, its effectiveness is not firmly established. A randomized controlled study of a model for training parents in problem behaviors in their children with AS showed that parents attending a one-day workshop or six individual lessons reported fewer behavioral problems, while parents receiving the individual lessons reported less intense behavioral problems in their AS children. Vocational training is important to teach job interview etiquette and workplace behavior to older children and adults with AS, and organization software and personal data assistants can improve the work and life management of people with AS.
No medications directly treat the core symptoms of AS. Although research into the efficacy of pharmaceutical intervention for AS is limited, it is essential to diagnose and treat comorbid conditions. Deficits in self-identifying emotions or in observing effects of one's behavior on others can make it difficult for individuals with AS to see why medication may be appropriate. Medication can be effective in combination with behavioral interventions and environmental accommodations in treating comorbid symptoms such as anxiety disorder, major depressive disorder, inattention and aggression. The atypical antipsychotic medications risperidone and olanzapine have been shown to reduce the associated symptoms of AS; risperidone can reduce repetitive and self-injurious behaviors, aggressive outbursts and impulsivity, and improve stereotypical patterns of behavior and social relatedness. The selective serotonin reuptake inhibitors (SSRIs) fluoxetine, fluvoxamine, and sertraline have been effective in treating restricted and repetitive interests and behaviors.
Care must be taken with medications, as side effects may be more common and harder to evaluate in individuals with AS, and tests of drugs' effectiveness against comorbid conditions routinely exclude individuals from the autism spectrum. Abnormalities in metabolism, cardiac conduction times, and an increased risk of type 2 diabetes have been raised as concerns with these medications, along with serious long-term neurological side effects. SSRIs can lead to manifestations of behavioral activation such as increased impulsivity, aggression, and sleep disturbance. Weight gain and fatigue are commonly reported side effects of risperidone, which may also lead to increased risk for extrapyramidal symptoms such as restlessness and dystonia and increased serum prolactin levels. Sedation and weight gain are more common with olanzapine, which has also been linked with diabetes. Sedative side-effects in school-age children have ramifications for classroom learning. Individuals with AS may be unable to identify and communicate their internal moods and emotions or to tolerate side effects that for most people would not be problematic.
There is some evidence that children with AS may see a lessening of symptoms; up to 20% of children may no longer meet the diagnostic criteria as adults, although social and communication difficulties may persist. As of 2006, no studies addressing the long-term outcome of individuals with Asperger syndrome are available and there are no systematic long-term follow-up studies of children with AS. Individuals with AS appear to have normal life expectancy, but have an increased prevalence of comorbid psychiatric conditions, such as major depressive disorder and anxiety disorder that may significantly affect prognosis. Although social impairment may be lifelong, the outcome is generally more positive than with individuals with lower functioning autism spectrum disorders; for example, ASD symptoms are more likely to diminish with time in children with AS or HFA. Most students with AS/HFA have average mathematical ability and test slightly worse in mathematics than in general intelligence, but some are gifted in mathematics and AS has not prevented some adults from major accomplishments, such as Vernon L. Smith winning the Nobel Prize.
Although many attend regular education classes, some children with AS may utilize special education services because of their social and behavioral difficulties. Adolescents with AS may exhibit ongoing difficulty with self care or organization, and disturbances in social and romantic relationships. Despite high cognitive potential, most young adults with AS remain at home, yet some do marry and work independently. The "different-ness" adolescents experience can be traumatic. Anxiety may stem from preoccupation over possible violations of routines and rituals, from being placed in a situation without a clear schedule or expectations, or from concern with failing in social encounters; the resulting stress may manifest as inattention, withdrawal, reliance on obsessions, hyperactivity, or aggressive or oppositional behavior. Depression is often the result of chronic frustration from repeated failure to engage others socially, and mood disorders requiring treatment may develop. Clinical experience suggests the rate of suicide may be higher among those with AS, but this has not been confirmed by systematic empirical studies.
Education of families is critical in developing strategies for understanding strengths and weaknesses; helping the family to cope improves outcomes in children. Prognosis may be improved by diagnosis at a younger age that allows for early interventions, while interventions in adulthood are valuable but less beneficial. There are legal implications for individuals with AS as they run the risk of exploitation by others and may be unable to comprehend the societal implications of their actions.
Prevalence estimates vary enormously. A 2003 review of epidemiological studies of children found autism prevalence rates ranging from 0.03 to 4.84 per 1,000, with the ratio of autism to Asperger syndrome ranging from 1.5:1 to 16:1; combining the geometric mean ratio of 5:1 with a conservative prevalence estimate for autism of 1.3 per 1,000 suggests indirectly that the prevalence of AS might be around 0.26 per 1,000. Part of the variance in estimates arises from differences in diagnostic criteria. For example, a relatively small 2007 study of 5,484 eight-year-old children in Finland found 2.9 children per 1,000 met the ICD-10 criteria for an AS diagnosis, 2.7 per 1,000 for Gillberg and Gillberg criteria, 2.5 for DSM-IV, 1.6 for Szatmari et al., and 4.3 per 1,000 for the union of the four criteria. Boys seem to be more likely to have AS than girls; estimates of the sex ratio range from 1.6:1 to 4:1, using the Gillberg and Gillberg criteria.
Anxiety disorder and major depressive disorder are the most common conditions seen at the same time; comorbidity of these in persons with AS is estimated at 65%. Reports have associated AS with medical conditions such as aminoaciduria and ligamentous laxity, but these have been case reports or small studies and no factors have been associated with AS across studies. One study of males with AS found an increased rate of epilepsy and a high rate (51%) of nonverbal learning disorder. AS is associated with tics, Tourette syndrome, and bipolar disorder, and the repetitive behaviors of AS have many similarities with the symptoms of obsessive–compulsive disorder and obsessive–compulsive personality disorder. However many of these studies are based on clinical samples or lack standardized measures; nonetheless, comorbid conditions are relatively common.
Named after the Austrian pediatrician Hans Asperger (1906–1980), Asperger syndrome is a relatively new diagnosis in the field of autism. As a child, Asperger appears to have exhibited some features of the very condition named after him, such as remoteness and talent in language. In 1944, Asperger described four children in his practice who had difficulty in integrating themselves socially. The children lacked nonverbal communication skills, failed to demonstrate empathy with their peers, and were physically clumsy. Asperger called the condition "autistic psychopathy" and described it as primarily marked by social isolation. Fifty years later, several standardizations of AS as a diagnosis were tentatively proposed, many of which diverge significantly from Asperger's original work.
Unlike today's AS, autistic psychopathy could be found in people of all levels of intelligence, including those with intellectual disability. In the context of the Nazi eugenics policy of sterilizing and killing social deviants and the mentally handicapped, Asperger passionately defended the value of autistic individuals, writing "We are convinced, then, that autistic people have their place in the organism of the social community. They fulfill their role well, perhaps better than anyone else could, and we are talking of people who as children had the greatest difficulties and caused untold worries to their care-givers." Asperger also called his young patients "little professors", and believed some would be capable of exceptional achievement and original thought later in life. His paper was published during wartime and in German, so it was not widely read elsewhere.
Lorna Wing popularized the term Asperger syndrome in the English-speaking medical community in her 1981 publication of a series of case studies of children showing similar symptoms, and Uta Frith translated Asperger's paper to English in 1991. Sets of diagnostic criteria were outlined by Gillberg and Gillberg in 1989 and by Szatmari et al. in the same year. AS became a standard diagnosis in 1992, when it was included in the tenth edition of the World Health Organization's diagnostic manual, International Classification of Diseases (ICD-10); in 1994, it was added to the fourth edition of the American Psychiatric Association's diagnostic reference, Diagnostic and Statistical Manual of Mental Disorders (DSM-IV).
Hundreds of books, articles and websites now describe AS, and prevalence estimates have increased dramatically for ASD, with AS recognized as an important subgroup. Whether it should be seen as distinct from high-functioning autism is a fundamental issue requiring further study, and there are questions about the empirical validation of the DSM-IV and ICD-10 criteria. In 2013, DSM-5 eliminated AS as a separate diagnosis, folding it into the autism spectrum on a severity scale.
People identifying with Asperger syndrome may refer to themselves in casual conversation as aspies (a term first used in print by Liane Holliday Willey in 1999). The word neurotypical (abbreviated NT) describes a person whose neurological development and state are typical, and is often used to refer to non-autistic people. The Internet has allowed individuals with AS to communicate and celebrate diversity with each other in a way that was not previously possible because of their rarity and geographic dispersal. A subculture of aspies has formed. Internet sites like Wrong Planet have made it easier for individuals to connect.
Autistic people have advocated a shift in perception of autism spectrum disorders as complex syndromes rather than diseases that must be cured. Proponents of this view reject the notion that there is an "ideal" brain configuration and that any deviation from the norm is pathological; they promote tolerance for what they call neurodiversity. These views are the basis for the autistic rights and autistic pride movements. There is a contrast between the attitude of adults with self-identified AS, who typically do not want to be cured and are proud of their identity, and parents of children with AS, who typically seek assistance and a cure for their children.
Some researchers have argued that AS can be viewed as a different cognitive style, not a disorder or a disability, and that it should be removed from the standard Diagnostic and Statistical Manual, much as homosexuality was removed. In a 2002 paper, Simon Baron-Cohen wrote of those with AS, "In the social world, there is no great benefit to a precise eye for detail, but in the worlds of maths, computing, cataloging, music, linguistics, engineering, and science, such an eye for detail can lead to success rather than failure." Baron-Cohen cited two reasons why it might still be useful to consider AS to be a disability: to ensure provision for legally required special support, and to recognize emotional difficulties from reduced empathy. Baron-Cohen argues that the genes for Asperger's combination of abilities have operated throughout recent human evolution and have made remarkable contributions to human history.
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Transgender is the state of one's gender identity or gender expression not matching one's assigned sex. Transgender is independent of sexual orientation; transgender people may identify as heterosexual, homosexual, bisexual, etc; some may consider conventional sexual orientation labels inadequate or inapplicable to them. The definition of transgender includes:
- "Of, relating to, or designating a person whose identity does not conform unambiguously to conventional notions of male or female gender roles, but combines or moves between these."
- "People who were assigned a sex, usually at birth and based on their genitals, but who feel that this is a false or incomplete description of themselves."
- "Non-identification with, or non-presentation as, the sex (and assumed gender) one was assigned at birth."
A transgender individual may have characteristics that are normally associated with a particular gender and identify elsewhere on the traditional gender continuum, or exist outside of it as other, agender, gender-neutral, genderqueer, non-binary, third gender, etc. Transgender people may also identify as bigender, pangender, or along several places on either the traditional transgender continuum or the more encompassing continuums that have been developed in response to recent, significantly more detailed studies. Furthermore, many transgender people experience a period of identity development that includes better understanding one's self-image, self-reflection, and self-expression. More specifically, the degree to which individuals feel genuine, authentic, and comfortable within their external appearance and accept their genuine identity is referred to as transgender congruence.
- 1 Evolution of the term transgender
- 2 Transgender identities
- 3 Transgender people and the LGBT community
- 4 Pride symbols
- 5 Transgender people and feminism
- 6 Transgender healthcare
- 7 Transgender people and the law
- 8 Transgender people and the U.S. military
- 9 Transgender people and religion
- 10 Transsexual people and science
- 10.1 Brain-based studies
- 10.2 Genetic studies
- 10.3 Terms and typology
- 11 By region
- 12 Coming out
- 13 See also
- 14 Notes
- 15 References
- 16 Further reading
- 17 External links
Evolution of the term transgender
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Writing for health professionals in the second edition of his reference work Sexual Hygiene and Pathology in 1965, psychiatrist John F. Oliven of Columbia University used the lexical compound trans+gender in the Transexualism section of "Primary Transvestism," noting "'transgenderism' is what is meant, because sexuality is not a major factor in primary transvestism." Crossdressing pioneer Virginia Charles Prince used the compound in the December 1969 issue of Transvestia, a national magazine for cross dressers founded by Prince. In the mid-1970s both trans-gender and trans people were in use as umbrella terms.[note 1] 'Transgenderist' was used to describe people who wanted to live cross-gender without sex reassignment surgery. By 1976, transgenderist was abbreviated as TG in educational materials.
In 1979, Christine Jorgensen publicly rejected transsexual and instead identified herself in newsprint as a trans-gender saying, "gender doesn't have to do with bed partners, it has to do with identity.” By 1984, the concept of a "transgender community" had developed, in which transgender was used as an umbrella term. In 1985, Richard Elkins established the "Trans-Gender Archive" at the University of Ulster. By 1992, the International Conference on Transgender Law and Employment Policy defined transgender as an expansive umbrella term including "transsexuals, transgenderists, cross dressers" and anyone transitioning.
Distinguishing transgender from transsexuality
Several somewhat ambiguous and possibly overlapping definitions can be found for the two terms: transgender and transsexual. Harry Benjamin invented a classification system for transsexuals and transvestites; he called his system the Sex Orientation Scale (SOS). In the SOS, Benjamin assigns transsexuals and transvestites to one of six categories based on their reasons for crossdressing, and the relative urgency of their need (if any) for sex reassignment surgery. Many transsexuals believe that to be a true transsexual, a person needs to have a desire for surgery. However, Benjamin's moderate intensity "true transsexual" needs either estrogen or testosterone as a "substitute for or preliminary to operation." There are also people who have had sexual reassignment surgery (SRS), but do not meet the definition of a transsexual, while other people do not desire SRS, yet clearly meet Benjamin Scale definition of a "true transsexual", such as Miriam Rivera.
In addition to the larger categories of transgender and transsexual, there is a wide range of gender expressions and identities which are contrary to the mainstream male-female binary. These include cross dressers, drag queens, drag kings, transvestites, genderqueer, etc. Some people take issue with transsexual because Virginia Charles Prince, who started the magazine Transvestia and built up the cross-dressing organization Tri-Ess, used transgender to distinguish cross-dressers from gay, bisexual and transsexual people. In "Men Who Choose to Be Women," Prince wrote "I, at least, know the difference between sex and gender and have simply elected to change the latter and not the former."
There is ample academic literature on the difference between sex and gender. For example, the Medilexicon Medical dictionary states that one's sex is a biological or physiological quality, while one's gender is a (psychological) "category to which an individual is assigned by self or others...". Therefore, transsexuality can be said to deal more with material aspects of one's sexuality, while transgender considerations can be said to deal more with one's internal gender disposition or predisposition, as well as the related social expectations that may accompany a given gender role. However, in pragmatic English, the sex and gender distinction is often ignored, so that gender is used to describe the categorical male/female difference and sex is used to describe sexual activity.
There exists political tension between the identities that fall under the "transgender umbrella." For example, transsexual men and women who can pay for medical treatments (or who have institutional coverage for their treatment) are likely to be concerned with medical privacy and establishing a durable legal status as their gender later in life. Extending insurance coverage for medical care is a coherent issue in the intersection of transsexuality and economic class.
While people self-identify as transgender, the transgender identity umbrella includes sometimes-overlapping categories. These include transsexual; transvestite or cross-dresser; genderqueer; androgyne; and bigender. Usually not included are transvestic fetishists (because it is considered to be a paraphilia rather than gender identification), and drag kings and drag queens, who are performers who cross-dress for the purpose of entertaining. In an interview, celebrity drag queen RuPaul talked about society's ambivalence to the differences in the people who embody these terms. "A friend of mine recently did the Oprah show about transgender youth," said RuPaul. "It was obvious that we, as a culture, have a hard time trying to understand the difference between a drag queen, transsexual, and a transgender, yet we find it very easy to know the difference between the American baseball league and the National baseball league, when they are both so similar."
The current definitions of transgender include all transsexual people, although this has been criticized. (See below.) Intersex people have genitalia or other physical sexual characteristics that do not conform to strict definitions of male and/or female, but intersex people are not necessarily transgender, since they do not all disagree with their assigned sex at birth. Transgender and intersex issues often overlap, however, because they both challenge the notion of rigid definitions of sex and gender.
The term trans man refers to female-to-male (FtM or F2M) transgender people, and trans woman refers to male-to-female (MtF or M2F) transgender people. It has been assumed that there are more trans women than trans men, but a Swedish study estimated a ratio of 1.4:1 in favour of trans women for those requesting sex reassignment surgery and a ratio of 1:1 for those who proceeded.
The term cisgender has been coined as an antonym referring to non-transgender people; i.e. those who identify with their gender assigned at birth. GLAAD notes that, when referring to a transgender person, using that person's preferred name and pronoun regardless of their legal gender status (as not all transgender people can afford surgery or other body modifications) is respectful. Unlike "transsexual", the word "transgender" should be used as an adjective rather than a noun — for example, "Max is transgender" or "Max is a transgender man" rather than "Max is a transgender."
Health-practitioner manuals, professional journalistic style guides, and LGBT advocacy groups advise the adoption by others of the name and pronouns identified by the person in question, including present references to the transgender person's past.
Transsexual people may undergo gender transition, the process of aligning one's gender expression or presentation with their internal gender identity. People who have transitioned may or may not necessarily identify as transgender or transsexual any longer, but simply as a man or a woman. Those who continue identifying as transsexual men or women may not want to ignore their pre-transition life, and may continue strong ties with other trans people and raising social consciousness.
The process of transition may involve some kind of medical gender reassignment therapy and often (but not always) includes hormone replacement therapy and/or sex reassignment surgery. References to "pre-operative", "post-operative" and "non-operative" transsexual people indicate whether they have had, or are planning to have sex reassignment surgery, although some trans people reject these terms as objectifying trans people based on their surgical status and not their mental gender identity.
Transvestite or cross-dresser
A transvestite is a person who cross-dresses, or dresses in clothes of the opposite sex. The term "transvestite" is used as a synonym for the term "cross-dresser", although "cross-dresser" is generally considered the preferred term. The term 'cross-dresser' is not exactly defined in the relevant literature. Michael A. Gilbert, professor at the Department of Philosophy, York University, Toronto, offers this definition: "[A cross-dresser] is a person who has an apparent gender identification with one sex, and who has and certainly has been birth-designated as belonging to [that] sex, but who wears the clothing of the opposite sex because it is that of the opposite sex." This definition excludes people "who wear opposite sex clothing for other reasons," such as "those female impersonators who look upon dressing as solely connected to their livelihood, actors undertaking roles, individual males and females enjoying a masquerade, and so on. These individuals are cross dressing but are not cross dressers." Cross-dressers may not identify with, or want to be the opposite gender, nor adopt the behaviors or practices of the opposite gender, and generally do not want to change their bodies medically. The majority of cross-dressers identify as heterosexual. People who cross-dress in public can have a desire to pass as the opposite gender, so as not to be detected as a cross-dresser, or may be indifferent.
The term "transvestite" and the associated outdated term "transvestism" are conceptually different from the term "transvestic fetishism", as "transvestic fetishist" describes those who intermittently use clothing of the opposite gender for fetishistic purposes. In medical terms, transvestic fetishism is differentiated from cross-dressing by use of the separate codes 302.3 in the DSM and F65.1 in the ICD.
Genderqueer is a recent attempt to signify gender experiences that do not fit into binary concepts, and refers to a combination of gender identities and sexual orientations. One example could be a person whose gender presentation is sometimes perceived as male, sometimes female, but whose gender identity is female, gender expression is butch, and sexual orientation is lesbian. It suggests nonconformity or mixing of gender stereotypes, conjoining both gender and sexuality, and challenges existing constructions and identities. In the binary sex/gender system, genderqueerness is unintelligible and abjected.
An androgyne is a person who cannot be classified into the typical gender roles of their society; androgyny is independent of orientation. Androgynes may identify as beyond gender, between genders, moving across genders, entirely genderless, or any or all of these, exhibiting a variety of male, female, and other characteristics. Androgyne identities include pangender, ambigender, non-gendered, agender, gender fluid or intergender. Androgyny can be either physical or psychological and is independent of birth sex. Occasionally, non-androgynous people adapt their physical appearance to look androgynous. This outward androgyny has been used in fashion, and the milder forms of it (women wearing men's pants or men wearing two earrings, for example) are not seen as transgender behavior.
A bigender (sometimes rendered as bi-gender, dual gender, or bi+gender) individual is one who moves between masculine and feminine gender roles. Such individuals fluidly move between two distinct personalities depending on context: whereas androgynous people retain the same gender-typed behaviour across situations, bigendered people consciously or unconsciously change their gender-role behaviour from primarily masculine to primarily feminine or vice versa.
Drag kings and queens
Drag is a term applied to clothing and make-up worn on special occasions for performing or entertaining, unlike those who are transgender or who cross-dress for other reasons. Drag performance includes overall presentation and behavior in addition to clothing and makeup. Drag can be theatrical, comedic, or grotesque. Drag queens have been considered caricatures of women by second-wave feminism. Drag artists have a long tradition in LGBT culture. Generally the terms drag queen covers men doing female drag, drag king covers women doing male drag, and faux queen covers women doing female drag. Nevertheless, there are drag artists of all genders and sexualities who perform for various reasons. Some drag performers, transvestites, and people in the gay community, have embraced the pornographically-derived term tranny to describe drag queens or people who engage in transvestism or cross-dressing, however this term is widely considered offensive if applied to transsexual people.
Transgender people and the LGBT community
The concepts of gender identity and transgender identity differ from that of sexual orientation. Sexual orientation describes an individual's enduring physical, romantic, emotional, and/or spiritual attraction to another person, while gender identity is one's personal sense of being a man or a woman. Transgender people have more or less the same variety of sexual orientations as cisgender people. In the past, the terms homosexual and heterosexual were incorrectly used to label transgender individuals' sexual orientation based on their birth sex. Professional literature now uses terms such as attracted to men (androphilic), attracted to women (gynephilic), attracted to both (bisexual) or attracted to neither (asexual) to describe a person's sexual orientation without reference to their gender identity. Therapists are coming to understand the necessity of using terms with respect to their clients' gender identities and preferences. For example, a person who is assigned male at birth, transitions to female, and is attracted to men would be identified as heterosexual.
Despite the distinction between sexual orientation and gender, throughout history the gay, lesbian, and bisexual subculture was often the only place where gender-variant people were socially accepted in the gender role they felt they belonged to; especially during the time when legal or medical transitioning was almost impossible. This acceptance has had a complex history. Like the wider world, the gay community in Western societies did not generally distinguish between sex and gender identity until the 1970s, and often perceived gender variant people more as homosexuals who behaved in a gender-variant way than as gender-variant people in their own right. Today, members of the transgender community often continue to struggle to remain part of the same movement as lesbian, gay and bisexual citizens, and to be included in rights protections.
Helms describes the meaning of the flag as follows:
The light blue is the traditional color for baby boys, pink is for girls, and the white in the middle is for those who are transitioning, those who feel they have a neutral gender or no gender, and those who are intersexed. The pattern is such that no matter which way you fly it, it will always be correct. This symbolizes us trying to find correctness in our own lives.[this quote needs a citation]
Transgender people and feminism
Some feminists and feminist groups are supportive of transgender people. Others are not.
Though second-wave feminism argued for the sex and gender distinction, some feminists believed there was a conflict between transgender identity and the feminist cause; e.g., they believed that male-to-female transition abandoned or devalued female identity, and that transgender people embraced traditional gender roles and stereotypes. Many transgender feminists, however, viewed themselves as contributing to feminism by questioning and subverting gender norms. Third wave and contemporary feminism more greatly accepts transgender people.
Feminist writer Janice Raymond asserts that sex determines gender, and that no practical difference is between the two. In her view, genitalia or "birth sex" or chromosomes deeply and permanently determine one's essential identity as a woman or man; trying to violate this divide is impossible, unnatural, and unhealthy. She argues that although transsexuals may claim to feel like a certain gender, only a biological female can genuinely feel what occupying a woman's body is; e.g., such experiences as childbirth.
Most mental health professionals recommend therapy for internal conflicts about gender identity or discomfort in an assigned gender role, especially if one desires to transition. People who experience discord between their gender and the expectations of others or whose gender identity conflicts with their body may benefit by talking through their feelings in depth; however, research on gender identity with regard to psychology, and scientific understanding of the phenomenon and its related issues, are relatively new. The terms transsexualism, dual-role transvestism, gender identity disorder in adolescents or adults and gender identity disorder not otherwise specified are listed as such in the International Statistical Classification of Diseases (ICD) or the American Diagnostic and Statistical Manual of Mental Disorders (DSM) under codes F64.0, F64.1, 302.85 and 302.6 respectively. The DSM-5 refers to the topic as gender dysphoria.
Transgender people may meet the criteria for a diagnosis of gender identity disorder (GID) "only if [being transgender] causes distress or disability." This distress is referred to as gender dysphoria and may manifest as depression or inability to work and form healthy relationships with others. This diagnosis is often misinterpreted as implying that transgender people suffer from GID; this misinterpretation has greatly confused transgender people and those who seek to either criticize or affirm them. Transgender people who are comfortable with their gender and whose gender is not directly causing inner frustration or impairing their functioning do not suffer from GID. Moreover, GID is not necessarily permanent and is often resolved through therapy and/or transitioning. Feeling oppressed by the negative attitudes and behaviors of such others as legal entities does not indicate GID. GID does not imply an opinion of immorality; the psychological establishment holds that people with any kind of mental or emotional problem should not receive stigma. The solution for GID is whatever will alleviate suffering and restore functionality; this solution often, but not always, consists of undergoing a gender transition.
Clinical training lacks relevant information needed in order to adequately help transgender clients, which only produces a series of practitioners who are not prepared to sufficiently work with this population of individuals. Many mental healthcare providers know little about transgender issues. Those who seek help from these professionals often educate the professional without receiving help. Many therapists who profess to know about transgender issues believe that transitioning from one sex to another – the standard transsexual model – is the best or only solution. This solution usually is good for transsexual people but is not the solution for other transgender people, particularly genderqueer people who lack an exclusively male or female identity. Instead, therapists can support their clients in whatever steps they choose to take to transition or support their decision to not transition while also addressing their clients' sense of congruence between gender identity and appearance.
Acknowledgment of the lack of clinical training has increased; however, research on the specific problems faced by the transgender community in mental health has focused on diagnosis and clinicians' experiences instead of transgender clients' experiences. Therapy was not always sought out by people due to mental health needs. Prior to the seventh version of the Standards of Care (SOC), an individual had to be diagnosed with gender identity disorder in order to proceed with hormone treatments or sexual reassignment surgery. The new version decreased the focus on diagnosis and instead emphasized the importance of flexibility in order to meet the diverse health care needs of transsexual, transgender, and all gender nonconforming people.
The purposes for seeking mental health services vary according to the individual, and simply because a transgender person seeks treatment does not mean their gender identity is problematic. The emotional strain on dealing with stigma and experiencing transphobia pushes many transgender people to seek treatment to improve their quality of life, as one transwoman reflected: "Transgendered individuals are going to come to a therapist and most of their issues have nothing to do, specifically, with being transgendered. It has to do because they've had to hide, they've had to lie, and they've felt all of this guilt and shame, unfortunately usually for years!" Struggling to deal with the stigma still attached to identifying as transgender, many people also seek mental health treatment for depression and anxiety, and some transgender people have stressed the importance of acknowledging their gender identity with a therapist in order to discuss other quality of life issues.
Problems still remain surrounding misinformation about transgender issues that hurt transgender people's mental health experiences. One transman who was enrolled as a student in a psychology graduate program highlighted the main concerns with modern clinical training: "Most people probably are familiar with the term transgender, but maybe that’s it. I don’t think I've had any formal training just going through [clinical] programs . . . I don’t think most [therapists] know. Most therapists—Master’s degree, PhD level—they've had . . . one diversity class on GLBT issues. One class out of the huge diversity training. One class. And it was probably mostly about gay lifestyle." Many health insurance policies do not cover treatment associated with gender transition, and numerous people are under or not insured, which raises concerns about the insufficient training most therapists receive prior to working with transgender clients, potentially increasing financial strain on clients without providing the treatment they need. Many clinicians who work with transgender clients only receive mediocre training on gender identity, but recently introductory training on interacting with transgender people have been made available to health care professionals to help remove barriers and increase the level of service for the transgender population.
The issues around psychological classifications and associated stigma (whether based in paraphilia or not) of cross dressers, transsexual men and women (and lesbian and gay children, who may resemble trans children early in life) have become more complex since CAMH (Centre for Addiction and Mental Health) colleagues Kenneth Zucker and Ray Blanchard were announced to be serving on the DSM-V's Sexual and Gender Identity Disorders Work Group. CAMH aims to 'cure' transgender people of their 'disorder', especially in children. Within the trans community, this intention has mostly produced shock and outrage with attempts to organize other responses. In February 2010, France became the first country in the world to remove transgender identity from the list of mental diseases.
Medical and surgical procedures exist for transsexual and some transgender people. (Most categories of transgender people as described above are not known for seeking the following treatments.) Hormone replacement therapy for trans men induces beard growth and masculinises skin, hair, voice, and fat distribution. Hormone replacement therapy for trans women feminises fat distribution and breasts. Laser hair removal or electrolysis removes excess hair for trans women. Surgical procedures for trans women feminise the voice, skin, face, adam's apple, breasts, waist, buttocks and genitals. Surgical procedures for trans men masculinise the chest and genitals and remove the womb and ovaries and fallopian tubes. The acronyms "GRS" and "SRS" refer to genital surgery. The term "sex reassignment therapy" (SRT) is used as an umbrella term for physical procedures required for transition. Use of the term "sex change" has been criticized for its emphasis on surgery, and the term "transition" is preferred. Availability of these procedures depends on degree of gender dysphoria, presence or absence of gender identity disorder, and standards of care in the relevant jurisdiction.
Trans men who have not had a hysterectomy and who take testosterone are at increased risk for endometrial cancer because androstenedione, which is made from testosterone in the body, can be converted into estrogen, and external estrogen is a risk factor for endometrial cancer.
Transgender people and the law
Legal procedures exist in some jurisdictions, allowing individuals to change their legal gender or name to reflect their gender identity. Requirements for these procedures vary from an explicit formal diagnosis of transsexualism to a diagnosis of gender identity disorder to a letter from a physician that attests the individual's gender transition or having established a different gender role. In 1994, the DSM IV entry was changed from "Transsexual" to "Gender Identity Disorder." In many places, transgender people are not legally protected from discrimination in the workplace or in public accommodations. A report released in February 2011 found that 90% of transgender people faced discrimination at work and were unemployed at double the rate of the general population. Over half had been harassed or turned away when attempting to access public services. Members of the transgender community also encounter high levels of discrimination in health care on an everyday basis.
In Canada, a private members bill protecting the rights of freedom of gender expression and gender identity passed in the House of Commons on February 9, 2011. It amends the Canada Human Rights code to help protect gender-variant people from discrimination by including gender identity and expression in the list of prohibited grounds for discrimination, as well as including gender identity and expression in the description of identifiable group, so that offences deliberately against gender-variant people can be punished to a similar extent as a racial-based crime. The bill may or may not be passed by the Senate.
In the U.S., a federal bill to protect workers from discrimination based on sexual orientation and gender identity – called the Employment Non-Discrimination Act – has stalled and failed several times over the past two decades. Still, individual states and cities have begun passing their own non-discrimination ordinances. In New York, for example, Governor David Paterson passed the first legislation to include transgender protections in September 2010.
Nicole Maines took a case of whether she is allowed to use her high school's girls' bathroom, as a transgender girl, to Maine's Supreme Court in June, 2013. She claims being denied such access is a violation of Maine's Human Rights Act, though a state judge has already disagreed with her.
Nicole Maines won her lawsuit against the Orono school district in January 2014 before the Maine Supreme Judicial Court.
In April 2014, the Supreme Court of India declared transgender to be the 'third gender' in Indian law. Justice KS Radhakrishnan noted in his decision that, "Seldom, our society realizes or cares to realize the trauma, agony and pain which the members of Transgender community undergo, nor appreciates the innate feelings of the members of the Transgender community, especially of those whose mind and body disown their biological sex", adding:
Non-recognition of the identity of Hijras/transgender persons denies them equal protection of law, thereby leaving them extremely vulnerable to harassment, violence and sexual assault in public spaces, at home and in jail, also by the police. Sexual assault, including molestation, rape, forced anal and oral sex, gang rape and stripping is being committed with impunity and there are reliable statistics and materials to support such activities. Further, non-recognition of identity of Hijras /transgender persons results in them facing extreme discrimination in all spheres of society, especially in the field of employment, education, healthcare etc.
Hijras/transgender persons face huge discrimination in access to public spaces like restaurants, cinemas, shops, malls etc. Further, access to public toilets is also a serious problem they face quite often. Since, there are no separate toilet facilities for Hijras/transgender persons, they have to use male toilets where they are prone to sexual assault and harassment. Discrimination on the ground of sexual orientation or gender identity, therefore, impairs equality before law and equal protection of law and violates Article 14 of the Constitution of India.
Transgender people and the U.S. military
United States Secretary of Defense Chuck Hagel is quoted as stating that the military should "continually" review its prohibition on transgender individuals and stating: "Every qualified American who wants to serve our country should have an opportunity if they fit the qualifications and can do it."
Transgender people and religion
James D. Whitehead and Evelyn Eaton Whitehead, educators and authors, discuss the links between spirituality and sexuality, and the frequent absence of compassion within the church community, in their case, the Catholic Church, in ministering to this community.
Transsexual people and science
Several studies have concentrated on whether sexually dimorphic brain structures in transsexuals are more similar to their preferred sex or to their birth sex. Researchers caution that there are known brain differences between homosexual and heterosexual persons and that the brain changes in response to hormone-treatment, which many transsexuals use. In order to know what in the brain is related to what feature of the person, studies of more uniform groups give clearer results than do studies of more mixed groups.
Androphilic male-to-female transsexuals
Studies have consistently shown that specifically androphilic male-to-female transsexuals (sometimes called homosexual MtF transsexuals in studies) show a shift towards the female direction in brain anatomy. In 2009, the German team of radiologists led by Gizewski compared 12 androphilic transsexuals with 12 biological males and 12 biological females. Using functional magnetic resonance imaging (fMRI), they found that when shown erotica, the biological men responded in several brain regions that the biological women did not, and that the sample of androphilic transsexuals was shifted towards the female direction in brain responses.
Rametti and colleagues used diffusion tensor imaging (DTI) to compare 18 androphilic male-to-female transsexuals with 19 gynephilic males and 19 typical (heterosexual) females. The androphilic transsexuals differed from both control groups in multiple brain areas, including the superior longitudinal fasciculus, the right anterior cingulum, the right forceps minor, and the right corticospinal tract. The study authors concluded that androphilic transsexuals are halfway between the patterns exhibited by male and female controls.
Gynephilic male-to-female transsexuals
Conversely, gynephilic male-to-female transsexuals also show differences in the brain from non-transsexual males, but in a unique pattern different from being shifted in a female direction. Researchers of the Karolinska Institute of Stockholm used MRI to compare 24 gynephilic male-to-female transsexuals with 24 non-transsexual male and 24 non-transsexual female controls. None of the study participants were on hormone treatment. The researchers found sex-typical differentiation between the MtF transsexuals and non-transsexual males, and the non-transsexual females; but the gynephilic transsexuals "displayed also singular features and differed from both control groups by having reduced thalamus and putamen volumes and elevated GM volumes in the right insular and inferior frontal cortex and an area covering the right angular gyrus."
These researchers concluded that:
Contrary to the primary hypothesis, no sex-atypical features with signs of 'feminization' were detected in the transsexual group....The present study does not support the dogma that [male-to-female transsexuals] have atypical sex dimorphism in the brain but confirms the previously reported sex differences. The observed differences between MtF-TR and controls raise the question as to whether gender dysphoria may be associated with changes in multiple structures and involve a network (rather than a single nodal area).
In Sweden, non-androphilic transsexual women were tested when they were smelling odorous steroids. The results showed that the transsexual women demonstrated "a pattern of activation away from the biological sex, occupying an intermediate position with predominantly female-like features."
Anne Lawrence, a sexologist, physician, and self-identified autogynephilic transsexual, has hypothesized that the desire by persons with autogynephilia, including some cross dressers and some transsexuals, to alter their body can be compared with apotemnophilia (alternately body integrity identity disorder if framed as an identity issue rather than a fetish). Some transsexuals argue that explanations that base on libido the desire to transition are unscientific or transphobic.
Mixed samples of male-to-female transsexuals
Several teams of researchers have examined the brains or brain functioning of MtF transsexuals without separating the samples into androphilic (or homosexual) and gynephilic (or heterosexual) types. Such studies have yielded contradictory results: some report differences between the (mixed groups of) MtF transsexuals and the non-transsexual controls, but other studies found no differences.
The corpus callosum was studied in MtF transsexuals because it is larger and differently shaped in men than in women. In 1991, a University of Texas team reported comparing the corpora callosa of 10 MtF transsexuals, 10 FtM transsexuals, 20 control males, and 20 control females. No significant differences were found.
In a pair of reports, the Dutch team that Dick Swaab led examined the volume and neuron count in the bed nucleus of the stria terminalis in six estrogen-treated transsexuals and one pre-treatment transsexual. They found the BSTc to be female-shifted (smaller) among the transsexuals than among the male control subjects. A subsequent study by Swaab found that the BSTc becomes sexually dimorphic only in adulthood, suggesting that differentiation of the BSTc does not cause transsexualism. Rather, the difference in the BSTc might instead be the result of a "failure to develop a male-like gender identity" (p. 1032). The BSTc has also been reported to be smaller in other sexually atypical populations unrelated to transsexualism.
Another team of Dutch researchers examined the effects of cross-gender hormone treatment on the brain in 8 male-to-female transsexuals and in 6 female-to-male transsexuals, finding that the hormones changed the sizes of the hypothalamus in a gender consistent manner. Treatment with male hormones shifted the hypothalamus towards the male direction in the same way as in male controls, and treatment with female hormones shifted the hypothalamus towards the female direction in the same way as female controls.
A 2003 study by Haraldsen and colleagues compared the performance of 52 persons with Gender Identity Disorder (33 from Norway and 19 from the U.S.) with that of 29 control subjects on a series of tests that tap into the functioning of different parts of the brain and on which men and women perform differently. The people in the GID sample "were either homosexually attracted by males or females (n=38), by both (n=3) or by neither (n=9)." No effects of transsexual status were detected.
Johns Hopkins researchers in 2005 reported on another test of brain functioning using test performance. The study subjects included 27 MtF transsexuals and 16 control men, and the authors reported that no female-typical patterns in cerebral lateralization or cognitive performance were found within the transsexual sample.
In 2009, UCLA researchers used MRIs to examine a mixed sample of 24 non-hormone-treated male-to-female transsexuals (6 were androphilic, and 18 were gynephilic), comparing them with 30 non-transsexual males and 30 non-transsexual females. The results "revealed that regional gray matter variation in MTF transsexuals is more similar to the pattern found in men than in women," except for the "right putamen.". They concluded that "These findings provide new evidence that transsexualism is associated with distinct cerebral pattern, which supports the assumption that brain anatomy plays a role in gender identity."
Gynephilic female-to-male transsexuals
Brain-based research has repeatedly shown that female-to-male transsexuals have several male-like characteristics in neuroanatomy. In 2010, a team of neuroscientists compared 18 female-to-male transsexuals with 24 male and 19 female gynephilic controls, using an MRI technique called diffusion tensor imaging or DTI. DTI is a specialized technique for visualizing white matter of the brain, and white matter structure is one of the differences in neuroanatomy between men and women. The study found that the white matter pattern in female-to-male transsexuals was shifted in the direction of biological males, even before the female-to-male transsexuals started taking male hormones (which can also modify brain structure).
Another team of neuroscientists, led by Nawata in Japan, used a technique called single-photon emission computed tomography (SPECT) compare the regional cerebral blood flow (rCBF) of 11 female-to-male transsexuals (attracted to women) with that of 9 biological females (attracted to men). Although the study did not include a sample of biological males so that a conclusion of "male shift" could be made, the study did reveal that the female-to-male transsexuals showed significant decrease in blood flow in the left anterior cingulate cortex and a significant increase in the right insula, two brain regions known to respond during sexual arousal.
Related developments in other fields
Brain structure differences associated with transsexualism do not exist in isolation. Similar brain structure differences have been noted between gay and heterosexual men, and between lesbian and heterosexual women.
More recent studies have found that circumstance, such as parenting, and repeated activities such as meditation modify brain structures in a process called brain plasticity or neuroplasticity. In May 2014, the Proceedings of the National Academy of Sciences reported that for fathers parenting "rewires the male brain".
In 2008, a study was performed to attempt to find a link between genes and transsexuality. The researchers compared 112 male-to-female transsexuals (both androphilic and gynephilic), mostly already undergoing hormone treatment, with 258 cisgender male controls. The male-to-female transsexuals were more likely than non-transsexual males to have a longer version of a receptor gene for the sex hormone androgen or testosterone. The research suggests reduced androgen and androgen signaling contributes to the female gender identity of male to female transsexuals. The authors say that a decrease in testosterone levels in the brain during development might prevent complete masculinization of the brain in male to female transsexuals and thereby cause a more feminized brain and a female gender identity.
Terms and typology
The use of homosexual transsexual and related terms have been applied to transgender people since the middle of the 20th century, though concerns about the terms have been voiced since then. Harry Benjamin said in 1966:
...it seems evident that the question "Is the transsexual homosexual?" must be answered "yes" and " no." "Yes," if his anatomy is considered; "no" if his psyche is given preference.
What would be the situation after corrective surgery has been performed and the sex anatomy now resembles that of a woman? Is the "new woman" still a homosexual man? "Yes," if pedantry and technicalities prevail. "No" if reason and common sense are applied and if the respective patient is treated as an individual and not as a rubber stamp.
Many sources, including some supporters of the typology, criticize this choice of wording as confusing and degrading. Biologist Bruce Bagemihl writes "..the point of reference for "heterosexual" or "homosexual" orientation in this nomenclature is solely the individual's genetic sex prior to reassignment (see for example, Blanchard et al. 1987, Coleman and Bockting, 1988, Blanchard, 1989). These labels thereby ignore the individual’s personal sense of gender identity taking precedence over biological sex, rather than the other way around." Bagemihl goes on to take issue with the way this terminology makes it easy to claim transsexuals are really homosexual males seeking to escape from stigma. Leavitt and Berger stated in 1990 that "The homosexual transsexual label is both confusing and controversial among males seeking sex reassignment. Critics argue that the term "homosexual transsexual" is "heterosexist", "archaic", and demeaning because it labels people by sex assigned at birth instead of their gender identity. Benjamin, Leavitt, and Berger have all used the term in their own work. Sexologist John Bancroft also recently expressed regret for having used this terminology, which was standard when he used it, to refer to transsexual women. He says that he now tries to choose his words more sensitively. Sexologist Charles Allen Moser is likewise critical of the terminology.
Use of androphilia and gynephilia was proposed and popularized by psychologist Ron Langevin in the 1980s. Psychologist Stephen T. Wegener writes, "Langevin makes several concrete suggestions regarding the language used to describe sexual anomalies. For example, he proposes the terms gynephilic and androphilic to indicate the type of partner preferred regardless of an individual's gender identity or dress. Those who are writing and researching in this area would do well to adopt his clear and concise vocabulary."
Psychiatrist Anil Aggrawal explains why the terms are useful in a glossary:
Androphilia – The romantic and/or sexual attraction to adult males. The term, along with gynephilia, is needed to overcome immense difficulties in characterizing the sexual orientation of transmen and transwomen. For instance, it is difficult to decide whether a transman erotically attracted to males is a heterosexual female or a homosexual male; or a transwoman erotically attracted to females is a heterosexual male or a lesbian female. Any attempt to classify them may not only cause confusion but arouse offense among the affected subjects. In such cases, while defining sexual attraction, it is best to focus on the object of their attraction rather than on the sex or gender of the subject.
Psychologist Rachel Ann Heath writes, "The terms homosexual and heterosexual are awkward, especially when the former is used with, or instead of, gay and lesbian. Alternatively, I use gynephilic and androphilic to refer to sexual preference for women and men, respectively. Gynephilic and androphilic derive from the Greek meaning love of a woman and love of a man respectively. So a gynephilic man is a man who likes women, that is, a heterosexual man, whereas an androphilic man is a man who likes men, that is, a gay man. For completeness, a lesbian is a gynephilic woman, a woman who likes other women. Gynephilic transsexed woman refers to a woman of transsexual background whose sexual preference is for women. Unless homosexual and heterosexual are more readily understood terms in a given context, this more precise terminology will be used throughout the book. Since homosexual, gay, and lesbian are often associated with bigotry and exclusion in many societies, the emphasis on sexual affiliation is both appropriate and socially just." Author Helen Boyd agrees, writing, "It would be much more accurate to define sexual orientation as either "androphilic" (loving men) and "gynephilic" (loving women) instead." Sociomedical scientist Rebecca Jordan-Young challenges researchers like Simon LeVay, J. Michael Bailey, and Martin Lalumiere, who she says "have completely failed to appreciate the implications of alternative ways of framing sexual orientation."
Blanchard's transsexualism typology characterizes trans women as having one of two motivations for transition. Whereas previous descriptions of transgenderism included very many combinations of sexual orientation, gender identity, and the desire to cross-dress, Blanchard interprets his evidence as suggesting that there were only two basic phenomena. One phenomenon was androphilia (male homosexuality), which ranged from typical gay men to, when extreme, androphilic or homosexual transsexualism. The other phenomenon was autogynephilia, which ranged from typical cross-dressers to, when extreme, autogynephilic transsexualism (or non-homosexual transsexualism). Androphilic male-to-female transsexuals are characterized by sexual attraction to males and by overt and obvious femininity since childhood, whereas autogynephilic transsexuals are characterized by sexual attraction to females (or sometimes to females and males, or by asexuality) and whose presentations are internal and typically unremarkable until they choose to disclose them, typically later in life. There are community activists who dislike the theory.
Scientific criticism of the theory includes papers from Veale, Nuttbrock, Moser, and others who argue that the theory is poorly representative of MTF transsexuals, non-instructive, the experiments poorly controlled, or contradicted by other data. Many sources, including some supporters of the theory, criticize Blanchard's choice of wording as confusing or degrading.
Also the DSM V workgroup has been quoted as saying:
In contemporary clinical practice, sexual orientation per se plays only a minor role in treatment protocols or decisions. Also, changes as to the preferred gender of sex partner occur during or after treatment (DeCuypere, Janes, & Rubens, 2005; Lawrence, 2005; Schroder & Carroll, 1999). It can be difficult to assess sexual orientation in individuals with a GI diagnosis, as they preoperatively might give incorrect information in order to be approved for hormonal and surgical treatment (Lawrence, 1999). Because sexual orientation subtyping is of interest to researchers in the field, it is recommended that reference to it be addressed in the text, but not as a specifier. It should also be assessed as a dimensional construct.
Blanchard is a member of the DSM V Sexual and Gender Identity Disorders Work Group chaired by Kenneth J. Zucker. Though it has supporters, the transsexual community has for the most part vehemently rejected Blanchard's typology theory.
In Latin American cultures, the travestis generally undergo hormonal treatment, use female gender expression including new names and pronouns from the masculine ones they were given when assigned a sex, and might use breast implants, but they are not offered and/or do not desire sex-reassignment surgery, and might be regarded as a gender in itself (a "third gender"), a mix between man and woman ("intergender/androgynes") or the presence of both masculine and feminine identities in a single person ("bigender").
They are framed as something entirely separate from transgender women, who possess the same gender identity of people assigned female at birth.
More recently, other transgender identities are becoming more known of, as a result of contact with other cultures of the Western world. These newer identities, sometimes known under the umbrella use of the term "genderqueer", along the older travesti one, are known as non-binary, that go along with binary transgenders (those traditionally diagnosed under the now obsolete "transsexualism") under the single umbrella of transgender, but not along crossdressers and drag queens and kings, that are held as nonconforming gender expressions rather than transgender gender identities when a distinction is made.
Nevertheless, deviating from the societal standards for sexual behavior, sexual orientation/identity, gender identity and gender expression have a single umbrella term that is known as sexodiverso or sexodiversa in both Spanish and Portuguese, with its most approximate translation to English being "queer".
Transgender people in non-Western cultures
In Thailand and Laos, the term kathoey is used to refer to male-to-female transgender people and effeminate gay men. The cultures of the Indian subcontinent include a third gender, referred to as hijra in Hindi. Transgender people have also been documented in Iran, Japan, Nepal, Indonesia, Vietnam, South Korea, Singapore, and the greater Chinese region, including Hong Kong, Taiwan, and the People's Republic of China.
In India, the Supreme Court on April 15, 2014, recognized a third gender that is neither male nor female, stating "Recognition of transgenders as a third gender is not a social or medical issue but a human rights issue."
On January 5, 2015, Reuters stated that the first transgender mayor was elected in central India.
In what is now the United States and Canada, many Native American and First Nations peoples recognised the existence of more than two genders, such as the Zuñi male-bodied Ła'mana, the Lakota male-bodied winkte and the Mohave male-bodied alyhaa and female-bodied hwamee. Such people were previously referred to as berdache but are now referred to as Two-Spirit, and their spouses would not necessarily have been regarded as gender-different. In Mexico, the Zapotec culture includes a third gender in the form of the Muxe.
In early Medina, gender-variant male-to-female Islamic people were acknowledged in the form of the Mukhannathun. In Ancient Rome, the Gallae were castrated followers of the Phrygian goddess Cybele and can be regarded as transgender in today's terms.
Among the ancient Middle Eastern Akkadian people, a salzikrum was a person who appeared biologically female but had distinct male traits. Salzikrum is a compound word meaning male daughter. According to the Code of Hammurabi, salzikrūm had inheritance rights like that of priestesses; they inherited from their fathers, unlike regular daughters. A salzikrum's father could also stipulate that she inherit a certain amount.
Transgender people vary greatly in choosing when, whether, and how to disclose their transgender status to family, close friends, and others. The prevalence of discrimination and violence against the transgender community can make coming out a risky decision. Fear of retaliatory behavior, such as being removed from the parental home while underage, is a cause for transgender people to not come out to their families until they have reached adulthood. Parental confusion and lack of acceptance of the child's transgenderism may be met with an effort to change their children back to "normal" by utilizing mental health services to alter the child's sexual orientation and what is seen as a "phase".
- History of transgenderism in the United States
- List of transgender people
- List of transgender-related topics
- List of transgender-rights organizations
- List of transgender, transsexual and intersex fictional characters
- List of unlawfully killed transgender people
- Transgender Day of Remembrance
- Transgender publications
- Transsexual pornography
- In April 1970, TV Guide published an article which referenced a post-operative transsexual movie character as being "transgendered."("Sunday Highlights". TV Guide. April 26, 1970. Retrieved 28 May 2012.
[R]aquel Welch (left), moviedom’s sex queen soon to be seen as the heroine/hero of Gore Vidal's transgendered "Myra Breckinridge"…)
- In the 1974 edition of Clinical Sexuality: A Manual for the Physician and the Professions, transgender was used as an umbrella term and the Conference Report from the 1974 "National TV.TS Conference" held in Leeds, West Yorkshire, UK used "trans-gender" and "trans.people" as umbrella terms.(Oliven, John F. (1974). Clinical sexuality: A Manual for the Physician and the Professions (3rd ed.). University of Michigan (digitized Aug 2008): Lippincott. pp. 110, 484–487. ISBN 9780397503292.
"Transgender deviance" p 110, "Transgender research" p 484, "transgender deviates" p 485, Transvestites not welcome at "Transgender Center" p 487), (2006). The Transgender Phenomenon (Elkins, Richard; King, Dave (2006). The Transgender Phenomenon. Sage. p. 13. ISBN 9780761971634.)
- However A Practical Handbook of Psychiatry (1974) references "transgender surgery" noting, "The transvestite rarely seeks transgender surgery, since the core of his perversion is an attempt to realize the fantasy of a phallic woman."(Novello, Joseph R. (1974). A Practical Handbook of Psychiatry. University of Michigan, digitized August 2008: C. C. Thomas. p. 176. ISBN 9780398028688.)
- In April 1970, TV Guide published an article which referenced a post-operative transsexual movie character as being "transgendered."("Sunday Highlights". TV Guide. April 26, 1970. Retrieved 28 May 2012.
- Gay and Lesbian Alliance Against Defamation. "GLAAD Media Reference Guide - Transgender glossary of terms", "GLAAD", USA, May 2010. Retrieved on 2011-02-24.
- Author unknown, (2004) "...Transgender, adj. Of, relating to, or designating a person whose identity does not conform unambiguously to conventional notions of male or female gender, but combines or moves between these..." Definition of transgender[dead link] from the Oxford English Dictionary, draft version March 2004. Retrieved on 2007-04-07.
- "USI LGBT Campaign - Transgender Campaign". Retrieved 11 January 2012.
- Stroud District Council "Gender Equality SCHEME AND ACTION PLAN 2007"
- "Layton, Lynne. In Defense of Gender Ambiguity: Jessica Benjamin. Gender & Psychoanalysis. I, 1996. Pp. 27–43". Retrieved 2007-03-06
- Kozee, H. B., Tylka, T. L., & Bauerband, L. A. (2012). Measuring transgender individuals' comfort with gender identity and appearance: Development and validation of the Transgender Congruence Scale. Psychology of Women Quarterly, 36, 179-196. doi: 10.1177/0361684312442161
- A., R. (August 1965). "Book Reviews and Notices: Sexual Hygiene and Pathology". American Journal of the Medical Sciences 250 (2): 235. doi:10.1097/00000441-196508000-00054. Retrieved 4 June 2012.
- Oliven, John F. (1965). Sexual Hygiene and Pathology. p. 514.
Where the compulsive urge reaches beyond female vestments, and becomes an urge for gender ("sex") change, transvestism becomes "transsexualism." The term is misleading; actually, "transgenderism" is what is meant, because sexuality is not a major factor in primary transvestism. Psychologically, the transsexual often differs from the simple cross-dresser; he is conscious at all times of a strong desire to be a woman, and the urge can be truly consuming.
- Elkins, Richard; King, Dave (2006). The Transgender Phenomenon. Sage. pp. 13–14. ISBN 9780761971634.
- Stryker, S. (2004), "... lived full-time in a social role not typically associated with their natal sex, but who did not resort to genital surgery as a means of supporting their gender presentation ..." in Transgender from the GLBTQ: an encyclopedia of gay, lesbian, bisexual, transgender and queer culture. Retrieved on 2007-04-10.
- The Radio Times (1979: 2 June)
- Parker, Jerry (October 18, 1979). "Christine Recalls Life as Boy from the Bronx". Newsday/Winnipeg Free Press. Retrieved 28 May 2012.
“If you understand trans-genders,” she says, (the word she prefers to transsexuals), “then you understand that gender doesn’t have to do with bed partners, it has to do with identity.”
- "News From California: 'Transgender'". Appeal-Democrat/Associate Press. May 11, 1982. pp. A–10. Retrieved 28 May 2012.
she describes people who have had such operations’ “transgender“ rather than transsexual. “Sexuality is who you sleep with, but gender is who you are,” she explained
- Peo, TV-TS Tapestry Board of Advisors, Roger E. (1984). "The ‘Origins’ and ‘Cures’ for Transgender Behavior". The TV-TS Tapestry (2). Retrieved 28 May 2012.
- "First International Conference on Transgender Law and Employment Policy (1992)". organizational pamphlet. ICTLEP/. 1992. Retrieved 28 May 2012.
Transgendered persons include transsexuals, transgenderists, and other crossdressers of both sexes, transitioning in either direction (male to female or female to male), of any sexual orientation, and of all races, creeds, religions, ages, and degrees of physical impediment.
- Benjamin, H. (1966). The transsexual phenomenon. New York: Julian Press, page 23.
- Gaughan, Sharon (2006-08-19). "What About Non-op Transsexuals? A No-op Notion". TS-SI. Retrieved 2008-09-30.[dead link]
- Conway, Lynn (2003). "The Strange Saga of Gregory Hemingway".
- Schoenberg, Nara (2001-11-19). "The Son Also Falls From elephant hunter to bejeweled exhibitionist, the tortured life of Gregory Hemingway". CHICAGO TRIBUNE. Archived from the original on 2001-11-20.
- "glbtq >> social sciences >> Prince, Virginia Charles". glbtq.com.
- Prince, V. (1969), Men Who Choose to be Women, Sexology, February, pp. 441–444. Use of the term "transgenderal".
- "Sex -- Medical Definition". medilexicon.com.
- UNCW: Developing and Implementing a Scale to Assess Attitudes Regarding Transsexuality
- Liberman, Mark. "Single-X Education". Language Log. Retrieved 28 June 2012.
- Boyd, Hellen. "The Umbrella". enGender. Retrieved 28 June 2012.
the only part of the gender binary we *necessarily* challenge is the notion that people are always assigned to the right side of the binary at birth, and don’t need sympathy or help if the assignment goes wrong.
- Ryan, Caitlin C; Futterman, Donna (1998). Lesbian and Gay Youth: Care and Counseling. Columbia University Press. p. 49. ISBN 0-231-11191-6
- Interview with RuPaul, David Shankbone, Wikinews, October 6, 2007.
- Landén, M., Wålinder, J., Lundstrom, B. (1996) "...Results: During the 20-year period of the study, 233 requests for sex reassignment were processed, and the incidence data were calculated on the basis of this group. This means that the average annual frequency was 11.6 cases. The number of inhabitants in Sweden over 15 years of age increased during the study period from 6.5 million to 7.1 million, i.e. there was a mean population of 6.8 million (12), which gives an annual incidence of request for sex reassignment of 0.17 per 100,000 inhabitants. The sex ratio (male:female) is 1.4 :1. To resolve the question of whether transsexualism increases or decreases, we divided the group into two 10-year periods. As can be seen from Table 1, not only do our results agree with the Swedish incidence data published in the 1970s, but also they remain remarkably stable over time. Separating from all applications the group with primary transsexualism yielded 188 cases, i.e. 9.4 cases annually. As is shown in Table 2, this corresponds to an incidence of primary transsexualism of 0.14 per 100,000 inhabitants over 15 years of age. It should also be noted that primary transsexualism is equally common in women and men..." in Incidence and sex ratio of transsexualism in Sweden from Acta Psychiatrica Scandanavica, Volume 93, pages 261-263. Retrieved on 2007-09-22.
- Crethar, H. C. & Vargas, L. A. (2007). Multicultural intricacies in professional counseling. In J. Gregoire & C. Jungers (Eds.), The counselor’s companion: What every beginning counselor needs to know. Mahwah, NJ: Lawrence Erlbaum. ISBN 0-8058-5684-6. p.61.
- Gay and Lesbian Alliance Against Defamation. "GLAAD's Transgender Resource Page", "GLAAD", USA. Retrieved on 2011-02-24.
- Glicksman, Eve (April 2013). "Transgender terminology: It's complicated". Vol 44, No. 4: American Psychological Association. p. 39. Retrieved 2013-09-17.
Use whatever name and gender pronoun the person prefers
- Sponsored by the American Medical Association and The Fenway Health with unrestricted support from Fenway Health and Pfizer. "Meeting the Health Care Needs of Lesbian, Gay, Bisexual, and Transgender (LGBT) People: The End to LGBT Invisibility" (PowerPoint Presentation). The Fenway Institute. p. 24. Retrieved 2013-09-17.
Use the pronoun that matches the person’s gender identity
- "Glossary of Gender and Transgender Terms" (PDF). Preface: Fenway Health. January 2010. p. 2. Retrieved 2013-09-17.
listen to your clients – what terms do they use to describe themselves
- "Therapists with Lesbian, Gay, Bisexual, and Transgender Clients" (Word Document). Association for Behavioral and Cognitive Therapies. 2010. p. 2. Retrieved 2013-09-17.
transsexuals prefer to be referred to using the pronoun of identified gender, regardless of their level of transition[dead link]
- Elizondo, Paul M. III, D.O.; Wilkinson, Willy, M.P.H.; Daley, Christopher, M.D. (6 September 2012). "Working With Transgender Persons". Phychiatric Times. Retrieved 2013-09-17.
If you are not sure which pronoun to use, you can ask the patient
- "Competencies for Counseling with Transgender Clients" (PDF). Association for Lesbian, Gay, Bisexual, and Transgender Issues in Counseling. 18 September 2009. p. 3.
honor the set of pronouns that clients select and use them throughout the counseling process
- "AP editors’ note on Manning". Associated Press. 22 August 2013. Retrieved 2013-09-17.
Use the pronoun preferred by the individuals who have acquired the physical characteristics of the opposite sex or present themselves in a way that does not correspond with their sex at birth.
- Division of Public Affairs (September 2011). "Style Guide". Vanderbilt University. p. 34. Retrieved 2013-09-17.
Use the pronoun preferred by the individuals who have acquired the physical characteristics of the opposite sex or present themselves in a way that does not correspond with their sex at birth.
- "Frequently Asked Questions on Trans Identity". Common Ground – Trans Etiquette. University of Richmond. Retrieved 2013-09-17.
be considerate of one’s gender identity by using the pronouns of the respective gender pronouns, or gender-‐neutral pronouns, they use
- "Journalists: Commit to Fair and Accurate Coverage of Transgender People, including Pvt. Chelsea Manning". Transgender Law Center. 2013. Retrieved 2013-09-17.
Avoid pronoun confusion when examining the stories and backgrounds of transgender people prior to their transition.
- "NAMES, PRONOUN USAGE & DESCRIPTIONS" (PDF). GLAAD Media Reference Guide. GLAAD. May 2010. p. 11. Retrieved 2013-09-17.
It is usually best to report on transgender people's stories from the present day instead of narrating them from some point or multiple points in the past, thus avoiding confusion and potentially disrespectful use of incorrect pronouns.
- "Transgender FAQ". Resources. Human Rights Campaign. Retrieved 2013-09-17.
should be identified with their preferred pronoun
- APA task force (1994) "...There must be evidence of a strong and persistent cross-gender identification, which is the desire to be, or the insistence that one is of the other sex..." in DSM-IV: Sections 302.6 and 302.85 published by the American Psychiatric Association. Retrieved via Mental Health Matters on 2007-04-08.
- World Health Organisation (1992) "...The desire to live and be accepted as a member of the opposite sex..." in ICD-10, Gender Identity Disorder, category F64.0 published by the World Health Organisation. Retrieved on 2007-04-09.
- Author and date unknown. "... For some, maintaining a link to their transness or their otherly-gendered past is highly significant, while for others, they view themselves as no longer trans, but now fully as a man or woman..." Post transition identification as a man or ftm or other[dead link] from FORGE (For Ourselves: Reworking Gender Expression), an American education, advocacy and support umbrella organization supporting FTMs and others. Retrieved 2007-04-03.
- E. D. Hirsch, Jr., E.D., Kett, J.F., Trefil, J. (2002) "Transvestite: Someone who dresses in the clothes usually worn by the opposite sex." in Definition of the word "transvestite" from The New Dictionary of Cultural Literacy, Third Edition[dead link]. Retrieved on 2007-08-13.
- various (2006) "trans·ves·tite...(plural trans·ves·tites), noun. Definition: somebody who dresses like opposite sex:" in Definition of the word "transvestite" from the Encarta World English Dictionary (North American Edition). Retrieved on 2007-08-13.
- Raj, R (2002) "transvestite (TV): n. Synonym: crossdresser (CD):" in Towards a Transpositive Therapeutic Model: Developing Clinical Sensitivity and Cultural Competence in the Effective Support of Transsexual and Transgendered Clients[dead link] from the International Journal of Transgenderism 6,2. Retrieved on 2007-08-13.
- Hall, B. et al. (2007) "...Many say this term (crossdresser) is preferable to transvestite, which means the same thing..." and "...transvestite (TV) - same as cross-dresser. Most feel cross-dresser is the preferred term..." in Discussion Paper: Toward a Commission Policy on Gender Identity from the Ontario Human Rights Commission Retrieved on 2007-08-13.
- Green, E., Peterson, E.N. (2006) "...The preferred term is 'cross-dresser', but the term 'transvestite' is still used in a positive sense in England..." in LGBTTSQI Terminology from Trans-Academics.org Retrieved on 2007-08-13.
- Swartz, Jacqueline (1999) "Professor in drag" in Ivory Tower[dead link] from Salon.com. Retrieved on 2007-10-09.
- Gilbert, Michael ‘Miqqi Alicia’ (2000) "The Transgendered Philosopher" in Special Issue on What is Transgender?[dead link] from The International Journal of Transgenderism, Special Issue July 2000[dead link]. Retrieved on 2007-10-09.
- Docter, Richard F., Prince, Virginia (1997). Transvestism: A survey of 1032 cross-dressers. Archives of Sexual Behavior 26(6), 589-605.
- World Health Organisation (1992) "...Fetishistic transvestism is distinguished from transsexual transvestism by its clear association with sexual arousal and the strong desire to remove the clothing once orgasm occurs and sexual arousal declines...." in ICD-10, Gender Identity Disorder, category F65.1 published by the World Health Organisation. Retrieved on 2007-08-13.
- APA task force (1994) "...The paraphiliac focus of Transvestic Fetishism involves cross-dressing. Usually the male with Transvestic Fetishism keeps a collection of female clothes that he intermittently uses to cross-dress. While cross dressed, he usually masturbates..." in DSM-IV: Sections 302.3 published by the American Psychiatric Association. Retrieved on 2007-08-13.
- Wilchins, Riki Anne (2002) ‘It’s Your Gender, Stupid’, pp.23-32 in Joan Nestle, Clare Howell and Riki Wilchins (eds.) Genderqueer: Voices from Beyond the Sexual Binary. Los Angeles:Alyson Publications, 2002.
- Nestle, J. (2002) "...pluralistic challenges to the male/female, woman/man, gay/straight, butch/femme constructions and identities..." from Genders on My Mind, pp.3-10 in Genderqueer: Voices from Beyond the Sexual Binary, edited by Joan Nestle, Clare Howell and Riki Wilchins, published by Los Angeles:Alyson Publications, 2002:9. Retrieved on 2007-04-07.
- Hale, J.C. (1998) "...[O]ur embodiments and our subjectivities are abjected from social ontology: we cannot fit ourselves into extant categories without denying, eliding, erasing, or otherwise abjecting personally significant aspects of ourselves ... When we choose to live with and in our dislocatedness, fractured from social ontology, we choose to forgo intelligibility: lost in language and in social life, we become virtually unintelligible, even to ourselves..." from Consuming the Living, Dis(Re)Membering the Dead in the Butch/FtM Borderlands in the Gay and Lesbian Quarterly 4:311, 336 (1998). Retrieved on 2007-04-07.
- androgyne. (n.d.). Merriam-Webster's Medical Dictionary. Retrieved 2008-04-07, from Dictionary.com website: http://dictionary.reference.com/browse/androgyne
- Is 'Tranny' Offensive? | The Bilerico Project
- Answers to Your Questions About Transgender Individuals and Gender Identity report from the website of the American Psychological Association - "What is the relationship between transgender and sexual orientation?"
- Tobin, H.J. (2003) "...It has become more and more clear that trans people come in more or less the same variety of sexual orientations as non-trans people..." Sexual Orientation from Sexuality in Transsexual and Transgender Individuals.
- Blanchard, R. (1989) The classification and labeling of nonhomosexual gender dysphorias from Archives of Sexual Behavior, Volume 18, Number 4, August 1989. Retrieved via SpringerLink on 2007-04-06.
- APA task force (1994) "...For sexually mature individuals, the following specifiers may be noted based on the individual’s sexual orientation: Sexually Attracted to Males, Sexually Attracted to Females, Sexually Attracted to Both, and Sexually Attracted to Neither..." in DSM-IV: Sections 302.6 and 302.85 published by the American Psychiatric Association. Retrieved via Mental Health Matters on 2007-04-06.
- Goethals, S.C. and Schwiebert, V.L. (2005) "...counselors to rethink their assumptions regarding gender, sexuality and sexual orientation. In addition, they supported counselors' need to adopt a transpositive disposition to counseling and to actively advocate for transgendered persons..." Counseling as a Critique of Gender: On the Ethics of Counseling Transgendered Clients from the International Journal for the Advancement of Counselling, Vol. 27, No. 3, September 2005. Retrieved via SpringerLink on 2007-04-06.
- Hines, Sally. TransForming gender: transgender practices of identity, intimacy and care. The Policy Press, 2007.
- Raymond, Janice G. (1980) The Transsexual Empire Women's Press, London, ISBN 0-7043-3857-2 (Pbk)
- Brown, M.L. & Rounsley, C.A. (1996) True Selves: Understanding Transsexualism - For Families, Friends, Coworkers, and Helping Professionals Jossey-Bass: San Francisco ISBN 0-7879-6702-5
- Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (1994)
- Answers to Your Questions About Transgender Individuals and Gender Identity report from the website of the American Psychological Association - "Is being transgender a mental disorder?"
- Carroll, L.; Gilroy, P.J.; Ryan, J. (2002). "Transgender issues in counselor education". Counselor Education and Supervision 41 (3): 233–242. doi:10.1002/j.1556-6978.2002.tb01286.x.
- Benson, H.E. (2013). "Seeking support: Transgender client experiences with mental health services". Journal of Feminist Family Therapy 25: 17–40. doi:10.1080/0895833.2013.755081.
- "Standards of care for the health of transsexual, transgender, and gender nonconforming people—7th version". The World Professional Association for Transgender Health. Retrieved 30 November 2014.
- Hanssmann, C.; Morrison, D.; Russian, E. (2008). "Talking, gawking, or getting it done: Providing trainings to increase cultural and clinical competence for transgender and gender-nonconforming patients and clients". Sexuality Research and Social Policy 5: 5–23. doi:10.1525/srsp.2008.5.1.5.
- Newsroom | APA DSM-5
- Gender Identity Disorder Reform
- eZ systems. "France: Transsexualism will no longer be classified as a mental illness in France". ilga.org.
- "Le transsexualisme n'est plus une maladie mentale en France". Le Monde.fr.
- Pfäfflin F., Junge A. (1998) "...This critique for the use of the term sex change in connection to sex reassignment surgery stems from the concern about the patient, to take the patient seriously...." in Sex Reassignment: Thirty Years of International Follow-Up Studies: A Comprehensive Review, 1961–1991[dead link] from the Electronic Book Collection[dead link] of the International Journal of Transgenderism[dead link]. Retrieved on 2007-09-06.
- APA task force (1994) "...preoccupation with getting rid of primary and secondary sex characteristics..." in DSM-IV: Sections 302.6 and 302.85 published by the American Psychiatric Association. Retrieved via Mental Health Matters on 2007-04-06.
- Committee on Health Care for Underserved Women (December 2011). "Health Care for Transgender Individuals: Committee Opinion No. 512". Obstetrics and Gynecology 118. American Committee for Obstetrics and Gynecology. pp. 1454–1458. PMID 22105293.
- Currah, Paisley; M. Juang, Richard; Minter, Shannon Price (eds.) (2006). Transgender Rights. Minnesota University Press. pp. 51–73. ISBN 0-8166-4312-1
- Whittle, Stephen. "Respect and Equality: Transsexual and Transgender Rights." Routledge-Cavendish, 2002.
- Gay and Lesbian Alliance Against Defamation. "Groundbreaking Report Reflects Persistent Discrimination Against Transgender Community", ‘’GLAAD’’, USA, February 4, 2011. Retrieved on 2011-02-24.
- Gay and Lesbian Alliance Against Defamation. "IN THE LIFE Follows LGBT Seniors as They Face Inequality in Healthcare", "GLAAD", USA, November 3, 2010. Retrieved on 2011-02-24.
- [dead link]
- Ibbitson, John (2011-02-10). "Transgendered-rights bill headed for defeat in Tory-held Senate". The Globe and Mail (Toronto).
- Gay and Lesbian Alliance Against Defamation. "LGBT Advocates Call for Action on ENDA", "GLAAD Blog", USA, May 2010. Retrieved on 2011-02-24.
- Gay and Lesbian Alliance Against Defamation. "Governor David Paterson Signs New York’s First Bill Ensuring Transgender Protections", "GLAAD Blog", USA, September 2010. Retrieved on 2011-02-24.
- Daniel June (13 June 2013). "Transgender Girl in Maine Seeks Supreme Court’s Approval to Use School’s Girls Room - JD Journal". JD Journal.
- "India recognises transgender people as third gender". The Guardian. 15 April 2014. Retrieved 15 April 2014.
- McCoy, Terrence (15 April 2014). "India now recognizes transgender citizens as ‘third gender’". Washington Post. Retrieved 15 April 2014.
- "Supreme Court recognizes transgenders as 'third gender'". Times of India. 15 April 2014. Retrieved 15 April 2014.
- National Legal Services Authority ... Petitioner Versus Union of India and others ... Respondents (Supreme Court of India 15 April 2014). Text
- Cooper, Helene. "Hagel ‘Open’ to Reviewing Military’s Ban on Transgender People". newspaper article. New York Times. Retrieved May 13, 2014.
- Whitehead, James D. and Evelyn Eaton. [<http://ncronline.org/news/people/epiphany-transgender-lives-reveals-diversity-body-christ> "An epiphany of transgender lives reveals diversity in body of Christ"]. article. National Catholic Reporter. Retrieved May 13, 2014.
- DeBernardo, Francis. "A Catholic Introduction to Transgender Issues". weblog. New Ways Ministry. Retrieved May 13, 2014.
- Gizewski, E. R., Krause, E., Schlamann, M., Happich, F., Ladd, M. E., Forsting, M., & Senf, W. (2009). Specific cerebral activation due to visual erotic stimuli in male-to-female transsexuals compared with male and female controls: An fMRI study. Journal of Sexual Medicine, 6, 440–448.
- Rametti, G., Carrillo, B., Gómez-Gil, E., Junque, C., Zubiarre-Elorza, L., Segovia, S., Gomez, Á. & Guillamon, A., (2010). The microstructure of white matter in male to female transsexuals before cross-sex hormonal treatment: A DTI study. Journal of Psychiatric Research. doi:10.1016/j.jpsychires.2010.11.007
- Savic, I., & Arver, S. (2011). Sex dimorphism of the brain in male-to-female transsexuals. Cerebral Cortex. doi:10.1093/cercor/bhr032
- H. Berglund, P. Lindström, C. Dhejne-Helmy & I. Savic (2008). Male-to-Female Transsexuals Show Sex-Atypical Hypothalamus Activation When Smelling Odorous Steroids. Cerebral Cortex. doi:10.1093/cercor/bhm216
- Lawrence, A. A. (2006). Clinical and theoretical parallels between desire for limb amputation and gender identity disorder. Archives of Sexual Behavior, 25, 263–278.
- McCloskey, D. (2003) "...The academics don't like Bailey's use of the mantle of Science to push a conservative, unscientific agenda worthy of National Review, or of The National Enquirer..." in Queer Science: A data-bending psychologist confirms what he already knew about gays and transsexuals from Reason, a libertarian magazine covering politics, culture, and ideas. Retrieved on 2007-09-22.
- Marks, J. (2004). "...The specific issue was whether the book (The Man Who Would Be Queen) was transphobic...The judges looked at the book more closely and decided it was..." quoted by Letellier, P (2004) in Group rescinds honor for disputed book from Advocate Online News on Gay.com, retrieved on 2007-09-11.
- Emory, L. E., Williams, D. H., Cole, C. M., Amparo, E. G., & Meyer, W. J. (1991). Anatomic variation of the corpus callosum in persons with gender dysphoria. Archives of Sexual Behavior, 20, 409-417.
- Zhou, J. N., Hofman, M. A., Gooren, L. J. G., & Swaab, D. F. (1995). A sex difference in the human brain and its relation to transsexuality. Nature, 378, 6552, 68–70.
- Kruijver, F.P., Zhou, J. N., Pool, C. W., Hofman, M. A., Gooren, L. J., & Swaab, D. F. (2000). Male-to-female transsexuals have female neuron numbers in a limbic nucleus.[dead link] Journal of Clinical Endocrinology Metabolism, 85, 2034–2041.
- Chung. W., De Vries, G., & Swaab, D. (2002). Sexual differentiation of the bed nucleus of the stria terminalis in humans may extend into adulthood. Journal of Neuroscience, 22, 1027–1033.
- Schiltz, K., Witzel, J., Northoff, G., Zierhut, K., Gubka, U., Fellman, H., Kaufmann, J., Tempelmann, C., Wiebking, C., & Bogerts, B. (2007). Brain pathology in pedophilic offenders: Evidence of volume reduction in the right amygdala and related diencephalic structures. Archives of General Psychiatry, 64, 737–746.
- Hulshoff Pol, H. E., Cohen-Kettenis, P. T., Van Haren, N. E., Peper, J. S., Brans, R. G., Cahn, W., et al. (2006). Changing your sex changes your brain: Influences of testosterone and estrogen on adult human brain structure. European Journal of Endocrinology, 155(Suppl. 1), S107-S114.
- Haraldsen, I. R., Opjordsmoen, S., Egeland, T., & Finset, A. (2003). Sex-sensitive performance in untreated patients with early onset gender identity disorder. Psychoneuroendocrinology, 28, 906–915.
- Wisniewski, A. B., Prendeville, M. T., & Dobs, A. S. (2005). Handedness, functional cerebral hemispheric lateralization, and cognition in male-to-female transsexuals receiving cross-sex hormone treatment. Archives of Sexual Behavior, 34, 167–172.
- Luders, E., Sanchez, F. J., Toga, A. W., Narr, K. L., Hamilton, L. S., & Vilain, E. (2009). Regional gray matter variation in male-to-female transsexualism. Neuroimage, 46, 904-907.
- Rametti, G., Carrillo, B., Gómez-Gil, E., Junque, C., Zubiarre-Elorza, L., Segovia, S., Gomez, Á, & Guillamon, A. (2011). White matter microstructure in female to male transsexuals before cross-sex hormonal treatment. A diffusion tensor imaging study. Journal of Psychiatric Research, 45, 199-204. doi:10.1016/j.jpsychires.2010.05.006
- Nawata, H., Ogomori, K., Tanaka, M., Nishimura, R., Urashima, H., Yano, R., Takano, K., & Kuwabara, Y. (2010). Regional cerebral blook flow changes in female to male gender identity disorder. Psychiatry and Clinical Neurosciences, 64, 157–161.
- LeVay S (August 1991). "A difference in hypothalamic structure between heterosexual and homosexual men". Science 253 (5023): 1034–7. doi:10.1126/science.1887219. PMID 1887219.
- Byne W, Tobet S, Mattiace LA, et al. (September 2001). "The interstitial nuclei of the human anterior hypothalamus: an investigation of variation with sex, sexual orientation, and HIV status". Horm Behav 40 (2): 86–92. doi:10.1006/hbeh.2001.1680. PMID 11534967.
- Eyal Abraham, Talma Hendler, Irit Shapira-Lichter, Yaniv Kanat-Maymon, Orna Zagoory-Sharon, and Ruth Feldman (May 2014). "Father's brain is sensitive to childcare experiences". Proceedings of the National Academy of Sciences 111 (27): 9792–9797. doi:10.1073/pnas.1402569111.
- "Transsexual study reveals genetic link". abc.net.au.
- Hare L, Bernard P, Sánchez FJ, Baird PN, Vilain E, Kennedy T, Harley VR (2009) Androgen receptor repeat length polymorphism associated with male-to-female transsexualism. Biol Psychiatry. 65(1):93-96
- Benjamin H (1966). The Transsexual Phenomenon. The Julian Press ASIN: B0007HXA76 (via Internet Archive)
- Bagemihl B. Surrogate phonology and transsexual faggotry: A linguistic analogy for uncoupling sexual orientation from gender identity. In Queerly Phrased: Language, Gender, and Sexuality. Anna Livia, Kira Hall (eds.) pp. 380 ff. Oxford University Press ISBN 0-19-510471-4
- Leavitt F, Berger JC (1990). Clinical patterns among male transsexual candidates with erotic interest in males. Archives of Sexual Behavior, full text Volume 19, Number 5 / October, 1990
- Morgan AJ Jr (1978). Psychotherapy for transsexual candidates screened out of surgery. Archives of Sexual Behavior. 7: 273-282.|
- Wahng SJ (2004). Double Cross: Transamasculinity Asian American Gendering in Trappings of Transhood. in Aldama AJ (ed.) Violence and the Body: Race, Gender, and the State. Indiana University Press. ISBN 0-253-34171-X
- Leiblum SR, Rosen RC (2000). Principles and Practice of Sex Therapy, Third Edition. ISBN 1-57230-574-6, Guilford Press of New York, c2000.
- Bancroft, John (2008). "Lust or Identity?". Archives of Sexual Behavior (Springer) 37 (3): 426–428. doi:10.1007/s10508-008-9317-1. PMID 18431640. Retrieved January 2009.
- Moser, Charles (July 2010). "Blanchard's Autogynephilia Theory: A Critique". Journal of Homosexuality (6 ed.) 57 (6): 790–809. doi:10.1080/00918369.2010.486241. PMID 20582803.
- Langevin R (1982). Sexual Strands: Understanding and Treating Sexual Anomalies in Men. Routledge, ISBN 978-0-89859-205-4
- Wegener ST (1984). Male sexual anomalies: the data (review of Sexual Strands) APA Review of Books: Volume 29, Issues 7-12, p. 783. Edwin Garrigues Boring, American Psychological Association
- Aggrawal, Anil (2008). Forensic and medico-legal aspects of sexual crimes and unusual sexual practices. CRC Press, ISBN 978-1-4200-4308-2
- Heath RA (2006). The Praeger handbook of transsexuality: Changing gender to match mindset. Greenwood Publishing Group, ISBN 978-0-275-99176-0
- Boyd H (2007). She's not the man I married: My life with a transgender husband, p. 102. Seal Press, ISBN 978-1-58005-193-4
- Jordan-Young RM (2010). Brain storm: the flaws in the science of sex differences. Harvard University Press, ISBN 978-0-674-05730-2
- Bailey, J. M. (2003). The Man Who Would Be Queen: The Science of Gender-Bending and Transsexualism. Joseph Henry Press, ISBN 0-309-08418-0, ISBN 978-0-309-08418-5
- Blanchard, R. (2005) "...Since the beginning of the last century, clinical observers have described the propensity of certain males to be erotically aroused by the thought or image of themselves as women..." in Early History of the Concept of Autogynephilia from the Archives of Sexual Behavior, Volume 34, Number 4, pages 439-446. Retrieved on 2007-09-22.
- Smith, Y.L.S., van Goozen, S.H.M., Kuiper, A.J., Cohen-Kettenis, P.T.. (2005) "...The present study was designed to investigate whether transsexuals can be validly subdivided into subtypes on the basis of sexual orientation..." in Transsexual subtypes: Clinical and theoretical significance from Psychiatry Research, Volume 137, Issue 3, pages 151-160. Retrieved on 2007-09-22.
- Serano, Julia (2007). Whipping girl: a transsexual woman on sexism and the scapegoating of femininity. Seal Press. p. 178. ISBN 978-1-58005-154-5.
While Blanchard's controversial theory is built upon a number of incorrect and unfounded assumptions, and there are many methodological flaws in the data he offers to support it, it has garnered some acceptance in the psychiatric literature...
- Moser, Charles (2010). "Blanchard's Autogynephilia Theory: A Critique". Journal of Homosexuality 57 (6): 790–809. doi:10.1080/00918369.2010.486241. PMID 20582803.
- Veale, Jaimie F.; Clarke, Dave E.; Lomax, Terri C. (2008). "Sexuality of Male-to-Female Transsexuals". Archives of Sexual Behavior 37 (4): 586–597. doi:10.1007/s10508-007-9306-9. PMID 18299976.
- Moser, Charles (2009). "Autogynephilia in Women". Journal of Homosexuality 56 (5): 539–547. doi:10.1080/00918360903005212. PMID 19591032.
- Nuttbrock, L; Bockting, W; Mason, M; Hwahng, S; Rosenblum, A; Macri, M; Becker, J (2010). "A Further Assessment of Blanchard's Typology of Homosexual Versus Non-Homosexual or Autogynephilic Gender Dysphoria". Archives of Sexual Behavior 40 (2): 247–257. doi:10.1007/s10508-009-9579-2. PMC 2894986. PMID 20039113.
- from DSM5.org rationale bullet 18. bullet 18 under rationale
- A nova geração gay nas Universidades dos EUA (Portuguese)
- Doussantousse, S. (2005) "...The Lao Kathoey’s characteristics appear to be similar to other transgenders in the region..." in Male Sexual Health: Kathoeys in the Lao PDR, South East Asia - Exploring a gender minority from the Transgender ASIA Research Centre. Retrieved on 2007-07-22.
- Jackson, P. (2003) Performative Genders, Perverse Desires: A Bio-History of Thailand's Same-Sex and Transgender Cultures in Intersections: Gender, History and Culture in the Asian Context, Issue 9, August 2003.
- Winter, S. and Udomsak, N. (2002) Male, Female and Transgender: Stereotypes and Self in Thailand[dead link] in the International Journal of Transgender, Volume 6, Number 1, January - March 2002.
- Author unknown, (2003) Human Rights Violations against the Transgender Community: A study of kothi and hijra sex workers in Bangalore, India, full text,summary, by the Peoples’ Union for Civil Liberties, Karnataka (PUCL-K), September 2003. Retrieved on 2007-04-07.
- Harrison, F. (2005) "...He shows me the book in Arabic in which, 41 years ago, Ayatollah Khomeini wrote about new medical issues like transsexuality. "I believe he was the first Islamic scientist in the world of Islam who raised the issue of sex change," says Hojatulislam Kariminia. The Ayatollah's ruling that sex-change operations were allowed has been reconfirmed by Iran's current spiritual leader..." in Iran's sex-change operations, from the BBC. Retrieved on 2007-07-22.
- Mitsuhashi, J. (2006) "...the male to female cross-dressing (MTFCD) community in Shinjuku, Tokyo, which plays an important role in the overall transgender world and how people in the community think and live..." in The transgender world in contemporary Japan: male to female cross-dressers, translated by Kasumi Hasegawa, from the Journal of Inter-Asia Cultural Studies, Vol. 7, No. 2. Retrieved on 2007-07-22.
- Haviland, C. (2005) "...The Gurung people of western Nepal have a tradition of men called maarunis, who dance in female clothes..." in Crossing sexual boundaries in Nepal, from the BBC. Retrieved on 2007-07-22.
- Graham, S. (2002) "...Among the Bugis of South Sulawesi, possibly four genders are acknowledged plus a fifth para-gender identity. In addition to male-men (oroane) and female-women (makunrai)..., there are calalai (masculine females), calabai (feminine males), and bissu..." in Priests and gender in South Sulawesi, Indonesia from the Transgender ASIA Research Centre. Retrieved on 2007-07-22.
- Walters, I. (2006) "...In Vietnam, male to female (MtF) transgender people are categorised as lai cai, bong cai, bong lai cai, dong co, or be-de..." in Vietnam Some notes by Ian Walters from the Transgender ASIA Research Centre. Retrieved on 2007-07-22.
- Shim, S. (2006) "...Rush, catering especially to crossdressers and transgenders, is a cafe owned by a 46-year-old man who goes by the female name Lee Cho-rong. "...Many people in South Korea don't really understand the difference between gay and transgender. I'm not gay. I was born a man but eager to live as a woman and be beautiful," said Lee..." in S. Korea in dilemma over transgender citizens right to choose from the Yonhap News Agency. Retrieved on 2007-07-22.
- Heng, R. (2005) "...Even if we take Bugis Street as a starting point, we should remember that cross-dressing did not emerge suddenly out of nowhere. Across Asia, there is a tradition of cross-dressing and other forms of transgender behaviour in many places with a rich local lexicon and rituals associated with them...." in Where queens ruled! - a history of gay venues in Singapore from IndigNation. Retrieved on 2007-07-22.
- Emerton, R. (2006) "...Hong Kong's transgender movement at its current stage, with particular reference to the objectives and activities of the Hong Kong Transgender Equality and Acceptance Movement..." in Finding a voice, fighting for rights: the emergence of the transgender movement in Hong Kong, from the Journal of Inter-Asia Cultural Studies, Vol. 7, No. 2. Retrieved on 2007-07-22.
- Hung, L. (2007) "...there are many archetypal flamboyant embodiments of female-to-male transgender physicality living and displaying their unrestrained, dashing iconic presence..." in Trans-Boy Fashion, or How to Tailor-Make a King[dead link] from the Gender Studies programme of The Chinese University of Hong Kong[dead link]. Retrieved on 2007-07-22.
- Ho, J. (2006) "...specificities of Taiwanese transgender existence in relation to body- and subject-formations, in hope to not only shed light on the actualities of trans efforts toward self-fashioning, but also illuminate the increasing entanglement between trans self-construction and the evolving gender culture that saturates it..." in Embodying gender: transgender body/subject formations in Taiwan, from the Journal of Inter-Asia Cultural Studies, Vol. 7, No. 2. Retrieved on 2007-07-22.
- Hahn, L. (2005) "...Aware that he often felt more like a woman than a man, Jin Xing underwent a sex change in 1995; a daring move in a conservative Chinese society..." in Jin Xing TalkAsia Interview Transcript - June 13, 2005 from CNN. Retrieved on 2007-07-22.
- Wang, Z. and Xie, F. (2006) "...While it is true that not everyone turns into a drag queen when they are feeling stressed out, many young people do seem to be caught up in the fad of androgyny..." in Cross-dressers captivate people across China from China Daily. Retrieved on 2007-07-22.
- Goldkorn, J. (2006) "...At one point in 2003, there was so much media coverage of transsexuals in China that Danwei started a special section for it..." in Transsexuals in the Chinese media again from Danwei. Retrieved on 2007-07-22.
- "Transgenders are the 'third gender', rules Supreme Court". NDTV. April 15, 2014. Retrieved April 15, 2014.
- "First transgender mayor elected in central India". January 5, 2015. Retrieved January 7, 2015.
- Fulton, R. and Anderson, S.W. (1992) The Amerindian "Man-Woman": Gender, Liminality, and Cultural Continuity in Current Anthropology: Vol. 33, No. 5, December 1992 pp. 603–610.
- Parsons, E.P. (1916) "...of these 'men-women'..." from Zuñi Ła'mana in the American Anthropologist, New Series, Vol. 18, No. 4. (Oct - Dec., 1916), pp. 521–528. Retrieved on 2007-05-21.
- Schützer, M.A.N. (1994) Winyanktehca: Two-souls person, a paper presented to the European Network of Professionals in Transsexualism, August 1994
- Parker, H.N. (2001) The myth of the heterosexual: anthropology and sexuality for classicists, from Arethusa 0004-0975, vol 34, p:313, 2001.
- Stryker, S. Berdache, from the GLBTQ: an encyclopedia of gay, lesbian, bisexual, transgender and queer culture.
- Medicine, B. (2002) Directions in Gender Research in American Indian Societies: Two Spirits and Other Categories, taken from Online Readings in Psychology and Culture Center for Cross-Cultural Research, Unit 3, Chapter 2, Western Washington University.
- Stephen, L (2002) Sexualities and Genders in Zapotec Oaxaca, Latin American Perspectives, Vol. 29, No. 2, pp. 41–59. Mar., 2002.
- Partial Translation of the Sunan Abu-Dawud, Book 41, Number 4910[dead link], USC-MSA Compendium of Muslim Texts, University of Southern California, translated by Prof. Ahmad Hasan.
- Rowsen, E.K. (1991) "...They played an important role in the development of Arabic music in Umayyad Mecca and, especially, Medina, where they were numbered among the most celebrated singers and instrumentalists..." from The Effeminates of Early Medina in the Journal of the American Oriental Society 111 (1991), pp. 671–93. Retrieved on 2007-04-07.
- Tillyard, E.M.W. (1917), A Cybele Altar in London, The Journal of Roman Studies, Vol. 7 (1917), pp. 284–288.
- Endres, N. Galli: Ancient Roman Priests from the GLBTQ: an encyclopedia of gay, lesbian, bisexual, transgender and queer culture.
- Brown, K. 20th Century Transgender History And Experience[dead link]
- Code of Hammurabi § 178 and following, and § 184 and following.
- Gay and Lesbian Alliance Against Defamation. , "GLAAD", USA, February 4, 2011. Retrieved on 2011-02-24.
- Gay and Lesbian Alliance Against Defamation. "Violence Toward Members of the Transgender Community"[dead link], "GLAAD", USA. Retrieved on 2011-02-25.
- Gay and Lesbian Alliance Against Defamation. "Sassafras Lowrey’s Kicked Out Anthology Shares Stories of LGBTQ Youth Homelessness", "GLAAD", USA, February 25, 2010. Retrieved 2011-02-25.
- "Coming Out to Family as Transgender". Human Rights Campaign. Retrieved 5 December 2010
- Bettcher, Talia Mae; Lombardi, Emilia (2005). "Lesbian, Gay, Bisexual, and Transgender/Transsexual Individuals". In Levy, Barry; Sidel, Victor. Social Injustice and Public Health. Oxford University Press.
- Sellers, Mitchell D. (2011). "Discrimination and the Transgender Population: A Description of Local Government Policies that Protect Gender Identity or Expression". Applied Research Projects. Texas State University-San Marcos. | <urn:uuid:7cbdb85e-5943-487b-9732-16289faeacce> | {
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What do we mean by newborns and stillbirths?
In this step we’ll outline and describe some of the terminology used throughout this week as there are distinct classifications that it’s important to get right.
Defining newborns and stillbirths
A baby in its first 28 days of life is referred to as a newborn. When a baby dies during the first 27 completed days after birth, it is referred to as a neonatal death.
A fetal death or stillbirth is defined as a baby born with no signs of life at or after 28 weeks’ gestation. The definition is taken from the International Classification of Diseases (ICD-10)1 which also provides thresholds to classify a stillbirth as either a late fetal death, early fetal death, or a miscarriage.
Figure 1 demonstrates the timeline for pregnancies, including definitions of the type of death by the stage at which they occur.
Problems with classification
If a baby is born alive and they show any sign of life before they die, they should be classed as a neonatal death, given a death certificate and included in national data systems. However, there is variation in the application of stillbirth definitions, especially in high income countries. Sometimes, and especially in settings without basic newborn care where the baby is not assessed properly to see if they are breathing or to check for a heartbeat, then a live birth may be misclassified as a stillbirth.
Preterm birth, small gestational age and low birthweight
The highest risks of death in utero, in the neonatal period, and throughout infancy and early childhood, are for small babies. Being born small is either due to being born preterm (‘Born Too Soon’), being born small for gestational age (SGA; ‘Born Too Small’) or a combination of the two.
Preterm birth is defined as before 37 completed weeks (see Figure 1). This is simplistic, and there are steep increases in risk of death at lower gestational ages and some up to 39 weeks so this cut-off may be debated.
Small for gestational age (SGA), defined as below the 10th centile for sex-specific, gestation-specific standards, depends on the standard used. Estimates were previously based on a US growth standard, but an international standard has now been provided by the InterGrowth study.3
Traditionally, low birthweight (<2500g) (LBW) has been used as a marker of small babies at highest risk of mortality and morbidity during the neonatal period and infancy, as well as of long-term developmental and physical health consequences, including effects on growth, insulin resistance and cardiovascular health. With around 20 million (15%) of all newborns worldwide born with a low birthweight each year, this group represents a substantial burden. The <2500g LBW cut-off is also simplistic due to risk being aligned to birth size and gestational age especially. More detailed studies are critical for understanding and reducing the burden. Unfortunately, in the highest burden settings, less than half of babies are weighed at birth, and fewer have accurate gestational age dating to delineate preterm and SGA. Whilst considerable progress has recently been made for estimating the burden of preterm and SGA, much remains to be done to improve the input data.
Stillbirths in your country
The definition used for stillbirths in some countries varies from the WHO standard of >1000 grams or >28 weeks gestation. What definition for stillbirth is used in your country? Are the data publicly available or hard to find? How would you describe attention for stillbirths in your country?
© London School of Hygiene & Tropical Medicine | <urn:uuid:7091e911-e572-4e5b-83e2-4169a84c2b0c> | {
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Chronic Kidney Disease and the Ways to Keep Your Kidney Healthy
Kidney has an important role in the body. It is responsible for filtering excess fluids and waste products from our blood and eliminated in the urine. The chronic kidney disease is progressive loss in the kidney function over a period of months or even years. ICD-10 code for chronic kidney disease is N18. You may have known the term of ICD already. It is the global health information standard that is used in clinical care and research to define diseases as well as chronic kidney. The ICD-10 code for chronic kidney disease is listed in Section C15-C26.
This disease occurs due to many factors such as diabetes and high blood pressure. It can also be caused by kidney infection or inflammation, congenital kidney diseases, obstruction of the urinary tract and autoimmune disorders. Then, you are at a higher risk of chronic kidney disease if you are a smoker and drinker. In addition, if you are obese, have diabetes or heart disease.
Early symptoms of this disease that you may notice are nausea, vomiting, loss of appetite, itching, chest pain, uncontrollable high blood pressure or unexpected weight loss. Later-stage symptoms include difficulty staying alert, weakness, numbness, fatigue, bad breath, cramps, bone pain, hiccups, swollen feet and ankles, and shortness of breath. Having a chronic kidney disease is awfully scary, isn’t it? So, it is important to keep your kidney healthy before any problem occurs. Here are several things you can do.
- Eat healthy foods. Foods are sources that will either help you or attack you. It is better if you consume super foods for your kidney such as apples, cauliflower, cabbage, cranberries, blueberries, fish and olive oil.
- Exercise regularly. Your healthy eating habit can be completed by exercising regularly. If you are having other health problems, be careful in choosing the kind of exercise.
- Quit smoking. One very bad habit that people commonly have is smoking. Smoking may damage blood vessels and it will decrease the flow of blood in your kidneys.
- Keep hydrate. Make sure that you drink enough water per day. The amount of water that people need is different between one and another based on several things. Make sure you know your amount and do not overdo it.
- Get regular kidney function screening. This point is for people who are at higher risk of chronic kidney. So, you must consult it with your doctor to check your kidney function regularly. | <urn:uuid:b2e6a4de-4999-4359-b4d3-f5230973f4fa> | {
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The patients with schizophrenia have higher mortality rates and shortened life span as compared to the general population.1,2 The literature reported that the major causes of this excess mortality are medical disease, unhealthy lifestyle, substance misuse, poor compliance or treatment refusal, and suicide among unnatural causes.3
This vulnerable group of patients does not receive the physical health care because of physical symptoms being misinterpreted as part of physical illness by professionals, lack of motivation, social isolation, poor social skills and cognitive impairment making them less likely to adhere to treatment.4 The peoples diagnosed with schizophrenia can expect to live 9-12 years fewer than those in the general population on average.5 Recent literature showed that men with schizophrenia die 20 years earlier and women die 15 years earlier than people without major mental illness.6 The common physical conditions found in patients with mental illness include diabetes, hyperlipidaemia, cardiovascular disease (hypertension, cardiac arrhythmias), obesity, malignant neoplasm, HIV/ AIDS, Hepatitis C, osteoporosis, hyperprolactinaemia and other physical illnesses.7 A study by Sokal et al reported greater odds of respiratory illnesses for persons with schizophrenia even after controlling for smoking and medical illnesses found to be more severe among them.8,9
Mortensen and Juel noted that some proportion of mortality in schizophrenia may be directly associated with side effects of neuroleptic medications.10 Several factors are known to increase the risk of medical disorders among mental illness. Among them are use of medications that contribute to weight gain, which is associated with diabetes and hypertension; poor attention to personal hygiene, which is associated with skin infections; high rates of smoking, which contributes to asthma, acute respiratory disease, heart disease, and lung cancer; reduced physical activity and fitness, which contributes to hypertension and heart disease; and use of medications with adverse gastrointestinal effects.9
Some variances associated with mental illness may remain unexplained. In our country, the study has not received much attention. Hence this study was undertaken to know the present scenario in the rural region.
The aims and objectives of the present study are as follows:
MATERIAL AND METHOD
Study design and sample
The cross-sectional study was conducted at Department of Psychiatry, Jawaharlal Nehru Medical College, Sawangi (M) Wardha, Maharashtra, India. The approval from Institutional ethics committee was obtained prior to the study. Total 100 patients diagnosed as schizophrenia as per International Classification of Diseases–10th revision of WHO (ICD-10) diagnostic criteria fulfilling the inclusion and exclusion criteria between Jan to Apr 2013 were included in the study. The majority of the physical illnesses were diagnosed by medical specialists within our hospital setup and documented in the medical records of the patients.
Patients in the age group of more than 18 and less than 55 years of age (due to increase risk of cognitive deficits in the patients).
Patients diagnosed to be suffering from Schizophrenia according to ICD 10 criteria.
Patients who were stable on medications since at least past three months.
Both inpatients and out patients.
A semi-structured proforma, designed for the study was used to collect the socio-demographic and clinical details. ICD-10 diagnostic criteria were used to validate the diagnosis of schizophrenia.
The patient and close relative were explained the nature of the study. The written consent obtained from the patient. The patient was then interviewed using the available tools. The relative was subsequently interviewed to obtain other relevant details along with previous medical records or documents. Whenever patient presented with any physical complaint he/she was referred to consultant physician at our Institute. The diagnosis and treatment given by physician was entered into the record. Those patients who were already having co-morbid physical illness were entered in proforma. Thus presences of medical co morbidities were assessed using family member report, patient self-report or previous medical records.
The sample consisted of 47 male and 53 female schizophrenia patients (Table 1). The mean age of onset of schizophrenia was 29.24 years (SD 13.07), mean duration of illness was 8.40 years (SD 8.60) and 93% patients had less than 20 years of duration of schizophrenia (Table 2). The result reported, 69% patients were exposed to psychotropic medications for less than 5 years while 23% were exposed for 6 to 10 years; 22.73% of patients had medical illness before onset of schizophrenia and 77.27% had developed medical illness after the onset of schizophrenia (Table 2). Among them medical illness worsened schizophrenia in 27.27% of patients (Table 2) and causes may include electrolyte disturbances such as hypocalcaemia, hyponatremia, hypernatremia, hypokalemia, hypomagnesemia; disorders causing the delirious state and endocrine disorders causing hormonal changes. It was found that schizophrenia patients who had higher age and exposure to psychotropic medications were significantly associated with medical co-morbidities (Table 3). The patients with schizophrenia developing medical illness were not significantly associated with duration of illness (Table 3). The co morbid medical illnesses were not associated with type of medication used, subtype of schizophrenia and family history of mental illness whereas reported significant association with history of substance use (Table 4). As shown in Figure 1, prevalence of medical co morbidities found to be 22%. The endocrine disorders were found to be highest (32%) followed by disorders of respiratory system (Figure 2). Figure 3 showed, 67% were exposed to atypical anti psychotics, 11% were exposed to typical anti psychotics while 22% were exposed to combination of both typical and atypical anti psychotic. Out of total patients, 78% were diagnosed as suffering from paranoid schizophrenia, 12% from undifferentiated schizophrenia, 3% from hebephrenic schizophrenia, 2% from catatonic schizophrenia and 5% from other types (Figure 4).
Schizophrenia has been described as a “life-shortening disease”. People with schizophrenia and other mental illnesses have high rates of preventable risk factors and physical co morbidity accounts for 60% of premature deaths.11 Koran et al estimated that 45% of patients in California’s public mental-health system had physical disease.12 A study by Koranyi et al of psychiatric clinic patients revealed that 43% of patients had physical illnesses.13 Hall et al found that 46% of patients admitted had an unrecognized physical illness that either caused or exacerbated their psychiatric illness.14 In our study we found 22% of medical co morbidity in schizophrenia patients. It is lower than that found in other studies. This disparity may be due to the fact that the present study setting was in rural area and low socio-economic strata, many people were not affording thorough medical investigations; bringing the percentage of medical co morbidity to lower levels.
A study by Holt and Pevler reported that diabetes occurred in 15% patients with schizophrenia lower as compared to present study.15
|Age (years)||Male (%)||Female (%)||Total (%)|
Increased risk in people with schizophrenia of developing glucose-regulation abnormalities, insulin resistance and type 2 diabetes mellitus found to be due to lifestyle factors (poor diet, sedentary behaviour); and all antipsychotic agents (atypical more than typical) increase the propensity to develop diabetes.16,17,18 People with severe mental illness have 2-3 times more risk for cardiovascular disorders than the general population. People with mental illness have higher rates of cardiovascular and respiratory disorders than the general population; antipsychotic agents contribute to metabolic syndrome X (hypertension, hyperlipidaemia, hyperglycaemia, insulin resistance and obesity); lifestyle factors (smoking, alcoholism, poor diet, and lack of exercise) contribute to increased risk of cardiac problems. Mortality due to ischaemic heart disease, cardiac arrhythmias and myocardial infarction is higher in people with mental illness.19,20,21,22 The present study reported prevalence of endocrinal abnormalities to be higher (31.82% especially diabetes mellitus type -2) than the cardiovascular morbidity at 9.09% and the patients who had higher age were associated with increased risk of physical illness. Our findings are consistent with a study conducted by Smith DJ et al who reported that people with schizophrenia had lower recorded rates of cardiovascular disease as compared to other physical health co morbidities.23 The variation as compared to other studies can be accounted to the fact of difference in sample demographics like variations in setting, as our study was on rural population.
It is a well-known fact that both typical and atypical antipsychotics though are main stay of treatment for schizophrenia, are also associated with their side effects. Gupta et al (2003) reported a prevalence rate of 30% for hypertension, 17% for diabetes and 43% for lipid abnormalities in 208 patients with psychotic disorders who were receiving anti-psychotic medications.24 Risk of metabolic syndrome also found to be higher in patients being treated with atypical antipsychotics. Heiskanen et al (2003) found that 37% of patients with schizophrenia receiving antipsychotic medications developed metabolic syndrome higher as compared to present study.25 Tarricone et al (2006) found that patients treated with atypical antipsychotics had higher mean glycaemia and triglyceridemia and a significantly higher risk of receiving a diagnosis of hyperglycemia and hypertriglyceridemia than the reference group.26 The above findings are consistent with the results reported in present study that patients who were exposed to psychotropic medications for longer periods of time, were more at risk of developing medical illness (majority of our patients i.e. 67% were being treated with atypical antipsychotics).
High alcohol use in schizophrenia is associated with more severe psychiatric symptoms and more disturbed behavior.27 Poor medication compliance, higher rates of re hospitalization and poor treatment response has been associated with comorbid drug abuse in schizophrenia.28,29 Smoking rates is found to be higher in schizophrenia subjects than in normal population.30 The present study also found that history of substance abuse in schizophrenia increased the risk of developing medical co-morbidities. This finding is in accordance with above mentioned studies.
Literature is limited for medical co-morbidity seen in different subtypes of schizophrenia as described in ICD-10. This study also did not find any difference in subtypes of schizophrenia and prevalence of medical co-morbidity. Similarly literature is very limited on prevalence of medical comorbidity in schizophrenia and its correlation with family history of mental illness. The present study found that having a family history of mental illness in patients with schizophrenia does not increase the likelihood of development of physical Illness.
The prevalence of medical co-morbidities was found to be lower than that in previous literature. As shown by this study schizophrenia patients reported co-morbid diabetes mellitus, C.O.P.D, hypertension, anaemia among many others. More the exposure to psychotropic mediations in term of duration increased the chances of developing medical illness. Sometimes the physical illnesses remain unrecognized in such patients so integrated approaches such as assessment of medical illness by physician and psychiatric diagnosis by psychiatrist require to prevent and treat the co-morbid disorders. Further research is needed to provide more insight into the risk factors and treatment modalities. | <urn:uuid:642c9f68-4fa7-4e28-ba7f-3536ca6c8050> | {
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Gender dysphoria(Redirected from Gender identity disorder)
Gender dysphoria (GD), or gender identity disorder (GID), is the distress a person experiences as a result of the sex and gender they were assigned at birth. In this case, the assigned sex and gender do not match the person's gender identity, and the person is transgender. There is evidence suggesting that twins who identify with a gender different from their assigned sex may do so not only due to psychological or behavioral causes, but also biological ones related to their genetics or exposure to hormones before birth.
|Synonyms||Gender identity disorder|
|Specialty||Psychiatry, psychology, psychotherapy|
|Symptoms||Distress related to one's assigned gender or sex|
|Complications||Eating disorders, suicide, depression, anxiety, social isolation|
|Differential diagnosis||Variance in gender identity or expression that isn't distressing|
|Medication||Hormones (e.g., androgens, antiandrogens, estrogens)|
GID was reclassified to gender dysphoria by the DSM-5. Some transgender people and researchers support declassification of GID because they say the diagnosis pathologizes gender variance, reinforces the binary model of gender, and can result in stigmatization of transgender individuals. The official reclassification as gender dysphoria in the DSM-5 may help resolve some of these issues, because the term gender dysphoria applies only to the discontent experienced by some persons resulting from gender identity issues. The American Psychiatric Association, publisher of the DSM-5, states that "gender nonconformity is not in itself a mental disorder. The critical element of gender dysphoria is the presence of clinically significant distress associated with the condition."
The main psychiatric approaches to treatment for persons diagnosed with gender dysphoria are psychotherapy or supporting the individual's preferred gender through hormone therapy, gender expression and role, or surgery.
Signs and symptoms
Symptoms of GD in children may include any of the following: disgust at their own genitalia, social isolation from their peers, anxiety, loneliness and depression. According to the American Psychological Association, transgender children are more likely to experience harassment and violence in school, foster care, residential treatment centers, homeless centers and juvenile justice programs than other children.
Adults with GD are at increased risk for stress, isolation, anxiety, depression, poor self-esteem and suicide. Studies indicate that transgender people have an extremely high rate of suicide attempts; one study of 6,450 transgender people in the United States found 41% had attempted suicide, compared to a national average of 1.6%. It was also found that suicide attempts were less common among transgender people who said their family ties had remained strong after they came out, but even transgender people at comparatively low risk were still much more likely to have attempted suicide than the general population. Transgender people are also at heightened risk for certain mental disorders such as eating disorders.
GID exists when a person suffers discontent due to gender identity, causing them emotional distress. Researchers disagree about the nature of distress and impairment in people with GID. Some authors have suggested that people with GID suffer because they are stigmatized and victimized; and that, if society had less strict gender divisions, transsexual people would suffer less.
A twin study (based on seven people in a 314 sample) suggested that GID may be 62% heritable, indicating the possibility of a genetic influence or prenatal development as its origin, in these cases.
The American Psychiatric Association permits a diagnosis of gender dysphoria if the criteria in the DSM-5 are met. The DSM-5 moved this diagnosis out of the sexual disorders category and into a category of its own. The DSM-5 states that at least two of the criteria for gender dysphoria must be experienced for at least six months' duration in adolescents or adults for diagnosis. The diagnosis was renamed from gender identity disorder to gender dysphoria, after criticisms that the former term was stigmatizing. Subtyping by sexual orientation was deleted. The diagnosis for children was separated from that for adults, as "gender dysphoria in children". The creation of a specific diagnosis for children reflects the lesser ability of children to have insight into what they are experiencing, or ability to express it in the event that they have insight. Other specified gender dysphoria or unspecified gender dysphoria can be diagnosed if a person doesn't meet the criteria for gender dysphoria but still has clinically significant distress or impairment.
The International Classification of Diseases (ICD-10) list three diagnostic criteria for "transsexualism" (F64.0):[not in citation given] Uncertainty about gender identity which causes anxiety or stress is diagnosed as sexual maturation disorder, according to the ICD-10.
Treatment for a person diagnosed with GID may include psychotherapy or to support the individual's preferred gender through hormone therapy, gender expression and role, or surgery. This may include psychological counseling, resulting in lifestyle changes, or physical changes, resulting from medical interventions such as hormonal treatment, genital surgery, electrolysis or laser hair removal, chest/breast surgery, or other reconstructive surgeries. The goal of treatment may simply be to reduce problems resulting from the person's transgender status, for example, counseling the patient in order to reduce guilt associated with cross-dressing, or counseling a spouse to help them adjust to the patient's situation.
Hormone treatment or surgery for gender dysphoria is somewhat controversial because of the irreversibility of certain[which?] physical changes. Guidelines have been established to aid clinicians. The World Professional Association for Transgender Health (WPATH) Standards of Care are used by some clinicians as treatment guidelines. Others use guidelines outlined in Gianna Israel and Donald Tarver's Transgender Care. Guidelines for treatment generally follow a "harm reduction" model.
The question of whether to counsel young children to be happy with their assigned sex, or to encourage them to continue to exhibit behaviors that do not match their assigned sex—or to explore a transsexual transition—is controversial. Some clinicians report that a significant proportion of young children diagnosed with gender dysphoria later do not exhibit any dysphoria.
Professionals who treat gender identity disorder in children have begun to refer and prescribe hormones, known as a puberty blocker, to delay the onset of puberty until a child is believed to be old enough to make an informed decision on whether hormonal gender reassignment leading to surgical gender reassignment will be in that person's best interest.
Until the 1970s, psychotherapy was the primary treatment for gender dysphoria, and generally was directed to helping the person adjust to the gender of the physical characteristics present at birth. Psychotherapy is any therapeutic interaction that aims to treat a psychological problem. Though some clinicians still use only psychotherapy to treat gender dysphoria, it may now be used in addition to biological interventions. Psychotherapeutic treatment of GID involves helping the patient to adapt. Attempts to cure GID by changing the patient's gender identity to reflect birth characteristics have been ineffective.:1568
Biological treatments physically alter primary and secondary sex characteristics to reduce the discrepancy between an individual's physical body and gender identity. Biological treatments for GID without any form of psychotherapy is quite uncommon. Researchers have found that if individuals bypass psychotherapy in their GID treatment, they often feel lost and confused when their biological treatments are complete.
Psychotherapy, hormone replacement therapy, and sex reassignment surgery together can be effective treating GID when the WPATH standards of care are followed.:1570 The overall level of patient satisfaction with both psychological and biological treatments is very high.
Estimated rates of those with a transgender identity range from a lower bound of 1:2000 (or about 0.05%) in the Netherlands and Belgium to 0.5% of Massachusetts adults. From a national survey of high-school students in New Zealand, 8,500 randomly selected secondary school students from 91 randomly selected high schools found 1.2% of students responded "yes" to the question "Do you think you are transgender?". These numbers are based on those who identify as transgender. It is estimated that about 0.005% to 0.014% of people assigned male at birth and 0.002% to 0.003% of people assigned female at birth would be diagnosed with gender dysphoria,[disputed ] based on 2013 diagnostic criteria, though this is considered a modest underestimate. Research indicates people who transition in adulthood are up to three times more likely to be male assigned at birth, but that among people transitioning in childhood the sex ratio is close to 1:1.
The term gender identity disorder is an older term for the condition. Some groups, including the American Psychiatric Association (APA), use the term gender dysphoria. The APA's Diagnostic and Statistical Manual first described the condition in the third publication ("DSM-III") in 1980.
In April 2011, the UK National Research Ethics Service approved prescribing monthly injection of puberty-blocking drugs to youngsters from 12 years old, in order to enable them to get older before deciding on formal sex change. The Tavistock and Portman NHS Foundation Trust (T&P) in North London has treated such children. Clinic director Dr. Polly Carmichael said, "Certainly, of the children between 12 and 14, there's a number who are keen to take part. I know what's been very hard for their families is knowing that there's something available but it's not available here." The clinic received 127 referrals for gender dysphoria in 2010.
The T&P completed a three-year trial to assess the psychological, social and physical benefits and risks involved for 12- to 14-year-old patients. The trial was deemed such a success that doctors have decided to make the drugs more widely available and to children as young as 9 years of age. As recently as 2009, national guidelines stated that treatment for gender dysphoria should not start until puberty had finished. Ferring Pharmaceuticals manufactures the drug Triptorelin, marketed under the name Gonapeptyl, at £82 per monthly dose. The treatment is reversible, which means the body will resume its previous state upon discontinuation of drugs.
Society and culture
Social "gender" characteristics are created and supported by the expectations of a culture, and are therefore only partially related to biological sex. For example, the association of particular colours with "girl" or "boy" babies begins extremely early in Western European-derived cultures. Other expectations relate to approved and allowable behaviors and emotional expression.
Some cultures have three defined genders: man, woman, and effeminate man. For example, in Samoa, the fa'afafine, a group of feminine males, are entirely socially accepted. The fa'afafine do not have any of the stigma or distress typically associated in most cultures with deviating from a male/female gender role. This suggests the distress so frequently associated with GID in a Western context is not caused by the disorder itself, but by difficulties encountered from social disapproval by one's culture. However, research has found that the anxiety associated with gender dysphoria persists in cultures, Eastern or otherwise, which are more accepting of gender nonconformity.
In Australia, a 2014 High Court of Australia judgment unanimously ruled in favor of a plaintiff named Norrie, who asked to be classified by a third gender category, 'non-specific', after a long court battle with the NSW Registrar of Births, Deaths and Marriages. However, the Court did not accept that gender was a social construction: it found that sex reassignment "surgery did not resolve her sexual ambiguity".:para 11
Classification as a disorder
The psychiatric diagnoses of gender identity disorder (now gender dysphoria) was introduced in the DSM-III in 1980. Some sources have characterized the addition as a political maneuver to re-stigmatize homosexuality. (Homosexuality was removed from the DSM-II in 1974.) By contrast, Kenneth Zucker and Robert Spitzer argue that gender identity disorder was included in the DSM-III because it "met the generally accepted criteria used by the framers of DSM-III for inclusion." Some researchers, including Robert Spitzer and Paul J. Fink, contend that the behaviors and experiences seen in transsexualism are abnormal and constitute a dysfunction.
Individuals with gender dysphoria may or may not regard their own cross-gender feelings and behaviors as a disorder. Advantages and disadvantages exist to classifying gender dysphoria as a disorder. Because gender dysphoria had been classified as a disorder in medical texts (such as the previous DSM manual, the DSM-IV-TR, under the name "gender identity disorder"), many insurance companies are willing to cover some of the expenses of sex reassignment therapy. Without the classification of gender dysphoria as a medical disorder, sex reassignment therapy may be viewed as cosmetic treatment, rather than medically necessary treatment, and may not be covered. In the United States, transgender people are less likely than others to have health insurance, and often face hostility and insensitivity from healthcare providers.
The DSM-IV-TR diagnostic component of distress is not inherent in the cross-gender identity; rather, it is related to social rejection and discrimination suffered by the individual. Psychology professor Darryl Hill insists that gender dysphoria is not a mental disorder, but rather that the diagnostic criteria reflect psychological distress in children that occurs when parents and others have trouble relating to their child's gender variance. Transgender people have often been harassed, socially excluded, and subjected to discrimination, abuse and violence, including murder.
In December 2002, the British Lord Chancellor's office published a Government Policy Concerning Transsexual People document that categorically states, "What transsexualism is not ... It is not a mental illness." In May 2009, the government of France declared that a transsexual gender identity will no longer be classified as a psychiatric condition, but according to French trans rights organizations, beyond the impact of the announcement itself, nothing changed. Denmark made a similar statement in 2016.
In the December 2016 draft of the ICD-11, GID is reclassified as gender incongruence.
This section is missing information about relationships of trans people with male partners.(December 2015)
Intimate relationships between lesbians and female-to-male people with GID will sometimes endure throughout the transition process, or shift into becoming supportive friendships. Intimate relationships between heterosexual women and male-to-female people with GID often suffer once the GID is known or revealed. Researchers say the fate of the relationship seems to depend mainly on the woman's adaptability. Problems often arise, with the cisgender partner becoming increasingly angry or dissatisfied, if her partner's time spent in a female role grows, if her partner's libido decreases, or if her partner is angry and emotionally cut-off when in the male role. Cisgender women sometimes also worry about social stigma and may be uncomfortable with the bodily feminization of their partner as the partner moves through transition. The cisgender women who are likeliest to accept and accommodate their partner's transition, researchers say, are those with a low sex drive or those who are equally sexually attracted to men and women.
Existing law prohibits public schools from discriminating on the basis of specified characteristics, including gender, gender identity, and gender expression, and specifies various statements of legislative intent and the policies of the state in that regard. Existing law requires that participation in a particular physical education activity or sport, if required of pupils of one sex, be available to pupils of each sex. This bill would require that a pupil be permitted to participate in sex-segregated school programs, activities, including athletic teams and competitions, and use facilities consistent with his or her gender identity, irrespective of the gender listed on the pupil's records.
The California Catholic Conference opposed the bill as unnecessary, as laws exist already to fight discrimination against transgender students. A spokeswoman for the conference said that the issue should be handled by school officials.
- "Gender Dysphoria" (PDF). American Psychiatric Publishing. Retrieved December 24, 2016.
- Coleman E (2011). "Standards of Care for the Health of Transsexual, Transgender, and Gender-Nonconforming People, Version 7" (PDF). International Journal of Transgenderism. Routledge Taylor & Francis Group. 13: 165–232. doi:10.1080/15532739.2011.700873. Archived from the original (PDF) on August 2, 2014. Retrieved August 30, 2014.
- Davidson, Michelle R. (2012). A Nurse's Guide to Women's Mental Health. Springer Publishing Company. p. 114. ISBN 0826171133.
- Heylens, G; De Cuypere, G; Zucker, K; Schelfaut, C; Elaut, E; Vanden Bossche, H; De Baere, E; T'Sjoen, G (2012). "Gender Identity Disorder in Twins: A Review of the Case Report Literature". The Journal of Sexual Medicine. 8 (3): 751–757. doi:10.1111/j.1743-6109.2011.02567.x.
- Fraser, L; Karasic, D; Meyer, W; Wylie, K (2010). "Recommendations for Revision of the DSM Diagnosis of Gender Identity Disorder in Adults". International Journal of Transgenderism. 12 (2): 80–85. doi:10.1080/15532739.2010.509202.
- Newman, L (1 July 2002). "Sex, Gender and Culture: Issues in the Definition, Assessment and Treatment of Gender Identity Disorder". Clinical Child Psychology and Psychiatry. 7 (3): 352–359. doi:10.1177/1359104502007003004.
- Ansara, Y. Gavriel; Hegarty, Peter (2012). "Cisgenderism in psychology: pathologising and misgendering children from 1999 to 2008". Psychology and Sexuality. 3 (2): 137–60. doi:10.1080/19419899.2011.576696.
- Grant; Jaime, M.; Mottet, Lisa; Tanis, Justin; Harrison, Jack; Herman, Jody; Keisling, Mara (2011). Injustice at Every Turn: A Report of the National Transgender Discrimination Survey (PDF). Washington: National Center for Transgender Equality and National Gay and Lesbian Task Force. Retrieved 10 May 2015.
- Reyes, Emily (January 28, 2014). "Transgender study looks at 'exceptionally high' suicide-attempt rate". Los Angeles Times. Retrieved 10 May 2015.
- O'Keefe, CarolynAnne (2007). Mentoring sexual orientation and gender identity minorities in a university setting. California: ProQuest Dissertations & Theses (PQDT). p. xvi. ISBN 9780542913112.
- Diemer, Elizabeth; Grant, Julia; Munn-Chernoff, Melissa; Patterson, David; Duncan, Alexis (April 28, 2015). "Gender Identity, Sexual Orientation, and Eating-Related Pathology in a National Sample of College Students". Journal of Adolescent Health. 57: 144–149. doi:10.1016/j.jadohealth.2015.03.003. PMC . PMID 25937471.
- Doyle, Kathryn (8 May 2015). "Sexual orientation, gender identity tied to eating disorder risk". reuters. Retrieved 10 May 2015.
- Bryant, Karl Edward (2007). The Politics of Pathology and the Making of Gender Identity Disorder. Ann Arbor, Michigan: ProQuest Dissertations & Theses (PQDT). p. 222. ISBN 9780549268161.
- Giordano, Simona (2012). Children with Gender Identity Disorder: A Clinical, Ethical, and Legal Analysis. New Jersey: Routledge. p. 147. ISBN 0415502713.
- Coolidge, F; Thede, L; Young, S (4 April 2002). "The Heritability of Gender Identity Disorder in a Child and Adolescent Twin Sample". Behavior Genetics. 32 (4): 251–257. doi:10.1023/A:1019724712983. PMID 12211624.
- "P 01 Gender Dysphoria in Adolescents or Adults". American Psychiatric Association. Retrieved April 2, 2012.
- "Gender Dysphoria". DSM-5. American Psychiatric Association. Retrieved 20 April 2014.
- "Gender Dysphoria in Children". American Psychiatric Association. May 4, 2011. Retrieved July 3, 2011.
- "P 00 Gender Dysphoria in Children". American Psychiatric Association. Retrieved April 2, 2012.
- Diagnostic and Statistical Manual of Mental Disorders 5. American Psychiatric Association. 2013. p. 459. ISBN 978-0-89042-555-8.
- Potts, S; Bhugra, D (1995). "Classification of sexual disorders". International Review of Psychiatry. 7 (2): 167–174. doi:10.3109/09540269509028323.
- Leiblum, Sandra (2006). Principles and Practice of Sex Therapy, Fourth Edition. The Guilford Press. pp. 488–9. ISBN 978-1-59385-349-5.
- Committee On, Adolescence (2013). "Office-based care for lesbian, gay, bisexual, transgender, and questioning youth". Pediatrics. 132 (1): 198–203. doi:10.1542/peds.2013-1282. PMID 23796746.
However, adolescents with multiple or anonymous partners, having unprotected intercourse, or having substance abuse issues should be tested at shorter intervals.
- "www.glma.org Compendium of Health Prof ession Association LGBT Policy & Position Statements" (PDF). GLMA. 2013. Retrieved August 27, 2013.
- "APA Policy Statements on Lesbian, Gay, Bisexual, & Transgender Concerns" (PDF). American Psychological Association. 2011. Retrieved August 27, 2013.
BE IT FURTHER RESOLVED that APA recognizes the efficacy, benefit, and necessity of gender transition treatments for appropriately evaluated individuals and calls upon public and private insurers to cover these medically necessary treatments;
- Spiegel, Alix (2008-05-08). "Q&A: Therapists on Gender Identity Issues in Kids". NPR. Retrieved 2008-09-16.
- The Transgendered Child: A Handbook for Families and Professionals (Brill and Pepper, 2008)[full citation needed][page needed]
- Gijs, L; Brawaeys, A (2007). "Surgical Treatment of Gender Dysphoria in Adults and Adolescents: Recent Developments, Effectiveness, and Challenges". Annual Review of Sex Research. 18 (178–224).
- George R. Brown, MD (20 July 2011). "Chapter 165 Sexuality and Sexual Disorders". In Robert S. Porter, MD; et al. The Merck Manual of Diagnosis and Therapy (19th ed.). Whitehouse Station, NJ, USA: Merck & Co., Inc. pp. 1567–1573. ISBN 978-0-911910-19-3.
- Bockting, W; Knudson, G; Goldberg, J (January 2006). "Counselling and Mental Health Care of Transgender Adults and Loved Ones".
- Hakeem, Az (2008). "Changing Sex or Changing Minds: Specialist Psychotherapy and Transsexuality". Group Analysis. 41 (2): 182–196. doi:10.1177/0533316408089883.
- Olyslager, Femke; Conway, Lynn (2008). "Transseksualiteit komt vaker voor dan u denkt. Een nieuwe kijk op de prevalentie van transseksualiteit in Nederland en België". Tijdschrift voor Genderstudies (in Dutch). Amsterdam: Amsterdam University Press. 11 (2): 39–51. ISSN 1388-3186. Retrieved August 27, 2013. Lay summary – How Frequently Does Transsexualism Occur?.
…it is safe to assume that the lower limit for the inherent prevalence of transsexualism in the Netherlands and Flanders is on order of 1:2000 to 1:1000 for transgender females and on the order of 1:4000 to 1:2000 for transgender males.
- Conron, KJ; Scott, G; Stowell, GS; Landers, S (January 2012), "Transgender Health in Massachusetts: Results from a Household Probability Sample of Adults", American Journal of Public Health, American Public Health Association, 102 (1): 118–222, doi:10.2105/AJPH.2011.300315, ISSN 1541-0048, OCLC 01642844, PMC , PMID 22095354, retrieved August 28, 2013,
Between 2007 and 2009, survey participants aged 18 to 64 years in the Massachusetts Behavioral Risk Factor Surveillance System (MA-BRFSS; N = 28 662) were asked: "Some people describe themselves as transgender when they experience a different gender identity from their sex at birth. For example, a person born into a male body, but who feels female or lives as a woman. Do you consider yourself to be transgender?" […] We restricted the analytic sample to 28176 participants who answered yes or no to the transgender question (excluding n=364, 1.0% weighted who declined to respond. […] Transgender respondents (n=131; 0.5%; 95% confidence interval [CI]=0.3%, 0.6%) were somewhat younger and more likely to be Hispanic than were nontransgender respondents.
- Clark, Terryann C.; Lucassen, Mathijs F.G.; Bullen, Pat; Denny, Simon J.; Fleming, Theresa M.; Robinson, Elizabeth M.; Rossen, Fiona V. (2014). "The Health and Well-Being of Transgender High School Students: Results From the New Zealand Adolescent Health Survey (Youth'12)". Journal of Adolescent Health. 55 (1): 93–9. doi:10.1016/j.jadohealth.2013.11.008. PMID 24438852.
Whether a student was transgender was measured by the question, "Do you think you are transgender? This is a girl who feels like she should have been a boy, or a boy who feels like he should have been a girl (e.g., Trans, Queen, Fa’faffine, Whakawahine, Tangata ira Tane, Genderqueer)?" […] Over 8,000 students (n = 8,166) answered the question about whether they were transgender. Approximately 95% of students did not report being transgender (n=7,731; 94.7%), 96 students reported being transgender (1.2%), 202 reported not being sure (2.5%), and 137 did not understand the question (1.7%).
- Diagnostic and Statistical Manual of Mental Disorders 5. American Psychiatric Association. 2013. p. 454. ISBN 978-0-89042-555-8.
- Landen, M; Walinder, J; Lundstrom, B (1996). "Prevalence, incidence and sex ratio of transsexualism". Acta Psychiatrica Scandinavica. 93 (4): 221–223. doi:10.1111/j.1600-0447.1996.tb10638.x. PMID 8712018.
On average, the male [to female]:female [to male] ratio in prevalence studies is estimated to be 3:1. However […] the incidence studies have shown a considerably lower male [to female] predominance. In Sweden and England and Wales a sex ratio of 1:1 has been reported. In the most recent incidence data from Sweden there is a slight male [to female] predominance among the group consisting of all applicants for sex reassignment, while in the group of primary [early onset] transsexuals there is no difference in incidence between men and women.
- "Gender Dysphoria Fact Sheet" (PDF). APA. Retrieved 2 September 2013.
- Koh, J (2012). "The history of the concept of gender identity disorder". Seishin Shinkeigaku Zasshi. 114 (6): 673–80. PMID 22844818.
- telegraph.co.uk: "Puberty blocker for children considering sex change", Telegraph (Alleyne) 15 Apr 2011
- Marecek, J., Crawford, M., & Popp, D. (2004). "On the Construction of Gender, Sex, and Sexualities". In A.H. Eagly, A.E. Beall, & R.J. Sternberg. The Psychology of Gender. New York: Guilford Press. pp. 192–216.
- Vasey, P; Bartlett, N (2007). "What Can the Samoan "Fa'afafine" Teach Us about the Western Concept of Gender Identity Disorder in Childhood?". Perspectives in Biology and Medicine. 50 (4): 481–490. doi:10.1353/pbm.2007.0056. PMID 17951883.
- Diagnostic and Statistical Manual of Mental Disorders 5. American Psychiatric Association. 2013. p. 459. ISBN 978-0-89042-555-8.
- NSW Registrar of Births, Deaths and Marriages v Norrie HCA 11 (2 April 2014), High Court (Australia).
- Arlene Istar Lev (2004). Transgender Emergence: Therapeutic Guidelines for Working with Gender-Variant People and Their Families. Haworth Press. p. 172. ISBN 978-0-7890-2117-5.
- Rudacille, Deborah (February 2005). The Riddle of Gender: Science, Activism, and Transgender Rights. Pantheon. ISBN 978-0-375-42162-4.[page needed]
- Zucker, KJ; Spitzer, RL (Jan–Feb 2005), "Was the gender identity disorder of childhood diagnosis introduced into DSM-III as a backdoor maneuver to replace homosexuality? A historical note.", Journal of Sex and Marital Therapy, 31 (1): 31–42, doi:10.1080/00926230590475251, PMID 15841704
- "Controversy Continues to Grow Over DSM's GID Diagnosis". Psychiatric News.
- Ford, Zack. "APA Revises Manual: Being Transgender is No Longer a Mental Disorder". Retrieved April 7, 2013.
- Mallon, Gerald P. (2009). Social Work Practice with Transgender and Gender Variant Youth. New Jersey: Routledge. ISBN 0415994829.
- "Government Policy concerning Transsexual People". People's rights/Transsexual people. U.K. Department for Constitutional Affairs. 2003. Archived from the original on 2008-05-11.
- "La transsexualité ne sera plus classée comme affectation psychiatrique". Le Monde. May 16, 2009.
- "«La France est très en retard dans la prise en charge des transsexuels»". Libération (in French). 2011-05-17.
En réalité, ce décret n'a été rien d'autre qu'un coup médiatique, un très bel effet d'annonce. Sur le terrain, rien n'a changé.
- "Denmark will become first country to no longer define being transgender as a mental illness". The Independent. 2016-05-14.
- "ICD-11 Beta Draft (Mortality and Morbidity Statistics) - Gender incongruence". World Health Organization. Retrieved December 23, 2016.
- Barrett, James (2007). Transexual and Other Disorders of Gender Identity: A Practical Guide to Management. RADCLIFFE MEDICAL PRESS LTD. p. 83. ISBN 185775719X.
- Los Angeles Times, "Assembly approves bill on gender identity in schools" by Chris Megerian, May 9, 2013; accessed April 11, 2014.
- Conway, Lynn (June 26, 2014). "Successful TransMen: Links and Photos". ai.eecs.umich.edu. Retrieved December 2, 2014.
- Conway, Lynn (February 5, 2011). "Transsexual Women's Successes: Links and Photos". ai.eecs.umich.edu. Retrieved December 2, 2014.
- Jacques, Juliet. "A Transgender Journey". The Guardian. Retrieved December 2, 2014.
- World Professional Association for Transgender Health (2012). Standards of Care for Gender Identity Disorders (PDF). Harry Benjamin International Gender Dysphoria Association. Archived from the original (PDF) on 2014-09-24. Includes a description of ICD-10 criteria.
- Health Law Standards of Care for Transsexualism - An alternative to the Benjamin Standards of Care proposed by the International Conference on Transgender Law and Employment Policy.
- The Lord Chancellor's Department Government Policy concerning Transsexual People | <urn:uuid:4ac3bc57-296d-4ad8-bbae-f34f0a05de6e> | {
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Multiple Chemical Sensitivity (MCS) is a chronic, physical illness affecting people of all ages and backgrounds. It causes sufferers to have allergic-type reactions to very low levels of chemicals in everyday products. Put simply the immune and detoxification systems stop working properly and the body cannot process toxins efficiently.
Besides reacting to things like cleaning products, shampoo, perfumes and pesticides, many sufferers are also sensitive to food, medicines, moulds and electromagnetic fields.
Who gets MCS?
MCS is a devastating and isolating illness that has many different triggers and can start at any age. It may develop after a single particular exposure to a toxic substance such as pesticides or industrial solvents (sometimes from a newly decorated home or office). Others develop sensitivities after a period of ill health or viral infection, with symptoms getting worse over several years.
Occasionally the illness arises gradually as a result of long term exposure to very low level toxins. Once sensitised, individuals often react to minute traces of chemicals at levels far below those usually considered to be harmful.
Some airborne irritants are odourless and sufferers may find themselves in the distressing position of having no idea what they are reacting to. Severe reactions can leave sufferers bedbound for several months, while many more become confined to their homes.
In 2003, research indicated over 12% of the US population was affected with severe MCS - over 36.5 million people - and statistics have continued to rise. Exact numbers of sufferers in the UK are still not known but include thousands of soldiers affected by Gulf War Syndrome. Despite this, the medical profession still varies widely in its support and there are currently no clinical guidelines for the treatment of patients.
Most people are familiar with mild forms of chemical sensitivity. Symptoms might include a rash from washing powder or shampoo, headaches from traffic fumes, asthma from perfume, or hyperactivity induced by chemicals in foods. These symptoms can usually be managed by avoiding the problem products.
Individuals with MCS react to far more than one or two items. Severe sufferers cannot tolerate any synthetic or petrochemical substances, and some even react to natural products. Because of modern manufacture, many people with MCS find themselves allergic to practically everything in their homes.
Exposure to very low levels of toxins and fragrances can lead to a wide range of symptoms including headaches, nausea, disorientation, confusion, breathing problems, exhaustion, muscle pains or collapse. Reactions vary in severity and can occur immediately or several hours later depending on which body systems are involved.
MCS affects family, relationships, employment, social interaction, and even simple things such as taking a bath, getting dressed or reading a book. Hypersensitive individuals may become intolerant of a great many foods and some find themselves unable to tolerate anything except liquid nutritional feeds. Others become sensitive to electromagnetic fields and are unable to use a telephone, computer, radio or TV - effectively becoming housebound without any form of outside communication.
Although symptoms can be managed and sometimes improved, there is currently no known cure.
Recovery involves avoidance of as many toxins and problem substances as practicably possible, to allow the body time to heal and prevent irreversible damage. This has a huge impact on everyday life but nutritional therapy and gentle detoxification can help repair the body’s systems. Some people also find specialist desensitisation and complementary therapies beneficial.
The easiest way to diagnose chemical sensitivity is to keep a Diary of symptoms, activities and what you eat or drink. After a couple of weeks look back and see if you can identify any recurring patterns. Once you've worked out what's triggering your symptoms, avoiding the product should help you feel a lot better. There's no need to go without, simply replace the item with an alternative. "Fragrance-free" and "environmentally-friendly" brands are less likely to contain allergic triggers
Early access to appropriate information, support, treatment and an individual approach is vital for any chance of recovery.
MCS is classified as a physical illness by the World Health Organisation (WHO) under the International Classification of Diseases ICD-10-SGB-V, T78.4. MCS is recognised as a serious medical illness in Germany, Denmark, Austria, Japan, Australia, Canada and the USA, where sufferers have access to appropriate medical treatment, housing and social support.
In the UK multiple sensitivities are listed as a symptom of ME, but MCS is not yet recognised as an illness in its own right. Medical support varies widely and there are no specialist NHS treatment facilities. Sufferers and their families are often left to cope as best they can without help - this is where we can make a difference!
What can be done?
First of all make sure your environment contains as few toxins as possible. Consider your diet, water and particularly the room you sleep in. Stop wearing perfume or aftershave and get rid of air-fresheners. Changing your laundry detergent and toiletries can make a significant difference. You can download a list of toiletries and cleaning products that are likely to be suitable form our leaflet: 'How to be Fragrance Free'.
Do you need to consider your environment and diet if you only have electro sensitivity? Yes. There is no miracle cure for either of these conditions and improving one aspect of your health will generally help you overall. Correcting leaky gut, and candida for example can make a big difference to both chemical and electro-senstivities.
At work or school ask if they will introduce a fragrance-free policy for staff/ pupils. Make sure the room is well ventilated and don't sit near the photocopier if you react to the fumes or electrical fields. Ideally open a window or if the air is too polluted invest in an air purifier. Support group members can request a helpsheet about air purifiers.Cabled internet will be less likely to exacerbate symptoms than Wi-Fi. Jobs that involve chemicals such as decorating, hairdressing or farming are likely to exacerbate symptoms and you will need to think carefully about how to limit this.
When you have removed the things you react to (as much as is practical) then start thinking about how to improve your immune and detoxification systems. An experienced practitioner can help you with this. Support group members can request a list of practitioners in the UK. There is no one method of treatment that suits everyone, as there are several different reasons you may have developed MCS. This means you have to learn about treatment options yourself and work with practitioners and qualified nutritional therapists to see what works for you. If illness or allergies run in your family then a DNA test may help to discover the root cause. You can then work with a practitioner to compensate for any issues with nutritional supplements. Probiotics are also worth investigating and there are certain supplements like magnesium, multi vitamins, B complexes and vitamin D3 that can help. When you have taken steps to repair your detoxification pathways it is time to start gently detoxifying.
When your body can't process toxins (xenobiotics) it will store them in your body until an occasion when it is able to process them. If you start detoxifying before you have repaired your pathways then you will simply loosen the toxins and they will circulate in your bloodstream until they can be stored again. This makes you feel awful, with headaches, flu symptoms, rashes etc. People with MCS often have a low tolerance for nutritional supplements and medicines for this reason. This applies to massage, saunas, and even a capsule of probiotics can wreak havoc if it is too much too soon (as it will kill off the 'bad' bacteria causing an increase in toxins). When we talk about 'gently detoxifying' we mean start any treatment at a low dose/ less time and see how you are. You cannot speed up this process. Your body will only be able to process and get rid of toxins at a certain rate.
There is much more information about the process of recovery and treatments in our helpsheets and you can read more about this here.
- Caress, S. and Steinemann, A. (2003). More than 12% of Population Reports Extreme Sensitivity to Low Levels of Common Chemicals. Published in Environmental Health Perspectives (EHP), the journal of the National Institute of Environmental Health Sciences, 11 September 2003 Retrieved 18/02/05, from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1241652/ | <urn:uuid:a371e582-3a4d-49a1-bfea-ba8a52e27d56> | {
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The Next Generation of Low Dead Space Disposable Syringes
A needlestick injury is a percutaneous piercing wound typically set by a needle point, but possibly also by other sharp instruments or objects. Commonly encountered by people handling needles in the medical setting, such injuries are an occupational hazard in the medical community. These events are of concern because of the risk to transmit blood-borne diseases through the passage of the hepatitis B virus (HBV), the hepatitis C virus (HCV), and the Human Immunodeficiency Virus (HIV), the virus which causes AIDS.
Despite their seriousness as a medical event, needlestick injuries have been neglected: most go unreported and ICD-10 coding is not available. On the other hand, as needlesticks have been recognized as occupational hazards, their prevention has become the subject of regulations in an effort to reduce and eliminate this preventable event.
Needlestick injuries are a common event in the healthcare environment. When drawing blood, administering an intramuscular or intravenous drug, or performing other procedures involving sharps, the needle can slip and injure the healthcare worker. This sets the stage to transmit viruses from the source person to the recipient. These injuries also commonly occur during needle recapping and as a result of failure to place used needles in approved sharps containers. During surgery, a surgical needle may inadvertendly penetrate the glove and skin of the surgeon or assistant. Penetrating accidents of the surgeon or assistant with the scalpel or other sharp instruments are also handled as a needlestick injury. Generally needlestick injuries cause only minor bleeding or visible trauma, however, even in the absence of bleeding the risk of viral infection remains. Scalpel injuries tend to be larger than a needlestick. In turn, a needlestick injury may also pose a risk for a patient if the injured health professional carries HBV, HCV or HIV. Needlestick injuries are not limited to the medical community. Any environment where sharps are encountered poses a risk.
The frequency of such events has been estimated to be about 800,000 cases in the USA alone (1999 report) Another investigation estimates the rates of injuries on a global level to affect about 3.5 million individuals. Among healthcare workers nurses and physicians appear especially at risk; an investigation among American surgeons indicates that almost every surgeon experienced at least one such injury during their training. Within the medical field specialties differ in regard to the risk of needlestick injury, thus surgery, anesthesia, ENT, internal medicine, and dermatology tend to show relatively high, and radiology and pediatrics relatively low rates of injury. Half or more events may go unreported as injured healthcare workers may not take the time to report, downplay the risk, or fear stigmatization and professional consequences.
Needlestick injuries may occur not only with freshly contaminated sharps, but also, after some time, with needles that carry dry blood. While the infectiousness of HIV and HCV decrease within a couple of hours, HBV remains stable during desiccation and infectious for more than a week.
Needlestick injuries are of significant concern to police workers. In San Diego 30% of police workers reported such injuries typically when searching suspects.
While needlestick injuries have the potential of transferring bacteria, protozoa, viruses and prions, from a practical point the transmission of the hepatitis B and hepatitis C viruses and the Human Immunodeficiency Virus (HIV) is important. It is estimated that annually as a consequence there are 66,000 infections with HBV, 16,000 with HCV, and 1,000 with HIV worldwide. In addition, a needlestick injury may lead to significant stress and anxiety for the affected injured person. Taking care of a needlestick injury is costly, estimated to be about $ 2,500 in the short term in the US.
Hepatitis B carries the greatest risk of transmission, with 37 to 62% of exposed workers eventually showing seroconversion and 22 to 31% showing clinical Hepatitis B infection. The hepatitis C transmission rate has been reported at 1.8%, but newer, larger surveys have shown only a 0.5% transmission rate. The overall risk of HIV infection after percutaneous exposure to HIV-infected material in the health care setting is 0.3%.
The specific risk of a single injury depends on a number of factors when the patients harbor the virus of concern. Injuries with a hollow-bore needle, deep penetration, visible blood on the needle, a needle that was located in a deep artery or vein, or with blood from terminally ill patients are known to increase the risk for HIV infection.
Estimates of the risk of a single injury indicate a risk of 300 HBV infections (30% risk), 30 HCV infection (3% risk) and 3 HIV infections (0.3% risk) per 1,000 respective exposures.
While the vast majority of needlestick injuries occur when the source-person does not carry the HBV, HCV, and HIV and thus do not carry a risk of infection, these events nevertheless cause stress and anxiety and signal a breakdown in protocol and prevention.
Preventive steps can be taken at several levels and include reduction or elimination of use of sharps as much as possible, engineering controls (i.e., needles or syringes with safety devices), administrative controls including training and provision of adequate resources, and work practice controls; the latter may include using instruments (not fingers) to grasp needles, load scalpels, and avoiding hand-to-hand passing of sharp instruments also preparing of medications especially removing cap. Removing cap from a needle generally causes needle stick injury. There are several ways to remove the cap from the needle but the most ideal and safest way to remove the cap is by carefully grasping the syringe and guiding the needle cap using the thumb and the pointing finger. Then gently push the cap away from the syringe to detach the cap from the hub. In this way needle stick injury can be prevented by avoiding the incidence of the rebound effect. Do not use the other hand as it increases the likeliness to have the syringe to rebound. Engineering advances include the development of safety needles and needle removers. The adherence to "no-touch" protocols that eliminate direct contact with needles in their use and disposal greatly reduce the risk of injury. In the surgical setting blunt-tip suture needles are able to reduce needlestick injuries. The American College of Surgeons (ACS) has endorsed the adoption of blunt-tip suture needles for suturing fascia.
Some countries have enacted legislation to protect healthcare workers. In the US, the Needlestick Safety Act was signed in 2000 and Bloodborne Pathogens Standard in 2001. These regulations mandate the use of safety devices and needle-removers with any sharps or needles. Discarded sharps enter the medical waste stream.
After a needlestick injury, certain procedures must be followed to minimize the risk of infection for the recipient. The affected area should be rinsed and washed thoroughly with soap and water; the practice to "milk out" more blood is controversial and not recommended by the CDC. Lab tests of the recipient are obtained for baseline studies: HIV, acute hepatitis panel (HAV IgM, HBsAg, HB core IgM, HCV) and for immunized individuals HB surface antibody. Unless already known, the infectious status of the source needs to be determined by checking for HBsAG, anti-HCV, and HIV antibody. Unless the source is known to be negative for HBV, HCV, and HIV post-exposure prophylaxis (PEP) should be initiated, ideally within one hour of the injury; typically this is done in the emergency department or the occupational health office. Guidelines for PEP have been updated over recent years in view of the introduction of new drugs, and protocols may differ somewhat between countries.
Current CDC guidelines call for the administration of hepatitis B immune globulin (HBIG) and/or hepatitis B vaccine. While the efficacy of the combination as not been evaluated in the needlestick injury setting, it has been shown to be the most efficacious approach in the perinatal setting. The approach has no contraindications during pregnancy and lactation.
CDC guidelines acknowledge that there is no active PEP for HCV, only recommendations intended to achieve early identification of chronic disease and, when detected, referral for evaluation of treatment options. According to the CDC identification of acute infection with HCV may not necessitate active intervention. However, there is some evidence that treatment with interferon alfa-2b may be beneficial preventing chronic hepatitis.
CDC guidelines generally recommend a PEP protocol with 3 or more antiviral drugs, when it is known that the donor was HIV positive; however, when the viral load was low and none of the above noted risk factors are met, the CDC protocol utilizes 2 antiviral drugs. Such a 2 drug protocol should also be considered when the donor status cannot be determined (i,e injury by a random needle in a used sharps' container), but there is an increased risk that the source was from a risk group for HIV. PEP drugs for prevention of HIV infection are given for 4 weeks and may include nucleoside reverse transcriptase inhibitors (NRTIs), nucleotide reverse transcriptase inhibitors (NtRTIs), nonnucleoside reverse transcriptase inhibitors (NNRTIs), protease inhibitors (PIs), and a single fusion inhibitor. PEP anti-HIV regimens are accompanied by significant side effects and their utilization is not indicated when there is evidence that HIV transmission is not involved; also, initiated protocols can be stopped when data appear indicating that the source-person is HIV-negative. Regardless whether PEP is instituted, follow-up of exposed individuals includes counseling and HIV testing by enzyme immunoassay to monitor for a possible seroconversion for at least 6 months after exposure. Such tests are done at baseline, 6 weeks, 12 weeks, and 6 months, and longer in specific circumstances, such as co-infection with HCV. | <urn:uuid:94b5ee4a-11ca-478f-9be8-469b32b6f3da> | {
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ICD-10-CM Coding: Cholesteatoma
Cholesteatoma is an abnormal skin growth in the middle ear, behind the eardrum. These develop as cysts or pouches that fill with old skin cells and other waste material. Typically, a cholesteatoma occurs because of Eustachian tube dysfunction, as well as infection in the middle ear, and can lead to deafness.
There are two types of cholesteatoma:
Acquired cholesteatoma is the most common. It is caused by accumulation of keratin in a pouch of tympanic membrane extending into the middle ear space. Cholesteatoma may also result from trauma, or metaplasia of the middle ear mucosa (metaplasia is the replacement of one differentiated cell type with another mature differentiated cell).
Congenital cholesteatoma are most commonly found in the anterior aspect of the eardrum.
Good clinical documentation should include the specific site or location of the Cholesteatoma (such as attic, tympanum, mastoid, and external ear). ICD-10-CM introduces the concept of laterality, and complete documentation should detail whether the Cholesteatoma is left, right, or bilateral. If laterality is not documented, you must use an unspecified code.
Example: The patient was brought to the OR and placed supine on the operating table. General anesthesia was established and the patient intubated. He was given antibiotics and turned 180degrees on the table. The facial nerve monitor was placed into the left facial muscles, and thereafter facial nerve monitoring was performed for the duration of the case. The left ear was then injected with 2 ml of 1 percent Lidocaine. After the left ear was prepped and draped, the operating microscope was brought in. A tympanomeatal flap was then created and elevated entering into the middle ear. We immediately encountered in the middle ear small cholesteatoma pearl adjacent to the scutal wall and was attached to the chora tympani. The scutum was curetted for further visualization and then the pearl, which was fairly well intact and was lifted out with a teratoma dissecting instrument. The chorda tympani was sacrificed and removed with the cholesteatoma. Otoendoscope revealed a clear area. Canal was packed with Gelfoam and a band-aid. The patient was turned back from anesthesia, awakened, extubated and brought to recovery in stable condition.
Findings: Small cholesteatoma pearl, fairly encapsulated and attached to chorda, and was removed along with the chorda.
This example contains documentation of the location of the cholesteatoma as tympanum, and the laterality as left ear.
H71.0 Cholesteatoma of attic
H71.1 Cholesteatoma of tympanum
H71.2 Cholesteatoma of mastoid
H71.3 Diffuse cholesteatoma
H71.9 Unspecified cholesteatoma
Additionally, category H71 contains an Excludes II note, which indicates that you may separate report the presence of additional conditions, when present:
Cholesteatoma of external ear (H60.4-)
Recurrent cholesteatoma of postmastiodectomy cavity (H95.0-)
Example: A twenty-two-year-old male presented with complaints of decreased hearing. Video otoscopic examination revealed keratin debris and “attic cerumen” in the right ear. CT scan indicated attic cholesteatoma with the beginnings of bone erosion. Left ear unremarkable.
In this example the patient is experiencing decreased hearing. Diagnostic testing confirms cholesteatoma in the right ear. The location is documented as “attic.” The correct code is H72.01.
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- Reporting Anesthesia Time Units - April 25, 2018 | <urn:uuid:07428977-ed80-4414-b31a-15995e6baaba> | {
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The Autism Spectrum Disorders (ASD), also known as Pervasive Developmental Disorders are a range of complex neurodevelopment disorders, characterized by social impairments, communication difficulties, and restricted, repetitive, and stereotyped patterns of behavior. Autistic disorder, sometimes called autism or classical ASD, is the most severe form of ASD, while other conditions along the spectrum include a milder form known as Asperger syndrome, and childhood disintegrative disorder and pervasive developmental disorder not otherwise specified (usually referred to as PDD-NOS). Although ASD varies significantly in character and severity, it occurs in all ethnic and socioeconomic groups and affects every age group. It is estimated that 1 out of 88 children will have an ASD. Males are four times more likely to have an ASD than females.
The diagnosis of Autism remains a clinical conundrum. Criteria laid down in DSM-IV and ICD-10 may be quite clear to an experienced person. But it can be quite confusing for the average clinician or caregiver. However, in the absence of any specific diagnostic laboratory or imaging studies, a clinical diagnosis remains the gold standard.
To read the full article, you need to Purchase this issue. CLICK HERE TO ORDER NOW. | <urn:uuid:55717dcb-9195-4e5b-a945-77935e96e0e7> | {
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Alcohol consumption is rampant in modern society. Alcohol abuse and addiction cause many problems, but is alcoholism deadly? Rarely does a person go to a group function without alcohol being served. Office parties, informal dinners, concerts and sporting events, even weddings involve beer, wine, or mixed drinks. It is no wonder there is so much alcoholism in our country.
According to the National Institute on Alcohol Abuse and Alcoholism (NIAAA) and the National Survey on Drug Use and Health (NSDUH):
- In 2014, 87.6 percent of people ages 18 or older reported that they drank alcohol at some point in their lifetime; 71.0 percent stated that they drank in the past year; 56.9 percent reported that they drank in the previous month.
- In 2014, 24.7 percent of people ages 18 or older reported that they engaged in binge drinking in the past month; 6.7 percent reported that they engaged in heavy drinking in the past month.
- Nearly 88,000 people (approximately 62,000 men and 26,000 women) die from alcohol-related causes annually, making it the fourth leading preventable cause of death in the United States.
- In 2014, alcohol-impaired driving fatalities accounted for 9,967 deaths (31 percent of overall driving fatalities).
What is Alcoholism?
Because individuals’ bodies and minds handle alcohol differently, alcoholism is not an assigned number or even a blood alcohol content reading. Making a clear call as to whether someone has an alcohol problem can be tricky.
‘Disease,’ ‘misuse,’ ‘impaired control over drinking,’ ‘malady,’ ‘mental obsession,’ and many other creative phrases are used to describe alcoholism. But the ICD-10 (International Classification of Diseases, 10th revision) – the handbook for medical billing – defines alcoholism as follows:
“A cluster of behavioural, cognitive, and physiological phenomena that develop after repeated alcohol use and that typically include a strong desire to consume, difficulties in controlling its use, persisting in its use despite harmful consequences, a higher priority given to alcohol consumption than to other activities and obligations, increased tolerance, and sometimes a physical withdrawal state.”
Nearly 14 million Americans are considered to abuse alcohol or are alcoholic, based on the above guidelines.
How Harmful are the Effects of Alcoholism?
Alcoholism is a habit of far-reaching consequences. About half of all convicted murderers were drinking at the time of their offense. Also, every 48 minutes, someone is killed by an alcohol-impaired driver (about 30 per day). From that point of view, certainly, alcoholism can be deadly!
But what about how alcohol affects the alcoholic himself? Sure it’s a bad habit, but can it kill a person?
Alcohol use can result in major health issues such as liver disease and high blood pressure. Likewise, there are results of drinking that are easily observed like impaired brain and physical function, that stem from alcohol’s interference with the communication pathways in our brains. But here are a few less-known facts:
- Up to 80% of alcoholics also suffer from Thiamine deficiency, which leaves their brain vulnerable to brain disorders such as hepatic encephalopathy and Korsakoff’s psychosis.
- Even a single incident of drinking can lower your immune system function for up to 24 hours afterward, leaving you susceptible to disease.
- Alcohol plays a part in 4% of the deaths worldwide each year – that’s 2.5 million.
- Alcohol consumption results in an estimated 18,200 to 21,300 cancer deaths per year in the United States alone.
Combine all this with increased risk of pancreatitis, cardiomyopathy and a host of other health complications – physical, mental and emotional. With this in mind, you should wonder “is alcoholism deadly”. Of course, the answer becomes appallingly clear.
What Can be Done to Combat Alcoholism?
Recovery can be achieved if the person wants to badly enough. Denial can prevent a person seeking treatment and soon the alcoholic will not be asking “is alcoholism deadly” because they may have already gotten that answer.
Inpatient facilities are the number one method of breaking alcoholism. They work in several ways:
- removing a patient’s access to alcohol
- guiding a patient through any withdrawal difficulties, they may have
- creating an atmosphere that allows the patient to focus 100% on healing
- diagnosing any medical issues that may be exacerbating a patient’s addiction
- re-training a patient into new, cleaner habits and better behavioral patterns
Going to an inpatient treatment facility is one of the best things an alcoholic can do for himself and his family. A person who completes a 30 day or longer inpatient treatment regime doubles their chance of long-term success. Multi-faceted treatment that doubles your chance of success is a smart decision.
If you are asking yourself “Is alcoholism deadly?”, call our toll-free number and one of our representatives can give you the information you need. | <urn:uuid:e764903c-0c53-4502-b9e7-215e0b41ef9a> | {
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The Aboriginal identity population includes people who reported that they identify with at least one Aboriginal group; that is, North American Indian, Métis or Inuit, and/or those who reported being a Treaty Indian or a Registered Indian, as defined by the Indian Act of Canada, and/or those who reported they were members of an Indian band or First Nations.
An adverse event following immunization (AEFI) is an unfavourable medical condition or reaction that occurs after an immunization is given. An adverse event that follows an immunization may or may not be due to that immunization. Reports of AEFIs from Middlesex-London are compiled and assessed as part of the provincial, national and international system of vaccine safety monitoring.
The number of live births to women in a given age group over the number of women in that age group.
Age-standardized rates may be used to compare different geographic areas or time frames to adjust for any differences in the age structure of the populations that could cause a difference in rates.
It reflects the number of events (e.g., deaths, hospitalizations) that would occur for a given population if that population had the same age distribution as the 1991 Canadian population.
Age-standardized rates have been used to make more valid comparisons than comparing crude rates. Standardization requires adjusting for the effects of varying age structures of different populations and over different periods of time. The importance of age-standardization can be illustrated by using Population X, which has a higher proportion of elderly persons than Population Y. The unadjusted or “crude” mortality rate for Population X would be significantly higher than Population Y solely because it has a higher proportion of elderly persons and the elderly have a much higher death rate than younger people. This concept also applies when comparing one population over different time periods if the age structure of the population changes over time. By standardizing the mortality rates for Population X, we can see what the mortality rate would be like if they had the same age structure as Population Y. The two different populations are now compared directly.
This index is based on six pollutants that have adverse effects on human health and the environment: ozone (O3), fine particulate matter (PM2.5), nitrogen dioxide (NO2), carbon monoxide (CO), sulphur dioxide (SO2), and total reduced sulphur (TRS) compounds.
AQI < 32 = good or very good; AQI 32-49 = moderate; AQI 50-99 = poor; AQI >99 = very poor
Air quality in the poor or very poor range can have adverse effects on a large portion of the animal/human population and can damage property and vegetation. (Ministry of the Environment, 2008)
The Association of Public Health Epidemiologists in Ontario is an organization of approximately 90 full members who practice epidemiology in Ontario's public health units, as well as more than 150 affiliate members. APHEO's mission is to advance and promote the discipline and professional practice of epidemiology in Ontario public health units.
Drinking five or more alcoholic drinks on one occasion.
The Body Mass Index (BMI) is a ratio of weight to height (kg/m2) and is considered the most useful indicator of population health risk associated with both overweight and underweight. (Health Canada, 2003)
Normal weight – BMI 18.5-24.9
Overweight – BMI 25.0-29.9
Obese – BMI 30.0 and above
The Canadian Community Health Survey (CCHS) is a national population household survey of Canadians aged 12 years and older. It provides self-reported information related to health status, health care utilization and health determinants. Data is generally available down to the level of health region. To produce accurate estimates at the health unit level, two-year period estimates (e.g. 2013 and 2014 data average) were used in this resource along with estimates from the 2003, 2005, 2007/8 , 2009/10 and 2011/12 data collection cycles.
‘Cardiovascular disease is a term that refers to more than one disease of the circulatory system including the heart and blood vessels, whether the blood vessels are affecting the lungs, the brain, kidneys or other parts of the body. The six types of cardiovascular disease are ischemic heart disease (heart attack), cerebrovascular disease (stroke), peripheral vascular disease, heart failure, rheumatic heart disease and congenital heart disease.’ Public Health Agency of Canada 2011 http://www.phac-aspc.gc.ca/cd-mc/cvd-mcv/index-eng.php
Data from the Canadian Census was provided by Statistics Canada. The census takes place every five years in Canada and is a reliable source of information for population and dwelling counts as well as demographic and other socio-economic characteristics.
Married and common-law couples, and the children, if any, of either or both spouses, who all live in the same dwelling. It also includes single parents with children living in the same dwelling. Children may be of any age or marital status as long as they live in the same dwelling as their parent(s).
The coefficient of variation (CV) is the measure used to indicate the sampling variability associated with survey estimates. The CV is obtained by dividing the standard deviation of the estimate by the estimate itself and it is expressed as a percentage of the estimate. Statistics Canada guidelines around the release of survey estimates, based on the magnitude of the CV, have been followed in this resource:
- A CV between 0 and 16.5% is considered acceptable and the estimate can be released without restriction;
- Estimates with a CV between 16.6 and 33.3% can be released, but with a cautionary note regarding high sampling variability;
- Estimates with a CV greater than 33.3% should be suppressed due to extreme sampling variability;
- Estimate release guidelines require at least 10 observations;
For CCHS survey estimates in this resource, CV’s have been calculated using the “bootstrap method”.
Confidence intervals (CIs) indicate the reliability of a statistical estimate or rate. A 95% confidence interval is interpreted as a range in which we can be 95% confident the true population value lies. Wide confidence intervals, suggest less reliable estimates than narrow confidence intervals. In general, the larger the population, the narrower the CI and hence, the more precise is the estimate. Confidence intervals can also be used as tests of statistical significance when comparing estimates – if the CIs for the estimates under comparison overlap, we can say the difference between the estimates is not statistically significant. For CCHS data, 95% CIs have been calculated using the “bootstrap method”.
Diagnoses are classified using the Canadian modification of the International Statistical Classification of Diseases and Related Health Problems, Tenth Revision (ICD-10-CA). For more information about what diagnoses are included in each ICD-10 chapter please consult http://apps.who.int/classifications/icd10/browse/2010/en
A small geographic area with a population of 400 to 700 persons. All of Canada is divided into dissemination areas which are used to report Census information.
Number of people aged 65 years and older divided by the number of people aged 20 to 64
People over the age of 15 years who did any work at all, or who had a job but were not at work, e.g., on leave.
A program designed to teach food handlers the general principles of safe food handling such as risk factors associated with food borne illness and to teach the skills necessary to handle food and prevent illness from occurring. The course is based on the principles of sanitary food service and hazard analysis critical control point (HACCP) procedures.
Food security exists when all people, at all times, have physical and economic access to sufficient, safe and nutritious food to meet their dietary needs and food preferences for an active and healthy life. http://www.fao.org/docrep/003/w3613e/w3613e00.htm The CCHS survey questions asked whether household members were able to afford the food they needed in the previous 12 months. Households were classified as food insecure if there was an indication of compromise in quality and/or quantity of food consumed or reduced food intake and disrupted eating patterns due to lack of money. | <urn:uuid:00326472-1288-4652-8b52-fa351bc0d9c0> | {
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About this issue
For more than a century, it was the norm for undergraduate and postgraduate teaching of psychiatry to start with a simple classification of mental disorders into five groups: organic mental disorders, (functional) psychotic disorders, neurotic disorders, personality disorders, and mental retardation. The key difference between functional psychotic disorders and disorders due to demonstrable brain damage was that the latter were characterised by symptoms indicating cognitive damage. Psychotic and neurotic disorders were called ‘functional’ disorders because it was thought that their origin was a disruption of function, as opposed to brain damage. National and international classification systems used the presence or absence of cognitive damage as one of the main criteria for the distinction of organic mental disorders from other mental disorders. The use of this criterion to distinguish organic mental disorders from, say psychotic disorders, was somewhat illogical, and yet no one seemed to worry that a person with cognitive functions, that were presumed to be perfectly in order, could have delusions. Rational thinking is the expression of good cognitive functioning, and it would seem that the difficulty of thinking rationally must be a sign that cognitive functioning is damaged.
Towards the end of the 20th century, this zeitgeist suddenly changed without any major discussion or opposition. Psychiatrists started speaking about the cognitive symptoms of schizophrenia and bipolar disorder; it was as if the previous generally-accepted distinction of organic and functional disorders by cognitive damage had never existed. Nonetheless, the World Health Organization maintained the distinction, and the tenth revision of the International Classification of Diseases (ICD-10) still lists groups of mental disorders in the order that was proposed when it was believed that organic mental disorders had cognitive symptoms and a poor prognosis. The most durable disorders are listed first (dementia, and consequences of brain trauma), followed by psychotic disorders (which were originally considered to be more treatable since there was no demonstrable brain damage), and then neurotic disorders. The description of schizophrenia states that: “Clear consciousness and intellectual capacity are usually maintained although certain cognitive deficits may evolve in the course of time”. Thus, this description acknowledges that some cognitive symptoms may be present, but it does not see them as the key feature of schizophrenia. Cognitive symptoms are not mentioned in the general description of affective disorders, although concentration and attention difficulties are listed in the descriptions of specific disorders without being given particular prominence.
In 1999, Andreasen wrote that a variety of causes may lead to “impairment in a fundamental cognitive process”, which then leads to “impairment in one or more second-order cognitive processes”, which in turn produces the symptoms of schizophrenia. This model has not been generally accepted, and the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders (DSM-5™) does not include cognitive impairment as a key symptom of schizophrenia. The presence of cognitive symptoms in depressive illnesses has been generally acknowledged and is usually ascribed to a lack of attention and concentration as a consequence of a preoccupation with affective symptoms.
The article by Höschl, Kane, Gaebel, Gorwood and Kennedy in this issue of the Institute Magazine takes the debate one step further. Taking for granted that cognitive symptoms are central to depression and schizophrenia, the author’s marshal arguments for and against the causal role that cognitive impairment might play in those disorders. This is an interesting issue: If, on the one hand, cognitive impairment is the cause of schizophrenia and depressive disorders, then much of our current effort to find effective treatments (and to make prevention possible) will have to change direction. If, on the other hand, cognitive impairment is just one more symptom of schizophrenia and depression, then research on cognitive impairment will have to focus on ways of dealing with it in much the same manner that we deal with other symptoms of these disorders. Thus, in either case the role of cognitive impairment in schizophrenia and affective disorders is of relevance either to direct research in new directions or to change the focus of treatment strategies from other symptoms to cognitive impairment.
This reorientation of our thinking and research from traditional targets, such as positive and negative symptoms to cognitive impairment, is a ‘silent revolution’ in our conceptualisation of schizophrenia and depressive disorders. This revolution may ultimately lead to a new understanding and successful management of these two disorders, which are among the ten most important causes of disability in our century. The Lundbeck Institute deserves credit for drawing attention to the role of cognitive impairment, both by placing it on the agenda of its faculty discussion and by paying particular attention to it in the array of courses and seminars that it organises to improve care for people with schizophrenia and affective disorders. | <urn:uuid:9864f817-a45d-4df7-9e58-dfd8e3c428ff> | {
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by June Bronnert, RHIA, CCS, CCS-P; Chip Masarie, MD; Frank Naeymi-Rad, PhD, MBA; Eric Rose, MD, FAAFP; and Greg Aldin
Terminologies ensure that the 'languages of medicine' can be understood by both humans and machines.
Electronic health records (EHRs) are the industry standard for documenting patient care. Industry initiatives and government legislation have facilitated EHR implementation and use. Most notable among them is the Health Information Technology for Economic and Clinical Health Act (HITECH) legislation, which incentivizes providers toward implementation and demonstration of meaningful EHR use. Ultimately, all of these efforts aim to improve patient outcomes.
Keeping the patient at the center of healthcare is vital. In order to provide patient-centered care, providers must be able to document patient care with sufficient clinical specificity. Sound EHR practices allow all providers to effectively engage in a patient's care delivery because electronic documentation supports patient-centered care in multiple fashions, most notably for decision-support capabilities and the exchange of data across providers and settings. A fundamental aspect of patient-centered care is having access to dependable data in order to make sound decisions. Accurate and reliable information in an electronic format requires all stakeholders to be engaged with the record.
An aspect of reliable and accurate information is ensuring that providers have the ability to capture their clinical intentions regarding patient care through terminologies. Healthcare terminology has long been called "the language of medicine," but, in the electronic age, this language has to be readable by both humans and computers. Various terminologies are used in defining associated terms. This article offers an overview of the different terminologies and how they affect documentation and, ultimately, patient care.
More Online-Audio Feature
http://journal.ahima.org. Hear authors June Bronnert and Chip Masarie discuss how terminology assists HIM professionals.
Terminology is a set of descriptions used to represent concepts specific to a particular discipline. It's also the foundation of EHR data. For example, the terms "heart attack" and "MI" describe the same concept of myocardial infarction. These concepts are in turn associated with codes that are used for a variety of purposes.
Different healthcare terminologies have their own unique features and purposes. For example, RxNorm encodes medications and Logical Observation Identifiers Names and Codes (LOINC) is used for laboratory results.
Many terminologies are required in today's healthcare environment which results in multiple coding systems being used in a single patient's electronic record. This creates an environment where the disparate systems must exchange as well as understand information to provide an effective, integrated healthcare system.
Terms related to terminology include:
Administrative code sets are designed to support administrative functions of healthcare, such as reimbursement and other secondary data aggregation. Common examples are the International Classification of Diseases (ICD) and the Current Procedural Terminology (CPT).1 Each system is fundamentally different; ICD's purpose is to aggregate, group, and classify conditions, whereas CPT is used for reporting medical services and procedures.
- Administrative code sets
- Clinical code sets
- Reference terminologies
- Interface terminologies
Clinical code sets have been developed to encode specific clinical entities involved in clinical work flow, such as LOINC and RxNorm. Clinical code sets have been developed to allow for meaningful electronic exchange and aggregation of clinical data for better patient care. For example, sending a laboratory test result using LOINC facilitates the receiving facility's ability to understand the result sent and make appropriate treatment choices based upon the laboratory result.
A reference terminology is defined as a "concept-based, controlled medical terminology."2 The Systematized Nomenclature of Medicine Clinical Terms (SNOMED CT) is an example of this kind of terminology. It maintains a common reference point in the healthcare industry. Reference terminologies also identify relationships between their concepts. Relationships can be hierarchically defined, such as a parent/child relationship. The reference terminology contains concept A and concept B, with a defined relationship of B as a child of A. SNOMED CT includes concepts such as heart disease and heart valve disorder, and their defined relationship identifies heart valve disorder as a child of heart disease.
Reference terminology allows healthcare systems to get value from clinical data coded at the point of care. In general, reference terms are useful for decision support and aggregate reporting and are more general than the highly detailed descriptions of actual patient conditions. For example, one patient may have severe calcific aortic stenosis and another might have mild aortic insufficiency; however, a healthcare enterprise might be interested in finding all patients with aortic valve disease. The reference terminology creates links between "medical concepts" that allow these types of data queries.
An important aspect of a well-constructed terminology is a concept, typically granular by nature and defined as "a unit of knowledge or thought created by a unique combination of characteristics." An example of a SNOMED CT concept is aortic valve disorder. Refer to the figure "Example of SNOMED CT Hierarchy Relationship" for the aortic valve hierarchical relationship.
Interface terminology is a set of clinically relevant terms mapped to the industry standard administrative and clinical code sets. Clinically relevant terms capture granularity and clinical intent in the documentation.
Example of SNOMED CT Hierarchy Relationship
SNOMED CT is an example of a reference terminology, a concept-based kind of terminology. Below is an example of the aortic valve hierarchical relationship in SNOMED CT.
Many clinicians are forced to use administrative coding sets (CPT, HCPCS, and ICD-9-CM codes) to capture clinical data. However, administrative code sets were designed to either group diagnoses and procedures or to contain broad categories with administrative technical terms with complex rules and guidelines. Examples of this are time durations or vascular branch orders directly stated in various terms.
Administrative codes and terms typically use language that is not natural or familiar for clinicians. For example, in ICD-10-PCS the root operation term "extirpation" is not routinely stated by surgeons. Administrative codes and descriptors also do not contain the different clinical, administrative, and colloquial terms used in healthcare, making it difficult for clinicians, information management professionals, and patients to find the terms they need when performing simple text searches. This disconnect between clinician language and coding sets creates concern over losing clinical intent in the documentation.
Forcing a physician to document in administrative terms is uncomfortable and disruptive. Interface terminology "bridges the gap between information that is in the physician's mind and information that can be interpreted by computer applications."3 Interface terminology helps clinicians find the right diagnosis and procedure terms to document and code more comprehensively and accurately within their normal workflow.
Interface Terminology Architecture
Clinicians interact with interface terminology when documenting diagnoses and procedures in the patient's electronic record. The physician performs searches using the search functionality in designated locations in the EHR, which returns terms to the provider to select the appropriate problem or procedure. The physician selects the appropriate term to capture the clinical intent. The term(s) populate predetermined fields in the electronic record. The selected term contains mappings to one or more industry standard terminologies, such as ICD or SNOMED CT. The "behind-the-scenes" mappings allow the physician to focus on patient care while at the same time capturing the necessary administrative and reference codes.
Each EHR vendor determines which codes are actually stored in the patient's record. By storing the interface terminology code, an EHR can always retrieve the most up-to-date administrative and reference codes in the future.
With interface terminology in place within an EHR, physicians find a number of beneficial impacts to their clinical workflow:
- Improved diagnostic search results for physicians to locate problems
- More clinically meaningful physician documentation
- Better and more complete problem lists are created
- Improved coding accuracy and reliability
The Problem List
Interface terminologies are important for problem lists. In practice, clinicians use many different synonyms, acronyms, eponyms, abbreviations, and other terms to describe the same diseases and problems. These alternate forms are often more familiar and frequently used in the clinical domain rather than the standard ICD-9-CM or ICD-10-CM terms. Interface terminology provides an interface to the standard ICD-9-CM-driven terminology in the EHR search. If the diagnosis was in standard ICD language, the clinician might have to alter the description or, depending upon the term, might even be unable to initially locate the diagnosis for selection.
The physician selects an interface terminology diagnosis. The selected diagnosis populates the patient's problem list. The associated ICD-9-CM mappings populate the organization's billing system for review and claims generation to increase efficiency and accuracy in the revenue cycle.
Clinical Interface to the Standards
Importance of Interface Terminology
The goal of interface terminology is to facilitate clinical documentation while streamlining other administrative functions of healthcare. Clinician-friendly terms with associated industry standard terminologies facilitate this goal. Interface terminology also supports the "capture once, use many times" philosophy of electronic health information. For example, if the term "CHF (congestive heart failure)" is captured with an associated ICD-9-CM code (428.0) or ICD-10-CM code (I50.9) and SNOMED CT code (42343007), the ICD code is routed to the financial system for review and claims generation, while the SNOMED CT code is available for other reporting.
ICD-10-CM/PCS codes may also be associated with the terms in an interface terminology. Having both ICD-9-CM and ICD-10-CM/PCS codes available for the terms frequently documented by an organization's providers can facilitate ICD-10-CM/PCS preparation. Interface terminology provides a stable and constant pivot point to meet the changing coding requirements of the healthcare industry. Depending upon the EHR functionality, organizations can extract the terms and associated codes for analysis.
Maintaining up-to-date and accurate information is just as vital to an organization as the implementation and design of the EHR. As industry standard terminologies are updated, organizations engage in a maintenance process. Interface terminology eases the maintenance process for organizations.
What happens if a diagnosis appears in a medical record, but the ICD code for that diagnosis is replaced? Interface terminology has the ability to have the diagnostic term remain active while the associated ICD code is updated to reflect the new code. No longer can physicians select diagnoses linked to out-of-date, incorrect, or non-billable codes. This helps reduce the amount of running back-and-forth between billing and clinicians to determine clinical intent and adjudicate coding discrepancies. The historical tags between the term and the prior ICD code stay intact for historical purposes.
Benefits of Interface Terminology
While there are many benefits of interface terminology, the most notable are:
- Uses familiar medical terms, which reduces search time and increases precision
- Improves charge capture as a result of accurate diagnostic codes
- Minimizes maintenance, which saves the expense of creating and maintaining a term dictionary and complicated term-to-code mappings
- Provides meaningful use compliance
- Enables accurate data capture at the point of care
- Increases patient safety through clarity of diagnosis, problem, and procedure descriptions
Health information management (HIM) professionals need to recognize the role of interface terminology in the EHR. Knowing how the terminology works in the EHR will help to ensure the organization is reaping all the benefits of the system.
The interface terminology affects how information is managed, from impacting the revenue cycle to the design of the physician's search experience and preservation of the clinical intent within the longitudinal EHR. HIM professionals, at a minimum, should be knowledgeable regarding:
- Which industry standard terminologies are associated with the terms
- The search functionality and the physician's search experience
- Where the coded information flows in the EHR once the physicians select the term
- How interface terminology is maintained along with documented procedures to resolve mapping discrepancies
- The use of interface terminology in natural language processing and auto-coding applications
- Where associated terminology is stored for secondary data uses and other data management activities as related to documentation workflow, data warehouse, patient active summary sheet, template, and other EHR documentation tools.
Interface Terminology and Patient-Centered Care
Patients are the heart of healthcare. Today there is a renewed focus on patients as the driving force behind their received care, as the industry is striving for a holistic, patient-centered approach to providing care. Recent government regulations, such as accountable care organizations (ACOs), support and reinforce this idea. The ACO is a new care delivery model focused on a provider team to coordinate and manage healthcare services for a defined patient population. This coordinated care team is the designed point of contact to ensure that all of the patient's healthcare needs are being addressed regardless of setting or specialty. Accurate information is critical to managing patient populations effectively. This drives the need for longitudinal data sharing, which has been a challenge for the healthcare industry.
Interface terminologies can play a large role in the ability to store and share data across provider settings, impacting these recent government regulations. They have the ability to capture clinical intent and create historical data to be available for longitudinal records. The needed level of clinical granularity is captured, which is important for continuity of care between providers. Having all associated maps for the terms also allows providers to know and manage their patient population. This robust data enables sound business practices for providers in addition to making the best decisions for their patients.
Interface terminology is vital to healthcare today and tomorrow, as terminology is the foundation of documentation improvements that will in turn improve patient care. The role of documentation does not change from paper to electronic. The saying "if it is not documented, it was not done" still applies. But how the documentation is accomplished does change in the electronic environment, and efficiencies are gained by using an interface terminology.
- Bowman, Sue. "Coordination of SNOMED-CT and ICD-10: Getting the Most out of Electronic Health Record Systems." Perspectives in Health Information Management, spring 2005 (May 25, 2005). Available at http://perspectives.ahima.org.
- Kanter, Andrew S., et al. "Interface Terminologies: Bridging the Gap between Theory and Reality for Africa." Studies in Health Technology and Informatics, vol. 136 (2008): p. 27-32. Available online at http://www.sim.hcuge.ch/helina/25.pdf.
June Bronnert (firstname.lastname@example.org) is director, terminology coding, Chip Masarie (email@example.com) is chief terminologist, Frank Naeymi-Rad (firstname.lastname@example.org) is chairman and CEO, Eric Rose (email@example.com) is director, clinical terminology, and Greg Aldin (firstname.lastname@example.org) is director, knowledge team operations at Intelligent Medical Objects, Inc.
Bronnert, June; Masarie, Chip; Naeymi-Rad, Frank; Rose, Eric; Aldin, Greg.
"Problem-Centered Care Delivery: How Interface Terminology Makes Standardized Health Information Possible"
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|Synonyms||Tourette's syndrome, Tourette's disorder, Gilles de la Tourette syndrome (GTS)|
|Georges Gilles de la Tourette (1857–1904), namesake of Tourette syndrome|
|Usual onset||Typically in childhood|
|Causes||Genetic with environmental influence|
|Diagnostic method||Based on history and symptoms|
|Treatment||Education, behavioral therapy|
|Medication||Usually none, occasionally antipsychotics|
|Prognosis||Improvement to disappearance of tics beginning in late teens|
Tourette syndrome (TS or simply Tourette's) is a common neuropsychiatric disorder with onset in childhood, characterized by multiple motor tics and at least one vocal (phonic) tic. These tics characteristically wax and wane, can be suppressed temporarily, and are typically preceded by an unwanted urge or sensation in the affected muscles. Some common tics are eye blinking, coughing, throat clearing, sniffing, and facial movements. Tourette's does not adversely affect intelligence or life expectancy.
Tourette's is defined as part of a spectrum of tic disorders, which includes provisional, transient and persistent (chronic) tics. While the exact cause is unknown, it is believed to involve a combination of genetic and environmental factors. There are no specific tests for diagnosing Tourette's; it is not always correctly identified because most cases are mild and the severity of tics decreases for most children as they pass through adolescence. Extreme Tourette's in adulthood, though sensationalized in the media, is a rarity; tics are often unnoticed by casual observers.
In most cases, medication for tics is not necessary. Education is an important part of any treatment plan, and explanation and reassurance alone are often sufficient treatment. Many individuals with Tourette's go undiagnosed or never seek medical care. Among those who are seen in specialty clinics, attention-deficit hyperactivity disorder (ADHD) and obsessive–compulsive disorder (OCD) are present at higher rates. These co-occurring diagnoses often cause more impairment to the individual than the tics; hence, it is important to correctly identify associated conditions and treat them.
About 1% of school-age children and adolescents have Tourette's. It was once considered a rare and bizarre syndrome, most often associated with coprolalia (the utterance of obscene words or socially inappropriate and derogatory remarks), but this symptom is present in only a small minority of people with Tourette's. The condition was named by Jean-Martin Charcot (1825–1893) on behalf of his resident, Georges Albert Édouard Brutus Gilles de la Tourette (1857–1904), a French physician and neurologist, who published an account of nine patients with Tourette's in 1885.
Tics are sudden, repetitive, nonrhythmic movements (motor tics) and utterances (phonic tics) that involve discrete muscle groups. Motor tics are movement-based tics, while phonic tics are involuntary sounds produced by moving air through the nose, mouth, or throat.
Tourette's was classified by the fourth version of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR) as one of several tic disorders "usually first diagnosed in infancy, childhood, or adolescence" according to type (motor or phonic tics) and duration (transient or chronic). Transient tic disorders consisted of multiple motor tics, phonic tics or both, with a duration between four weeks and twelve months. Chronic tic disorder was either single or multiple, motor or phonic tics (but not both), which were present for more than a year. Tourette's is diagnosed when multiple motor tics, and at least one phonic tic, are present for more than a year. The fifth version of the DSM (DSM-5), published in May 2013, reclassified Tourette's and tic disorders as motor disorders listed in the neurodevelopmental disorder category, and replaced transient tic disorder with provisional tic disorder, but made few other significant changes.
Tic disorders are defined only slightly differently by the World Health Organization International Statistical Classification of Diseases and Related Health Problems, ICD-10; code F95.2 is for combined vocal and multiple motor tic disorder [de la Tourette].
Although Tourette's is the more severe expression of the spectrum of tic disorders, most cases are mild. The severity of symptoms varies widely among people with Tourette's, and mild cases may be undetected.
Tics are movements or sounds "that occur intermittently and unpredictably out of a background of normal motor activity", having the appearance of "normal behaviors gone wrong". The tics associated with Tourette's change in number, frequency, severity and anatomical location. Waxing and waning—the ongoing increase and decrease in severity and frequency of tics—occurs differently in each individual. Tics may also occur in "bouts of bouts", which vary for each person.
Coprolalia (the spontaneous utterance of socially objectionable or taboo words or phrases) is the most publicized symptom of Tourette's, but it is not required for a diagnosis of Tourette's and only about 10% of Tourette's patients exhibit it. Echolalia (repeating the words of others) and palilalia (repeating one's own words) occur in a minority of cases, while the most common initial motor and vocal tics are, respectively, eye blinking and throat clearing.
In contrast to the abnormal movements of other movement disorders (for example, choreas, dystonias, myoclonus, and dyskinesias), the tics of Tourette's are temporarily suppressible, nonrhythmic, and often preceded by an unwanted premonitory urge. Immediately preceding tic onset, most individuals with Tourette's are aware of an urge, similar to the need to sneeze or scratch an itch. Individuals describe the need to tic as a buildup of tension, pressure, or energy which they consciously choose to release, as if they "had to do it" to relieve the sensation or until it feels "just right". Examples of the premonitory urge are the feeling of having something in one's throat, or a localized discomfort in the shoulders, leading to the need to clear one's throat or shrug the shoulders. The actual tic may be felt as relieving this tension or sensation, similar to scratching an itch. Another example is blinking to relieve an uncomfortable sensation in the eye. These urges and sensations, preceding the expression of the movement or vocalization as a tic, are referred to as "premonitory sensory phenomena" or premonitory urges. Because of the urges that precede them, tics are described as semi-voluntary or "unvoluntary", rather than specifically involuntary; they may be experienced as a voluntary, suppressible response to the unwanted premonitory urge. Published descriptions of the tics of Tourette's identify sensory phenomena as the core symptom of the syndrome, even though they are not included in the diagnostic criteria.
|Video clips of tics|
While individuals with tics are sometimes able to suppress their tics for limited periods of time, doing so often results in tension or mental exhaustion. People with Tourette's may seek a secluded spot to release their symptoms, or there may be a marked increase in tics after a period of suppression at school or at work. Some people with Tourette's may not be aware of the premonitory urge. Children may be less aware of the premonitory urge associated with tics than are adults, but their awareness tends to increase with maturity. They may have tics for several years before becoming aware of premonitory urges. Children may suppress tics while in the doctor's office, so they may need to be observed while they are not aware they are being watched. The ability to suppress tics varies among individuals, and may be more developed in adults than children.
Although there is no such thing as a "typical" case of Tourette syndrome, the condition follows a fairly reliable course in terms of the age of onset and the history of the severity of symptoms. Tics may appear up to the age of eighteen, but the most typical age of onset is from five to seven. A 1998 study published by Leckman and colleagues from the Yale Child Study Center showed that the ages of highest tic severity are eight to twelve (average ten), with tics steadily declining for most patients as they pass through adolescence. The most common, first-presenting tics are eye blinking, facial movements, sniffing and throat clearing. Initial tics present most frequently in midline body regions where there are many muscles, usually the head, neck and facial region. This can be contrasted with the stereotyped movements of other disorders (such as stims and stereotypies of the autism spectrum disorders), which typically have an earlier age of onset, are more symmetrical, rhythmical and bilateral, and involve the extremities (e.g., flapping the hands). Tics that appear early in the course of the condition are frequently confused with other conditions, such as allergies, asthma, and vision problems: pediatricians, allergists and ophthalmologists are typically the first to see a child with tics.
Most cases of Tourette's in older individuals are mild and almost unrecognizable. When symptoms are severe enough to warrant referral to clinics, obsessive–compulsive disorder (OCD) and attention-deficit hyperactivity disorder (ADHD) are often associated with Tourette's. In children with tics, the additional presence of ADHD is associated with functional impairment, disruptive behavior, and tic severity. Compulsions resembling tics are present in some individuals with OCD; "tic-related OCD" is hypothesized to be a subgroup of OCD, distinguished from non-tic related OCD by the type and nature of obsessions and compulsions. Not all persons with Tourette's have ADHD or OCD or other comorbid conditions, although in clinical populations, a high percentage of patients presenting for care do have ADHD. One author reports that a ten-year overview of patient records revealed about 40% of patients with Tourette's have "TS-only" or "pure TS", referring to Tourette syndrome in the absence of ADHD, OCD and other disorders. Another author reports that 57% of 656 patients presenting with tic disorders had uncomplicated tics, while 43% had tics plus comorbid conditions. People with "full-blown Tourette's" have significant comorbid conditions in addition to tics.
The exact cause of Tourette's is unknown, but it is well established that both genetic and environmental factors are involved. Genetic epidemiology studies have shown that the overwhelming majority of cases of Tourette's are inherited, although the exact mode of inheritance is not yet known and no gene has been identified. In other cases, tics are associated with disorders other than Tourette's, a phenomenon known as tourettism.
A person with Tourette's has about a 50% chance of passing the gene(s) to one of his or her children, but Tourette's is a condition of variable expression and incomplete penetrance. Thus, not everyone who inherits the genetic vulnerability will show symptoms; even close family members may show different severities of symptoms, or no symptoms at all. The gene(s) may express as Tourette's, as a milder tic disorder (provisional or chronic tics), or as obsessive–compulsive symptoms without tics. Only a minority of the children who inherit the gene(s) have symptoms severe enough to require medical attention. Gender appears to have a role in the expression of the genetic vulnerability: males are more likely than females to express tics.
Non-genetic, environmental, post-infectious, or psychosocial factors—while not causing Tourette's—can influence its severity. Autoimmune processes may affect tic onset and exacerbation in some cases. In 1998, a team at the US National Institute of Mental Health proposed a hypothesis based on observation of 50 children that both obsessive–compulsive disorder (OCD) and tic disorders may arise in a subset of children as a result of a poststreptococcal autoimmune process. Children who meet five diagnostic criteria are classified, according to the hypothesis, as having Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal infections (PANDAS). This contentious hypothesis is the focus of clinical and laboratory research, but remains unproven.
Some forms of OCD may be genetically linked to Tourette's. A subset of OCD is thought to be causally related to Tourette's and may be a different expression of the same factors that are important for the expression of tics. The genetic relationship of ADHD to Tourette syndrome, however, has not been fully established.
The exact mechanism affecting the inherited vulnerability to Tourette's has not been established, and the precise cause is unknown. Tics are believed to result from dysfunction in cortical and subcortical regions, the thalamus, basal ganglia and frontal cortex. Neuroanatomic models implicate failures in circuits connecting the brain's cortex and subcortex, and imaging techniques implicate the basal ganglia and frontal cortex. After 2010, the role of histamine and the H3-receptor came into focus in the pathophysiology of TS, as "key modulators of striatal circuitry". A reduced level of histamine in the H3-receptor may disrupt other neurotransmitters, causing tics.
According to the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5), Tourette’s may be diagnosed when a person exhibits both multiple motor and one or more vocal tics over the period of a year; the motor and vocal tics need not be concurrent. The onset must have occurred before the age of 18, and cannot be attributed to the effects of another condition or substance (such as cocaine). Hence, other medical conditions that include tics or tic-like movements—such as autism or other causes of tourettism—must be ruled out before conferring a Tourette's diagnosis. Since 2000, the DSM has recognized that clinicians see patients who meet all the other criteria for Tourette's, but do not have distress or impairment.
There are no specific medical or screening tests that can be used in diagnosing Tourette's; it is frequently misdiagnosed or underdiagnosed, partly because of the wide expression of severity, ranging from mild (the majority of cases) or moderate, to severe (the rare, but more widely recognized and publicized cases). Coughing, eye blinking, and tics that mimic unrelated conditions such as asthma are commonly misdiagnosed.
The diagnosis is made based on observation of the individual's symptoms and family history, and after ruling out secondary causes of tic disorders. In patients with a typical onset and a family history of tics or obsessive–compulsive disorder, a basic physical and neurological examination may be sufficient.
There is no requirement that other comorbid conditions (such as ADHD or OCD) be present, but if a physician believes that there may be another condition present that could explain tics, tests may be ordered as necessary to rule out that condition. An example of this is when diagnostic confusion between tics and seizure activity exists, which would call for an EEG, or if there are symptoms that indicate an MRI to rule out brain abnormalities. TSH levels can be measured to rule out hypothyroidism, which can be a cause of tics. Brain imaging studies are not usually warranted. In teenagers and adults presenting with a sudden onset of tics and other behavioral symptoms, a urine drug screen for cocaine and stimulants might be necessary. If a family history of liver disease is present, serum copper and ceruloplasmin levels can rule out Wilson's disease. Most cases are diagnosed by merely observing a history of tics.
Secondary causes of tics (not related to inherited Tourette syndrome) are commonly referred to as tourettism. Dystonias, choreas, other genetic conditions, and secondary causes of tics should be ruled out in the differential diagnosis for Tourette syndrome. Other conditions that may manifest tics or stereotyped movements include developmental disorders, autism spectrum disorders, and stereotypic movement disorder; Sydenham's chorea; idiopathic dystonia; and genetic conditions such as Huntington's disease, neuroacanthocytosis, Hallervorden-Spatz syndrome, Duchenne muscular dystrophy, Wilson's disease, and tuberous sclerosis. Other possibilities include chromosomal disorders such as Down syndrome, Klinefelter syndrome, XYY syndrome and fragile X syndrome. Acquired causes of tics include drug-induced tics, head trauma, encephalitis, stroke, and carbon monoxide poisoning. The symptoms of Lesch-Nyhan syndrome may also be confused with Tourette syndrome. Most of these conditions are rarer than tic disorders, and a thorough history and examination may be enough to rule them out, without medical or screening tests.
Although not all people with Tourette's have comorbid conditions, most Tourette's patients presenting for clinical care at specialty referral centers may exhibit symptoms of other conditions along with their motor and phonic tics. Associated conditions include attention-deficit hyperactivity disorder (ADD or ADHD), obsessive–compulsive disorder (OCD), learning disabilities and sleep disorders. Disruptive behaviors, impaired functioning, or cognitive impairment in patients with comorbid Tourette's and ADHD may be accounted for by the comorbid ADHD, highlighting the importance of identifying and treating comorbid conditions. Disruption from tics is commonly overshadowed by comorbid conditions that present greater interference to the child. Tic disorders in the absence of ADHD do not appear to be associated with disruptive behavior or functional impairment, while impairment in school, family, or peer relations is greater in patients who have more comorbid conditions and often determines whether therapy is needed.
Because comorbid conditions such as OCD and ADHD can be more impairing than tics, these conditions are included in an evaluation of patients presenting with tics. "It is critical to note that the comorbid conditions may determine functional status more strongly than the tic disorder," according to Samuel Zinner, MD. The initial assessment of a patient referred for a tic disorder should include a thorough evaluation, including a family history of tics, ADHD, obsessive–compulsive symptoms, and other chronic medical, psychiatric and neurological conditions. Children and adolescents with TS who have learning difficulties are candidates for psychoeducational testing, particularly if the child also has ADHD. Undiagnosed comorbid conditions may result in functional impairment, and it is necessary to identify and treat these conditions to improve functioning. Complications may include depression, sleep problems, social discomfort, self-injury, anxiety, personality disorders, oppositional defiant disorder, and conduct disorders.
The treatment of Tourette's focuses on identifying and helping the individual manage the most troubling or impairing symptoms. Most cases of Tourette's are mild, and do not require pharmacological treatment; instead, psychobehavioral therapy, education, and reassurance may be sufficient. Treatments, where warranted, can be divided into those that target tics and comorbid conditions, which, when present, are often a larger source of impairment than the tics themselves. Not all people with tics have comorbid conditions, but when those conditions are present, they often take treatment priority.
There is no cure for Tourette's and no medication that works universally for all individuals without significant adverse effects. Knowledge, education and understanding are uppermost in management plans for tic disorders. The management of the symptoms of Tourette's may include pharmacological, behavioral and psychological therapies. While pharmacological intervention is reserved for more severe symptoms, other treatments (such as supportive psychotherapy or cognitive behavioral therapy) may help to avoid or ameliorate depression and social isolation, and to improve family support. Educating a patient, family, and surrounding community (such as friends, school, and church) is a key treatment strategy, and may be all that is required in mild cases.
Medication is available to help when symptoms interfere with functioning. The classes of medication with the most proven efficacy in treating tics—typical and atypical neuroleptics including risperidone (trade name Risperdal), ziprasidone (Geodon), haloperidol (Haldol), pimozide (Orap) and fluphenazine (Prolixin)—can have long-term and short-term adverse effects. The antihypertensive agents clonidine (trade name Catapres) and guanfacine (Tenex) are also used to treat tics; studies show variable efficacy, but a lower side effect profile than the neuroleptics. Stimulants and other medications may be useful in treating ADHD when it co-occurs with tic disorders. Drugs from several other classes of medications can be used when stimulant trials fail, including guanfacine (trade name Tenex), atomoxetine (Strattera) and tricyclic antidepressants. Clomipramine (Anafranil), a tricyclic, and SSRIs—a class of antidepressants including fluoxetine (Prozac), sertraline (Zoloft), and fluvoxamine (Luvox)—may be prescribed when a Tourette's patient also has symptoms of obsessive–compulsive disorder. Several other medications have been tried, but evidence to support their use is unconvincing.
Because children with tics often present to physicians when their tics are most severe, and because of the waxing and waning nature of tics, it is recommended that medication not be started immediately or changed often. Frequently, the tics subside with explanation, reassurance, understanding of the condition and a supportive environment. When medication is used, the goal is not to eliminate symptoms: it should be used at the lowest possible dose that manages symptoms without adverse effects, given that these may be more disturbing than the symptoms for which they were prescribed.
Cognitive behavioral therapy (CBT) is a useful treatment when OCD is present, and there is increasing evidence supporting the use of habit reversal (HRT) in the treatment of tics. There is evidence that HRT reduces tic severity, but there are methodological limitations in the studies, and a need for more trained specialists and better large-scale studies.
Relaxation techniques, such as exercise, yoga or meditation, may be useful in relieving the stress that may aggravate tics, but the majority of behavioral interventions (such as relaxation training and biofeedback, with the exception of habit reversal) have not been systematically evaluated and are not empirically supported therapies for Tourette's. Deep brain stimulation has been used to treat adults with severe Tourette's that does not respond to conventional treatment, but it is regarded as an invasive, experimental procedure that is unlikely to become widespread.
Tourette syndrome is a spectrum disorder—its severity ranges over a spectrum from mild to severe. The majority of cases are mild and require no treatment. In these cases, the impact of symptoms on the individual may be mild, to the extent that casual observers might not know of their condition. The overall prognosis is positive, but a minority of children with Tourette syndrome have severe symptoms that persist into adulthood. A study of 46 subjects at 19 years of age found that the symptoms of 80% had minimum to mild impact on their overall functioning, and that the other 20% experienced at least a moderate impact on their overall functioning. The rare minority of severe cases can inhibit or prevent individuals from holding a job or having a fulfilling social life. In a follow-up study of thirty-one adults with Tourette's, all patients completed high school, 52% finished at least two years of college, and 71% were full-time employed or were pursuing higher education.
Regardless of symptom severity, individuals with Tourette's have a normal life span. Although the symptoms may be lifelong and chronic for some, the condition is not degenerative or life-threatening. Intelligence is normal in those with Tourette's, although there may be learning disabilities. Severity of tics early in life does not predict tic severity in later life, and prognosis is generally favorable, although there is no reliable means of predicting the outcome for a particular individual. The gene or genes associated with Tourette's have not been identified, and there is no potential "cure". A higher rate of migraines than the general population and sleep disturbances are reported.
Several studies have demonstrated that the condition in most children improves with maturity. Tics may be at their highest severity at the time that they are diagnosed, and often improve with understanding of the condition by individuals and their families and friends. The statistical age of highest tic severity is typically between eight and twelve, with most individuals experiencing steadily declining tic severity as they pass through adolescence. One study showed no correlation with tic severity and the onset of puberty, in contrast with the popular belief that tics increase at puberty. In many cases, a complete remission of tic symptoms occurs after adolescence. However, a study using videotape to record tics in adults found that, although tics diminished in comparison with childhood, and all measures of tic severity improved by adulthood, 90% of adults still had tics. Half of the adults who considered themselves tic-free still displayed evidence of tics.
Many people with TS may not realize they have tics; because tics are more commonly expressed in private, TS may go unrecognized or undetected. It is not uncommon for the parents of affected children to be unaware that they, too, may have had tics as children. Because Tourette's tends to subside with maturity, and because milder cases of Tourette's are now more likely to be recognized, the first realization that a parent had tics as a child may not come until their offspring is diagnosed. It is not uncommon for several members of a family to be diagnosed together, as parents bringing children to a physician for an evaluation of tics become aware that they, too, had tics as a child.
Children with Tourette's may suffer socially if their tics are viewed as "bizarre". If a child has disabling tics, or tics that interfere with social or academic functioning, supportive psychotherapy or school accommodations can be helpful. Because comorbid conditions (such as ADHD or OCD) can cause greater impact on overall functioning than tics, a thorough evaluation for comorbidity is called for when symptoms and impairment warrant.
A supportive environment and family generally gives those with Tourette's the skills to manage the disorder. People with Tourette's may learn to camouflage socially inappropriate tics or to channel the energy of their tics into a functional endeavor. Accomplished musicians, athletes, public speakers, and professionals from all walks of life are found among people with Tourette's. Outcomes in adulthood are associated more with the perceived significance of having severe tics as a child than with the actual severity of the tics. A person who was misunderstood, punished, or teased at home or at school will fare worse than children who enjoyed an understanding and supportive environment.
Tourette syndrome is found among all social, racial and ethnic groups and has been reported in all parts of the world; it is three to four times more frequent among males than among females. The tics of Tourette syndrome begin in childhood and tend to remit or subside with maturity; thus, a diagnosis may no longer be warranted for many adults, and observed prevalence rates are higher among children than adults. As children pass through adolescence, about one-quarter become tic-free, almost one-half see their tics diminish to a minimal or mild level, and less than one-quarter have persistent tics. Only 5 to 14% of adults experience worse tics in adulthood than in childhood.
Up to 1% of the overall population experiences tic disorders, including chronic tics and transient tics of childhood. Chronic tics affect 5% of children, and transient tics affect up to 20%. Prevalence rates in special education populations are higher.
The reported prevalence of TS varies "according to the source, age, and sex of the sample; the ascertainment procedures; and diagnostic system", with a range reported between .4% and 3.8% for children ages 5 to 18. Robertson (2011) says that 1% of school-age children have Tourette's. According to Lombroso and Scahill (2008), the emerging consensus is that .1 to 1% of children have Tourette's, with several studies supporting a tighter range of .6 to .8%. Bloch and Leckman (2009) and Swain (2007) report a range of prevalence in children of .4 to .6%, Knight et al. (2012) estimate .77% in children, and Du et al. (2010) report that 1 to 3% of Western school-age children have Tourette's.
Singer (2011) states the prevalence of TS in the overall population at any time is .1% for impairing cases and .6% for all cases, while Bloch and colleagues (2011) state the overall prevalence as between .3 and 1%. Robertson (2011) also suggests that the rate of Tourette's in the general population is 1%. Using year 2000 census data, a prevalence range of .1 to 1% yields an estimate of 53,000–530,000 school-age children with Tourette's in the US, and a prevalence estimate of .1% means that in 2001 about 553,000 people in the UK age 5 or older would have Tourette's.
Tourette syndrome was once thought to be rare: in 1972, the US National Institutes of Health (NIH) believed there were fewer than 100 cases in the United States, and a 1973 registry reported only 485 cases worldwide. However, multiple studies published since 2000 have consistently demonstrated that the prevalence is much higher than previously thought. Discrepancies across current and prior prevalence estimates come from several factors: ascertainment bias in earlier samples drawn from clinically referred cases, assessment methods that may fail to detect milder cases, and differences in diagnostic criteria and thresholds. There were few broad-based community studies published before 2000 and until the 1980s, most epidemiological studies of Tourette syndrome were based on individuals referred to tertiary care or specialty clinics. Individuals with mild symptoms may not seek treatment and physicians may not confer an official diagnosis of TS on children out of concern for stigmatization; children with milder symptoms are unlikely to be referred to specialty clinics, so prevalence studies have an inherent bias towards more severe cases. Studies of Tourette syndrome are vulnerable to error because tics vary in intensity and expression, are often intermittent, and are not always recognized by clinicians, patients, family members, friends or teachers; approximately 20% of persons with Tourette syndrome do not recognize that they have tics. Newer studies—recognizing that tics may often be undiagnosed and hard to detect—use direct classroom observation and multiple informants (parent, teacher, and trained observers), and therefore record more cases than older studies relying on referrals. As the diagnostic threshold and assessment methodology have moved towards recognition of milder cases, the result is an increase in estimated prevalence.
Tourette's is associated with several comorbid conditions, or co-occurring diagnoses, which are often the major source of impairment for an affected child. Most individuals with tics do not seek medical attention, so epidemiological studies of TS "reflect a strong ascertainment bias", but among those who do warrant medical attention, the majority have other conditions, and up to 50% have ADHD or OCD.
The first presentation of Tourette syndrome is thought to be in the book, Malleus Maleficarum ("Witch's hammer") by Jakob Sprenger and Heinrich Kraemer, published in the late 15th century and describing a priest whose tics were "believed to be related to possession by the devil". A French doctor, Jean Marc Gaspard Itard, reported the first case of Tourette syndrome in 1825, describing Marquise de Dampierre, an important woman of nobility in her time. Jean-Martin Charcot, an influential French physician, assigned his resident Georges Albert Édouard Brutus Gilles de la Tourette, a French physician and neurologist, to study patients at the Salpêtrière Hospital, with the goal of defining an illness distinct from hysteria and from chorea.
In 1885, Gilles de la Tourette published an account in Study of a Nervous Affliction describing nine persons with "convulsive tic disorder", concluding that a new clinical category should be defined. The eponym was later bestowed by Charcot after and on behalf of Gilles de la Tourette.
Little progress was made over the next century in explaining or treating tics, and a psychogenic view prevailed well into the 20th century. The possibility that movement disorders, including Tourette syndrome, might have an organic origin was raised when an encephalitis epidemic from 1918–1926 led to a subsequent epidemic of tic disorders.
During the 1960s and 1970s, as the beneficial effects of haloperidol (Haldol) on tics became known, the psychoanalytic approach to Tourette syndrome was questioned. The turning point came in 1965, when Arthur K. Shapiro—described as "the father of modern tic disorder research"—treated a Tourette’s patient with haloperidol, and published a paper criticizing the psychoanalytic approach.
Since the 1990s, a more neutral view of Tourette's has emerged, in which biological vulnerability and adverse environmental events are seen to interact. In 2000, the American Psychiatric Association published the DSM-IV-TR, revising the text of DSM-IV to no longer require that symptoms of tic disorders cause distress or impair functioning, recognizing that clinicians often see patients who meet all the other criteria for Tourette's, but do not have distress or impairment.
Findings since 1999 have advanced TS science in the areas of genetics, neuroimaging, neurophysiology, and neuropathology. Questions remain regarding how best to classify Tourette syndrome, and how closely Tourette's is related to other movement disorders or psychiatric disorders. Good epidemiologic data is still lacking, and available treatments are not risk free and not always well tolerated. High-profile media coverage focuses on treatments that do not have established safety or efficacy, such as deep brain stimulation, and alternative therapies involving unstudied efficacy and side effects are pursued by many parents.
Society and culture
Not everyone with Tourette's wants treatment or a "cure", especially if that means they may "lose" something else in the process. Researchers Leckman and Cohen, and former US Tourette Syndrome Association (TSA) national board member Kathryn Taubert, believe that there may be latent advantages associated with an individual's genetic vulnerability to developing Tourette syndrome, such as a heightened awareness and increased attention to detail and surroundings that may have adaptive value. There is evidence to support the clinical lore that children with "TS-only" (Tourette's in the absence of comorbid conditions) are unusually gifted: neuropsychological studies have identified advantages in children with TS-only. Children with TS-only are faster than the average for their age group on timed tests of motor coordination.
Notable individuals with Tourette syndrome are found in all walks of life, including musicians, athletes, media figures, teachers, physicians, and authors. The best-known example of a person who may have used obsessive–compulsive traits to advantage is Samuel Johnson, the 18th-century English man of letters, who likely had Tourette syndrome as evidenced by the writings of James Boswell. Johnson wrote A Dictionary of the English Language in 1747, and was a prolific writer, poet, and critic. Tim Howard, described by the Chicago Tribune as the "rarest of creatures – an American soccer hero" and by the TSA as the "most notable individual with Tourette Syndrome around the world" says that his neurological makeup gave him an enhanced perception and an ability to hyper-focus that contributed to his success on the field.
Although it has been speculated that Mozart had Tourette's, no Tourette's expert or organization has presented credible evidence to support such a conclusion, and there are problems with the arguments supporting the diagnosis: tics are not transferred to the written form, as is supposed with Mozart's scatological writings; the medical history in retrospect is not thorough; side effects due to other conditions may be misinterpreted; "it is not proven whether written documents can account for the existence of a vocal tic" and "the evidence of motor tics in Mozart's life is doubtful."
Pre-dating Gilles de la Tourette's 1885 publication, likely portrayals of TS or tic disorders in fictional literature are Mr. Pancks in Little Dorrit by Charles Dickens and Nikolai Levin in Anna Karenina by Leo Tolstoy. The entertainment industry has been criticized for depicting those with Tourette syndrome as social misfits whose only tic is coprolalia, which has furthered stigmatization and the public's misunderstanding of those with Tourette's. The coprolalic symptoms of Tourette's are also fodder for radio and television talk shows in the US and in the British media.
- "Tourette Syndrome Fact Sheet". NINDS. 16 April 2014. Archived from the original on March 23, 2005. Retrieved 18 October 2016.
- Singer HS. "Tourette syndrome and other tic disorders". Handb Clin Neurol. 2011;100:641–57. doi:10.1016/B978-0-444-52014-2.00046-X PMID 21496613. Also see Singer HS. "Tourette's syndrome: from behaviour to biology". Lancet Neurol. 2005 Mar;4(3):149–59. doi:10.1016/S1474-4422(05)01012-4 PMID 15721825.
- Robertson MM. "Gilles de la Tourette syndrome: the complexities of phenotype and treatment". Br J Hosp Med (Lond). 2011 Feb;72(2):100–7. PMID 21378617
- Jankovic J. Movement Disorders, An Issue of Neurologic Clinics. The Clinics: Radiology: Elsevier, 2014, p. viii
- Peterson BS, Cohen DJ. "The treatment of Tourette's Syndrome: multimodal, developmental intervention". J Clin Psychiatry. 1998;59 Suppl 1:62–72; discussion 73–74. PMID 9448671. Quote: "Because of the understanding and hope that it provides, education is also the single most important treatment modality that we have in TS." Also see Zinner 2000.
- Du JC, Chiu TF, Lee KM, et al. "Tourette syndrome in children: an updated review". Pediatr Neonatol. 2010 Oct;51(5):255–64. doi:10.1016/S1875-9572(10)60050-2 PMID 20951354
- Leckman JF, Bloch MH, King RA, Scahill L. "Phenomenology of tics and natural history of tic disorders". Adv Neurol. 2006;99:1–16. PMID 16536348
- "Tourette's Disorder, 307.23 (F95.2)". Diagnostic and Statistical Manual of Mental Disorders, 2013, Fifth edition. American Psychiatric Association, p. 81.
- Neurodevelopmental disorders. American Psychiatric Association. Retrieved on December 29, 2011.
- Moran, M. "DSM-5 provides new take on neurodevelopment disorders". Psychiatric News. 18 January 2013;48(2):6–23. doi:10.1176/appi.pn.2013.1b11
- "Highlights of changes from DSM-IV-TR to DSM-5" (PDF). American Psychiatric Association. 2013. Retrieved on June 5, 2013.
- Du, Chiu, Lee, et al. 2010. See also ICD version 2007. World Health Organization. Retrieved on December 29, 2011.
- Bagheri MM, Kerbeshian J, Burd L. "Recognition and management of Tourette's syndrome and tic disorders". Archived March 31, 2005, at the Wayback Machine. American Family Physician. 1999; 59:2263–74. PMID 10221310 Retrieved on October 28, 2006.
- The Tourette Syndrome Classification Study Group. "Definitions and classification of tic disorders". Arch Neurol. 1993 Oct;50(10):1013–16. PMID 8215958 Archived April 26, 2006.
- Dure LS 4th, DeWolfe J. "Treatment of tics". Adv Neurol. 2006;99:191–96. PMID 16536366
- Malone DA Jr, Pandya MM. "Behavioral neurosurgery". Adv Neurol. 2006;99:241–47. PMID 16536372
- Jankovic J. "Differential diagnosis and etiology of tics". Adv Neurol. 2001;85:15–29. PMID 11530424
- Cohen AJ, Leckman JF. "Sensory phenomena associated with Gilles de la Tourette's syndrome". J Clin Psychiatry. 1992 Sep;53(9):319–23. PMID 1517194
- Prado HS, Rosário MC, Lee J, Hounie AG, Shavitt RG, Miguel EC. "Sensory phenomena in obsessive–compulsive disorder and tic disorders: a review of the literature". CNS Spectr. 2008;13(5):425–32. PMID 18496480.
- Bliss J. "Sensory experiences of Gilles de la Tourette syndrome". Arch Gen Psychiatry. 1980 Dec;37(12):1343–47. PMID 6934713
- Kwak C, Dat Vuong K, Jankovic J. "Premonitory sensory phenomenon in Tourette's syndrome". Mov Disord. 2003 Dec;18(12):1530–33. doi:10.1002/mds.10618 PMID 14673893
- Swain JE, Scahill L, Lombroso PJ, King RA, Leckman JF. "Tourette syndrome and tic disorders: a decade of progress". J Am Acad Child Adolesc Psychiatry. 2007 Aug;46(8):947–68 doi:10.1097/chi.0b013e318068fbcc PMID 17667475
- Scahill LD, Leckman JF, Marek KL. "Sensory phenomena in Tourette's syndrome". Adv Neurol. 1995;65:273–80. PMID 7872145
- Miguel EC, do Rosario-Campos MC, Prado HS, et al. "Sensory phenomena in obsessive–compulsive disorder and Tourette's disorder". J Clin Psychiatry. 2000 Feb;61(2):150–56. PMID 10732667
- Black, KJ. Tourette Syndrome and Other Tic Disorders. eMedicine (March 30, 2007). Retrieved on August 10, 2009.
- Zinner SH. "Tourette disorder". Pediatr Rev. 2000;21(11):372–83. PMID 11077021
- Leckman JF, Zhang H, Vitale A, et al. "Course of tic severity in Tourette syndrome: the first two decades. (PDF). Pediatrics. 1998;102 (1 Pt 1):14–19. PMID 9651407.
- Rapin I. "Autism spectrum disorders: relevance to Tourette syndrome". Adv Neurol. 2001;85:89–101. PMID 11530449
- Robertson MM. "The prevalence and epidemiology of Gilles de la Tourette syndrome. Part 1: the epidemiological and prevalence studies". J Psychosom Res. 2008 Nov;65(5):461–72. doi:10.1016/j.jpsychores.2008.03.006 PMID 18940377
- Robertson MM. "The prevalence and epidemiology of Gilles de la Tourette syndrome. Part 2: tentative explanations for differing prevalence figures in GTS, including the possible effects of psychopathology, aetiology, cultural differences, and differing phenotypes". J Psychosom Res. 2008 Nov;65(5):473–86. doi:10.1016/j.jpsychores.2008.03.007 PMID 18940378
- Hounie AG, do Rosario-Campos MC, Diniz JB, et al. "Obsessive-compulsive disorder in Tourette syndrome". Adv Neurol. 2006;99:22–38. PMID 16536350
- Spencer T, Biederman J, Harding M, et al. "Disentangling the overlap between Tourette's disorder and ADHD". J Child Psychol Psychiatry. 1998 Oct;39(7):1037–44. doi:10.1111/1469-7610.00406 PMID 9804036
- Denckla MB. "Attention-deficit hyperactivity disorder (ADHD) comorbidity: a case for "pure" Tourette syndrome?" J Child Neurol. 2006 Aug;21(8):701–3. PMID 16970871
- Denckla MB. "Attention deficit hyperactivity disorder: the childhood co-morbidity that most influences the disability burden in Tourette syndrome". Adv Neurol. 2006;99:17–21. PMID 16536349
- Walkup, JT, Mink, JW, Hollenback, PJ, (eds). Advances in Neurology, Tourette syndrome. Lippincott, Williams & Wilkins, Philadelphia, PA. 2006;99:xv. ISBN 0-7817-9970-8 Google books.
- Bloch M, State M, Pittenger C. "Recent advances in Tourette syndrome". Curr. Opin. Neurol. 2011 Apr;24(2):119–25. doi:10.1097/WCO.0b013e328344648c PMID 21386676
- O'Rourke JA, Scharf JM, Yu D, et al. "The genetics of Tourette syndrome: A review". J Psychosom Res. 2009 Dec;67(6):533–545. doi:10.1016/j.jpsychores.2009.06.006 PMID 19913658
- Mejia NI, Jankovic J. "Secondary tics and tourettism" (PDF). Rev Bras Psiquiatr. 2005;27(1):11–17. PMID 15867978
- van de Wetering BJ, Heutink P. "The genetics of the Gilles de la Tourette syndrome: a review". J Lab Clin Med. 1993 May;121(5):638–45. PMID 8478592
- Tourette Syndrome: Frequently Asked Questions. Tourette Syndrome Association. Retrieved on May 8, 2013.
- PANDAS. NIH. Retrieved on November 25, 2006.
- Swerdlow, NR. "Tourette Syndrome: Current Controversies and the Battlefield Landscape". Curr Neurol Neurosci Rep. 2005, 5:329–31. doi:10.1007/s11910-005-0054-8 PMID 16131414
- Pauls DL, Towbin KE, Leckman JF, et al. "Gilles de la Tourette's syndrome and obsessive–compulsive disorder. Evidence supporting a genetic relationship". Arch Gen Psychiatry. 1986 Dec;43(12):1180–82. PMID 3465280
- Miguel EC, do Rosario-Campos MC, Shavitt RG, et al. "The tic-related obsessive–compulsive disorder phenotype and treatment implications". Adv Neurol. 2001;85:43–55. PMID 11530446
- Rapanelli M, Pittenger C. “Histamine and Histamine Receptors in Tourette Syndrome and Other Neuropsychiatric Conditions”. Neuropharmacology, 2016 Jul;106:85–90. PMID 26282120 doi:10.1016/j.neuropharm.2015.08.019
- Rapanelli, Maximiliano. “The Magnificent Two: Histamine and the H3 Receptor as Key Modulators of Striatal Circuitry”. Progress in Neuro-Psychopharmacology and Biological Psychiatry, 2017 Feb 6;73:36–40. PMID 27773554 doi:10.1016/j.pnpbp.2016.10.002
- Bolam, J. Paul, and Tommas J. Ellender. “Histamine and the Striatum.” Neuropharmacology, 2016 Jul;106:74–84. PMID 26275849 doi:10.1016/j.neuropharm.2015.08.013
- Sadek B, Saad A, Sadeq A, Jalal F, Stark H. “Histamine H3 Receptor as a Potential Target for Cognitive Symptoms in Neuropsychiatric Diseases.” Behavioural Brain Research 2016 Oct 1;312:415–30. PMID 27363923 doi:10.1016/j.bbr.2016.06.051
- Walkup JT, Ferrão Y, Leckman JF, Stein DJ, Singer H. "Tic disorders: some key issues for DSM-V". Depress Anxiety. 2010 Jun;27(6):600–10. doi:10.1002/da.20711 PMID 20533370
- Summary of Practice: Relevant changes to DSM-IV-TR. American Psychiatric Association. Retrieved from May 11, 2008 archive.org version on December 29, 2011.
- What is DSM-IV-TR? Retrieved on October 28, 2006.
- Scahill L, Erenberg G, Berlin CM Jr, Budman C, Coffey BJ, Jankovic J, Kiessling L, King RA, Kurlan R, Lang A, Mink J, Murphy T, Zinner S, Walkup J; Tourette Syndrome Association Medical Advisory Board: Practice Committee. "Contemporary assessment and pharmacotherapy of Tourette syndrome" (PDF). NeuroRx. 2006 Apr;3(2):192–206. doi:10.1016/j.nurx.2006.01.009 PMID 16554257
- Ringman JM, Jankovic J. "Occurrence of tics in Asperger's syndrome and autistic disorder". J Child Neurol. 2000 Jun;15(6):394–400. PMID 10868783
- Jankovic J, Mejia NI. "Tics associated with other disorders". Adv Neurol. 2006;99:61–68. PMID 16536352
- Freeman, RD. Tourette's Syndrome: minimizing confusion. Roger Freeman, MD, blog. Retrieved on February 8, 2006.
- Scahill L, Williams S, Schwab-Stone M, Applegate J, Leckman JF. "Disruptive behavior problems in a community sample of children with tic disorders". Adv Neurol. 2006;99:184–90. PMID 16536365
- Robertson MM. "Tourette syndrome, associated conditions and the complexities of treatment" (PDF). Brain. 2000;123 Pt 3:425–62. doi:10.1093/brain/123.3.425 PMID 10686169
- Stern JS, Burza S, Robertson MM. "Gilles de la Tourette's syndrome and its impact in the UK". Postgraduate Medicine Journal. 2005 Jan;81(951):12–19. doi:10.1136/pgmj.2004.023614 PMID 15640424
- Medication trade names may differ between countries. In general, this article uses North American trade names.
- Bloch, State, Pittenger 2011. See also Schapiro NA. "Dude, you don't have Tourette's:" Tourette's syndrome, beyond the tics. Pediatr Nurs. 2002 May–Jun;28(3):243–46, 249–53. PMID 12087644 Full text (free registration required).
- Coffey BJ, Shechter RL. "Treatment of co-morbid obsessive compulsive disorder, mood, and anxiety disorders". Adv Neurol. 2006;99:208–21. PMID 16536368
- Hwang GC, Tillberg CS, Scahill L. Habit reversal training for children with tourette syndrome: update and review. J Child Adolesc Psychiatr Nurs. 2012 Nov;25(4):178–83. PMID 23121140 doi:10.1111/jcap.12002
- Dutta N, Cavanna AE. The effectiveness of habit reversal therapy in the treatment of Tourette syndrome and other chronic tic disorders: a systematic review. Funct Neurol. 2013 Jan–Mar;28(1):7–12. PMID 23731910
- Woods DW, Himle MB, Conelea CA. "Behavior therapy: other interventions for tic disorders". Adv Neurol. 2006;99:234–40. PMID 16536371
- Statement: Deep Brain Stimulation and Tourette Syndrome. Tourette Syndrome Association. Retrieved on February 26, 2005.
- Viswanathan A, Jimenez-Shahed J, Baizabal Carvallo JF, Jankovic J. Deep brain stimulation for Tourette syndrome: target selection. Stereotact Funct Neurosurg. 2012;90(4):213–24. PMID 22699684 doi:10.1159/000337776
- Kammer T. "Mozart in the neurological department—who has the tic?" (PDF). Front Neurol Neurosci. 2007;22:184–92. doi:10.1159/0000102880 PMID 17495512
- What is Tourette Syndrome? Tourette Syndrome Foundation of Canada. Retrieved on July 2, 2013.
- Todd, Olivier. Malraux: A Life. Knopf, 2005.
- Guidotti TL. André Malraux: a medical interpretation (PDF). J R Soc Med. 1985 May;78(5):401–6. PMID 3886907
- Liebmann, Lisa. Lisa Liebmann on the Mona Lisa. TATEetc. Issue 6 / Spring 2006. Retrieved on March 1, 2008.
- Pappert EJ, Goetz CG, Louis ED, et al. "Objective assessments of longitudinal outcome in Gilles de la Tourette's syndrome." Neurology. 2003 Oct 14;61(7):936–40. PMID 14557563
- Singer HS. "Tourette's syndrome: from behaviour to biology". Lancet Neurol. 2005 Mar;4(3):149–59. doi:10.1016/S1474-4422(05)01012-4 PMID 15721825
- Burd L, Kerbeshian PJ, Barth A, et al. "Long-term follow-up of an epidemiologically defined cohort of patients with Tourette syndrome". J Child Neurol. 2001;16(6):431–37. PMID 11417610
- Howard, Tim. Tim Howard: Growing up with Tourette syndrome and my love of football. The Guardian. December 6, 2014. Retrieved on March 21, 2015.
- Knight T, Steeves T, Day L, Lowerison M, Jette N, Pringsheim T. Prevalence of tic disorders: a systematic review and meta-analysis. Pediatr Neurol. 2012 Aug;47(2):77–90. PMID 22759682 doi:10.1016/j.pediatrneurol.2012.05.002
- Leckman JF, Cohen DJ. Tourette's Syndrome—Tics, Obsessions, Compulsions: Developmental Psychopathology and Clinical Care. John Wiley & Sons, Inc., New York. 1999:37. ISBN 0-471-16037-7 Google books. "For example, individuals who were misunderstood and punished at home and at school for their tics or who were teased mercilessly by peers and stigmatized by their communities will fare worse than a child whose interpersonal environment was more understanding and supportive."
- Cohen DJ, Leckman JF, Pauls D. "Neuropsychiatric disorders of childhood: Tourette’s syndrome as a model". Acta Paediatr Suppl 422; 106–11, Scandinavian University Press, 1997. "The individuals with TS who do the best, we believe, are: those who have been able to feel relatively good about themselves and remain close to their families; those who have the capacity for humor and for friendship; those who are less burdened by troubles with attention and behavior, particularly aggression; and those who have not had development derailed by medication."
- Bloch MH, Leckman JF. "Clinical course of Tourette syndrome". J Psychosom Res. 2009 Dec;67(6):497–501. doi:10.1016/j.jpsychores.2009.09.002 PMID 19913654
- Lombroso PJ, Scahill L. "Tourette syndrome and obsessive–compulsive disorder". Brain Dev. 2008 Apr;30(4):231–37. doi:10.1016/j.braindev.2007.09.001 PMID 17937978
- Cohen DJ, Jankovic J, Goetz CG, (eds). Advances in neurology, Tourette syndrome. Lippincott, Williams & Wilkins, Philadelphia, PA. 2001;85:xviii. ISBN 0-7817-2405-8
- Abuzzahab FE, Anderson FO. "Gilles de la Tourette's syndrome; international registry". Minnesota Medicine. 1973 Jun;56(6):492–96. PMID 4514275
- Scahill, L. "Epidemiology of Tic Disorders". Medical Letter: 2004 Retrospective Summary of TS Literature. Tourette Syndrome Association. The first page (PDF), is available at archive.org without subscription. Retrieved on June 11, 2007.
- Bloch, State, Pittenger 2011. See also Zohar AH, Apter A, King RA, et al. "Epidemiological studies". In Leckman JF, Cohen DJ. Tourette's Syndrome—Tics, Obsessions, Compulsions: Developmental Psychopathology and Clinical Care. John Wiley & Sons, Inc., New York. 1999:177–92. ISBN 0-471-16037-7
- Bloch, State, Pittenger 2011. See also Schapiro 2002 and Coffey BJ, Park KS. "Behavioral and emotional aspects of Tourette syndrome". Neurol Clin. 1997 May;15(2):277–89. PMID 9115461
- Hawley, JS. Tourette Syndrome. eMedicine (June 23, 2008). Retrieved on August 10, 2009.
- Leckman JF. "Tourette's syndrome". Lancet. 2002 Nov 16;360(9345):1577–86. doi:10.1016/S0140-6736(02)11526-1 PMID 12443611
- Teive HA, Chien HF, Munhoz RP, Barbosa ER. "Charcot's contribution to the study of Tourette's syndrome". Arq Neuropsiquiatr. 2008 Dec;66(4):918–21. PMID 19099145 as reported in Finger S. "Some movement disorders." In Finger S (ed). Origins of neuroscience: the history of explorations into brain function. New York: Oxford University Press, 1994:220–239.
- Germiniani FM, Miranda AP, Ferenczy P, Munhoz RP, Teive HA. Tourette's syndrome: from demonic possession and psychoanalysis to the discovery of gene. Arq Neuropsiquiatr. 2012 Jul;70(7):547–9. PMID 22836463
- Itard JMG. "Mémoire sur quelques functions involontaires des appareils de la locomotion, de la préhension et de la voix". Arch Gen Med. 1825;8:385–407. From Newman, Sara. "Study of several involuntary functions of the apparatus of movement, gripping, and voice" by Jean-Marc Gaspard Itard (1825) History of Psychiatry. 2006;17:333–39. doi:10.1177/0957154X06067668
- What is Tourette syndrome? Tourette Syndrome Association. Retrieved on January 14, 2012.
- Gilles de la Tourette G, Goetz CG, Llawans HL, trans. "Étude sur une affection nerveuse caractérisée par de l'incoordination motrice accompagnée d'echolalie et de coprolalie". In: Friedhoff AJ, Chase TN, eds. Advances in Neurology: Volume 35. Gilles de la Tourette syndrome. New York: Raven Press; 1982;1–16. Discussed at Black, KJ. Tourette Syndrome and Other Tic Disorders. eMedicine (March 30, 2007). Retrieved on August 10, 2009. Original text (in French). Retrieved on August 10, 2009.
- Robertson MM, Reinstein DZ. "Convulsive tic disorder: Georges Gilles de la Tourette, Guinon and Grasset on the phenomenology and psychopathology of Gilles de la Tourette syndrome". Behavioural Neurology, 1991;4(1), 29–56.
- Enersen, Ole Daniel. Georges Albert Édouard Brutus Gilles de la Tourette. Archived March 9, 2005, at the Wayback Machine. WhoNamedIt.com Retrieved on May 14, 2007.
- Blue, Tina. Tourette syndrome. Essortment 2002. Pagewise Inc. Retrieved on August 10, 2009.
- Rickards H, Hartley N, Robertson MM. "Seignot's paper on the treatment of Tourette's syndrome with haloperidol. Classic Text No. 31". Hist Psychiatry. 1997 Sep;8 (31 Pt 3):433–36. PMID 11619589
- Gadow KD, Sverd J. "Attention deficit hyperactivity disorder, chronic tic disorder, and methylphenidate". Adv Neurol. 2006;99:197–207. PMID 16536367
- Walkup, JT, Mink, JW, Hollenback, PJ, (eds). Advances in Neurology, Tourette syndrome. Lippincott, Williams & Wilkins, Philadelphia, PA. 2006;99:xvi–xviii. ISBN 0-7817-9970-8 Google books.
- Sacks, O. The man who mistook his wife for a hat: and other clinical tales. Harper and Row, New York. 1985:92–100. ISBN 0-684-85394-9
- Leckman JF, Cohen DJ. Tourette's Syndrome—Tics, Obsessions, Compulsions: Developmental Psychopathology and Clinical Care. John Wiley & Sons, Inc., New York. 1999:408. ISBN 0-471-16037-7
- Leckman JF, Cohen DJ. Tourette's Syndrome—Tics, Obsessions, Compulsions: Developmental Psychopathology and Clinical Care. John Wiley & Sons, Inc., New York. 1999:18–19, 148–151; 408. ISBN 0-471-16037-7
- Schuerholz LJ, Baumgardner TL, Singer HS, et al. "Neuropsychological status of children with Tourette's syndrome with and without attention deficit hyperactivity disorder". Neurology. 1996 Apr;46(4):958–65. PMID 8780072
- Schuerholz LJ, Cutting L, Mazzocco MM, et al. "Neuromotor functioning in children with Tourette syndrome with and without attention deficit hyperactivity disorder". J Child Neurol. 1997 Oct;12(7):438–42. PMID 9373800
- Portraits of adults with TS. Tourette Syndrome Association. Retrieved from July 16, 2011 archive.org version on December 21, 2011.
- Samuel Johnson. Tourette Syndrome Association. Retrieved from April 7, 2005 archive.org version on December 30, 2011.
- Pearce JM. "Doctor Samuel Johnson: 'the great convulsionary' a victim of Gilles de la Tourette's syndrome" (PDF). Journal of the Royal Society of Medicine. 1994 Jul;87(7):396–9. PMID 8046726
- Keilman, John. Reviews: The Game of Our Lives by David Goldblatt, The Keeper by Tim Howard. Chicago Tribune. January 22, 2015. Retrieved on March 21, 2015.
- Tim Howard receives first-ever Champion of Hope Award from the National Tourette Syndrome Association. Archived March 30, 2015, at the Wayback Machine. Tourette Syndrome Association. October 14, 2014. Retrieved on March 21, 2015.
- Simkin B. "Mozart's scatological disorder". BMJ. 1992 Dec 19–26;305(6868):1563–7. PMID 1286388 Also see: Simkin, Benjamin. Medical and Musical Byways of Mozartiana. Fithian Press. 2001. ISBN 1-56474-349-7 Review, Retrieved on May 14, 2007.
- Did Mozart really have TS? Tourette Syndrome Association. Retrieved from April 7, 2005 archive.org version on December 30, 2011.
- Kammer T. "Mozart in the neurological department—who has the tic?" (PDF). Front Neurol Neurosci. 2007;22:184–92. PMID 17495512 doi:10.1159/0000102880 Retrieved on February 7, 2012.
- Ashoori A, Jankovic J. "Mozart's movements and behaviour: a case of Tourette's syndrome?" J Neurol Neurosurg Psychiatry. 2007 Nov;78(11):1171–5 doi:10.1136/jnnp.2007.114520 PMID 17940168.
- Sacks O. "Tourette's syndrome and creativity". BMJ. 1992 Dec 19–26;305(6868):1515–6. doi:10.1136/bmj.305.6868.1515 PMID 1286364
- Voss H. The representation of movement disorders in fictional literature. J Neurol Neurosurg Psychiatry. 2012 Oct;83(10):994–9. PMID 22752692 doi:10.1136/jnnp-2012-302716
- Holtgren, Bruce. "Truth about Tourette's not what you think". Cincinnati Enquirer. January 11, 2006. "As medical problems go, Tourette's is, except in the most severe cases, about the most minor imaginable thing to have. ... the freak-show image, unfortunately, still prevails overwhelmingly. The blame for the warped perceptions lies overwhelmingly with the video media – the Internet, movies and TV. If you search for 'Tourette' on Google or YouTube, you'll get a gazillion hits that almost invariably show the most outrageously extreme examples of motor and vocal tics. Television, with notable exceptions such as Oprah, has sensationalized Tourette's so badly, for so long, that it seems beyond hope that most people will ever know the more prosaic truth."
- US media:
- Oprah and Dr. Laura – Conflicting Messages on Tourette Syndrome. Oprah Educates; Dr. Laura Fosters Myth of TS as "Cursing Disorder". Tourette Syndrome Association. May 31, 2001. Retrieved from October 6, 2001 archive.org version on December 21, 2011.
- Letter of response to Dr. Phil. Tourette Syndrome Association. Retrieved from August 31, 2008 archive.org version on December 21, 2011.
- Letter of response to Garrison Keillor radio show. Tourette Syndrome Association. Retrieved from February 7, 2009 archive.org version on December 21, 2011.
- UK media:
- Kushner, HI. A Cursing Brain?: The Histories of Tourette Syndrome. Harvard University Press. 2000. ISBN 0-674-00386-1.
- Olson, S. "Making Sense of Tourette's" (PDF). Science. 2004 Sep 3;305(5689):1390–92. doi:10.1126/science.305.5689.1390 PMID 15353772
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This page uses content from Wikipedia and is licensed under CC BY-SA.
|Synonyms||Intellectual developmental disability (IDD), general learning disability|
|Children with intellectual disabilities or other developmental conditions can compete in the Special Olympics.|
|Frequency||153 million (2015)|
Intellectual disability (ID), also known as general learning disability, and mental retardation (MR), is a generalized neurodevelopmental disorder characterized by significantly impaired intellectual and adaptive functioning. It is defined by an IQ under 70 in addition to deficits in two or more adaptive behaviors that affect everyday, general living.
Once focused almost entirely on cognition, the definition now includes both a component relating to mental functioning and one relating to individuals' functional skills in their environments. As a result of this focus on the person's abilities in practice, a person with an unusually low IQ may not be considered to have intellectually disability.
Intellectual disability is subdivided into syndromic intellectual disability, in which intellectual deficits associated with other medical and behavioral signs and symptoms are present, and non-syndromic intellectual disability, in which intellectual deficits appear without other abnormalities. Down syndrome and fragile X syndrome are examples of syndromic intellectual disabilities.
Intellectual disability affects about 2–3% of the general population. Seventy-five to ninety percent of the affected people have mild intellectual disability. Non-syndromic or idiopathic cases account for 30–50% of cases. About a quarter of cases are caused by a genetic disorder, and about 5% of cases are inherited from a person's parents. Cases of unknown cause affect about 95 million people as of 2013.
Intellectual disability (ID) begins during childhood and involves deficits in mental abilities, social skills, and core activities of daily living (ADLs) when compared to same-aged peers. There often are no physical signs of mild forms of ID, although there may be characteristic physical traits when it is associated with a genetic disorder (e.g., Down syndrome).
The level of impairment ranges in severity for each person. Some of the early signs can include:
In early childhood, mild ID (IQ 50–69) may not be obvious or identified until children begin school. Even when poor academic performance is recognized, it may take expert assessment to distinguish mild intellectual disability from specific learning disability or emotional/behavioral disorders. People with mild ID are capable of learning reading and mathematics skills to approximately the level of a typical child aged nine to twelve. They can learn self-care and practical skills, such as cooking or using the local mass transit system. As individuals with intellectual disability reach adulthood, many learn to live independently and maintain gainful employment.
Moderate ID (IQ 35–49) is nearly always apparent within the first years of life. Speech delays are particularly common signs of moderate ID. People with moderate intellectual disability need considerable supports in school, at home, and in the community in order to fully participate. While their academic potential is limited, they can learn simple health and safety skills and to participate in simple activities. As adults, they may live with their parents, in a supportive group home, or even semi-independently with significant supportive services to help them, for example, manage their finances. As adults, they may work in a sheltered workshop.
People with severe or profound ID need more intensive support and supervision their entire lives. They may learn some ADLs, but an intellectual disability is considered severe or profound when individuals are unable to independently care for themselves without ongoing significant assistance from a caregiver throughout adulthood. Individuals with profound ID are completely dependent on others for all ADLs and to maintain their physical health and safety, although they may be able to learn to participate in some of these activities to limited degree.
Among children, the cause of intellectual disability is unknown for one-third to one-half of cases. About 5% of cases are inherited from a person's parents. Genetic defects that cause intellectual disability but are not inherited can be caused by accidents or mutations in genetic development. Examples of such accidents are development of an extra chromosome 18 (trisomy 18) and Down syndrome, which is the most common genetic cause. Velocardiofacial syndrome and fetal alcohol spectrum disorders are the two next most common causes. However, doctors have found many other causes. The most common are:
According to both the American Association on Intellectual and Developmental Disabilities(Intellectual Disability: Definition, Classification, and Systems of Supports (11th Edition) and the American Psychiatric Association Diagnostic and Statistical Manual of Mental Disorders (DSM-IV), three criteria must be met for a diagnosis of intellectual disability: significant limitation in general mental abilities (intellectual functioning), significant limitations in one or more areas of adaptive behavior across multiple environments (as measured by an adaptive behavior rating scale, i.e. communication, self-help skills, interpersonal skills, and more), and evidence that the limitations became apparent in childhood or adolescence. In general, people with intellectual disability have an IQ below 70, but clinical discretion may be necessary for individuals who have a somewhat higher IQ but severe impairment in adaptive functioning.
It is formally diagnosed by an assessment of IQ and adaptive behavior. A third condition requiring onset during the developmental period is used to distinguish intellectual disability from other conditions dementia such as Alzheimer's disease or traumatic brain injuries.
The first English-language IQ test, the Stanford–Binet Intelligence Scales, was adapted from a test battery designed for school placement by Alfred Binet in France. Lewis Terman adapted Binet's test and promoted it as a test measuring "general intelligence." Terman's test was the first widely used mental test to report scores in "intelligence quotient" form ("mental age" divided by chronological age, multiplied by 100). Current tests are scored in "deviation IQ" form, with a performance level by a test-taker two standard deviations below the median score for the test-taker's age group defined as IQ 70. Until the most recent revision of diagnostic standards, an IQ of 70 or below was a primary factor for intellectual disability diagnosis, and IQ scores were used to categorize degrees of intellectual disability.
Since current diagnosis of intellectual disability is not based on IQ scores alone, but must also take into consideration a person's adaptive functioning, the diagnosis is not made rigidly. It encompasses intellectual scores, adaptive functioning scores from an adaptive behavior rating scale based on descriptions of known abilities provided by someone familiar with the person, and also the observations of the assessment examiner who is able to find out directly from the person what he or she can understand, communicate, and such like. IQ assessment must be based on a current test. This enables diagnosis to avoid the pitfall of the Flynn effect, which is a consequence of changes in population IQ test performance changing IQ test norms over time.
Clinically, intellectual disability is a subtype of cognitive deficit or disabilities affecting intellectual abilities, which is a broader concept and includes intellectual deficits that are too mild to properly qualify as intellectual disability, or too specific (as in specific learning disability), or acquired later in life through acquired brain injuries or neurodegenerative diseases like dementia. Cognitive deficits may appear at any age. Developmental disability is any disability that is due to problems with growth and development. This term encompasses many congenital medical conditions that have no mental or intellectual components, although it, too, is sometimes used as a euphemism for intellectual disability.
Adaptive behavior, or adaptive functioning, refers to the skills needed to live independently (or at the minimally acceptable level for age). To assess adaptive behavior, professionals compare the functional abilities of a child to those of other children of similar age. To measure adaptive behavior, professionals use structured interviews, with which they systematically elicit information about persons' functioning in the community from people who know them well. There are many adaptive behavior scales, and accurate assessment of the quality of someone's adaptive behavior requires clinical judgment as well. Certain skills are important to adaptive behavior, such as:
By most definitions, intellectual disability is more accurately considered a disability rather than a disease. Intellectual disability can be distinguished in many ways from mental illness, such as schizophrenia or depression. Currently, there is no "cure" for an established disability, though with appropriate support and teaching, most individuals can learn to do many things. Causes, such as congenital hypothyroidism, if detected early may be treated to prevent development of an intellectual disability.
There are thousands of agencies around the world that provide assistance for people with developmental disabilities. They include state-run, for-profit, and non-profit, privately run agencies. Within one agency there could be departments that include fully staffed residential homes, day rehabilitation programs that approximate schools, workshops wherein people with disabilities can obtain jobs, programs that assist people with developmental disabilities in obtaining jobs in the community, programs that provide support for people with developmental disabilities who have their own apartments, programs that assist them with raising their children, and many more. There are also many agencies and programs for parents of children with developmental disabilities.
Beyond that, there are specific programs that people with developmental disabilities can take part in wherein they learn basic life skills. These "goals" may take a much longer amount of time for them to accomplish, but the ultimate goal is independence. This may be anything from independence in tooth brushing to an independent residence. People with developmental disabilities learn throughout their lives and can obtain many new skills even late in life with the help of their families, caregivers, clinicians and the people who coordinate the efforts of all of these people.
There are four broad areas of intervention that allow for active participation from caregivers, community members, clinicians, and of course, the individual(s) with an intellectual disability. These include psychosocial treatments, behavioral treatments, cognitive-behavioral treatments, and family-oriented strategies. Psychosocial treatments are intended primarily for children before and during the preschool years as this is the optimum time for intervention. This early intervention should include encouragement of exploration, mentoring in basic skills, celebration of developmental advances, guided rehearsal and extension of newly acquired skills, protection from harmful displays of disapproval, teasing, or punishment, and exposure to a rich and responsive language environment. A great example of a successful intervention is the Carolina Abecedarian Project that was conducted with over 100 children from low SES families beginning in infancy through pre-school years. Results indicated that by age 2, the children provided the intervention had higher test scores than control group children, and they remained approximately 5 points higher 10 years after the end of the program. By young adulthood, children from the intervention group had better educational attainment, employment opportunities, and fewer behavioral problems than their control-group counterparts.
Core components of behavioral treatments include language and social skills acquisition. Typically, one-to-one training is offered in which a therapist uses a shaping procedure in combination with positive reinforcements to help the child pronounce syllables until words are completed. Sometimes involving pictures and visual aids, therapists aim at improving speech capacity so that short sentences about important daily tasks (e.g. bathroom use, eating, etc.) can be effectively communicated by the child. In a similar fashion, older children benefit from this type of training as they learn to sharpen their social skills such as sharing, taking turns, following instruction, and smiling. At the same time, a movement known as social inclusion attempts to increase valuable interactions between children with an intellectual disability and their non-disabled peers. Cognitive-behavioral treatments, a combination of the previous two treatment types, involves a strategical-metastrategical learning technique[clarification needed] that teaches children math, language, and other basic skills pertaining to memory and learning. The first goal of the training is to teach the child to be a strategical thinker through making cognitive connections and plans. Then, the therapist teaches the child to be metastrategical by teaching them to discriminate among different tasks and determine which plan or strategy suits each task. Finally, family-oriented strategies delve into empowering the family with the skill set they need to support and encourage their child or children with an intellectual disability. In general, this includes teaching assertiveness skills or behavior management techniques as well as how to ask for help from neighbors, extended family, or day-care staff. As the child ages, parents are then taught how to approach topics such as housing/residential care, employment, and relationships. The ultimate goal for every intervention or technique is to give the child autonomy and a sense of independence using the acquired skills he/she has.
Although there is no specific medication for intellectual disability, many people with developmental disabilities have further medical complications and may be prescribed several medications. For example, autistic children with developmental delay may be prescribed antipsychotics or mood stabilizers to help with their behavior. Use of psychotropic medications such as benzodiazepines in people with intellectual disability requires monitoring and vigilance as side effects occur commonly and are often misdiagnosed as behavioral and psychiatric problems.
Intellectual disability affects about 2–3% of the general population. 75–90% of the affected people have mild intellectual disability. Non-syndromic or idiopathic ID accounts for 30–50% of cases. About a quarter of cases are caused by a genetic disorder. Cases of unknown cause affect about 95 million people as of 2013. It is more common in males and in low to middle income countries.
Intellectual disability has been documented under a variety of names throughout history. Throughout much of human history, society was unkind to those with any type of disability, and people with intellectual disability were commonly viewed as burdens on their families.
Greek and Roman philosophers, who valued reasoning abilities, disparaged people with intellectual disability as barely human. The oldest physiological view of intellectual disability is in the writings of Hippocrates in the late fifth century BCE, who believed that it was caused by an imbalance in the four humors in the brain.
Until the Enlightenment in Europe, care and asylum was provided by families and the church (in monasteries and other religious communities), focusing on the provision of basic physical needs such as food, shelter and clothing. Negative stereotypes were prominent in social attitudes of the time.
In the 13th century, England declared people with intellectual disability to be incapable of making decisions or managing their affairs. Guardianships were created to take over their financial affairs.
In the 17th century, Thomas Willis provided the first description of intellectual disability as a disease. He believed that it was caused by structural problems in the brain. According to Willis, the anatomical problems could be either an inborn condition or acquired later in life.
In the 18th and 19th centuries, housing and care moved away from families and towards an asylum model. People were placed by, or removed from, their families (usually in infancy) and housed in large professional institutions, many of which were self-sufficient through the labor of the residents. Some of these institutions provided a very basic level of education (such as differentiation between colors and basic word recognition and numeracy), but most continued to focus solely on the provision of basic needs of food, clothing, and shelter. Conditions in such institutions varied widely, but the support provided was generally non-individualized, with aberrant behavior and low levels of economic productivity regarded as a burden to society. Individuals of higher wealth were often able to afford higher degrees of care such as home care or private asylums. Heavy tranquilization and assembly line methods of support were the norm, and the medical model of disability prevailed. Services were provided based on the relative ease to the provider, not based on the needs of the individual. A survey taken in 1891 in Cape Town, South Africa shows the distribution between different facilities. Out of 2046 persons surveyed, 1,281 were in private dwellings, 120 in jails, and 645 in asylums, with men representing nearly two thirds of the number surveyed. In situations of scarcity of accommodation, preference was given to white men and black men (whose insanity threatened white society by disrupting employment relations and the tabooed sexual contact with white women).
In the late 19th century, in response to Charles Darwin's On the Origin of Species, Francis Galton proposed selective breeding of humans to reduce intellectual disability. Early in the 20th century the eugenics movement became popular throughout the world. This led to forced sterilization and prohibition of marriage in most of the developed world and was later used by Adolf Hitler as a rationale for the mass murder of people with intellectual disability during the holocaust. Eugenics was later abandoned as an evil violation of human rights, and the practice of forced sterilization and prohibition from marriage was discontinued by most of the developed world by the mid-20th century.
Although ancient Roman law had declared people with intellectual disability to be incapable of the deliberate intent to harm that was necessary for a person to commit a crime, during the 1920s, Western society believed they were morally degenerate.
Ignoring the prevailing attitude, Civitans adopted service to people with developmental disabilities as a major organizational emphasis in 1952. Their earliest efforts included workshops for special education teachers and daycamps for children with disabilities, all at a time when such training and programs were almost nonexistent. The segregation of people with developmental disabilities was not widely questioned by academics or policy-makers until the 1969 publication of Wolf Wolfensberger's seminal work "The Origin and Nature of Our Institutional Models", drawing on some of the ideas proposed by SG Howe 100 years earlier. This book posited that society characterizes people with disabilities as deviant, sub-human and burdens of charity, resulting in the adoption of that "deviant" role. Wolfensberger argued that this dehumanization, and the segregated institutions that result from it, ignored the potential productive contributions that all people can make to society. He pushed for a shift in policy and practice that recognized the human needs of those with intellectual disability and provided the same basic human rights as for the rest of the population.
The publication of this book may be regarded as the first move towards the widespread adoption of the social model of disability in regard to these types of disabilities, and was the impetus for the development of government strategies for desegregation. Successful lawsuits against governments and an increasing awareness of human rights and self-advocacy also contributed to this process, resulting in the passing in the U.S. of the Civil Rights of Institutionalized Persons Act in 1980.
From the 1960s to the present, most states have moved towards the elimination of segregated institutions. Normalization and deinstitutionalization are dominant. Along with the work of Wolfensberger and others including Gunnar and Rosemary Dybwad, a number of scandalous revelations around the horrific conditions within state institutions created public outrage that led to change to a more community-based method of providing services.
By the mid-1970s, most governments had committed to de-institutionalization, and had started preparing for the wholesale movement of people into the general community, in line with the principles of normalization. In most countries, this was essentially complete by the late 1990s, although the debate over whether or not to close institutions persists in some states, including Massachusetts.
In the past, lead poisoning and infectious diseases were significant causes of intellectual disability. Some causes of intellectual disability are decreasing, as medical advances, such as vaccination, increase. Other causes are increasing as a proportion of cases, perhaps due to rising maternal age, which is associated with several syndromic forms of intellectual disability.
Along with the changes in terminology, and the downward drift in acceptability of the old terms, institutions of all kinds have had to repeatedly change their names. This affects the names of schools, hospitals, societies, government departments, and academic journals. For example, the Midlands Institute of Mental Subnormality became the British Institute of Mental Handicap and is now the British Institute of Learning Disability. This phenomenon is shared with mental health and motor disabilities, and seen to a lesser degree in sensory disabilities.
The terms used for this condition are subject to a process called the euphemism treadmill. This means that whatever term is chosen for this condition, it eventually becomes perceived as an insult. The terms mental retardation and mentally retarded were invented in the middle of the 20th century to replace the previous set of terms, which included "imbecile" and "moron" and are now considered offensive. By the end of the 20th century, these terms themselves have come to be widely seen as disparaging, politically incorrect, and in need of replacement. The term intellectual disability is now preferred by most advocates and researchers in most English-speaking countries. As of 2015[update], the term "mental retardation" is still used by the World Health Organization in the ICD-10 codes, which have a section titled "Mental Retardation" (codes F70–F79). In the next revision, the ICD-11 is expected to replace the term mental retardation with either intellectual disability or intellectual developmental disorder, which the DSM-5 already uses. Because of its specificity and lack of confusion with other conditions, the term "mental retardation" is still sometimes used in professional medical settings around the world, such as formal scientific research and health insurance paperwork.
The several traditional terms that long predate psychiatry are simple forms of abuse in common usage today; they are often encountered in such old documents as books, academic papers, and census forms. For example, the British census of 1901 has a column heading including the terms imbecile and feeble-minded.
Negative connotations associated with these numerous terms for intellectual disability reflect society's attitude about the condition. Some elements of society seek neutral medical terms, while others want to use such terms as weapons of abuse.
Today, new expressions like developmentally disabled, special, or challenged are replacing the term mentally retarded. The term developmental delay is popular among caretakers and parents of individuals with intellectual disability because delay suggests that a person is slowly reaching his or her full potential rather than having a lifelong condition.
Usage has changed over the years and differed from country to country. For example, mental retardation in some contexts covers the whole field but previously applied to what is now the mild MR group. Feeble-minded used to mean mild MR in the UK, and once applied in the US to the whole field. "Borderline intellectual functioning" is not currently defined, but the term may be used to apply to people with IQs in the 70s. People with IQs of 70 to 85 used to be eligible for special consideration in the US public education system on grounds of intellectual disability.
The American Association on Mental Retardation changed its name to the American Association on Intellectual and Developmental Disabilities (AAIDD) in 2007, and soon thereafter changed the names of its scholarly journals to reflect the term "intellectual disability." In 2010, the AAIDD released its 11th edition of its terminology and classification manual, which also used the term intellectual disability
In the UK, mental handicap had become the common medical term, replacing mental subnormality in Scotland and mental deficiency in England and Wales, until Stephen Dorrell, Secretary of State for Health for the United Kingdom from 1995–97, changed the NHS's designation to learning disability. The new term is not yet widely understood, and is often taken to refer to problems affecting schoolwork (the American usage), which are known in the UK as "learning difficulties." British social workers may use "learning difficulty" to refer to both people with intellectual disability and those with conditions such as dyslexia. In education, "learning difficulties" is applied to a wide range of conditions: "specific learning difficulty" may refer to dyslexia, dyscalculia or developmental coordination disorder, while "moderate learning difficulties", "severe learning difficulties" and "profound learning difficulties" refer to more significant impairments.
In England and Wales between 1983 and 2008, the Mental Health Act 1983 defined "mental impairment" and "severe mental impairment" as "a state of arrested or incomplete development of mind which includes significant/severe impairment of intelligence and social functioning and is associated with abnormally aggressive or seriously irresponsible conduct on the part of the person concerned." As behavior was involved, these were not necessarily permanent conditions: they were defined for the purpose of authorizing detention in hospital or guardianship. The term mental impairment was removed from the Act in November 2008, but the grounds for detention remained. However, English statute law uses mental impairment elsewhere in a less well-defined manner—e.g. to allow exemption from taxes—implying that intellectual disability without any behavioral problems is what is meant.
A BBC poll conducted in the United Kingdom came to the conclusion that 'retard' was the most offensive disability-related word. On the reverse side of that, when a contestant on Celebrity Big Brother live used the phrase "walking like a retard", despite complaints from the public and the charity Mencap, the communications regulator Ofcom did not uphold the complaint saying "it was not used in an offensive context [...] and had been used light-heartedly". It was, however, noted that two previous similar complaints from other shows were upheld.
In the past, Australia has used British and American terms interchangeably, including "mental retardation" and "mental handicap". Today, "intellectual disability" is the preferred and more commonly used descriptor.
People with intellectual disabilities are often not seen as full citizens of society. Person-centered planning and approaches are seen as methods of addressing the continued labeling and exclusion of socially devalued people, such as people with disabilities, encouraging a focus on the person as someone with capacities and gifts as well as support needs. The self-advocacy movement promotes the right of self-determination and self-direction by people with intellectually disabilities, which means allowing them to make decisions about their own lives.
Until the middle of the 20th century, people with intellectual disabilities were routinely excluded from public education, or educated away from other typically developing children. Compared to peers who were segregated in special schools, students who are mainstreamed or included in regular classrooms report similar levels of stigma and social self-conception, but more ambitious plans for employment. As adults, they may live independently, with family members, or in different types of institutions organized to support people with disabilities. About 8% currently live in an institution or a group home.
In the United States, the average lifetime cost of a person with an intellectual disability amounts to $1,014,000 per person, in 2003 US dollars. This is slightly more than the costs associated with cerebral palsy, and double that associated with serious vision or hearing impairments. About 14% is due to increased medical expenses (not including what is normally incurred by the typical person), 10% is due to direct non-medical expenses, such as the excess cost of special education compared to standard schooling, and 76% is indirect costs accounting for reduced productivity and shortened lifespans. Some expenses, such as costs associated with being a family caregiver or living in a group home, were excluded from this calculation.
People with intellectual disability as a group have higher rates of adverse health conditions such as epilepsy and neurological disorders, gastrointestinal disorders, and behavioral and psychiatric problems compared to people without disabilities. Adults also have a higher prevalence of poor social determinants of health, behavioral risk factors, depression, diabetes, and poor or fair health status than adults without intellectual disability. In the United Kingdom people with intellectual disability live on average 16 years less than the general population.
The term general learning disability is now used in the UK instead of terms such as mental handicap or mental retardation. The degree of disability can vary significantly, being classified as mild, moderate, severe or profound.
Decades-long quest by disabilities advocates finally persuades state, federal governments to end official use of 'retarded'.
Figure 8-3. Estimated full-scale IQ distributions for SCA and control children: 47,XXX (mean ~83), 45,X & Variant (mean ~85), 47,XXY (mean ~95), 47,XYY (mean ~100), Controls and SCA Mosaics (mean ~104)
The resolution ... urges a change from the old term to "developmental disability"
The term intellectual disability covers the same population of individuals who were diagnosed previously with mental retardation in number, kind, level, type, duration of disability, and the need of people with this disability for individualized services and supports.
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Japan and South Korea have already abandoned the term.
According to the Schizophrenia and Related Disorders Alliance of America (SARDAA), about 3.5 million people in the United States have been diagnosed with schizophrenia, and the disorder can be found in approximately 1.1 percent of the world’s population.
But according to psychiatry professor Jim van Os of the Maastricht University Medical Centre, “schizophrenia” does not exist.
Professor Os argues that the term “schizophrenia” connotates a hopeless chronic brain disease, and that the word should be replaced with something like “psychosis spectrum syndrome” in order to be more accurate. Japan and South Korea have already abandoned the term “schizophrenia.”
The term can be found in both of the official reference texts used to diagnose patients — ICD-10 (International Classification of Diseases, 10th revision) and DSM-5 (Diagnostic and Statistical Manual of Mental Disorders, fifth edition). However, Professor Os argues that it should be dropped.
Why? Psychotic illnesses are classified among a number of different categories, including schizophrenia, bipolar disorder with psychotic features, delusional disorder, schizoaffective disorder, etc. However, these categories "do not represent diagnoses of discrete diseases, because these remain unknown; rather, they describe how symptoms can cluster, to allow grouping of patients,” Os said in a press release.
He further explains that grouping and diagnosing patients based on clustering symptoms allows clinicians to say, for instance, "You have symptoms of psychosis and mania, and we classify that as schizoaffective disorder." However, if the psychotic symptoms disappear, it could then be reclassified as bipolar disorder, or if the mania symptoms disappear, it could be re-diagnosed as schizophrenia. The psychotic disorders tend to have a lot of overlapping symptoms and this classification system doesn’t always lead to a solid diagnosis.
"That is how our classification system works. We don't know enough to diagnose real diseases, so we use a system of symptom based classification,” Os explains.
Interestingly, Os highlights the language used to typically describe schizophrenia: the American Psychiatric Association (who publishes the DSM) describes schizophrenia as a “chronic brain disorder” on its website, and academic journals describe it as a “devastating, highly heritable brain disorder,” a “debilitating neurological disorder,” or a “brain disorder with predominantly genetic risk factors.”
Os says that this language strongly depicts schizophrenia as a distinct, genetic brain disease, but oddly, this language isn’t used for the other categories of psychotic illness, despite the fact that they constitute 70 percent of psychotic illnesses.
It’s time to forget about “devastating” schizophrenia as the only category that matters, says Os, and "and start doing justice to the broad and heterogeneous psychosis spectrum syndrome that really exists."
Os isn’t the first to highlight the problems with the term “schizophrenia,” and in his paper, published in the British Medical Journal, he argues that “schizophrenia” should be dropped from ICD-11, which is due by 2018. | <urn:uuid:25186b5d-85c6-42f0-839a-f9498eee2877> | {
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International Classification of Diseases (ICD), in medicine, diagnostic tool that is used to classify and monitor causes of injury and death and that maintains information for health analyses, such as the study of mortality (death) and morbidity (illness) trends. The ICD is designed to promote international compatibility in health data collecting and reporting.
History of the ICD
Some of the first attempts to systematically classify diseases were made in the 1600s and 1700s, though the resulting classifications were considered to be of little utility, largely as a result of inconsistencies in nomenclature and poor statistical data. During the 1800s the importance of creating a uniform system was realized, and several medical statisticians commissioned the completion of that task. The International Statistical Institute adopted the first international classification of diseases in 1893. The system was based on the Bertillon Classification of Causes of Death, developed by French statistician and demographer Jacques Bertillon. In 1898 the American Public Health Association recommended that Canada, Mexico, and the United States use that system and that it be revised every decade. In the following years Bertillon’s classification became known as the International List of Causes of Death and ultimately as the ICD.
The ICD became increasingly detailed through repeated revision, particularly after 1948, when the World Health Organization (WHO) assumed responsibility for publishing the ICD and began collecting international data for all general epidemiological surveillance and health management purposes. WHO significantly revised the ICD in the 1980s and early ’90s. The resulting three-volume work, known as ICD-10 (International Statistical Classification of Diseases and Related Health Problems), was published in 1992; it eventually replaced the two-volume ICD-9 in countries worldwide that used the classification. The ICD became a core classification of the WHO Family of International Classifications (WHO-FIC).
Design of the ICD
The ICD contains a description of all known diseases and injuries. Each disease is detailed with diagnostic characteristics and given a unique identifier that is used to code mortality data on death certificates and morbidity data from patient and clinical records. The core of the ICD-10 uses one single list of four-alphanumeric-character codes from A00.0 to Z99.0 . The first letter of the code designates a different chapter; there are 22 chapters in total (several letters are included in a single chapter together). Within each chapter, the four-character codes are divided so that they specify different classification axes. The fourth character (the number after the decimal) is not required for reporting and is used in various ways.
Use of the ICD
Every country subscribing to the ICD system uses it in varying degrees. Most countries subscribe to the entirety of the ICD system, whereas some use the ICD in hospitals only and others for morbidity only. Some countries have chosen to implement partial code use. Differences in mortality classification coding between ICD-9 and ICD-10 prevented direct comparisons between the two, though a method to adjust for the change was introduced.
The U.S. Department of Health and Human Services felt that the ICD needed to provide better clinical information and developed a system that was referred to as ICD 9th revision: Clinical Modification (ICD-9-CM). The CM codes were more precise and allowed for strong analyses. The ICD-9-CM was used by hospitals and other health care facilities, particularly for reporting morbidity (the ICD-10 was used to report mortality data). The ICD-9-CM was replaced by the ICD-10-CM in 2015. | <urn:uuid:73263565-284e-4e53-905f-13b83aa10a69> | {
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Influenza, commonly known as the flu, is a contagious respiratory illness caused by influenza viruses resulting in mild to severe influenza-like illness. Seasonal influenza affects persons of all ages. Each year, between 5% and 15% of the worlds population is affected by seasonal influenza (WHO, 2013). Complications of influenza include pneumonia, bronchitis, ear infections, sinus infections, and worsening of chronic medical conditions such as congestive heart failure, asthma, or diabetes. Vaccination has been shown to reduce influenza morbidity and mortality and high economic burden associated with influenza illness.
GlobalData epidemiologists identified country-specific population-based studies and government-collated surveillance data to build the influenza forecast, and utilized appropriate proxy data where applicable. Moreover, clinically relevant segmentations are provided for diagnosed incident cases of seasonal influenza, including influenza-like illness (ILI) cases, lab confirmed cases, hospitalized cases, and averted cases. Lastly, uniform diagnostic criteria are utilized for all segmentations across the 7MM using ICD-10 codes J09-J10, and seasonal versus calendar year influenza cases were reconciled, for example, by applying rates from the 2007-2008 influenza season to the 2007 calendar year population.
In the 7MM, GlobalData epidemiologists forecast that the seasonal influenza vaccination coverage will increase from 323,457,073 people in 2015 to 344,202,999 people in 2025, at an Annual Growth Rate (AGR) of 0.64%. The US will have the largest population vaccinated for seasonal influenza among the 7MM throughout the forecast period, while Spain will have the lowest. In the 7MM, GlobalData epidemiologists forecast that the diagnosed outpatient ILI incident cases will increase from 38,432,598 cases in 2015 to 38,686,403 cases in 2025, at an AGR of 0.07%. GlobalData epidemiologists forecast that the influenza cases averted by seasonal influenza vaccinations will increase from 1,801,663 cases in 2015 to 1,858,033 cases in 2025.
- The Seasonal Influenza EpiCast Report provides an overview of the risk factors, comorbidities, and the global and historical trends for seasonal influenza in the sevenmajor markets (7MM) (US, France, Germany, Italy, Spain, UK, and Japan). It includes a 10-year epidemiological forecast for the diagnosed incident cases of seasonal influenza segmented by age and sex in the 7MM. Moreover, clinically relevant segmentations are provided for diagnosed incident cases of seasonal influenza, including influenza-like illness (ILI) cases, lab confirmed cases, hospitalized cases, and averted cases. In addition, the report also includes the number of individuals who received the influenza vaccination in the 7MM. For all the 7MM, diagnosed incident cases are segmented by age (0-4 years, 5-17 years, 18-64 years, and =65 years) and sex.
- The seasonal influenza epidemiology report is written and developed by Masters- and PhD-level epidemiologists.
- The EpiCast Report is in-depth, high quality, transparent and market-driven, providing expert analysis of disease trends in the 8MM.
Reasons to buy
The Seasonal Influenza EpiCast report will allow you to -
- Develop business strategies by understanding the trends shaping and driving the global seasonal influenza market.
- Quantify patient populations in the global seasonal influenza market to improve product design, pricing, and launch plans.
- Organize sales and marketing efforts by identifying the age groups and sex that present the best opportunities for seasonal influenza therapeutics in each of the markets covered.
Table of Contents
1 Table of Contents 7
1.1 List of Tables 8
1.2 List of Figures 10
2 Epidemiology 11
2.1 Disease Background 11
2.2 Risk Factors and Comorbidities 12
2.3 Global Trends 13
2.3.1 Historical Perspective of Vaccination Coverage 14
2.3.2 Laboratory Confirmed Influenza Cases 17
2.3.3 Hospitalization Due to Influenza 17
2.3.4 Influenza Averted Cases 18
2.4 Forecast Methodology 18
2.4.1 Sources Used Tables 19
2.4.2 Forecast Assumptions and Methods 23
2.4.3 Sources Not Used 38
2.5 Epidemiological Forecast for Seasonal Influenza (2015-2025) 38
2.5.1 Seasonal Influenza Vaccination 38
2.5.2 Seasonal Influenza Vaccination Rates 45
2.5.3 Diagnosed Outpatient Influenza-Like Illness Incident Cases 47
2.5.4 Lab Confirmed Incident Cases of Seasonal Influenza 54
2.5.5 Influenza-Related Hospitalized Incident Cases 60
2.5.6 Cases Averted by Seasonal Influenza Vaccinations 65
2.6 Discussion 69
2.6.1 Epidemiological Forecast Insight 69
2.6.2 Limitations of the Analysis 70
2.6.3 Strengths of the Analysis 71
3 Appendix 72
3.1 Bibliography 72
3.2 About the Authors 83
3.2.1 Epidemiologists 83
3.2.2 Reviewers 84
3.2.3 Global Director of Therapy Analysis and Epidemiology 85
3.3 About GlobalData 86
3.4 About EpiCast 86
3.5 Disclaimer 87
MarketResearchReports.biz is the most comprehensive collection of market research reports. MarketResearchReports.Biz services are specially designed to save time and money for our clients. We are a one stop solution for all your research needs, our main offerings are syndicated research reports, custom research, subscription access and consulting services. We serve all sizes and types of companies spanning across various industries. | <urn:uuid:2d563718-daec-449a-8183-6d279d9cbbf5> | {
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Several viruses of the family Filoviridae cause severe and frequently fatal viral hemorrhagic fevers in humans. Introduction of filoviruses into human populations is an extremely rare event that most likely occurs by direct or indirect contact with healthy mammalian filovirus hosts or by contact with infected, sick, or deceased nonhuman primates. Filoviruses are highly infectious but not very contagious. Natural human-to-human transmission takes place through direct person-to-person (usually skin-to-skin) contact or exposure to infected bodily fluids and tissues; there is no evidence of such transmission by aerosol or respiratory droplets. Infections progress rapidly from influenza-like to hemorrhagic manifestations and typically culminate in multiple-organ dysfunction syndrome and shock. Treatment of filovirus infections is of necessity entirely supportive because no specific efficacious antiviral agents or vaccines are yet available.
Filoviruses are categorized as World Health Organization (WHO) Risk Group 4 Pathogens. Consequently, all work with material suspected of containing filoviruses should be conducted only in maximal containment (biosafety level 4) laboratories. Experienced personnel handling these viruses must wear appropriate personal protective gear (see “Prevention,” below) and follow rigorous standard operating procedures. The proper authorities and WHO reference laboratories should be contacted immediately when filovirus infections are suspected.
The family Filoviridae includes three genera: Cuevavirus, Ebolavirus, and Marburgvirus (Table 234-1 and Fig. 234-1). The available data suggest that the only known cuevavirus, Lloviu virus (LLOV), and one ebolavirus, Reston virus (RESTV), are not pathogenic for humans. The remaining four ebolaviruses—Bundibugyo virus (BDBV), Ebola virus (EBOV), Sudan virus (SUDV), and Taï Forest virus (TAFV)—cause Ebola virus disease (EVD; International Classification of Disease, Tenth Revision [ICD-10], code A98.4). The two marburgviruses, Marburg virus (MARV) and Ravn virus (RAVV), are the etiologic agents of Marburg virus disease (MVD; ICD-10 code A98.3).
Filoviruses have linear, nonsegmented, single-stranded, negative-sense RNA genomes that are ~19 kb in length. These genomes contain six or seven genes that encode the following seven structural proteins: nucleoprotein, polymerase cofactor (VP35), matrix protein (VP40), glycoprotein (GP1,2), transcriptional cofactor (VP30), secondary matrix protein (VP24), and RNA-dependent RNA polymerase (L protein). Cuevaviruses and ebolaviruses, but not marburgviruses, also encode three nonstructural proteins of unknown function (sGP, ssGP, and Δ-peptide). Filovirions are unique among human virus particles in that they are predominantly pleomorphic filaments but also assume torus- or 6-like shapes (width, ~80 nm; average length, ≥790 nm). These enveloped virions contain helical ribonucleocapsids and are covered with GP1,2 spikes (Fig. 234-2).
TABLE 234-1Filovirus Taxonomy |Favorite Table|Download (.pdf) TABLE 234-1Filovirus Taxonomy
|Current Taxonomy and Nomenclature ||Previous Taxonomy and Nomenclature |
Species Marburg marburgvirus
Virus 1: Marburg virus (MARV)
Virus 2: Ravn virus (RAVV)
Species Taï Forest ebolavirus
Virus: Taï Forest virus (TAFV)
Species Reston ebolavirus
Virus: Reston virus (RESTV)
Species Sudan ebolavirus
Virus: Sudan ...
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Rosenhan's study has changed the classifications systems vastly nine healthy people presented themselves at different psychiatric hospitals and said that they were hearing voices saying things like 'empty and 'thud' all were admitted and all , except one were diagnosed as suffering from schizophrenia apart from. I description and classification schizophrenia is a serious mental illness that afflicts about 1% of the population at some point in their lifetime in the current diagnostic and statistical manual of mental disorders (dsm-iv), it is described as an illness that is characterized by psychotic symptoms and significant interpersonal. Autistic spectrum disorders were also thought to be a type of childhood schizophrenia as prof frances puts it in an essay on the topic called psychiatric diagnosis: “our classification of mental disorders is no more than a collection of fallible and limited constructs that seek but never find an elusive truth. Many critics have pointed out problems in the dsm-5 my biggest concern: the new dsm-5 makes it easy for anybody to diagnose anybody with anything, including schizophrenia. Diagnostic classification systems diagnostic manuals contain the information needed for clinicians to make objective, reliable diagnoses they contain: classifications of disorders into different types for example, psychoses like schizophrenia involve a break from reality but neuroses like depression involve. Explains why classification/diagnosis systems are often updated and revised ethical consideration is the main weakness of classification systems the effects of labeling leads to stigmatisation prejudice and discrimination self psychiatrists from new york had a higher likelihood of diagnosing schizophrenia.
This is a summary sheet including all information needed for aqa new specification psychology 'classification of schizophrenia' it is best used as a hand out in lessons to summarise the key information students should learn for the exam, or as a re. It provides a biological explanation of schizophrenia including genetics - twin and adoption studies, dopamine hypothesis and neuro developmental hypothesis includes detailed discuss issues surrounding the classification and diagnosis of schizophrenia, including reliability and validity 2 essay. Diagnosis involves matching the results of the psychological assessment with classification systems such as dsm-iv-tr and icd-10 the purpose of diagnosis is to find a treatment the aim of the study was to investigate reliability of diagnosis of depression and schizophrenia the researchers asked american and british.
New 2nd edition psya4 schizophrenia model essay answers psya4r june 2015 (replacement paper): outline one issue relating to the classification and/or diagnosis of schizophrenia (4 marks) psya4r june 2015 (replacement paper): outline and evaluate one or more biological explanations for. This essay will be a critical evaluation of the diagnosis and classification of abnormality and the intrinsic problems involved the term shortly after admission they stopped claiming that they could hear voices and all were eventually discharged after varying lengths of stay, with the diagnosis of ' schizophrenia in remission.
In 2013 the diagnostic and statistical manual of mental disorders 5th edition ( dsm-v) changed the method of classification to bring all these categories under a single heading: schizophrenia according to the american psychiatric association (apa), the decision to eliminate these various subtypes was. According to the diagnostic and statistical manual of mental disorders, fifth edition, (dsm-5), to meet the criteria for diagnosis of schizophrenia, the patient must have experienced at least 2 of the following symptoms : delusions hallucinations disorganized speech disorganized or catatonic behavior.
Not only the classification systems that determine the reliability of a diagnosis the psychiatrist's role is vital • test-retest reliability: seeman (2007) – test- retest reliability for schizophrenia initial diagnosis of schizophrenia, especially in women, was often changed as the psychiatrists got to know their. A summary of classification in 's psychological disorders learn exactly what perfect for acing essays, tests, and quizzes, as well as for writing lesson plans psychologists and psychiatrists use a reference book called the diagnostic and statistical manual of mental disorders (dsm) to diagnose psychological disorders. | <urn:uuid:55b48034-9763-4ca8-9feb-6a3a26f91f7c> | {
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Borderline personality disorder refers to an emotionally unstable state characterized by impulsiveness, low self-control, emotionality, a strong level
, unstable connection with reality and highanxiety. Borderline personality disorder, being a mental illness, is marked by a sharp drop in mood, impulsive behavior and serious problems with self-esteem and relationships. Individuals with this disease often also have other health problems: eating disorders,
, alcohol and drug abuse. The first signs of the disease appear in young years. According to available statistics, borderline pathology is observed in 3% of the adult population, of which 75% are representatives of the fair sex. An essential sign of the disease is self-damaging or suicidal behavior, completed
reach about 8-10%.
Causes of borderline personality disorder
Of the 100 people, two have a borderpersonality disorder and experts to this day doubt the causes of this condition. It can be caused by an imbalance of chemicals in the brain, called neurotransmitters, which help in regulating mood. Also, the mood is influenced by the environment and genetics.
Borderline personality disorder is five times more likelyis noted in those people whose relatives suffered from this ailment. This condition is often found in families where other diseases associated with mental ill health are noted. These are problems associated with the abuse of alcohol and drugs, antisocial personality disorder, depressive conditions. Often, patients experienced severe trauma in childhood. It can be physical, sexual, emotional violence; ignoring, sharing with the parent or his early loss. If such trauma is noted in combination with some personality traits (anxiety, lack of stress-resistance), the risk in the development of the borderline state is significantly increased. Researchers recognize that individuals with borderline personality disorder have a worsened functioning of parts of the brain, which still does not allow to know: these problems are the consequences of the condition or its cause.
Borderline personality disorder symptoms
Patients with a borderline personality state often have unstable relationships, problems with impulsiveness,
, which begin to manifest from childhood.
The emergence of a borderline disorderpersonality is due to the efforts of American psychologists from 1968 to 1980, which enabled the inclusion of a borderline personality type in DSM-III, and then in ICD-10. But the studies and theoretical work carried out by psychologists were devoted to justifying and isolating the intermediate personality type between
The sign of the disorder is low-risksuicide attempts due to insignificant incidents and occasionally dangerous suicide attempts due to comorbid depression. Often provoke attempts of suicides interpersonal situations.
Common for this disorder is the
be left alone or abandoned,even if it is an imaginary threat. This fear can provoke a desperate attempt to hold on to those who are close to such a person. Sometimes a person rejects others first, responding to the fear of being abandoned. Such eccentric behavior can provoke problematic relationships in any life sphere.
Diagnosis of borderline personality disorder
This state must be differentiated from
, anxiety-phobic, schizotypic and affective states.
DSM-IV to the signs of borderline disorder includes the instability of interpersonal relationships, pronounced impulsivity, emotional instability, impaired internal preferences.
All these signs occur at a young age and make themselves felt in different situations. Diagnostics includes, in addition to basic, the presence of five or more of the following features:
- applying excessive efforts to avoid the imaginary or real fate of being abandoned;
- the prerequisites to be drawn into tense, intense, unstable relationships characterized by an alternation of extremes: depreciation and idealization;
- personality identity disorder: persistent, marked instability of the image, as well as feelings of the Self; - impulsiveness, which manifests itself in the waste of money, violation of traffic rules; sexual behavior, overeating, substance abuse;
- Suicidal recurrent behavior, threats and hints of suicide, acts of self-harm;
- changeability of mood -
; affective instability;
- a constantly felt feeling of emptiness;
- Inadequacy in the manifestation of strong anger, as well as difficulties caused by the need to control feelings of anger;
- expressed dissociative symptoms or paranoid ideas.
Not every individual with fiveor more of these symptoms, a borderline pathology will be established. For the diagnosis to be established, the symptoms should be marked with a sufficiently long time period.
Borderline personality disorder is often confused with other conditions that have similar symptoms (antisocial or dramatic personality disorder).
Among individuals with borderline pathology oftenthere have been attempts at suicidal behavior, with 10% of them committing suicide. Emerging other conditions along with borderline personality pathology also require treatment. These additional conditions can complicate the treatment.
Conditions that arise with borderline pathology include:
- depression or
- food disorders;
- problems with alcohol and drug abuse;
- attention deficit hyperactivity disorder.
In addition to this disease, other disorders can also join. Some of them are:
- dramatic personality disorder, leading to emotional excess reactions;
- anxious personality disorder, which includes avoiding social contacts;
- antisocial personality disorder.
Treatment of borderline personality disorder
This state is included in the DSM-IV and ICD-10. The classification of borderline pathology as an independent personality disorder is controversial. Treatment is often very difficult and time-consuming. This is because it is very difficult to deal with problems that are associated with behavior and emotions. However, treatment can give good results immediately after the start of therapy.
How to help yourself with a borderline disorderpersonality? Psychotherapy plays a significant role in the treatment. Psychopharmacotherapy is used in the treatment of various combinations of pathology, for example, such as depression.
How to live with a person who has a borderpersonality disorder? This question is often asked by relatives, because the patient always has an increased impressionability and a sensitivity to all on the way to obstacles, they often experience a feeling peculiar to the situation of stress, and relatives do not know how to help them. Such individuals experience difficulties in controlling their thoughts and emotions, are very impulsive and irresponsible in their behavior, are unstable in their relationships with other people.
When practicing psychotherapy, the most difficultthe task is to maintain and create a psychotherapeutic relationship. It can be very difficult for patients to maintain certain limits of the psychotherapeutic union, since the leading symptom is their tendency to get involved in intense, intense, unstable relationships marked by alternating extremes. Sometimes psychotherapists themselves try to distance themselves from complex patients, thereby protecting themselves from problems. | <urn:uuid:52e4ca76-6e78-4888-aaa6-7f6b7cd1feff> | {
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A bone fracture (sometimes abbreviated FRX or Fx, Fx, or #) is a medical condition in which there is a damage in the continuity of the bone. A bone fracture may be the result of high force impact or stress, or a minimal trauma injury as a result of certain medical conditions that weaken the bones, such as osteoporosis, bone cancer, or osteogenesis imperfecta, where the fracture is then properly termed a pathologic fracture.
|Synonyms||broken bone, bone break|
|Internal and external views of an arm with a compound fracture, both before and after surgery|
|Classification and external resources|
|ICD-10||Sx2 (where x=0–9 depending on the location of the fracture)|
Signs and symptomsEdit
- Breaking in the continuity of the periosteum, with or without similar discontinuity in endosteum, as both contain multiple pain receptors
- Edema of nearby soft tissues caused by bleeding of torn periosteal blood vessels evokes pressure pain
- Muscle spasms trying to hold bone fragments in place. Sometimes also followed by cramping
Damage to adjacent structures such as nerves or vessels, spinal cord, and nerve roots (for spine fractures), or cranial contents (for skull fractures) may cause other specific signs and symptoms.
The natural process of healing a fracture starts when the injured bone and surrounding tissues bleed, forming a fracture hematoma. The blood coagulates to form a blood clot situated between the broken fragments. Within a few days, blood vessels grow into the jelly-like matrix of the blood clot. The new blood vessels bring phagocytes to the area, which gradually remove the non-viable material. The blood vessels also bring fibroblasts in the walls of the vessels and these multiply and produce collagen fibres. In this way the blood clot is replaced by a matrix of collagen. Collagen's rubbery consistency allows bone fragments to move only a small amount unless severe or persistent force is applied.
At this stage, some of the fibroblasts begin to lay down bone matrix in the form of collagen monomers. These monomers spontaneously assemble to form the bone matrix, for which bone crystals (calcium hydroxyapatite) are deposited in amongst, in the form of insoluble crystals. This mineralization of the collagen matrix stiffens it and transforms it into bone. In fact, bone is a mineralized collagen matrix; if the mineral is dissolved out of bone, it becomes rubbery. Healing bone callus on average, is sufficiently mineralized to show up on X-ray within 6 weeks in adults and less in children. This initial "woven" bone does not have the strong mechanical properties of mature bone. By a process of remodeling, the woven bone is replaced by mature "lamellar" bone. The whole process may take up to 18 months, but in adults, the strength of the healing bone is usually 80% of normal by 3 months after the injury.
Several factors may help or hinder the bone healing process. For example, any form of nicotine hinders the process of bone healing, and adequate nutrition (including calcium intake) will help the bone healing process. Weight-bearing stress on bone, after the bone has healed sufficiently to bear the weight, also builds bone strength.
Effects of smokingEdit
Smokers generally have lower bone density than non-smokers, so have a much higher risk of fractures. There also is evidence that smoking delays bone healing.
A bone fracture may be diagnosed based on the history given and the physical examination performed. Radiographic imaging often is performed to confirm the diagnosis. Under certain circumstances, radiographic examination of the nearby joints is indicated in order to exclude dislocations and fracture-dislocations. In situations where projectional radiography alone is insufficient, Computed Tomography (CT) or Magnetic Resonance Imaging (MRI) may be indicated.
In orthopedic medicine, fractures are classified in various ways. Historically they are named after the physician who first described the fracture conditions, however, there are more systematic classifications in place currently.
- Traumatic fracture – This is a fracture due to sustained trauma. e.g., fractures caused by a fall, road traffic accident, fight, etc.
- Pathologic fracture – A fracture through a bone that has been made weak by some underlying disease is called pathological fracture. e.g., a fracture through a bone weakened by metastasis. Osteoporosis is the most common cause of pathological fracture.
- Periprosthetic fracture – This is a fracture at the point of mechanical weakness at the end of an implant
- Closed fractures are those in which the overlying skin is intact
- Open/compound fractures involve wounds that communicate with the fracture, or where fracture hematoma is exposed, and may thus expose bone to contamination. Open injuries carry a higher risk of infection.
- Clean fracture
- Contaminated fracture
- Translated, or ad latus, with sideways displacement.
- Linear fracture: A fracture that is parallel to the bone's long axis
- Transverse fracture: A fracture that is at a right angle to the bone's long axis
- Oblique fracture: A fracture that is diagonal to a bone's long axis (more than 30°)
- Spiral fracture: A fracture where at least one part of the bone has been twisted
- Compression fracture/Wedge fracture: usually occurs in the vertebrae, for example when the front portion of a vertebra in the spine collapses due to osteoporosis (a medical condition which causes bones to become brittle and susceptible to fracture, with or without trauma)
- Impacted fracture: A fracture caused when bone fragments are driven into each other
- Avulsion fracture: A fracture where a fragment of bone is separated from the main mass
- Incomplete fracture: Is a fracture in which the bone fragments are still partially joined, in such cases, there is a crack in the osseous tissue that does not completely traverse the width of the bone.
- Complete fracture: Is a fracture in which bone fragments separate completely.
- Comminuted fracture: Is a fracture in which the bone has broken into several pieces.
An anatomical classification may begin with specifying the involved body part, such as the head or arm, followed with more specific localization. Fractures that have additional definition criteria than merely localization often may be classified as subtypes of fractures, such as a Holstein-Lewis fracture being a subtype of a humerus fracture. Most typical examples in an orthopedic classification given in previous section cannot be classified appropriately into any specific part of an anatomical classification, however, as they may apply to multiple anatomical fracture sites.
- Skull fracture
- Spinal fracture
- Cervical fracture
- Clay-shoveler fracture – fracture through the spinous process of a vertebra occurring at any of the lower cervical or upper thoracic vertebrae
- Burst fracture – in which a vertebra breaks from a high-energy axial load
- Compression fracture – a collapse of a vertebra, often in the form of wedge fractures due to larger compression anteriorly
- Chance fracture – compression injury to the anterior portion of a vertebral body with concomitant distraction injury to posterior elements
- Holdsworth fracture – an unstable fracture dislocation of the thoracolumbar junction of the spine
- Rib fracture
- Sternal fracture
- Shoulder fracture
- Arm fracture
- Humerus fracture (fracture of upper arm)
- Forearm fracture
- Ulnar fracture
- Radius fracture
- Essex-Lopresti fracture – a fracture of the radial head with concomitant dislocation of the distal radio-ulnar joint with disruption of the interosseous membrane
- Distal radius fracture
- Galeazzi fracture – a fracture of the radius with dislocation of the distal radioulnar joint
- Colles' fracture – a distal fracture of the radius with dorsal (posterior) displacement of the wrist and hand
- Smith's fracture – a distal fracture of the radius with volar (ventral) displacement of the wrist and hand
- Barton's fracture – an intra-articular fracture of the distal radius with dislocation of the radiocarpal joint
- Hand fracture
- Scaphoid fracture
- Rolando fracture – a comminuted intra-articular fracture through the base of the first metacarpal bone
- Bennett's fracture – a fracture of the base of the first metacarpal bone which extends into the carpometacarpal (CMC) joint
- Boxer's fracture – a fracture at the neck of a metacarpal
- Pelvic fracture
- Femoral fracture
- Patella fracture
- Crus fracture
- Tibia fracture
- Pilon fracture
- Tibial plateau fracture
- Bumper fracture – a fracture of the lateral tibial plateau caused by a forced valgus applied to the knee
- Segond fracture – an avulsion fracture of the lateral tibial condyle
- Gosselin fracture – a fractures of the tibial plafond into anterior and posterior fragments
- Toddler's fracture – an undisplaced and spiral fracture of the distal third to distal half of the tibia
- Fibular fracture
- Maisonneuve fracture – a spiral fracture of the proximal third of the fibula associated with a tear of the distal tibiofibular syndesmosis and the interosseous membrane
- Le Fort fracture of ankle – a vertical fracture of the antero-medial part of the distal fibula with avulsion of the anterior tibiofibular ligament
- Bosworth fracture – a fracture with an associated fixed posterior dislocation of the proximal fibular fragment that becomes trapped behind the posterior tibial tubercle; the injury is caused by severe external rotation of the ankle
- Combined tibia and fibula fracture
- Tibia fracture
- Foot fracture
The Orthopaedic Trauma Association Committee for Coding and Classification published its classification system in 1996, adopting a similar system to the 1987 AO Foundation system. In 2007, they extended their system, unifying the two systems regarding wrist, hand, foot, and ankle fractures.
Classifications named after peopleEdit
A number of classifications are named after the person (eponymous) who developed it.
- "Denis classification" for spinal fractures
- "Frykman classification" for forearm fractures (fractures of radius and ulna)
- "Gustilo open fracture classification"
- "Letournel and Judet Classification" for Acetabular fractures
- "Neer classification" for humerus fractures
- Seinsheimer classification, Evans-Jensen classification, Pipkin classification, and Garden classification for hip fractures
Treatment of bone fractures are broadly classified as surgical or conservative, the latter basically referring to any non-surgical procedure, such as pain management, immobilization or other non-surgical stabilization. A similar classification is open versus closed treatment, in which open treatment refers to any treatment in which the fracture site is opened surgically, regardless of whether the fracture is an open or closed fracture.
Since bone healing is a natural process that will occur most often, fracture treatment aims to ensure the best possible function of the injured part after healing. Bone fractures typically are treated by restoring the fractured pieces of bone to their natural positions (if necessary), and maintaining those positions while the bone heals. Often, aligning the bone, called reduction, in good position and verifying the improved alignment with an X-ray is all that is needed. This process is extremely painful without anesthesia, about as painful as breaking the bone itself. To this end, a fractured limb usually is immobilized with a plaster or fiberglass cast or splint that holds the bones in position and immobilizes the joints above and below the fracture. When the initial post-fracture edema or swelling goes down, the fracture may be placed in a removable brace or orthosis. If being treated with surgery, surgical nails, screws, plates, and wires are used to hold the fractured bone together more directly. Alternatively, fractured bones may be treated by the Ilizarov method which is a form of external fixator.
Occasionally smaller bones, such as phalanges of the toes and fingers, may be treated without the cast, by buddy wrapping them, which serves a similar function to making a cast. By allowing only limited movement, fixation helps preserve anatomical alignment while enabling callus formation, toward the target of achieving union.
Splinting results in the same outcome as casting in children who have a distal radius fracture with little shifting.
Surgical methods of treating fractures have their own risks and benefits, but usually surgery is performed only if conservative treatment has failed, is very likely to fail, or likely to result in a poor functional outcome. With some fractures such as hip fractures (usually caused by osteoporosis), surgery is offered routinely because non-operative treatment results in prolonged immobilisation, which commonly results in complications including chest infections, pressure sores, deconditioning, deep vein thrombosis (DVT), and pulmonary embolism, which are more dangerous than surgery. When a joint surface is damaged by a fracture, surgery is also commonly recommended to make an accurate anatomical reduction and restore the smoothness of the joint.
Infection is especially dangerous in bones, due to the recrudescent nature of bone infections. Bone tissue is predominantly extracellular matrix, rather than living cells, and the few blood vessels needed to support this low metabolism are only able to bring a limited number of immune cells to an injury to fight infection. For this reason, open fractures and osteotomies call for very careful antiseptic procedures and prophylactic use of antibiotics.
Occasionally, bone grafting is used to treat a fracture.
Sometimes bones are reinforced with metal. These implants must be designed and installed with care. Stress shielding occurs when plates or screws carry too large of a portion of the bone's load, causing atrophy. This problem is reduced, but not eliminated, by the use of low-modulus materials, including titanium and its alloys. The heat generated by the friction of installing hardware can accumulate easily and damage bone tissue, reducing the strength of the connections. If dissimilar metals are installed in contact with one another (i.e., a titanium plate with cobalt-chromium alloy or stainless steel screws), galvanic corrosion will result. The metal ions produced can damage the bone locally and may cause systemic effects as well.
A Cochrane review of low-intensity pulsed ultrasound to speed healing in newly broken bones found insufficient evidence to justify routine use. Other reviews have found tentative evidence of benefit. It may be an alternative to surgery for established nonunions.
Vitamin D supplements combined with additional calcium marginally reduces the risk of hip fractures and other types of fracture in older adults; however, vitamin D supplementation alone did not reduce the risk of fractures.
Some fractures may lead to serious complications including a condition known as compartment syndrome. If not treated, eventually, compartment syndrome may require amputation of the affected limb. Other complications may include non-union, where the fractured bone fails to heal or mal-union, where the fractured bone heals in a deformed manner.
Complications of fractures may be classified into three broad groups, depending upon their time of occurrence. These are as follows –
- Immediate complications – occurs at the time of the fracture
- Early complications – occurring in the initial few days after the fracture
- Late complications – occurring a long time after the fracture
|Immediate complications||Early complications||Late complications|
||Imperfect union of the fracture
In children, whose bones are still developing, there are risks of either a growth plate injury or a greenstick fracture.
- A greenstick fracture occurs due to mechanical failure on the tension side. That is, since the bone is not so brittle as it would be in an adult, it does not completely fracture, but rather exhibits bowing without complete disruption of the bone's cortex in the surface opposite the applied force.
- Growth plate injuries, as in Salter-Harris fractures, require careful treatment and accurate reduction to make sure that the bone continues to grow normally.
- Plastic deformation of the bone, in which the bone permanently bends, but does not break, also is possible in children. These injuries may require an osteotomy (bone cut) to realign the bone if it is fixed and cannot be realigned by closed methods.
- Certain fractures mainly occur in children, including fracture of the clavicle and supracondylar fracture of the humerus.
- Witmer, Daniel K.; Marshall, Silas T.; Browner, Bruce D. (2016). "Emergency Care of Musculoskeletal Injuries". In Townsend, Courtney M.; Beauchamp, R. Daniel; Evers, B. Mark; Mattox, Kenneth L. Sabiston Textbook of Surgery (20th ed.). Elsevier. pp. 462–504. ISBN 978-0-323-40163-0.
- MedicineNet – Fracture Archived 2008-12-21 at the Wayback Machine. Medical Author: Benjamin C. Wedro, MD, FAAEM.
- Sloan, A.; Hussain, I.; Maqsood, M.; Eremin, O.; El-Sheemy, M. (2010). "The effects of smoking on fracture healing". The Surgeon. 8 (2): 111–6. doi:10.1016/j.surge.2009.10.014. PMID 20303894.
- Pountos, Ippokratis; Georgouli, Theodora; Calori, Giorgio M.; Giannoudis, Peter V. (2012). "Do Nonsteroidal Anti-Inflammatory Drugs Affect Bone Healing? A Critical Analysis". The Scientific World Journal. 2012: 606404. doi:10.1100/2012/606404. PMC . PMID 22272177.
- Kanis, J. A.; Johnell, O.; Oden, A.; Johansson, H.; De Laet, C.; Eisman, J. A.; Fujiwara, S.; Kroger, H.; McCloskey, E. V.; Mellstrom, D.; Melton, L. J.; Pols, H.; Reeve, J.; Silman, A.; Tenenhouse, A. (2004). "Smoking and fracture risk: A meta-analysis". Osteoporosis International. 16 (2): 155–62. doi:10.1007/s00198-004-1640-3. PMID 15175845.
- Roberto Schubert. "Fractures of the extremities (general rules and nomenclature)". Radiopaedia. Retrieved 2018-02-21.
- Essex Lopresti fracture Archived 2009-10-01 at the Wayback Machine. at Wheeless' Textbook of Orthopaedics online
- Hunter, Tim B.; Peltier, Leonard F.; Lund, Pamela J. (2000). "Radiologic History Exhibit". RadioGraphics. 20 (3): 819–36. doi:10.1148/radiographics.20.3.g00ma20819. PMID 10835130.
- Mellick, Larry B.; Milker, Laura; Egsieker, Erik (1999). "Childhood accidental spiral tibial (CAST) fractures". Pediatric Emergency Care. 15 (5): 307–9. doi:10.1097/00006565-199910000-00001. PMID 10532655.
- Perry, C. R.; Rice, S; Rao, A; Burdge, R (1983). "Posterior fracture-dislocation of the distal part of the fibula. Mechanism and staging of injury". The Journal of Bone and Joint Surgery. American Volume. 65 (8): 1149–57. doi:10.2106/00004623-198365080-00016. PMID 6630259.
- TheFreeDictionary > Lisfranc's fracture Citing: Mosby's Medical Dictionary, 8th edition. Copyright 2009
- "Fracture and dislocation compendium. Orthopaedic Trauma Association Committee for Coding and Classification". Journal of Orthopaedic Trauma. 10 Suppl 1: v–ix, 1–154. 1996. PMID 8814583.
- Müller ME, Nazarian S, Koch P (1987). Classification AO des fractures. Tome I. Les os longs. Berlin: Springer-Verlag.[page needed]
- Marsh, J. L.; Slongo, T. F.; Agel, J; Broderick, J. S.; Creevey, W; Decoster, T. A.; Prokuski, L; Sirkin, M. S.; Ziran, B; Henley, B; Audigé, L (2007). "Fracture and dislocation classification compendium - 2007: Orthopaedic Trauma Association classification, database and outcomes committee". Journal of Orthopaedic Trauma. 21 (10 Suppl): S1–133. PMID 18277234.
- Rüedi, etc. all; Thomas P. Rüedi; Richard E. Buckley; Christopher G. Moran (2007). AO principles of fracture management, Volume 1. Thieme. p. 96. ISBN 3-13-117442-0.
- "Fractures of the Acetabulum". wheelessonline.com. Archived from the original on 2009-09-26.
- Mourad, L (1997). "Neer classification of fractures of the proximal humerus". Orthopedic nursing. 16 (2): 76. PMID 9155417.
- Proximal Humerus Fractures at eMedicine
- Drendel, Amy L.; Gorelick, Marc H.; Weisman, Steven J.; Lyon, Roger; Brousseau, David C.; Kim, Michael K. (2009). "A Randomized Clinical Trial of Ibuprofen Versus Acetaminophen with Codeine for Acute Pediatric Arm Fracture Pain". Annals of Emergency Medicine. 54 (4): 553–60. doi:10.1016/j.annemergmed.2009.06.005. PMID 19692147.
- Boutis, K.; Willan, A.; Babyn, P.; Goeree, R.; Howard, A. (2010). "Cast versus splint in children with minimally angulated fractures of the distal radius: A randomized controlled trial". Canadian Medical Association Journal. 182 (14): 1507–12. doi:10.1503/cmaj.100119. PMC . PMID 20823169.
- Griffin, XL; Parsons, N; Costa, ML; Metcalfe, D (23 June 2014). "Ultrasound and shockwave therapy for acute fractures in adults". The Cochrane Database of Systematic Reviews (6): CD008579. doi:10.1002/14651858.CD008579.pub3. PMID 24956457.
- Lou, S.; Lv, H.; Li, Z.; Zhang, L.; Tang, P (1 September 2017). "The effects of low-intensity pulsed ultrasound on fresh fracture: A meta-analysis". Medince. 96 (39): e8181. doi:10.1097/MD.0000000000008181. PMC . PMID 28953676.
- Leighton, R.; Watson, J.T; Giannoudis, P.; Papakostidis, C.; Harrison, A.; Steen, R.G. (May 2017). "Healing of fracture nonunions treated with low-intensity pulsed ultrasound (LIPUS): A systematic review and meta-analysis". Injury. 48 (7): 1339–1347. doi:10.1016/j.injury.2017.05.016. PMID 28532896.
- Avenell, Alison; Mak, Jenson C. S.; O'Connell, Dianne (2014-04-14). "Vitamin D and vitamin D analogues for preventing fractures in post-menopausal women and older men". The Cochrane Database of Systematic Reviews (4): CD000227. doi:10.1002/14651858.CD000227.pub4. ISSN 1469-493X. PMID 24729336. | <urn:uuid:45ce2ca7-970b-4125-b892-d7480bfe5782> | {
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In addition to being associated with characteristic physical and behavioural features, Fragile-X syndrome causes intellectual disabilities ranging from mild to severe. It is the most common cause of inherited intellectual disability and is second only to Down's syndrome as the most common genetic cause of intellectual disability.
Manga Sabaratnam (UK) and Yogesh Thakker (UK)
Fragile X syndrome (FXS) is the most common inherited cause of intellectual disability worldwide. It is caused by a mutation of the FMR-1 (fragile-X mental retardation) gene located on the X chromosome. This contribution explores the genetic and molecular basis of the disease and methods for its detection, as well as neuropathological findings. The issues involved in genetic counselling and screening are also discussed. The presentation of FXS is variable, but common physical, behavioural and developmental features are outlined. The specific deficits, in terms of intellectual disability, are also explored; for example, males with FXS have particular difficulties in sequential processing of information. Broad differences between male and female intellectual disability have also been discovered. The relationship between FXS and autistic spectrum disorders is mentioned, as are comorbidities with other neurological (epilepsy) and psychiatric disorders. There is no definitive treatment for FXS, but a number of interventions can raise the quality of life of the individual and their family and carers. These include pharmacological treatments for comorbid conditions such as epilepsy and attention deficit hyperactivity disorder, as well as behavioural and cognitive interventions. Newly developed targeted treatments for FXS like mGluR5 antagonists, GABA agonists and MMP-9 inhibitors have been described. However, there is still much scope for new research into both the molecular basis and the potential treatments of FXS.
FXS is an X-linked semi-dominant condition with reduced penetrance. It is caused by an expansion of an unstable CGG trinucleotide repeat in the fragile X gene (FMR-1). In addition to being associated with characteristic physical and behavioural features, causes intellectual disability ranging from mild to severe. It is the most common cause of inherited intellectual disability and is second only to Down’s syndrome as the most common genetic cause of intellectual disability. There is a wide spectrum of clinical features, but life expectancy is not greatly reduced.
There are about 100–200 affected births in the UK each year. The population prevalence is estimated at 1 in 4000 males and 1 in 8000 females (Hagerman and Hagerman, 2002). It occurs in all races and ethnic groups. It accounts for approximately 10% of all males with severe intellectual disability and 10% of mild intellectual disability. The average age at diagnosis of FXS is 35 to 37 months (Bailey et al., 2009).
FXS was first documented by Martin and Bell in 1943. They described a pedigree with 11 affected males and four mildly affected females in three generations. They believed that this pedigree suggested X linked inheritance since males were more severely affected than females. The break on the long arm of the chromosome (the fragile site) was first demonstrated in 1969 by Lubs, but was not confirmed until 1977, with the discovery that a folate-deficient culture medium was required to show the fragile site. Verkerk et al. isolated the long-awaited FMR-1 (fragile-X mental retardation) gene using a positional cloning strategy in 1991 and it became diagnostic test for FXS.
The fragile site was found at region Xq27.3 on the long arm of the X chromosome
Genetics and Aetiology
After the detection of FMR-1 gene by Verkerk et al (1991) it was identified that FXS is caused by abnormal expansion of a trinucleotide repeat (CGG) in the FMR-1 gene. The diagnosis of FXS was originally made by visualizing the folate-sensitive fragile site at Xq27.3 (FRAXA) induced by culturing the cells in folate-deficient culture media. The mutational basis of FRAXA was recognized to be due to the expansion of a trinucleotide repeat (CGG)n present in the 5' untranslated region of the identified gene. The lack of expression of the FMR-1 gene results in non-production of the protein (fragile-X mental retardation protein, or FMRP), resulting in FXS. FMR-1 is the first cloned gene to be linked to human intelligence.
Ninety-five per cent of cases of FXS are due to expansion in the CGG sequence (Fu et al., 1991). Normal individuals carry between 5 and 54 copies of CGG repeat. In normal carriers, the number of CGG repeats (the premutation) is between 55 and 200. In individuals clinically manifesting the syndrome (full mutation), the CGG repeats increase to 200–2000 or more. Such a large mutation is usually accompanied by hypermethylation of the DNA sequence, whereby methyl groups attach to the CGG triplets. This renders the FMR-1 gene transcriptionally inactive.
It is also possible for the CGG expansions to vary from cell to cell, resulting in somatic heterogeneity in allele size. Up to 40% of affected males are ‘mosaics’ – i.e. they exhibit both a premutation and a full mutation in the blood (Nolin et al., 1994). There are two kinds of mosaicism in FXS: repeat size mosaicism and methylation mosaicism. In repeat size mosaicism, an individual has some cells that have a full mutation and some cells that have a premutation. In methylation mosaicism, all the cells have a full mutation, but the methylation pattern may not be the same in all cells.
Under normal circumstances, the FMR-1 gene encodes FMRP. The absence of FMRP is likely to be responsible for the development of the Fragile X phenotype. The exact role of FMRP is unknown, but it is thought to act to regulate protein synthesis. FMRP usually helps the connection between neurons that underlie learning and memory; absence of FMRP seems to delay the development of such neurons. In normal individuals, FMRP is ubiquitously expressed, but at higher levels in the brain and the testes. The major characteristics in affected individuals with FXS relate to the functioning of the brain and macro-orchidism. People with the premutation make FMRP; those with the full mutation do not. Females with the full mutation on one X chromosome and normal FMR-1 on the other make a reduced amount of FMRP.
The identification of the FMR-1 gene led to an increased understanding of the unusual and previously unexplained features of its inheritance. FXS is an X-linked, dominantly inherited disorder, with reduced penetrance, but its pattern of inheritance is atypical. Both females and males can be affected, although it is less common and often less severe in females. In addition, both males and females can be unaffected carriers. Four-fifths of males with the full mutation are clinically affected, while only half the females with the full mutation are affected. In females with the premutation, the CGG trinucleotide expansion in the FMR-1 gene is hereditarily unstable. There is, therefore, a high risk of the premutation expanding to a full mutation when it is transmitted from a woman to her children. However, when the premutation is passed through men (also known as carrier males or normal-transmitting males), it does not significantly increase in size. The sons of an unaffected man do not receive the X chromosome and so are neither affected nor carriers. His daughters, on the other hand, receive the premutation and are all unaffected carriers, although their own children are at risk of inheriting the full mutation. Heterozygous females who receive the full mutation from their mothers may have clinical features of FXS. The transmission of the mutation through phenotypically normal daughters to their grandchildren, (the so-called Sherman paradox, or ‘genetic anticipation’) occurs when the disease severity increases through successive generations. About 25% of female carriers have intellectual disability, and they are more likely to have similarly affected offspring than are intellectually normal carrier females.
As the fragility at Xq27.3 is visible under the microscope in only 4–50% of cells, cytogenetic testing has been superseded by more accurate DNA tests. These are less expensive, less time-consuming and can accurately detect both full mutation and premutation and provide details about the allele size and methylation in affected individuals as well as normal-transmitting males and carrier females.
The following tests are available to detect FXS:
- Polymerase chain reaction (PCR) is the routine screening test used on Fragile X samples. It is particularly effective for small increases (premutation) but is not very sensitive in detecting full mutations.
- If PCR fails, Southern blotting is performed. This can detect full mutations and methylation status of the regulatory site and the presence of mosaicism. It is more labour-intensive than PCR and requires larger amounts of genomic DNA. Southern blot analysis detects alleles in all size ranges, but precise sizing is not possible. The technique looks for amplification of the length of the FMR-1 gene.
- Willemsen et al. (1995) developed a diagnostic test based on use of antibody to FMR protein (product of FMR-1 gene) to detect presence or absence of FMR protein in lymphocytes or hair root. This can detect the full mutation in males; it is not useful in mosaic males or females as some FMRP is still formed.
- A method recently developed, called methylation-specific melting curve analysis (MS-MCA), relies on the fact that the transcription errors seen on the FMR1 gene results in hypermethylation of the genetic material (Dahl et al., 2007). It can be used in males only, but allows rapid and reliable identification of patients.
Other fragile sites
Of the other nearby fragile sites identified on the X chromosome, namely FRAX-D, FRAX-E and FRAX-F, only the FRAX-E mutation is associated with intellectual disability (Figure 2). Distinguishing these sites from FRAX-A on standard chromosome cultures has become easier with improving techniques, especially fluorescent in situ hybridization (FISH).
Other Fragile X conditions:
In addition to FXS, there are other two genetic conditions caused by changes in the FMR1 gene has been described.
- Fragile X-associated tremor/ataxia syndrome (FXTAS) is a progressive neurodegenerative disorder that affects older adult carriers, predominantly males. FXTAS is found among carriers of premutation (55-200 CGG repeats) alleles of the FMR1 gene. Clinical features of FXTAS include progressive intention tremor and gait ataxia, accompanied by characteristic white matter abnormalities on MRI. (Greco et al., 2006)
- Fragile X-associated primary ovarian insufficiency (FXPOI) affects ovarian functioning and can lead to fertility and early menopause. Carriers of the FMR1 premutation (55-200 CGG repeats) are at risk for FXPOI.
The common physical, behavioural and developmental features of FXS are shown in Table 1. The somatic phenotype is well formed and easily distinguishable in adults
FIGURE 3: Men and boys with fragile-X syndrome, showing classical facial features.
- Pregnancy is usually unremarkable, and affected babies are normally born at full term. The failure to achieve normal developmental milestones may first alert parents to intellectual handicap. Macro-orchidism is rare before puberty, but the phenotype is more evident as the child grows
- In typical Fragile X males characteristic physical features are long, narrow face, prominent ears, joint hypermobility and flat feet (Hagerman et al., 1984). The forehead is large and quadrangular with relative macrocephaly.
- Macro-orchidism is almost invariable in DNA-confirmed post-pubertal males (Lachiewicz & Dawson 1994). This phenotype has also been described in patients with acquired central nervous system lesions, patients with no abnormality of the FMR-1 gene, and it sometimes co-occurs in Klinefelter, Prader-Willi, Sotos, Rubenstein-Taybi and Down’s syndromes.
- Affected females usually resemble affected males, though with enlarged ovaries. Unaffected (premutation) females have high rates of premature ovarian failure and dizygous twinning.
- Previous studies have consistently reported a high risk (30–40%) for ocular problems in FXS individuals (Storm et al., 1987; Maino et al., 1990). Refractive errors of various degrees up to 93% and strabismus ranging from 30% to 40% have been reported (Storm et al. 1987). Musculoskeletal manifestations such as pes planus (flat feet), excessive joint laxity with hyperextensible metacarpophalangeal joints and scoliosis are common. The skin is usually soft and smooth, but there may be calluses from hand-biting. Cardiac abnormalities include mitral valve prolapse and aortic root dilatation, hypoplasia of the aorta and post-ductal coarctation. These are thought to develop during late childhood and adolescence, as in the general population. Taken together, these findings may suggest an underlying connective tissue dysplasia.
Males: Although the level of severity of intellectual disability among boys is equally distributed between mild and severe, the majority of men with FXS have moderate-to-severe degrees of intellectual disability. The average IQ in adult men with the completely methylated full mutation is approximately 40 (Merenstein et al., 1996). Specific cognitive profiles show that they have particular difficulties in sequential processing, with short-term memory deficits manifesting as a weakness in arithmetic. In spite of the reported decline in IQ test scores with age, adaptive behaviour improves with appropriate training. Although there is no correlation between the size of the CGG repeat (within the full mutation range) and degree of intellectual impairment in males, lower expression of FMRP is thought to correlate with IQ in mosaic males and males with a partially methylated full mutation.
Females: Approximately 50 percent of women with the full mutation have IQs in the borderline or mild intellectual disability range (Hagerman et al., 1992). Affected females without intellectual disability may have specific deficits in the areas of attention, visuo-spatial skills and executive functions. The less serious effects in females may be due to the fact that they have two X chromosomes, of which only one is active in each cell. This increases the chances a normal FMR-1 gene owing to random X chromosome inactivation.
Speech and language delay is an early symptom, with first words appearing at about 2 years and short sentences at 3 years. Some children do not develop speech at all. Language ability may be appropriate for an individual’s cognitive level, but others often display ‘jocular litanic phraseology’ with echolalia and speech dysfluency, or ‘cluttering’.
Epilepsy and EEG findings
Individuals with FXS have increased risk for seizures, with rates of 13% to 18% for boys and ~5% for girls (Hagerman et al., 2009). They are usually generalized and usually in the first 15 years of life. They respond well to anticonvulsants, particularly carbamazepine, and half of them disappear by age 20. The most common abnormal EEG findings are rhythmic theta activity, and slowing of background activity. Initial reports of characteristic sleep EEG patterns, such as quasi-rhythmic temporal lobe spikes of medium/high voltage, have not been replicated. (Sabaratnam 2001)
Pathological and neuropathological findings
Pathological findings include abnormal mitral valves with mucoid degeneration and excess mucopolysaccharide; ventricular hypertrophy; cardiac enlargement; and interstitial cell hyperplasia, which causes megalo-testes (Sabaratnam 2000)
Neuropathological findings include increased brain weight; mildly dilated cerebral ventricles; and loss of Purkinje cells in the cerebellum (which normally shows high expression of FMRP).
Lee et al. (2007) studied the brain structure in 36 subjects with FXS using tensor-based morphometry (TBM). The results of the study showed that subjects with FXS had 10% increase in caudate and 19% increase in lateral ventricle volumes compared to controls. The authors also found structural abnormalities in the cerebellum in the form of mainly small volumes bilaterally.
The amygdala plays an important role in social behaviour and emotion processing and shows significant enlargement in children with idiopathic autism (Lightbody & Reiss, 2009). As individuals with FXS often display these behaviours, many studies focused on studying size of amygdala in individuals with FXS. Hazlett et al. (2009) investigated this relationship in their study of brain development in FXS. Overall, the young boys with FXS (18–42 months) demonstrated smaller amygdala volumes than the control group by 8%.
In ICD-10, FXS is noted as one of the medical conditions associated with pervasive developmental disorder (PDD). In children, it is the behavioural features such as hand-flapping, hand-biting, tactile defensiveness, poor eye contact, hyperactivity and perseverative speech that are more notable. Most boys have attentional problems and hyperactivity. Only a minority of males with FXS have autism, although autism-like behavioural features are seen in almost all people with FXS. The prevalence rate of autism in FXS ranges between 21% and 33% (Hatton et al. 2006, Rogers et al. 2001). The majority show the characteristic profile of social anxiety, gaze aversion to strangers, vocal perseveration, delayed echolalia, and stereotypies such as hand-biting and hand-flapping.
Associated psychiatric disorders
In a 10 years follow up study by Sabaratnam et al. (2003), it was found that there was ten-fold increase in the prevalence of psychiatric morbidity in the individuals with FXS compared to general population. The most common DSM-IV diagnosis among the Fragile X boys is ADHD (73%), followed by oppositional defiant disorder, anxiety disorders (Baumgardner et al., 1995).
The discovery of the FMR-1 gene means that, theoretically, DNA-based screening for the premutation could forewarn all potentially affected families. Population-based screening is neither feasible nor ethicalmainly because of the current inability to distinguish full-mutation female fetuses with mental impairment from fetuses whose intelligence is not affected. Therefore, screening would be targeted at individuals who are at a higher risk. The various proposed strategies include preconceptual testing and routine prenatal screening of all carrier pregnancies. Other strategies could include systematic testing in affected families (‘cascade’ screening or extended family follow-up); case finding in paediatric or adult practice; or a combination of these.
Barriers to implementing even limited paediatric screening and cascade screening in affected families include inadequate resources, difficulties in counselling those with intermediate-range alleles, and the need to achieve uniformly high standards in the existing screening programmes as a prerequisite for any population-based programme.
While there is no cure for FXS, many areas of intervention can improve the lives of those affected and their families. All affected people can make progress with proper education, therapy and support. A multidisciplinary approach is necessary to manage the multifaceted problems encountered. Each child should be formally assessed to establish his or her needs. Speech therapists, behavioural therapists, special educators and paediatricians are all likely to be involved.
The early years are of vital importance for stimulating maximum learning in children with the syndrome, and intervention at this stage can prevent many problems later. Services that can be offered include family training to encourage physical, speech and sensory training, and the promotion of a routine for the child, which helps to alleviate anxiety.
If a positive FXS test is discovered, the proband and family should be referred for genetic counselling and cascade testing of family members at risk of carrying a full mutation or permutation (McConkie-Rosell et al., 2007). Genetic counselling aims to educate families about the syndrome, its implications and prognosis, supporting them in making informed decisions about the future and in dealing with the emotional impact of the diagnosis. Counselling also identifies others who might need to be alerted about the diagnosis and the availability of testing.
Family education and counselling is essential to facilitate parents’ acceptance and understanding of the child and to encourage patience and persistence with a child who may seem uncooperative. Despite the wealth of knowledge regarding the behavioural phenotype of FXS, there are almost no empirical studies on the effectiveness of behavioural treatments among patients with FXS (Reiss and Hall, 2007). Both animal and human studies have shown that variations in the environment have an impact on behaviour (Restivo et al., 2005). A higher-quality home environment is associated with fewer autistic behaviours, better adaptive behaviour, and higher IQ scores in children with FXS (Glaser et al., 2003). Weiskop et al. (2005) evaluated a parent training programme using behavioural principles to reduce sleep problems in children with autism or FXS. The authors found that as a result of the programme settling problems, night waking, and co-sleeping were effectively reduced.
Psychotherapy and counselling has been applied for higher functioning individuals with FXS (Hills-Epstein et al., 2002). Psychotherapy or cognitive-behavioural interventions can focus on anxiety reduction through desensitization and other behavioural tools, the discussion and treatment of sexuality issues (especially fetishism and other paraphilias), or management of depression (Schneider et al., 2009).
As autism-like behavioural features are commonly found in the individuals with FXS treatment models used in individuals with autism can be modified and applied to the individuals with FXS. Treatment models that are well established in autism management like Treatment and Education of Autistic and Related Communication-Handicapped Children model (Schopler et al., 1984), Denver model (Rogers et al., 2001) and Applied Behavior Analysis model (Smith et al., 2007) can be effective in management of individuals with FXS (Hagerman et al., 2009).
- Treatment of ADHD: Hagerman et al. (1988) did a controlled trial of stimulant medication in children with the FXS. The authors found that in addition to behavioural intervention and individualized therapies, stimulants were shown to improve symptoms of ADHD in individuals with FXS. Stimulants may not be helpful for children under the age of five as they may cause increased irritability. Hagerman et al. (1995) did a survey of clonidine use among 35 children with FXS. They found that 63% of parents thought that clonidine was very helpful for their child.
Among the nonstimulants, two controlled trials demonstrated that L-acetyl-carnitine was beneficial for the treatment of ADHD symptoms in children with FXS. In both the studies, effects were more remarkable in the parent report rather than teacher report. (Torrioli et al., 2008, Torrioli et al., 1999)
- Treatment of Aggressive behaviour: Antipsychotic medications have been frequently used to address challenging behaviours like aggression and irritability. In a study by Berry-Kravis & Potanos (2004), about 80% of individuals with FXS responded to one or more antipsychotic drugs, without significant adverse effects. Risperidone has been the most frequently prescribed antipsychotic medication and has been found to be safe and effective for aggressive individuals with FXS (McCracken et al., 2002). Aripiprazole is also used in individuals with FXS (Berry-Kravis & Sumis, 2006) with good response rate.
- Treatment of Anxiety: Selective serotonin reuptake inhibitors (SSRI) like Fluoxetine have been used in individuals with FXS with co-morbid social anxiety, autism, or selective mutism (Berry-Kravis & Potanos, 2004). In about 20% of individuals with FXS, Fluoxetine use may result in disinhibited behaviour, irritability or aggression (Hagerman et al. 1994).
- Treatment of Epilepsy: Seizures in FXS generally are easily controlled with a single anticonvulsant. (Hagerman et al., 2009). Medications like Carbamazipine and Valproate have been used historically to achieve good seizure control. More recently, medications like Lamotrigine, Oxcabazepine, Zonisamide and Levetiracetam have proven to be effective anticonvulsants for patients with seizures that are difficult to control, with the advantage of minimal cognitive adverse effects (Hagerman et al., 2009). Side effect profile of the antiepileptic medication should be taken into consideration before prescribing to individuals with FXS.
Other targeted treatments for FXS
- Metabotropic glutamate receptor (mGluR5) antagonists: mGluR theory of Fragile X pathogenesis has been proposed by Bear et al. (2004). It has been hypothesised that many psychiatric and neurological symptoms of FXS could be due to unchecked activation of mGluR5. It has been suggested that mGluR5 antagonists would be an effective treatment for FXS (Bear, 2005). Fenobam, selective mGluR5 antagonist has been found to have anxiolytic properties and have been used safely in the trials in non- FXS populations. New mGluR5 antagonists are being developed and will be tried in the individuals with FXS in the future.
Berry-Kravis et al. (2008) did open-label treatment trial of lithium to target the underlying defect in FXS. Lithium has been found to down regulate the mGluR5 system. The study found that lithium can be helpful for stabilising mood in FXS and provides functional benefit. The study results were consistent with the results of previous animal studies.
Gamma-amino butyric acid (GABA) agonists: GABA is the main inhibitory neurotransmitter in brain. Animal studies have demonstrated that there is reduced GABA inhibition in brains of the individuals with FXS. Aarbaclofen is a selective GABA-B receptor agonist. Aarbaclofen inhibits glutamate signalling in the brain and thereby indirectly inhibit excessive mGluR mediated protein synthesis in FXS. Aarbaclofen is currently been studied in clinical trial in individuals with FXS.
- Matrix metalloproteinase-9 (MMP-9) inhibitor: Minocycline belongs to a group of antibiotics called synthetic tetracyclines. Minocycline inhibits MMP-9 protein. MMPs are involved in normal development and physiological processes such as wound repair and tissue remodelling. Excessive MMP-9 activity is believed to contribute to the lax connective tissue phenotype often seen in children with FXS. A recent pilot open-label trial suggest that minocycline has positive effects on behavioural symptoms in individuals with FXS (Paribello et al., 2010)
Managing associated medical conditions
Cardiac functioning of individuals with FXS needs to be assessed because of the increased incidence of mitral valve prolapse and cardiomegaly. Individuals with FXS should also be tested for conductive hearing loss which could result from frequent ear infections.
There have been significant developments in FXS research in the last two decades. It is now possible to diagnose FXS early in its course by molecular genetic techniques. Despite in the advances in the genetic testing many individuals with FXS continue to remain undiagnosed. In the future we may see further efforts to implement newborn or infant screening for FXS. While there is no cure for FXS yet, interventions with multidisciplinary approach can improve quality of life of those affected and their families. There has been growing excitement in the Fragile X research community and among the families of people that have FXS about new developments in the targeted treatments for FXS. It is hoped that future molecular therapies, whether they are aimed at mGluR5, the AMPA receptor, or other molecular targets, will be directed at preventing the development of some of the symptoms of FXS. In future we may also see Gene therapy interventions developed which may involve placing a functioning copy of the FMR1 gene into the cells of the brain so that the right form of FMRP could be produced in the right place at the right time and in the right amounts.
1. Bailey DB Jr, Raspa M, Bishop E, et al. No change in the age of diagnosis for FXS: findings from a national parent survey. Pediatrics. 2009;124 (2):527 –533
2. Baumgardner T, Reiss A, Freund L, et al. Specification of the neurobehavioral phenotype in males with FXS. Pediatrics 1995;95(5):744–52
3. Bear MF, Huber KM, Warren ST. The mGluR theory of fragile X mental retardation. Trends Neurosci. 2004;27 (7):370 –377
4. Bear MF. Therapeutic implications of the mGluR theory of fragile X mental retardation. Genes Brain Behav. 2005;4 (6):393 –398
5. Berry-Kravis E, Potanos K. Psychopharmacology in FXS: present and future. Ment Retard Dev Disabil Res Rev. 2004;10 (1):42 –48
6. Berry-Kravis E, Sumis A, Hervey C, et al. Open-label treatment trial of lithium to target the underlying defect in FXS. J Dev Behav Pediatr 2008, 29:293-302.
7. Berry-Kravis E, Sumis A. Clinic-based retrospective analysis of psychopharmacology for behavior in FXS. Presented at the 10th International Fragile X Conference; July 19–23, 2006; Atlanta, GA
8. Dahl C, Gronskov K, Larsen LA, et al; A homogeneous assay for analysis of FMR1 promoter methylation in patients with FXS. Clin Chem. 2007 Apr; 53(4):790-3. Epub 2007 Jan 26.
9. Fu YH, Kuhl DP, Pizzuti A, et al. Variation of the CGG repeat at the fragile X site results in genetic instability: resolution of the Sherman paradox. Cell. 1991 Dec 20;67(6):1047–1058
10. Glaser B, Hessl D, Dyer-Friedman J, et al. Biological and environmental contributions to adaptive behavior in FXS. Am J Med Genet A. 2003;117A (1):21 –29
11. Greco CM, Berman RF, Martin RM, et al. Neuropathology of fragile X-associated tremor/ataxia syndrome (FXTAS). Brain 2006; 129: 243–55.
12. Hagerman RJ, Berry-Kravis E, Kaufmann WE, et al. Advances in the treatment of fragile X syndrome. Pediatrics 2009, 123:378-390.
13. Hagerman RJ, Fulton MJ, Leaman A, et al. A survey of fluoxetine therapy in FXS. Dev Brain Dysfunct. 1994;7 :155 –164
14. Hagerman RJ, Hagerman PJ, editors. FXS: diagnosis, treatment, and research. Baltimore (MD): Johns Hopkins University Press; 2002.
15. Hagerman RJ, Jackson C, Amiri K, et al. Girls with FXS: physical and neurocognitive status and outcome. Pediatrics. 1992;89:395 – 400
16. Hagerman RJ, Murphy MA, Wittenberger MD. A controlled trial of stimulant medication in children with the FXS. Am J Med Genet. 1988;30 (1–2):377 –392
17. Hagerman RJ, Riddle JE, Roberts LS, et al. A survey of the efficacy of clonidine in FXS. Dev Brain Dysfunct. 1995;8 (4–6):336 –344
18. Hagerman RJ, Van Housen K, Smith AC, et al.: Consideration of connective tissue dysfunction in the FXS. Am J Med Genet 1984; 17: 111 – 121
19. Hatton D, Hooper SR, et al. Problem behavior in boys with FXS. American Journal of Medical Genetics. 2002;108(2):105–116.
20. Hazlett HC, Poe MD, Lightbody AA, et al. Teasing apart the heterogeneity of autism: same behavior, different brains in toddlers with FXS and autism. J Neurodev Disord. 2009;1(1):81-90.
21. Hills-Epstein, J, Riley, K, Sobesky, W. The treatment of emotional and behavioral problems. In: FXS: Diagnosis, treatment, and research, 3rd ed, Hagerman, RJ, Hagerman, PJ (Eds), Johns Hopkins University Press, Baltimore 2002. p.339-362
22. Lachiewicz AM, Dawson DV. Do young boys with FXS have macro-orchidism? Pediatrics 1994; 93: 992–5.
23. Lee AD, Leow AD, Lu A, et al. 3D pattern of brain abnormalities in FXS visualized using tensor-based morphometry. Neuroimage. 2007;34:924–938
24. Lightbody AA, Reiss AL. Gene, brain, and behavior relationships in FXS: evidence from neuroimaging studies. Dev Disabil Res Rev 2009; 15:343–352.
25. Lubs H. A marker X chromosome. Am J Hum Genet 1969; 21: 231–44.
26. Maino DM, Maino JH, Maino SA. Mental retardation syndromes with associated ocular defects. J Am Optom Assoc 1990; 61:707-16.
27. Martin J P, Bell J. A pedigree of mental defect showing sex‐linkage. J Neurol Psychiatry 1943. 6:154-157.
28. McConkie-Rosell A, Abrams L, Finucane B et al: Recommendations from multi-disciplinary focus groups on cascade testing and genetic counseling for fragile X-associated disorders. J Genet Couns 2007; 16: 593 – 606.
29. McCracken JT, McGough J, Shah B, et al. Risperidone in children with autism and serious behavioral problems. N Engl J Med. 2002;347 (5):314 –321
30. Merenstein SA, Sobesky WE, Taylor AK, et al. Molecular-clinical correlations in males with an expanded FMR1 mutation. Am J Med Genet. 1996; 64:388–394.
31. Paribello C, Tao L, Folino A, et al. Open-label add-on treatment trial of minocycline in FXS. BMC Neurol. 2010;10:91.
32. Reiss AL, Hall SS. FXS: assessment and treatment implications. Child Adolesc Psychiatr Clin N Am. 2007;16 (3):663 –675
33. Restivo L, Ferrari F, Passino E, et al. Enriched environment promotes behavioral and morphological recovery in a mouse model for the FXS. Proc Natl Acad Sci U S A. 2005;102 (32):11557 –11562
34. Rogers SJ, Hall T, Osaki D, et al. The Denver model: a comprehensive, integrated educational approach to young children with autism and their families. In: Handelman JS, Harris SL, eds. Preschool Education Programs for Children with Autism. 2nd ed. Austin, TX: Pro-ed; 2001:95–134
35. Rogers SJ, Wehner EA, et al. The Behavioral Phenotype in Fragile X: Symptoms of Autism in Very Young Children with FXS, Idiopathic Autism, and other Developmental Disorders. Journal of Developmental and Behavioral Pediatrics. 2001;22(6):409–417.
36. Sabaratnam M. Pathological and neuropathological findings in two males with FXS. J Intellect Disabil Res. 2000; 44:81–85.
37. Sabaratnam M, Murthy NV, Wijeratne A, Buckingham A, Payne S. Autistic-like behaviour profile and psychiatric morbidity in FXS: a prospective ten-year follow-up study. Eur Child Adolesc Psychiatry. 2003; 12(4):172–177.
38. Sabaratnam M, Vroegop PG, Gangadharan SK: Epilepsy and EEG findings in 18 males with FXS. Seizure 2001, 10:60-63.
39. Schneider A, Hagerman RJ, Hessl D. FXS — From genes to cognition. Dev Disabil Res Rev. 2009; 15:333–342.
40. Schopler E, Mesibov G, Shigley R, et al. Helping autistic children through their parents: the TEACCH model. In: Reynolds CR, Gutkin TR, eds. The Handbook of School Psychology. New York, NY: Wiley; 1984:629–643
41. Smith T, Mozingo D, Mruzek DW, et al. Applied behavior analysis in the treatment of autism. In: Hollander E, Anagnostou E, eds. Clinical Manual for the Treatment of Autism. Washington, DC: American Psychiatric Publishing; 2007:153–177
42. Storm RL, PeBenito R, Ferretti C. Ophthalmologic findings in the FXS. Arch Ophthalmol 1987 Aug; 105(8):1099-102.
43. Torrioli MG, Vernacotola S, Mariotti P, et al. Double-blind, placebo-controlled study of L-acetylcarnitine for the treatment of hyperactive behavior in FXS [letter]. Am J Med Genet.1999;87 (4):366 –368
44. Torrioli MG, Vernacotola S, Peruzzi L, et al. A double-blind, parallel, multicenter comparison of L-acetylcarnitine with placebo on the attention deficit hyperactivity disorder in FXS boys. Am J Med Genet A. 2008; 146 (7):803 –812
45. Verkerk AJ, Pieretti M, Sutcliffe JS, et al. Identification of a gene (FMR-1) containing a CGG repeat coincident with a breakpoint cluster region exhibiting length variation in FXS. Cell. 1991; 65:905-914.
46. Weiskop S, Richdale A, Matthews J. Behavioural treatment to reduce sleep problems in children with autism or FXS. Dev Med Child Neurol. 2005;47 (2):94 –104
47. Willemsen R, Mohkamsing S, de Vries B, et al. Rapid antibody test for FXS. Lancet. 1995; 345:1147–1148.
The Fragile X Society, 53 Winchelsea Lane, Hastings, East Sussex TN35 4LG, UK. Tel: 01424 813147. Website: www.fragilex.org.uk
TABLE 1: Common physical, behavioural and developmental features of fragile-X syndrome
|Physical features||Behavioural Features||Developmental Features|
Large, prominent ears
High arched palate
Malocclusion of teeth
Hand calluses (due to self-injury)
Mitral valve prolapse, cardiomegaly, hypoplasia and dilation of aorta, post-ductal coarctation
Soft, fleshy skin
Scoliosis, pes planus, joint laxity and hyperextensible joints
↑Size of fourth ventricle
↓Volume of superior temporal gyrus
↓Posterior cerebellar vermis
Epileptic seizures (25%)
Attention deficit hyperactivity disorder
Short attention span
Psychiatric disordersIncreased incidence of familial bipolar affective disorders
Fine and gross motor delay
Problems with co-ordination
|First published in Psychiatry; Volume 2:8 August 2003 and reprinted with the kind permission of The Medicine Publishing Company.|
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The following technical terms are used in Public Health data publications.
Age-adjusted mortality rate - A mortality rate statistically modified to eliminate the effect of different age distributions in the different populations.
Age-specific mortality rate - A mortality rate limited to a particular age group. The numerator is the number of deaths in that age group; the denominator is the number of persons in that age group in the population.
Comparability ratio - Mortality data are coded using the International Classification of Diseases, Tenth Revision (ICD-10). Before 1999, deaths were coded using ICD-9. To ensure reliable trending of data over time, comparability ratios are applied to ICD-9 data so that they may be compared to the death data coded with ICD-10.
Confidence interval - A range of values for a variable of interest, e.g., a rate, constructed so that this range has a specified probability of including the true value of the variable. The specified probability is called the confidence level, and the end points of the confidence interval are called the confidence limits. Confidence intervals can be used to approximate statistical significance.
Demographic information - The "person" characteristics — age, sex, race, and occupation — of descriptive epidemiology used to characterize the populations at risk.
Health indicator - A measure that reflects, or indicates, the state of health of persons in a defined population, e.g., the infant mortality rate.
Incidence rate - A measure of the frequency with which an event, such as a new case of illness, occurs in a population over a period of time. The denominator is the population at risk; the numerator is the number of new cases occurring during a given time period.
Increase/decrease - The terms "increase" and "decrease" indicate that a rate has had a statistically significant change over time.
Mortality rate - A measure of the frequency of occurrence of death in a defined population during a specified interval of time.
Prevalence - The number or proportion of cases or events or conditions in a given population.
Prevalence rate - The proportion of persons in a population who have a particular disease or attribute at a specified point in time or over a specified period of time.
Proportion - A type of ratio in which the numerator is included in the denominator. The ratio of a part to the whole, expressed as a "decimal fraction"(e.g., 0.2), as a fraction (1/5), or, loosely, as a percentage (20%).
Public health surveillance - The systematic collection, analysis, interpretation, and dissemination of health data on an ongoing basis, to gain knowledge of the pattern of disease occurrence and potential in a community, in order to control and prevent disease in the community.
Rate - An expression of the frequency with which an event occurs in a defined population.
Risk factor - An aspect of personal behavior or lifestyle, an environmental exposure, or an inborn or inherited characteristic that is associated with an increased occurrence of disease or other health-related event or condition.
Sample - A selected subset of a population. A sample may be random or non-random and it may be representative or non-representative.
Similar - When data are described as "similar" this indicates the difference is likely due to chance as opposed to a real difference between two populations, even if the data points are different. For example, if the rate for any given year or group of years is significantly higher or lower than the HP 2010 goal (using 95% confidence intervals) the rate is described as significantly higher or lower than the goal. If the goal falls within the confidence interval, the rate is described as similar to the goal.
Statistical significance - Data analysis includes a measure of whether an apparent difference between two figures (e.g., rates of disease for county and state) represents a real difference between the two figures, versus being due to chance. If statistical analysis determines that there is less than a 5% likelihood that the difference between two data points is due to chance, we say that the difference is "statistically significant", and we consider the two data points to be different.
Trend - A long-term movement or change in frequency, usually upwards or downwards.
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2.2 Diagnostic criteria for autism
Profiles of characteristics necessary for a diagnosis of classic autism or an ASD are called diagnostic criteria. These criteria appear within general systems for the classification and diagnosis of psychological problems such as the Diagnostic and Statistical Manual prepared by the American Psychiatric Association (last revised in 2000 and known as DSM-IV-TR™), and the International Classification of Diseases, prepared by the World Health Organization (currently in its tenth edition and known as ICD-10).
We will first look at the diagnostic criteria for ‘classic’ autism. In Section 3 of this course we will highlight the way this ‘classic’ picture must be modified to take into account varying symptom patterns across the spectrum.
Box 1: Diagnostic criteria for classic autism according to DSM-IV-TR™
A A total of six (or more) items from (1), (2) and (3), with at least two from (1), and one each from (2) and (3):
Qualitative impairment in social interaction, as manifested by at least two of the following:
(a) Marked impairment in the use of multiple nonverbal behaviours such as eye-to-eye gaze, facial expression, body postures, and gestures to regulate social interaction.
(b) Failure to develop peer relationships appropriate to developmental level.
(c) A lack of spontaneous seeking to share enjoyment, interests, or achievements with other people (e.g. by a lack of showing, bringing or pointing out objects of interest).
(d) Lack of social or emotional reciprocity.
Qualitative impairments in communication as manifested by at least one of the following:
(a) Delay in, or total lack of, the development of spoken language (not accompanied by an attempt to compensate through alternative modes of communication such as gesture or mime).
(b) In individuals with adequate speech, marked impairment in the ability to initiate or sustain a conversation with others.
(c) Stereotyped and repetitive use of language or idiosyncratic language.
(d) Lack of varied, spontaneous make-believe play or social imitative play appropriate to developmental level.
Restricted repetitive and stereotyped patterns of behaviour, interests, and activities, as manifested by at least one of the following:
(a) Encompassing preoccupation with one or more stereotyped and restricted patterns of interest that is abnormal either in intensity or focus.
(b) Apparently inflexible adherence to specific, non-functional routines or rituals.
(c) Stereotyped and repetitive motor mannerisms (e.g. hand or finger flapping or twisting, or complex whole-body movements).
(d) Persistent preoccupation with parts of objects.
B Delays or abnormal functioning in at least one of the following areas, with onset prior to age 3 years: (a) social interaction, (b) language as used in social communication, (c) symbolic or imaginative play.
C The disturbance is not better accounted for by Rett's Disorder or Childhood Disintegrative Disorder.*
* Rett's Disorder and Childhood Disintegrative Disorder are syndromes with some symptoms overlapping with autism. Discussion is beyond the scope of this course.
Diagnostic criteria: A formally agreed profile of symptoms and characteristics, typifying a syndrome or disorder, used in diagnosis.
Reflect on the four accounts of autism at the beginning of this course in light of the diagnostic criteria. Make a list of those diagnostic criteria represented in the different accounts, and compare your list to the discussion below.
Christopher: lack of eye contact and loss of language indicating qualitative impairments in communication (Area 2) and possibly a lack of social reciprocity (Area 1). Symptoms developed below 36 months.
Alison: ‘living in own world’ suggesting qualitative impairments in both social interaction (Area 1, particularly not sharing interests, lack of social reciprocity) and communication (Area 2, apparently she does not speak). Rocking indicates repetitive activities, and musical interests could reflect a preoccupation (Area 3).
Gunilla: her rather idiosyncratic understanding and use of language could reflect a subtle communication impairment (Area 2). However her difficulties, which are not well captured by the diagnostic criteria, probably reflect a less severe spectrum disorder – see Section 3.
Tito: fascination with calendars suggests a preoccupation (Area 3). However, his command of language to describe this obsession seems at odds with several criteria in Area 2. Tito also has areas of outstanding talent – especially poetry, which fits with the descriptions of ‘savant’ skills in Sections 2.3 and 3.3. He is almost certainly in the small minority of individuals whose autism goes together with ‘savant syndrome’. | <urn:uuid:9594041d-95ce-4bbc-9ce9-e1ec843dae9d> | {
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Diabetes is a number of diseases that involve problems with the hormone insulin. Medically referred to as diabetes mellitus, diabetes describes a group of metabolic diseases in which the person has high blood glucose (blood sugar), either because insulin production is inadequate, or because the body’s cells do not respond properly to insulin, or both.
Normally, the pancreas (an organ behind the stomach) releases insulin to help your body store and use the sugar and fat from the food and every this you consume. Diabetes can then occur when the pancreas produces very little or no insulin, or when the body does not respond appropriately to the insulin produced by the pancreas.
Patients with high blood sugar will typically experience frequent urination (polyuria), they will become increasingly thirsty (polydipsia) and hungry (polyphagia).
If left untreated, diabetes can cause many complications.
Acute complications can include diabetic ketoacidosis, hyperosmolar hyperglycemic state, or death.
Serious long-term complications include cardiovascular disease, stroke, chronic kidney disease, foot ulcers and damage to the eyes.
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The most common diabetes symptoms include frequent urination, intense thirst and hunger, weight gain, unusual weight loss, fatigue, cuts and bruises that do not heal, male sexual dysfunction, numbness and tingling in hands and feet.
TYPE 1 DIABETES
Some people do refer to this type as insulin-dependent diabetes, juvenile diabetes, or early-onset diabetes.
Type 1 diabetes happens when your immune system destroys cells in your pancreas called beta cells which are the ones that produce insulin. hence, the body does not produce insulin.
DamageS to beta cells from type 1 diabetes throws the process off. Glucose doesn’t move into your cells because insulin isn’t there to do it.
Instead it builds up in your blood and your cells starve. This causes high blood sugar.
Medically, patients with type 1 diabetes will need to take insulin injections for the rest of their life. They must also ensure proper blood-glucose levels by carrying out regular blood tests and following a special diet.
However, natural remedies that work on preparing the damages to the beta cell and the pancreas have been proven to be helpful to type 1 diabetic patients.
You can click here to read about such natural remedy.
Sensitivity and responsiveness to insulin are usually normal, especially in the early stages of type 1 diabetes.
Type 1 diabetes can also be accompanied by irregular and unpredictable high blood sugar levels, frequently with ketosis and sometimes with serious low blood sugar levels.
Other complications include an impaired counter-regulatory response to low blood sugar, infection, gastroparesis (which leads to erratic absorption of dietary carbohydrates), and endocrinopathies.
Symptoms of type1 diabetes are often subtle, but they can become severe. They include:
- Heavy thirst
- Increased hunger (especially after eating)
- Dry mouth
- Nausea and vomiting
- Pain in your belly
- Frequent urination
- Unexplained weight loss (even though you’re eating and feel hungry)
- Fatigue (weak, tired feeling)
- Blurred vision
- Heavy, laboured breathing (your doctor will call this Kussmaul respiration)
- Frequent infections of the skin, urinary tract, or vagina
Signs of an emergency with type 1 diabetes include:
- Shaking and confusion
- Rapid breathing
- Fruity smell to your breath
- Pain in your belly
- Loss of consciousness (rare)
The key to good health is to keep your blood sugar levels within the range your doctor gives you.
You’ll need to check them often and adjust insulin, food, and activities to make that happen.
TYPE 2 DIABETES
Type 2 diabetes is the most common type of diabetes mellitus.
It begins with insulin resistance; a condition in which cells fail to respond to insulin properly. As the disease progresses, a lack of insulin may also develop.
The most common cause is excessive body weight and insufficient exercise. The defective responsiveness of body tissues to insulin is believed to involve the insulin receptor.
In the early stage of type 2 diabetes, the predominant abnormality is reduced insulin sensitivity. At this stage, high blood sugar can be reversed by a variety of measures and medications that improve insulin sensitivity or reduce the liver’s glucose production.
Type 2 diabetes is primarily due to lifestyle factors and genetics. A number of lifestyle factors are known to be important to its development, including obesity (defined by a body mass index of greater than 30), lack of physical activity, poor diet, stress, and urbanization.
Dietary factors also influence the risk of developing type 2 diabetes. Consumption of sugar-sweetened drinks in excess is associated with an increased risk. The type of fats in the diet is also important, with saturated fat and trans fats increasing the risk and polyunsaturated and monounsaturated fat decreasing the risk.
Eating lots of white rice, and other starches, also may increase the risk of diabetes. A lack of physical activity is believed to cause 7% of cases.
Gestational diabetes is the third main form and occurs when pregnant women without a previous history of diabetes develop high blood sugar levels.
Gestational diabetes mellitus resembles type 2 diabetes in several respects involving a combination of relatively inadequate insulin secretion and responsiveness.
It occurs in about 2 -10% of all pregnancies and may improve or disappear after delivery.
However, after pregnancy approximately 5 – 10% of women with gestational diabetes are found to have diabetes, most commonly type 2.
Gestational diabetes is fully treatable, but requires careful medical supervision throughout the pregnancy because of the baby.
Management may include dietary changes, blood glucose monitoring, and in some cases, insulin may be required.
Though it may be transient, untreated gestational diabetes can damage the health of the foetus or mother.
Risks to the baby include macrosomia (high birth weight), congenital heart and central nervous system abnormalities, and skeletal muscle malformations.
Increased levels of insulin in a foetus’s blood may inhibit foetal surfactant production and cause infant respiratory distress syndrome. A high blood bilirubin level may result from red blood cell destruction.
In severe cases, perinatal death may occur, most commonly as a result of poor placental perfusion due to vascular impairment.
Other Types of Diabetes
Prediabetes indicates a condition that occurs when a person’s blood glucose levels are higher than normal but not high enough for a diagnosis of type 2 diabetes. Many people who later develop type 2 diabetes spend many years in a state of prediabetes.
Latent autoimmune diabetes of adults (LADA) is a condition in which type 1 diabetes develops in adults. Adults with LADA are frequently initially misdiagnosed as having type 2 diabetes, based on age rather than cause.
Any disease that causes extensive damage to the pancreas may lead to diabetes (for example, chronic pancreatitis and cystic fibrosis).
Diseases associated with excessive secretion of insulin-antagonistic hormones can cause diabetes (which is typically resolved once the hormone excess is removed).
Many drugs impair insulin secretion and some toxins damage pancreatic beta cells. The ICD-10 (1992) diagnostic entity, malnutrition-related diabetes mellitus (MRDM or MMDM, ICD-10 code E12), was deprecated by the World Health Organization (WHO) when the current taxonomy was introduced in 1999.
Other forms of diabetes mellitus include congenital diabetes, which is due to genetic defects of insulin secretion, cystic fibrosis-related diabetes, steroid diabetes induced by high doses of glucocorticoids, and several forms of monogenic diabetes.
Prevention and treatment involve maintaining a healthy diet, regular physical exercise, a normal body weight, and avoiding use of tobacco.
Control of blood pressure and maintaining proper foot care are important for people with the disease.
Low blood sugar (hypoglycemia), is common in people with type 1 and type 2 diabetes. Most cases are mild and are not considered medical emergencies. Effects can range from feelings of unease, sweating, trembling, and increased appetite in mild cases to more serious effects such as confusion, changes in behaviour such as aggressiveness, seizures, unconsciousness, and (rarely) permanent brain damage or death in severe cases.
Moderately low blood sugar may easily be mistaken for drunkenness; rapid breathing and sweating, cold, pale skin are characteristic of low blood sugar but not definitive.
Mild to moderate cases are self-treated by eating or drinking something high in sugar. Severe cases can lead to unconsciousness and must be treated with intravenous glucose or injections with glucagon.
People (usually with type 1 diabetes) may also experience episodes of diabetic ketoacidosis (DKA), a metabolic disturbance characterised by nausea, vomiting and abdominal pain, the smell of acetone on the breath, deep breathing known as Kussmaul breathing, and in severe cases a decreased level of consciousness.
A rare but equally severe possibility is hyperosmolar hyperglycemic state (HHS), which is more common in type 2 diabetes and is mainly the result of dehydration
The major long-term complications relate to damage to blood vessels. Diabetes doubles the risk of cardiovascular disease and about 75% of deaths in diabetics are due to coronary artery disease.
Other macrovascular diseases include stroke, and peripheral artery disease.
The primary complications of diabetes due to damage in small blood vessels include damage to the eyes, kidneys, and nerves.
Damage to the eyes, known as diabetic retinopathy, is caused by damage to the blood vessels in the retina of the eye, and can result in gradual vision loss and eventual blindness.
Diabetes also increases the risk of having glaucoma, cataracts, and other eye problems. It is recommended that diabetics visit an eye doctor once a year.
Damage to the kidneys, known as diabetic nephropathy, can lead to tissue scarring, urine protein loss, and eventually chronic kidney disease, sometimes requiring dialysis or kidney transplantation.
NB: You can contact us for potent natural remedies for kidney issues.
Damage to the nerves of the body, known as diabetic neuropathy, is the most common complication of diabetes. The symptoms can include numbness, tingling, pain, and altered pain sensation, which can lead to damage to the skin.
Diabetes-related foot problems (such as diabetic foot ulcers) may occur, and can be difficult to treat, occasionally requiring amputation (contact us for a guaranteed natural remedy for treating wounds relating to diabetes, no matter how long it’s been there).
Additionally, proximal diabetic neuropathy causes painful muscle atrophy and weakness.
There is a link between cognitive deficit and diabetes. Compared to those without diabetes, those with the disease have a 1.2 to 1.5-fold greater rate of decline in cognitive function.
Being diabetic, especially when on insulin, increases the risk of falls in older people.
How to determine whether you have diabetes, prediabetes or neither
Doctors can determine whether a patient has a normal metabolism, prediabetes or diabetes in one of three different ways – there are three possible tests:
The A1C test
- at least 6.5% means diabetes
- between 5.7% and 5.99% means prediabetes
- less than 5.7% means normal
The FPG (fasting plasma glucose) test (also called fasting blood sugar)
- at least 126 mg/dl means diabetes
- between 100 mg/dl and 125.99 mg/dl means prediabetes
- less than 100 mg/dl means normal
An abnormal reading following the FPG means the patient has impaired fasting glucose (IFG)
The OGTT (oral glucose tolerance test)
- at least 200 mg/dl means diabetes
- between 140 and 199.9 mg/dl means prediabetes
- less than 140 mg/dl means normal
An abnormal reading following the OGTT means the patient has impaired glucose tolerance (IGT)
The above is the detail of everything important that you need to know about diabetes.
Stay healthy and never give up
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This tool provides information on the causes of death and age groups that are driving inequalities in life expectancy at local area level. Targeting the causes of death which contribute most to the life expectancy gap should have the biggest impact on reducing inequalities.
The tool provides data tables and charts showing the breakdown of the life expectancy gap in 2015-17 for two comparisons:
The tool includes data for the following geographies:
The tool was last updated on 14th January 2020.
The following changes were made in the most recent update:
Use the tabs at the top of the screen to move between pages of the tool.
The context page provides information on life expectancy and life expectancy gaps. This can be used as a guide to which comparison(s) to select on the Breakdowns page.
Select a geography type and geography from the dropdown box.
Two tables are then displayed. The first shows life expectancy in the selected geography, in England as a whole, and the absolute gap in life expectancy between the two. The second shows life expectancy in the most deprived and least deprived quintiles of the selected geography, and the absolute gap between the two.
The breakdowns page provides information on the causes of death and age groups which are driving the gaps in life expectancy, either within the selected geography, or between the selected geography and England.
Select from the dropdown boxes to display data and charts of interest:
Geography type and geography - select a geography type and geography from the dropdown box.
Comparator area - select ‘England’ to view the breakdown of the gap between the selected geography as a whole and England as a whole, or ‘Within area’ to view the breakdown of the gap between the most and least deprived quintile of the selected geography. The England comparator is likely to be most useful to areas where the life expectancy is lower than England, however, areas with a lower life expectancy than England should also consider within area inequalities. Scarf charts are not available where life expectancy of an area is higher than England, however, bar chart data are available for all areas, since even in areas with a higher life expectancy than England, there may be specific causes of death which are causing a reduction in life expectancy which could be targeted locally.
Segment gap by - select to view breakdowns by either cause of death or age group.
Chart type - select the chart type of interest.
Move between viewing charts and data tables using the tabs.
Detailed guidance on interpreting the results is available on the guidance and FAQs tab. This includes information on the data and methods used to construct the tool. A set of frequently asked questions is also available.
Numbers of deaths are based on Office for National Statistics (ONS) death registration data. Deaths were extracted for the relevant geographies for years 2015, 2016 and 2017 and pooled.
Cause groups have been defined using International Classification of Diseases, Tenth Revision (ICD-10) codes and the groupings used are specified in the table below. Broad causes of death are consistent with those used in previous versions of the Segment Tool and are based on ICD-10 chapters. Detailed causes of death include the top 10 leading causes of death (in 2016) for males and females. In addition to the 10 leading causes, the External cause group has been further broken down to include groups for land transport accidents, accidental poisoning, and suicide, as these causes of death make up a considerable proportion of deaths amongst younger adults.
Table 1: Causes of death and ICD-10 codes used in the tool
|Broad cause||ICD 10 code||Detailed cause||ICD10 code|
|Other circulatory||Rest of I00-I99|
|Leukaemia & lymphoma||C81-C96|
|Other cancer||Rest of C00-C97|
|Mental and behavioural||F00-F99, G30||Dementia and Alzheimer’s disease||F01, F03, G30|
|Other mental and behavioural||Rest of F00-F99|
|Respiratory||J00-J99||Chronic lower respiratory diseases||J40-J47|
|Influenza and pneumonia||J09-J18|
|Other respiratory||Rest of J00-J99|
|Digestive||K00-K93||Cirrhosis and other diseases of liver||K70-K76|
|Other digestive||Rest of K00-K93|
|External causes||V00-Y98||Land transport accidents||V01-V89|
|Suicide and injury of undetermined intent||X60-X84 (age 10+), Y10-Y34 (age 15+)|
|Other external causes||Rest of V00-Y98|
|Under 28 days||No code assigned||Under 28 days||No code assigned|
|Other||All other codes||Urinary disease||N00-N39|
|Other||All other codes|
For the breakdown of the gap between each area as a whole and England, ONS mid-year estimates for the relevant geography for the years 2015, 2016 and 2017 were pooled.
For the breakdown of the gap between the most deprived quintile and the least deprived quintile in each area, ONS mid-year estimates for LSOAs for the years 2015, 2016 and 2017 were aggregated to quintiles and pooled.
Data for upper and lower tier local authorities in England are based on boundaries at March 2019. Data for City of London have not been included because of the small number of deaths in this area. Data for Isles of Scilly local authority have been combined with Cornwall local authority.
Data for NHS geographies are based on boundaries at April 2019, and resident populations.
The tool also contains data for England and the English regions.
Index of Multiple Deprivation (IMD) 2015 scores have been used to define deprivation quintiles.
Each local authority/CCG/region/England was divided into quintiles based on Lower Super Output Area (LSOA) level IMD scores, using the standard PHE method described on this page: https://fingertips.phe.org.uk/profile/guidance
Life expectancy was calculated based on quinary age bands up to a maximum of 90+ (0, 1-4, 5-9,…,85-89, 90+), using the standard PHE method. A template life expectancy calculator can be downloaded from this page: https://fingertips.phe.org.uk/profile/guidance
The contribution of different age bands or causes of death to the gap in life expectancy between two areas (due to differences in age or cause specific death rates) have been calculated using a method of ‘life expectancy decomposition’.
For the Segment Tool, the Arriaga III method has been used, as described by Ponnapalli . The method is based on a life table divided into 5-year age groups. The contributions of each age group are then distributed into causes of death using a method described by Preston and others . Contributions are distributed proportionately according to the difference in mortality between the selected areas by cause of death within each age group.
This method is consistent with the analysis published in the PHE Health Profile for England on the causes of trends and inequalities in life expectancy. It replaces the previous method used to breakdown the gap for consistency, and also because the method distributes the life expectancy gap exactly between causes and age groups, whereas the previous method resulted in some discrepancies.
For each cause of death and age group, the number of expected deaths is also provided. Excess deaths are the number of ‘extra’ deaths occurring over and above those that are expected. Expected deaths are the number of deaths which would be expected to occur if the area had the same age specific mortality rate for that cause of death/age group as the comparator area.
The scarf charts show, for each broad cause of death or each broad age group, the percentage contribution that it makes to the overall life expectancy gap between the areas selected. For the England comparison, scarf charts are only available for areas where the life expectancy in the area is lower than the life expectancy in England (ie where there is a gap to segment). For the within area comparison, scarf charts are only available for areas where the life expectancy in the most deprived quintile is lower than life expectancy in the least deprived quintile.
Causes of death/age groups are only included in the scarf chart if they make a contribution to the gap in life expectancy (ie. where the mortality rate is higher for that cause of death or age group in the selected area compared to the comparator area). If a cause of death or age group is not displayed in the chart (or percentage contribution shows as “-” in the data table), this means that the cause of death or age group does not make any contribution to the life expectancy gap.
The gap in life expectancy is broken down so that the percentage contribution of causes will sum to 100 per cent. In some areas, particularly where the gap in life expectancy is small, or where only a few causes of death or age groups have excess mortality, care should be taken in interpreting the results. Some causes of death may be highlighted as contributing a large percentage of the life expectancy gap, even though the gap itself may be small.
To aid interpretation, numbers of deaths are included in the data table. The table shows the total number of deaths in the selected area (or most deprived quintile of the selected area if the within area comparison is used) for each cause or age group in the period 2015-17, and the number of excess deaths for each cause or age group. If the mortality rate for a particular cause of death or age group is lower than the comparator area, then the number of excess deaths will be negative.
When interpreting the within area breakdown, it is also important to consider the mortality rate for each cause in the area as a whole. For example, if a local authority has a very high mortality rate for cancer, the within area breakdown may not highlight cancer as a significant contributor to the within area gap because the mortality rates are consistently high across the whole local authority. In this case, cancer would still be an issue requiring consideration in the local authority, even though it had not been highlighted in the within area analysis.
The broad bar charts show the amount that life expectancy would increase (in years) in the selected area (or the most deprived quintile of the selected area) if its mortality rate for each age group or cause of death was changed to that of the comparator area, assuming all other rates remained constant.
Contributions that widen the inequality gap (that is, where the mortality rate is higher in the selected area than the comparator area) are represented with a positive value, while contributions that offset the gap (that is, where the mortality rate is lower in the selected area than the comparator area) are represented with a negative value.
Bar charts are available for all areas, regardless of whether life expectancy is lower in the selected area than the comparator area.
The analysis of broad causes of death can be used to give an indication of the drivers of inequality in the area. The broad cause data should be used as a starting point, but this analysis can mask variation between causes of death within a broad cause group. For example, the contribution of cancer to inequalities in an area may be a result of very high mortality rates from lung cancer, whereas mortality rates for other cancers may be similar to the comparator.
The detailed bar charts show the same information as the broad bar charts, and are calculated using the same methods, but for a more detailed list of causes of death.
There is potential to further develop the tool. We would welcome feedback on what development would be most useful in order to inform future work. Please contact us at firstname.lastname@example.org
No, the outputs are not directly comparable because of changes to the methodology and cause of death groupings used.
Life expectancy at birth is an estimate of the average number of years a new-born baby would survive if he or she experienced the particular area’s age-specific mortality rates for that time period throughout his or her life. The figures in the tool therefore reflect mortality among those living in each area in 2015-17, rather than mortality among those born in each area. It is not therefore the number of years a baby born in the area in 2015-17 could actually expect to live, both because the death rates of the area are likely to change in the future and because many of those born in the area will live elsewhere for at least some part of their lives.
The Segment Tool breaks down the gap in life expectancy between the most deprived quintile and the least deprived quintile of each area. This gap looks at life expectancy at two extreme points within an area, without considering life expectancy between those points.
The overarching measure of inequality in life expectancy in the Public Health Outcomes Framework (PHOF), is the slope index of inequality (SII). This measures variation in life expectancy across the whole range of deprivation, rather than just considering the extreme groups. The calculation takes into account life expectancy in each deprivation decile within an area, and summarises the variation into a single number. These data are available from the PHOF data tool https://fingertips.phe.org.uk/profile/public-health-outcomes-framework
This means that the difference between the most and least deprived quintile will be different to the slope index of inequality in life expectancy.
The within area comparison uses the most deprived and least deprived quintile in each area, rather than the most and least deprived decile. These larger groups are used to improve the robustness of the results by reducing the number of small numbers in each cause of death or age group category.
Scarf charts are only displayed when life expectancy in the selected area (or most deprived quintile of the selected area), is lower than the comparator area. In some areas, life expectancy is lower than the comparator area for one sex but not for the other. In these cases, a scarf chart will be available, but a scarf will only be shown for the sex where life expectancy is lower than the comparator area.
In a small number of cases, the output tables in the Segment Tool show that, in some areas, for a particular cause of death, there is a positive contribution to the life expectancy gap (meaning the cause makes a contribution to the life expectancy gap), and yet there are 0 or a negative number of excess deaths associated with that cause.
The number of excess deaths provided in the tables is a summary for all ages within the selected area for a given cause. However, although the area may have no excess deaths overall, the life expectancy calculation takes into account the age at which deaths occur.
Therefore, if deaths for that cause of death occur at younger ages in the selected area compared to the comparator area, this will have a greater impact on life expectancy, and therefore the life expectancy gap.
Public Health Outcomes Framework data tool: https://fingertips.phe.org.uk/profile/public-health-outcomes-framework
Health inequality tools (including the Health Inequality Dashboard): https://fingertips.phe.org.uk/profile/inequality-tools
Health Profile for England: https://www.gov.uk/government/publications/health-profile-for-england-2018
Health Equity report: https://www.gov.uk/government/publications/health-equity-in-england
Health Equity collection: https://www.gov.uk/government/collections/health-equity
Ponnapalli K (2005) A comparison of different methods for decomposition of changes in expectation of life at birth and differentials in life expectancy at birth. Demographic Research 12:141 to 172.
Preston S, Heuveline P, Guillot M (2000) Demography: Measuring and Modelling Population Processes. Blackwell Publishing.
We are happy to answer any questions you may have, and invite your feedback on the tool to help inform future development.
Please contact the Population Health Analysis team by email at: email@example.com | <urn:uuid:216a899b-c675-4eed-9488-3dd2db22f0c5> | {
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Hypochondriasis, also known as hypochondria, health anxiety or illness anxiety disorder, refers to worry about having a serious illness. This debilitating condition is the result of an inaccurate perception of the condition of body or mind despite the absence of an actual medical condition. An individual suffering from hypochondriasis is known as a hypochondriac. Hypochondriacs become unduly alarmed about any physical or psychological symptoms they detect, no matter how minor the symptom may be, and are convinced that they have, or are about to be diagnosed with, a serious illness.
Often, hypochondria persists even after a physician has evaluated a person and reassured them that their concerns about symptoms do not have an underlying medical basis or, if there is a medical illness, their concerns are far in excess of what is appropriate for the level of disease. Many hypochondriacs focus on a particular symptom as the catalyst of their worrying, such as gastro-intestinal problems, palpitations, or muscle fatigue. To qualify for the diagnosis of hypochondria the symptoms must have been experienced for at least 6 months.
The DSM-IV-TR defines this disorder, "Hypochondriasis", as a somatoform disorder and one study has shown it to affect about 3% of the visitors to primary care settings. The newly published DSM-5 replaces the diagnosis of hypochondriasis with the diagnoses of "Somatic Symptom Disorder" and "Illness Anxiety Disorder".
Hypochondria is often characterized by fears that minor bodily or mental symptoms may indicate a serious illness, constant self-examination and self-diagnosis, and a preoccupation with one's body. Many individuals with hypochondriasis express doubt and disbelief in the doctors' diagnosis, and report that doctors’ reassurance about an absence of a serious medical condition is unconvincing, or short-lasting. Additionally, many hypochondriacs experience elevated blood pressure, stress, and anxiety in the presence of doctors or while occupying a medical facility, a condition known as "white coat syndrome". Many hypochondriacs require constant reassurance, either from doctors, family, or friends, and the disorder can become a disabling torment for the individual with hypochondriasis, as well as his or her family and friends. Some hypochondriacal individuals completely avoid any reminder of illness, whereas others frequently visit medical facilities, sometimes obsessively. Other victims of this disease will never speak about it.
Hypochondriasis is categorized as a somatic amplification disorder—a disorder of "perception and cognition"—that involves a hyper-vigilance of situation of the body or mind and a tendency to react to the initial perceptions in a negative manner that is further debilitating. Hypochondriasis manifests in many ways. Some people have numerous intrusive thoughts and physical sensations that push them to check with family, friends, and physicians. For example, a person who has a minor cough may think that they have tuberculosis. Or sounds produced by organs in the body, such as those made by the intestines, might be seen as a sign of a very serious illness to patients dealing with hypochondriasis.
Other people are so afraid of any reminder of illness that they will avoid medical professionals for a seemingly minor problem, sometimes to the point of becoming neglectful of their health when a serious condition may exist and go undiagnosed. Yet others live in despair and depression, certain that they have a life-threatening disease and no physician can help them. Some consider the disease as a punishment for past misdeeds.
Hypochondriasis is often accompanied by other psychological disorders. Bipolar disorder, clinical depression, obsessive-compulsive disorder (OCD), phobias, and somatization disorder are the most common accompanying conditions in people with hypochondriasis, as well as a generalized anxiety disorder diagnosis at some point in their life.
Many people with hypochondriasis experience a cycle of intrusive thoughts followed by compulsive checking, which is very similar to the symptoms of obsessive-compulsive disorder. However, while people with hypochondriasis are afraid of having an illness, patients with OCD worry about getting an illness or of transmitting an illness to others. Although some people might have both, these are distinct conditions.
Patients with hypochondriasis often are not aware that depression and anxiety produce their own physical symptoms, and mistake these symptoms for manifestations of another mental or physical disorder or disease. For example, people with depression often experience changes in appetite and weight fluctuation, fatigue, decreased interest in sex and motivation in life overall. Intense anxiety is associated with rapid heartbeat, palpitations, sweating, muscle tension, stomach discomfort, dizziness, and numbness or tingling in certain parts of the body (hands, forehead, etc.).
In some cases, hypochondriasis responds well to antipsychotics, particularly the newer atypical antipsychotic medication.
If a person is ill with a medical disease such as diabetes or arthritis, there will often be psychological consequences, such as depression. Some even report being suicidal. In the same way, someone with psychological issues such as depression or anxiety will sometimes experience physical manifestations of these affective fluctuations, often in the form of medically unexplained symptoms. Common symptoms include headaches; abdominal, back, joint, rectal, or urinary pain; nausea; fever and/or night sweats; itching; diarrhea; dizziness; or balance problems. Many people with hypochondriasis accompanied by medically unexplained symptoms feel they are not understood by their physicians, and are frustrated by their doctors’ repeated failure to provide symptom relief.
The ICD-10 defines hypochondriasis as follows:
A. Either one of the following:
B. Preoccupation with the belief and the symptoms causes persistent distress or interference with personal functioning in daily living, and leads the patient to seek medical treatment or investigations (or equivalent help from local healers).
C. Persistent refusal to accept medical advice that there is no adequate physical cause for the symptoms or physical abnormality, except for short periods of up to a few weeks at a time immediately after or during medical investigations.
D. Most commonly used exclusion criteria: not occurring only during any of the schizophrenia and related disorders (F20-F29, particularly F22) or any of the mood disorders (F30-F39).
The DSM-IV defines hypochondriasis according to the following criteria:
A. Preoccupation with fears of having, or the idea that one has, a serious disease based on the person's misinterpretation of bodily symptoms.
B. The preoccupation persists despite appropriate medical evaluation and reassurance.
C. The belief in Criterion A is not of delusional intensity (as in Delusional Disorder, Somatic Type) and is not restricted to a circumscribed concern about appearance (as in Body Dysmorphic Disorder).
D. The preoccupation causes clinically significant distress or impairment in social, occupational, or other important areas of functioning.
E. The duration of the disturbance is at least 6 months.
F. The preoccupation is not better accounted for by Generalized Anxiety Disorder, Obsessive-Compulsive Disorder, Panic Disorder, a Major Depressive Episode, Separation Anxiety, or another Somatoform Disorder.
The newly published DSM-5 replaces the diagnosis of hypochondriasis with "illness anxiety disorder".
Hypochondria is currently considered a psychosomatic disorder, as in a mental illness with physical symptoms. Cyberchondria is a colloquial term for hypochondria in individuals who have researched medical conditions on the Internet. The media and the Internet often contribute to hypochondria, as articles, TV shows and advertisements regarding serious illnesses such as cancer and multiple sclerosis often portray these diseases as being random, obscure and somewhat inevitable. Inaccurate portrayal of risk and the identification of non-specific symptoms as signs of serious illness contribute to exacerbating the hypochondriac’s fear that they actually have that illness.
Major disease outbreaks or predicted pandemics can also contribute to hypochondria. Statistics regarding certain illnesses, such as cancer, will give hypochondriacs the illusion that they are more likely to develop the disease.
Overly protective caregivers and an excessive focus on minor health concerns have been implicated as a potential cause of hypochondriasis development.
It is common for serious illnesses or deaths of family members or friends to trigger hypochondria in certain individuals. Similarly, when approaching the age of a parent's premature death from disease, many otherwise healthy, happy individuals fall prey to hypochondria. These individuals believe they are suffering from the same disease that caused their parent's death, sometimes causing panic attacks with corresponding symptoms.
Family studies of hypochondriasis do not show a genetic transmission of the disorder. Among relatives of people suffering from hypochondriasis only somatization disorder and generalized anxiety disorder were more common than in average families. Other studies have shown that the first degree relatives of patients with OCD have a higher than expected frequency of a somatoform disorder (either hypochondriasis or body dysmorphic disorder).
Most research indicates that cognitive behavioral therapy (CBT) is an effective treatment for hypochondriasis. Much of this research is limited by methodological issues. A small amount of evidence suggests that selective serotonin reuptake inhibitors can also reduce symptoms, but further research is needed.
Among the regions of the abdomen, the hypochondrium is the uppermost part. The word derives from the Greek term ὑποχόνδριος hypokhondrios, meaning "of the soft parts between the ribs and navel" from hypo ("under") and khondros, or cartilage (of the sternum). Hypochondria in Late Latin meant "the abdomen".
The term hypochondriasis for a state of disease without real cause reflected the ancient belief that the viscera of the hypochondria were the seat of melancholy and sources of the vapor that caused morbid feelings. Until the early 18th century, the term referred to a "physical disease caused by imbalances in the region that was below your rib cage" (i.e., of the stomach or digestive system). For example, Robert Burton's The Anatomy of Melancholy (1621) blamed it "for everything from 'too much spittle' to 'rumbling in the guts'".
Immanuel Kant discussed hypochondria in his 1798 book, Anthropology like this:
The disease of the hypochondriac consists in this: that certain bodily sensations do not so much indicate a really existing disease in the body as rather merely excite apprehensions of its existence: and human nature is so constituted – a trait which the animal lacks – that it is able to strengthen or make permanent local impressions simply by paying attention to them, whereas an abstraction – whether produced on purpose or by other diverting occupations – lessen these impressions, or even effaces them altogether.Anthropology by Immanuel Kant, 1798 Journal of Speculative Philosophy Vol. XVI edited by William Torrey Harris p. 395-396 | <urn:uuid:61e772c7-f382-468e-9f1a-75cb149eb55a> | {
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Christian Jonathan Haverkampf M.D.
Psychiatry is the medical specialty devoted to the diagnosis, prevention, study, and treatment of mental disorders. These include various abnormalities related to mood, behaviour, cognition, and perceptions. Working on internal and external communication is a central focus in psychiatric treatment.
Keywords: psychiatry, psychotherapy, communication, medicine
The question what psychiatry is begins with the definition of the term ‘psyche’. The term “psychiatry” was first coined by the German physician Johann Christian Reil in 1808. The ancient Greek term ‘psyche’ is often translated as ‘soul’. However, it can also mean ‘butterfly’. While psychiatry was up until about a century ago more an occult art than a science, this has changed dramatically in the twentieth century. Within the last century, psychiatry began to make its terms, observations and inquiry much more structured and ‘scientific’.
Psychiatric illnesses all have in common that communication with others and the own person is disturbed. (Haverkampf, 2010b) These maladaptive communication patterns lead to the symptoms which are commonly observed. For example, in a case of schizophrenia the source of incoming information can no longer be correctly attributed to the outside world or the inside, and in a case of anxiety emotional signals are no longer correctly identified and processed. Communication, the transmission of messages, adheres to rules like any other natural phenomena and is relied on in nature from information carried in a beam of light to cells exchanging DNA. Humans can observe and reflect on these flows of information, also on information flows within themselves. The sense of self and the attribution of a mind to someone or oneself is a result of the ability to observe these flows of information, and as such of the communication one has with oneself or the world around.
Psychiatry refers to a field of medicine focused specifically on the mind, aiming to study, prevent, and treat mental disorders in humans. It is devoted to the diagnosis, prevention, study, and treatment of mental disorders. These include various abnormalities related to mood, behaviour, cognition, and perceptions. Psychiatry focuses on the interaction between patients and therapists in a way, which no other medical specialty does. While it is true that psychiatry has become more biologically based over the last century, it has also begun to look at the finer details of information transmission in the neuronal networks of the brain. Fortunately, gone are the times of lobotomies, where parts of the brain were removed, to make way for much more specific and finer treatment interventions, whether with psychotherapy or medication that works on specific neurotransmitter receptors or mimics certain neurotransmitters. The elaboration of the information transmission at the synaptic level has given us clues on how psychiatric illness is maintained, and medication works, within the larger system of an individual’s neuronal network.
The 20th century introduced a new psychiatry into the world, with different perspectives of looking at mental disorders. For Emil Kraepelin, the initial ideas behind biological psychiatry, stating that the different mental disorders are all biological in nature, evolved into a new concept of “nerves”, and psychiatry linked up with neurology and neuropsychiatry. Sigmund Freud, who early in his career searched intensively for explanations of psychiatric phenomena on a neuronal level, initiated the development of psychoanalysis, which shifted the emphasis on communication as an important instrument in the healing process. The psychoanalytic theory became popular among psychiatrists because it allowed the patients to be treated in private practices at a time when effective psychiatric medication was still in its infancy.
Psychopharmacology became an integral part of psychiatry starting with Otto Loewi’s discovery of the neuromodulatory properties of acetylcholine, which became the first neurotransmitter to be described. The discovery of chlorpromazine’s effectiveness in treating schizophrenia in 1952 revolutionized treatment of the disorder, as did lithium carbonate’s ability to stabilize mood highs and lows in bipolar disorder in 1948. Neuroimaging became an investigatory tool in psychiatry in the 1980s.
Psychopharmacological changes in the neurotransmission systems, the information interfaces where electrical signals are translated into chemical signals, and back again, affect how and what information is being transmitted. This in turn has an effect on a person’s internal communication and his or her communication with the external world, which are also the target of psychotherapy. (Haverkampf, 2010a, 2017c) Medication and psychotherapy can thus work together synergistically.
Unlike physicians in other medical specialties, psychiatrists specialize in the doctor–patient relationship and should be trained extensively in the use of psychotherapy and other therapeutic communication techniques. Unfortunately, this is not always the case, which can reduce the effectiveness in treating a mental health condition significantly, because treatment of a mental health condition implies working with and understanding communication on different levels. The patient uses communication with other people and the self-talk with him or herself to meat own needs, values, wishes, desires and aspirations, requiring a holistic approach to the communication patterns and mechanisms a patient uses.
Since communication plays such a central role in psychiatric treatment, the author has developed communication-focused therapy (CFT), which focuses on internal and external communication patterns to relieve the symptoms of a wide variety of mental health conditions (Haverkampf, 2017a, 2018c).
Psychiatry is the most multidisciplinary medical specialty using research in the field of neuroscience, psychology, medicine, biology, biochemistry, even physics, and pharmacology. Since psychiatry looks at the patient who is interacting with the larger world around, the social and communication sciences, including even behavioural economics, and the humanities can make important contributions to the field of psychiatry. If one considers psychiatry as a specialty that focuses on improving meaningful communication within wider information systems, the biological and social viewpoints merely represent looking at the same processes with different magnifications.
Psychiatry addresses internal and external communication issues, which are usually multifactorial in their aetiology. Compliance and the effects of medication and psychotherapy depend on the interactions between the patient and the environment. There are branches of psychiatry which look at different environments and how they influence the mental well-being of a patient. Unfortunately, psychiatric hospitals and various public health clinics have been notoriously slow at implementing any recommendations from this research.
Psychiatric illnesses can be conceptualized in several different ways. The biomedical approach examines signs and symptoms and compares them with diagnostic criteria. However, unlike the other fields of medicine, psychiatric diagnoses say little about underlying causes on a biological level but are mostly groupings of symptoms which seem to appear together. This is not to say that such groupings are not helpful. They can make it easier to describe conditions and often make it easier to pick specific therapeutic approaches and types of medication. However, since individual symptoms overlap and due to the complexity of the neural networks, it is usually not possible to follow a group of symptoms back to a specific biological variation. Since the brain is highly plastic, synapses rearrange their connections with each other all the time and assign varying weights to them. This means that a symptom of anxiety, for example, can be triggered by information stored over millions of nerve cells, and merely understanding how a biological component, such as a receptor, works does not help in understanding or treating the symptom.
Psychiatry is both ‘software’ and ‘hardware’ oriented, where ‘software’ refers to the information stored in the neural network and ‘hardware’ to the cellular network on a biological level. In the latter, there is an overlap with neurology and other medical sciences. What sets psychiatry apart is particularly the concern with information, the flows of information and how information is processed. New diagnostic systems and schemata have been developed on the psychotherapy side, which pay greater attention to the information dynamics. These models and systems can provide additional information to an experienced clinician who can then integrate these additional aspects with the diagnostic systems from the traditional medico-psychiatric side.
The biopsychosocial model is commonly used to describe the three factors that play a role in the development and maintenance of a psychiatric condition:
- Environment (social)
What is striking about these three domains is that all consist of the transmission of information in one way or another. Some describe more the internal communication (biology, neuroscience, psychology), while others describe the external communication (psychology, sociology, economics and others), but all work in parallel all of the time. Psychiatry thus works with very complex systems, which are much more elaborate than in any other field of medicine. This may also be the reasons why psychiatry was the field within medicine to develop rather late, because it uses the insight gained in several other fields.
Psychiatric diagnoses take place in a wide variety of settings and are performed by many different health professionals. Therefore, the diagnostic procedure may vary greatly based upon these factors. Typically, though, a psychiatric diagnosis utilizes a differential diagnosis procedure where a mental status examination and physical examination is conducted, with pathological, psychopathological or psychosocial histories obtained, and sometimes neuroimages or other neurophysiological measurements are taken, or personality tests or cognitive tests administered. In some cases, a brain scan might be used to rule out other medical illnesses, but at this time relying on brain scans alone cannot accurately diagnose a mental illness or tell the risk of getting a mental illness in the future. A few psychiatrists are beginning to utilize genetics during the diagnostic process but on the whole, this remains a research topic.
The problem with most diagnostic systems in psychiatry is that they do not address the underlying causes of an illness but focus instead on bundles of symptoms. As a descriptive system this makes sense in many instances. However, from a treatment perspective this is often unhelpful. Since medication works on underlying neurotransmission system within a vast network of interconnected neurons, a system that makes diagnosis based on properties within that system and on the individual neuronal level would be more helpful. From a psychotherapeutic perspective, a focus on internal and external communication would be helpful. Both perspectives could lead to systems that would be compatible with each other or even to one system that combines features of the two.
Three main diagnostic manuals used to classify mental health conditions are in use today. The International Classification of Diseases (ICD-10) is produced and published by the World Health Organization, includes a section on psychiatric conditions, and is used worldwide. The Diagnostic and Statistical Manual of Mental Disorders (DSM-V), produced and published by the American Psychiatric Association, is primarily focused on mental health conditions and is the main classification tool in the United States, although the ICD-10 has official status there as well. It is currently in its fifth revised edition and is also used worldwide. As already mentioned, the diagnostic systems are based on bundles of symptoms. Psychiatry has “a syndrome-based disease classification, which is not based on mechanisms and does not guide treatment, which largely depends on trial and error” (Stephan et al., 2016). The author of this article would not go so far. Greater clarity about a diagnosis or several diagnoses, even if we do not understand fully the underlying biological and psychological mechanisms, can be an important tool in formulating a treatment plan, which often also includes medication (Haverkampf, 2018a)
The diagnostic manuals overlap to a significant degree. One reason is that they describe groups of symptoms which are often seen together, and over time the use of their diagnostic terms has made it easier to provide treatment and conduct research. However, both suffer from the critiques mentioned above. They can give a rough idea of the symptoms, a suitable therapy and the prognosis. However, since the diagnostic systems say nothing about the underlying causes, the actual therapy needs to be individualized and its success depends on several factors inside the person and in the environment. Looking at the patient’s internal and external communication can help individualize the therapy. (Haverkampf, 2010b, 2012, 2013a, 2013b)
It is important to keep in mind the purpose served by diagnosis. It is ultimately to help a patient and raise his or her quality of life. While there may be other uses of it for forensic, insurance or other purposes, they should not lead to a different interpretation of what a diagnosis is for in a treatment context. Diagnoses can at least help to raise the probability that a specific medication or group of medication will alleviate certain symptoms (Haverkampf, 2018a, 2018f).
The first step in treatment is traditionally assessment. This usually involves interviewing the person and often obtaining information from other sources such as other health and social care professionals, relatives, associates, law enforcement personnel, emergency medical personnel, and psychiatric rating scales. A mental status examination is carried out, and a physical examination is usually performed to establish or exclude other illnesses that may be contributing to the alleged psychiatric problems. A physical examination may also serve to identify any signs of self-harm; this examination is often performed by someone other than the psychiatrist, especially if blood tests and medical imaging are performed.
However, especially in psychotherapeutic treatment, assessment can still take place after the therapy has commenced. While it is important to have a working hypothesis for the condition, it is important to remain open to any new insights gained from observing and interacting with the patient over time. For this, it is important to be in the interaction with the patient, yet also to be able to take a step outside of the interaction and reflect on the communication dynamics.
Assessment with a focus on the internal and external communication can identify problems which are leading to the symptoms. This information is then helpful to make better decisions with respect to medication and psychotherapy. Communication-Focused Therapy, as developed by the author, focuses on communication patterns an individual uses, whether in everyday life or in a therapeutic setting (Haverkampf, 2010b, 2017a). Rather than looking primarily at the content of what is being communicated, the how it is communicated assumes an additional particularly important role. Since people, and all other living organisms, meet their needs and aspirations through the exchange of information withing themselves and with the world, it is important to encourage awareness, reflection and experimentation with communication to make it more efficient and satisfying for the individual. As life aligns more with the basic parameters, the needs, values and aspirations, as a result of better communication, the symptoms of a mental health condition often receded (Haverkampf, 2017f, 2017b, 2017d) .
Psychiatric medication represents a very heterogenous group of substances, which are among the most widely prescribe in the world. Psychiatric medication was usually available before one had an understanding for its effects on a cellular or neural network level. However, in all cases it has been shown that psychiatric medication affects the information transmission in the brain. This is a point where psychotherapy and medication could go well with each other hand in hand (Haverkampf, 2018f).
The efficacy of medication can often very significantly among individuals. One antidepressant from the most popular group of antidepressants, the selective serotonin reuptake inhibitor (SSRI), for example, may help against the symptoms of depression and anxiety, while another from the same group does not work in the same patient. The outcome is not always easy to predict, although one can have a sense of the medication that is most likely to work. It requires a proper assessment in the first place, but also a solid understanding of the desired changes and the expectations of the patient.
Like most medications, psychiatric medications can cause adverse effects in patients, and some require ongoing therapeutic drug monitoring, for instance, full blood counts serum drug levels, renal function, liver function, and thyroid function. Electroconvulsive therapy (ECT) is sometimes administered for severe and disabling conditions, such as those unresponsive to medication. Although the literature reports on successes in treatment-resistant cases, its use remains controversial. Often, the available treatment options with medication and psychotherapy have not been fully exhausted when considering ECT.
To summarize, one may say that the support available form medication can be life-changing in some cases and increase the quality of life significantly. In contrast, in others, it may do little or lead to side effects, or there can be both positive and negative effects side by side. Several parameters have been studied to shape the recommendations of the professional. For example, in a study on the variables that could predict a successful treatment outcome in depression, chronic depression, older age, and lower intelligence, each predicted relatively weak response across psychotherapy and medication. On the other hand, marriage, unemployment, and having experienced a higher number of recent life events each predicted superior response to cognitive therapy relative to antidepressant medications (Fournier et al., 2009).
As already mentioned, increasingly psychiatrists are limiting their practices to psychopharmacology (prescribing medications), as opposed to previous practice in which a psychiatrist would provide traditional 50-minute psychotherapy sessions, of which psychopharmacology would be a part, but most of the consultation sessions consisted of “talk therapy.” This shift began in the early 1980s and accelerated in the 1990s and 2000s. A major reason for this change was the advent of managed care insurance plans, which began to limit reimbursement for psychotherapy sessions provided by psychiatrists. The underlying assumption was that psychopharmacology was at least as effective as psychotherapy, and it could be delivered more efficiently because less time is required for the appointment. For example, most psychiatrists schedule three or four follow-up appointments per hour, as opposed to seeing one patient per hour in the traditional psychotherapy model. Because of this shift in practice patterns, psychiatrists often refer patients whom they think would benefit from psychotherapy to other mental health professionals, e.g., clinical social workers and psychologists.
However, this approach is short-sighted. It may be easier to prescribe medication, which is a concept familiar to most patients, than to explain how psychotherapy works, whose basic premises, tools and approaches are less well known. Psychotherapy often delivers a lasting effect in the long-term in cases of anxiety, mild to moderate depression and several other conditions, which goes beyond the ongoing support medication can offer (Haverkampf, 2017a). The reason is that changes in the internal and external communications usually bring about changes in a patient’s symptoms (Haverkampf, 2018d). While medication also has an effect on these communication patterns and, through learning effects, it can even last for some time after the drug is discontinued, the changes are usually less specifically tailored to the needs and personal history of the patient.
Psychiatric treatments have changed over the past several decades. In the past, psychiatric patients were often hospitalized for six months or more, with some cases involving hospitalization for many years. Today, people receiving psychiatric treatment are more likely to be seen as outpatients. In many cases, a combination of psychotherapy and medication can prevent relapse longer than either treatment type on its own. (Haverkampf, 2018f, 2018e) There is a substantial synergism between the two. Medication can provide the support which facilitates psychotherapy, while psychotherapy can increase the compliance with medication.
Most unethical treatments in psychiatry have been a result of neglecting the importance of communication in treatment and seeing properties of interactions as being localized in a particular area of the brain rather than occurring in a network internally and through interactions with the world externally. Much unethical behaviour in psychiatry can be summarised by saying that the physician failed to interact, communicate and understand a patient in any meaningful way. When knowledge about psychiatric conditions is seen separate from the interaction with the patient, it becomes akin to playing the lottery of sorts. Treatment requires a focus on how the patient communicates internally and externally and how the world responds to these messages.
When a psychiatrist is connected on emotional and cognitive levels with himself or herself as well as the patient and has healthy boundaries in place, ethical lapses become less likely. However, this often requires substantial experience and skills in a psychotherapeutic technique that focuses on insight. It requires an interest in and experience with human communication.
To have a definition of illness, one needs a definition of health. Psychiatry is not only concerned with psychiatric illness but largely also with the maintenance of mental health. Insight into the aetiology and pathogenesis of burnout, for example, helps to prevent it, (Haverkampf, 2013a, 2013c, 2017g, 2018b) which is not only good for the individual but society and the economy as a whole. (Haverkampf, 2013c) Knowledge about which work and communication environments are helpful in preventing a relapse of psychosis can help a person arrange life in ways which keep him or her mentally healthy for as long as possible. (Haverkampf, 2017e) Skills in connecting with oneself can help to understand the information contained in emotional signals underlying episodes of anxiety. (Haverkampf, 2012)
The biopsychosocial model reduces to the communication model. Internal communication and external communication are, to some extent, arbitrary distinctions because communication still adheres to the basic rules and laws of communication, whether it unfolds in a person or without. However, this requires an integrated and more universal view of mental health. What makes us all human are the mental processes which give us the ability to observe and reflect on these flows of information. Psychotherapy and medication are the tools to bring about change in these communication patterns, internal and external ones. Other supportive therapies, such as occupational therapy, meditation and various forms of bodywork, can provide crucial additional support towards a satisfied, content and happy life, one in which personal needs, values, wishes, desires and aspirations can be met.
Dr Jonathan Haverkampf, M.D. (Vienna) MLA (Harvard) LL.M. psychoanalytic psychotherapy (Zurich) trained in medicine, psychiatry and psychotherapy and works in private practice for psychotherapy, counselling and psychiatric medication in Dublin, Ireland. He is the author of several books and over a hundred articles. Dr Haverkampf has developed Communication-Focused Therapy® and written extensively about it. He also has advanced degrees in management and law. The author can be reached by email at email@example.com or on the websites www.jonathanhaverkampf.ie and www.jonathanhaverkampf.com.
World Health Organisation (1992). The ICD-10 Classification of Mental and Behavioural Disorders: Clinical Descriptions and Diagnostic Guidelines. Geneva: World Health Organisation. ISBN 978-92-4-154422-1.
American Psychiatric Association (2000). Diagnostic and Statistical Manual of Mental Disorders (4th, text revision ed.). Washington, DC: American Psychiatric Publishing, Inc. ISBN 978-0-89042-025-6.
Chen, Yan-Fang (March–June 2002). “Chinese classification of mental disorders (CCMD-3): Towards integration in international classification”. Psychopathology. 35 (2–3): 171–5. PMID 12145505. doi:10.1159/000065140.
Essen-Möller, Eric (September 1961). “On classification of mental disorders”Paid subscription required. Acta Psychiatrica Scandinavica. 37 (2): 119–26. doi:10.1111/j.1600-0447.1961.tb06163.x.
Mezzich, Juan E. (February 1979). “Patterns and issues in multiaxial psychiatric diagnosis”. Psychological Medicine. 9 (1): 125–37. PMID 370861. doi:10.1017/S0033291700021632.
Guze, SB (June 1970). “The need for toughmindedness in psychiatric thinking”. Southern Medical Journal. 63 (6): 662–71. PMID 5446229. doi:10.1097/00007611-197006000-00012.
Dalal, PK; Sivakumar, T (October–December 2009). “Moving towards ICD-11 and DSM-5: Concept and evolution of psychiatric classification”. Indian Journal of Psychiatry. 51 (4): 310-9. PMC 2802383 Freely accessible. PMID 20048461. doi:10.4103/0019-5545.58302
Kendell, Robert; Jablensky, Assen (January 2003). “Distinguishing Between the Validity and Utility of Psychiatric Diagnoses”. American Journal of Psychiatry. 160 (1): 4–12. PMID 12505793. doi:10.1176/appi.ajp.160.1.4
Baca-Garcia E, Perez-Rodriguez MM, Basurte-Villamor I, Fernandez del Moral AL, Jimenez-Arriero MA, Gonzalez de Rivera JL, Saiz-Ruiz J, Oquendo MA (February 2007). “Diagnostic stability of psychiatric disorders in clinical practice”. The British Journal of Psychiatry. 190 (3): 210–6. PMID 17329740. doi:10.1192/bjp.bp.106.024026
Pincus HA, Zarin DA, First M (December 1998). “‘Clinical Significance’ and DSM-IV”Paid subscription required. Letters to the Editor. Archives of General Psychiatry. 55 (12): 1145. PMID 9862559. doi:10.1001/archpsyc.55.12.1145.
Greenberg, Gary (29 January 2012). “The D.S.M.’s Troubled Revision”. The Opinion Pages. The New York Times.
Moncrieff, Joanna; Wessely, Simon; Hardy, Rebecca (26 January 2004). “Active placebos versus antidepressants for depression”. Cochrane Database of Systematic Reviews (1): CD003012. PMID 14974002. doi:10.1002/14651858.CD003012.pub2.
Hopper, Kim; Wanderling, Joseph (January 2000). “Revisiting the developed versus developing country distinction in course and outcome in schizophrenia: results from ISoS, the WHO collaborative follow-up project. International Study of Schizophrenia” (PDF). Schizophrenia Bulletin. 26 (4): 835–46. PMID 11087016. doi:10.1093/oxfordjournals.schbul.a033498.
Unzicker, Rae E.; Wolters, Kate P.; Robinson, Debra (20 January 2000). “From Privileges to Rights: People Labeled with Psychiatric Disabilities Speak for Themselves”. National Council on Disability. Retrieved on 01-10-2017.
Jiang, H. Joanna; Barrett, Marguerite L.; Sheng, Minya (November 2014). Characteristics of Hospital Stays for Nonelderly Medicaid Super-Utilizers, 2012 (Healthcare Cost and Utilization Project (HCUP) Statistical Brief). Rockville, MD: Agency for Healthcare Research and Quality. 184.
Treatment Protocol Project (2003). Acute inpatient psychiatric care: A source book. Darlinghurst, Australia: World Health Organisation. ISBN 0-9578073-1-7. OCLC 223935527.
Mojtabai R, Olfson M (4 August 2008). “National trends in psychotherapy by office-based psychiatrists”. Archives of General Psychiatry. 65 (8): 962–70. PMID 18678801. doi:10.1001/archpsyc.65.8.962 Freely accessible.
Clemens, Norman A. (March 2010). “New parity, same old attitude towards psychotherapy?”. Journal of Psychiatric Practice. 16 (2): 115–9. PMID 20511735. doi:10.1097/01.pra.0000369972.10650.5a.
Mellman, Lisa A. (March 2006). “How endangered is dynamic psychiatry in residency training?”. The Journal of the American Academy of Psychoanalysis and Dynamic Psychiatry. 34 (1): 127–33. PMID 16548751. doi:10.1521/jaap.2006.34.1.127.
Stone, Alan A. (July 2001). “Psychotherapy in the managed care health market”. Journal of Psychiatric Practice. 7 (4): 238–43. PMID 15990529. doi:10.1097/00131746-200107000-00003.
Pasnau, Robert O. (March 2000). “Can the patient-physician relationship survive in the era of managed care?”. Journal of Psychiatric Practice. 6 (2): 91–6. PMID 15990478. doi:10.1097/00131746-200003000-00004.
Mojtabai R, Olfson M (January 2010). “National trends in psychotropic medication polypharmacy in office-based psychiatry”. Archives of General Psychiatry. 67 (1): 26–36. PMID 20048220. doi:10.1001/archgenpsychiatry.2009.175
Olfson M, Marcus SC, Druss B, Elinson L, Tanielian T, Pincus HA (9 January 2002). “National trends in the outpatient treatment of depression”. JAMA. 287 (2): 203–9. PMID 11779262. doi:10.1001/jama.287.2.203
Harris, Gardiner (March 5, 2011). “Talk Doesn’t Pay, So Psychiatry Turns to Drug Therapy”. The New York Times. Retrieved 01-10-2017.
Scull, Andrew, ed. (2014). Cultural Sociology of Mental Illness: An A-to-Z Guide. 1. Sage Publications. p. 386. ISBN 978-1-4833-4634-2. OCLC 955106253.
Levinson, David; Gaccione, Laura (1997). Health and Illness: A Cross-cultural Encyclopedia. Santa Barbara, CA: ABC-CLIO. p. 42. ISBN 978-0-87436-876-5. OCLC 916942828.
Koenig, Harold G. (2005). “History of Mental Health Care”. Faith and Mental Health: Religious Resources for Healing. West Conshohocken: Templeton Foundation Press. p. 36. ISBN 978-1-59947-078-8. OCLC 476009436.
Elkes, Alexander; Thorpe, James Geoffrey (1967). A Summary of Psychiatry. London: Faber & Faber. p. 13. OCLC 4687317.
Burton, Robert (1881). The Anatomy of Melancholy: What it is with All the Kinds, Causes, Symptoms, Prognostics, and Several Cures of it: in Three Partitions, with Their Several Sections, Members and Subsections Philosophically, Medicinally, Historically Opened and Cut Up. London: Chatto & Windus. pp. 22, 24. OL 3149647W.
Dumont, Frank (2010). A history of personality psychology: Theory, science and research from Hellenism to 21th century. New York: Cambridge University Press. ISBN 978-0-521-11632-9. OCLC 761231096.
Mohamed, Wael M.Y. (August 2008). “History of Neuroscience: Arab and Muslim Contributions to Modern Neuroscience” (PDF). International Brain Research Organization. Retrieved on 01-10-2017.
Fournier, J. C., DeRubeis, R. J., Shelton, R. C., Hollon, S. D., Amsterdam, J. D., & Gallop, R. (2009). Prediction of Response to Medication and Cognitive Therapy in the Treatment of Moderate to Severe Depression. Journal of Consulting and Clinical Psychology, 77(4), 775–787. https://doi.org/10.1037/a0015401
Haverkampf, C. J. (2010a). A Primer on Interpersonal Communication (3rd ed.). Dublin: Psychiatry Psychotherapy Communication Publishing Ltd.
Haverkampf, C. J. (2010b). Communication and Therapy (3rd ed.). Retrieved from http://www.jonathanhaverkampf.com
Haverkampf, C. J. (2012). A Case of Severe Anxiety. J Psychiatry Psychotherapy Communication, 1(2), 35–40.
Haverkampf, C. J. (2013a). A Case of Burnout. J Psychiatry Psychotherapy Communication, 2(3), 80–87.
Haverkampf, C. J. (2013b). A Case of Depression. J Psychiatry Psychotherapy Communication, 2(3), 88–90.
Haverkampf, C. J. (2013c). Economic Costs of Burnout. J Psychiatry Psychotherapy Communication, 2(3), 88–94.
Haverkampf, C. J. (2017a). Communication-Focused Therapy (CFT) (2nd ed.). Dublin: Psychiatry Psychotherapy Communication Publishing Ltd.
Haverkampf, C. J. (2017b). Communication-Focused Therapy (CFT) for ADHD. J Psychiatry Psychotherapy Communication, 6(4), 110–115.
Haverkampf, C. J. (2017c). Communication-Focused Therapy (CFT) for Bipolar Disorder. J Psychiatry Psychotherapy Communication, 6(4), 125–129.
Haverkampf, C. J. (2017d). Communication-Focused Therapy (CFT) for Depression. J Psychiatry Psychotherapy Communication, 6(4), 101–104.
Haverkampf, C. J. (2017e). Communication-Focused Therapy (CFT) for Psychosis. J Psychiatry Psychotherapy Communication, 6(4), 116–119.
Haverkampf, C. J. (2017f). Communication-Focused Therapy (CFT) for Social Anxiety and Shyness. J Psychiatry Psychotherapy Communication, 6(4), 107–109.
Haverkampf, C. J. (2017g). Healing Burnout.
Haverkampf, C. J. (2018a). An Overview of Psychiatric Medication (3rd ed.). Dublin: Psychiatry Psychotherapy Communication Publishing Ltd.
Haverkampf, C. J. (2018b). Burnout and Happiness at the Workplace (2nd ed.). Dublin: Psychiatry Psychotherapy Communication Publishing Ltd.
Haverkampf, C. J. (2018c). Communication-Focused Therapy (CFT) – Specific Diagnoses (Vol II) (2nd ed.). Dublin: Psychiatry Psychotherapy Communication Publishing Ltd.
Haverkampf, C. J. (2018d). Communication Patterns and Structures.
Haverkampf, C. J. (2018e). Psychiatric Conditions, Psychotherapy and Medication (1st ed.). Dublin: Psychiatry Psychotherapy Communication Publishing Ltd.
Haverkampf, C. J. (2018f). Psychiatric Medication and Psychotherapy (1st ed.). Psychiatry Psychotherapy Communication Publishing Ltd.
Stephan, K. E., Bach, D. R., Fletcher, P. C., Flint, J., Frank, M. J., Friston, K. J., … Breakspear, M. (2016, January 1). Charting the landscape of priority problems in psychiatry, part 1: Classification and diagnosis. The Lancet Psychiatry, Vol. 3, pp. 77–83. https://doi.org/10.1016/S2215-0366(15)00361-2
Haque, Amber (December 2004). “Psychology from Islamic Perspective: Contributions of Early Muslim Scholars and Challenges to Contemporary Muslim Psychologists”. Journal of Religion and Health. 43 (4): 357–377 . doi:10.1007/s10943-004-4302-z.
Verhagen, Peter; Van Praag, Herman M.; López-Ibor, Juan José, Jr.; Cox, John; Moussaoui, Driss, eds. (2010). Religion and Psychiatry: Beyond Boundaries. World Psychiatric Association. Chichester: John Wiley & Sons. p. 202. ISBN 978-0-470-69471-8. OCLC 761549866.
Laffey, Paul (November 2003). “Psychiatric therapy in Georgian Britain”Paid subscription required. Psychological Medicine. 33: 1285–97. PMID 14580082. doi:10.1017/S0033291703008109.
Gerard, Donald L. (September 1997). “Chiarugi and Pinel considered: Soul’s brain/person’s mind”Paid subscription required. Journal of the History of the Behavioral Sciences. 33 (4): 381–403. doi:10.1002/(SICI)1520-6696(199723)33:4<381::AID-JHBS3>3.0.CO;2-S.
Suzuki, Akihito (January 1995). “The politics and ideology of non-restraint: the case of the Hanwell Asylum”. Medical History. London: Wellcome Institute. 39 (1): 1–17. PMC 1036935 Freely accessible. PMID 7877402. doi:10.1017/s0025727300059457.
Bynum, W.F.; Porter, Roy; Shepherd, Michael, eds. (1988). The Asylum and its psychiatry. The Anatomy of Madness: Essays in the history of psychiatry. 3. London: Routledge. ISBN 978-0-415-00859-4. OCLC 538062123.
Yanni, Carla (2007). The Architecture of Madness: Insane Asylums in the United States. Minneapolis: Minnesota University Press. ISBN 978-0-8166-4939-6.
Rothman, D.J. (1990). The Discovery of the Asylum: Social Order and Disorder in the New Republic. Boston: Little Brown. p. 239. ISBN 978-0-316-75745-4.
Borch-Jacobsen, Mikkel (7 October 2010). “Which came first, the condition or the drug?”. London Review of Books. 32 (19): 31–33.
Turner, Trevor (2007). “Chlorpromazine: Unlocking psychosis”. BMJ. 334 (suppl): s7. PMID 17204765. doi:10.1136/bmj.39034.609074.94
Cade, JFJ (3 September 1949). “Lithium salts in the treatment of psychotic excitement”. Medical Journal of Australia. 2 (10): 349–52. PMID 18142718.
Burns, Tom (2006). Psychiatry: A very short introduction. Oxford: Oxford University Press. ISBN 978-0-19-280727-4. OCLC 706088927.
Backes, Katherine A.; Borges, Nicole J.; Binder, S. Bruce; Roman, Brenda (2013), “First-year medical student objective structured clinical exam performance and specialty choice”, International Journal of Medical Education, 4: 38–40, doi:10.5116/ijme.5103.b037
Alarcón, Renato D. (2016), “Psychiatry and Its Dichotomies”, Psychiatric Times, 33 (5): 1
“Information about Mental Illness and the Brain (Page 3 of 3)”. The Science of Mental Illness. National Institute of Mental Health. January 31, 2006. Retrieved 01-10-20172007.
Kupfer DJ, Regier DA (2010). “Why all of medicine should care about DSM-5”. JAMA. 303 (19): 1974–1975. PMID 20483976. doi:10.1001/jama.2010.646.
Gabbard GO (2007). “Psychotherapy in psychiatry”. International Review of Psychiatry. 19 (1): 5–12. PMID 17365154. doi:10.1080/09540260601080813.
James, F.E. (July 1991). “Psyche”. Psychiatric Bulletin. 15 (7): 429–31. doi:10.1192/pb.15.7.429
Storrow, Hugh A. (1969). Outline of Clinical Psychiatry. New York: Appleton-Century-Crofts. p. 1. ISBN 978-0-390-85075-1. OCLC 599349242.
Pietrini, Pietrini (November 2003). “Toward a Biochemistry of Mind?”. Editorial. American Journal of Psychiatry. 160 (11): 1907–8. PMID 14594732. doi:10.1176/appi.ajp.160.11.1907.
“Madrid Declaration on Ethical Standards for Psychiatric Practice”. World Psychiatric Association. Retrieved 01-10-2017.
López-Muñoz F, Alamo C, Dudley M, Rubio G, García-García P, Molina JD, Okasha A (9 May 2007). Cecilio Alamoa, Michael Dudleyb, Gabriel Rubioc, Pilar García-Garcíaa, Juan D. Molinad and Ahmed Okasha. “Progress in Neuro-Psychopharmacology and Biological Psychiatry: Psychiatry and political–institutional abuse from the historical perspective: The ethical lessons of the Nuremberg Trial on their 60th anniversary”. Progress in Neuro-Psychopharmacology and Biological Psychiatry. 31 (4): 791–806. PMID 17223241. doi:10.1016/j.pnpbp.2006.12.007.
Gluzman, Semyon F. (December 1991). “Abuse of psychiatry: analysis of the guilt of medical personnel”. Journal of Medical Ethics. 17 (Suppl): 19–20. PMC 1378165 Freely accessible. PMID 1795363. doi:10.1136/jme.17.Suppl.19
Debreu, Gerard (1988). “Introduction”. In Corillon, Carol. Science and Human Rights. The National Academies Press. p. 21. doi:10.17226/9733 Freely accessible. Retrieved 01-10-2017.
Kirk, Stuart A.; Gomory, Tomi; Cohen, David (2013). Mad Science: Psychiatric Coercion, Diagnosis, and Drugs. New Brunswick, NJ: Transaction Publishers. ISBN 978-1-4128-4976-0. OCLC 935892629.
Verhulst J, Tucker G (May 1995). “Medical and narrative approaches in psychiatry”. Psychiatric Services. 46 (5): 513–4. PMID 7627683. doi:10.1176/ps.46.5.513
McLaren, N (February 1998). “A critical review of the biopsychosocial model”. The Australian and New Zealand Journal of Psychiatry. 32 (1): 86–96. PMID 9565189. doi:10.1046/j.1440-1614.1998.00343.x.
McLaren, Niall (2007). Humanizing Madness. Ann Arbor, MI: Loving Healing Press. ISBN 1-932690-39-5.
McLaren, Niall (2009). Humanizing Psychiatry. Ann Arbor, MI: Loving Healing Press. ISBN 1-61599-011-9.
Hurst, Michael. “Humanistic Therapy”. CRC Health Group. Retrieved 01-10-2016.
McLeod, Saul (2014). “Psychoanalysis”. Simply Psychology. Retrieved 01-10-2016.
Cherry, Kendra (9 June 2017). “What’s the Difference Between a Psychologist and a Psychiatrist?”. VeryWell. Dotdash.
Brown, Menna; Barnes, Jacob; Silver, Katie; Williams, Nicholas; Newton, Philip M. (April 2016). “The Educational Impact of Exposure to Clinical Psychiatry Early in an Undergraduate Medical Curriculum”. Academic Psychiatry. 40 (2): 274–281. PMID 26077010. doi:10.1007/s40596-015-0358-1 – via SpringerLink.
Japsen, Bruce (15 September 2015). “Psychiatrist Shortage Worsens Amid ‘Mental Health Crisis’”. Forbes.
Thiele, Jonathan S.; Doarn, Charles R.; Shore, Jay H. (27 May 2015). “Locum Tenens and Telepsychiatry: Trends in Psychiatric Care”. Telemedicine Journal and e-Health. 21 (6): 510–3. PMID 25764147. doi:10.1089/tmj.2014.0159.
Hausman, Ken (6 December 2013). “Brain Injury Medicine Gains Subspecialty Status”. Psychiatric News. 48 (23): 10. doi:10.1176/appi.pn.2013.11b29.
Gandey, Allison (12 November 2010). “New Epilepsy and Emergency Medicine Subspecialties Launched”. Medscape Medical News. WebMD, LLC. Retrieved 2017-08-20.
“About AACP”. American Association of Community Psychiatrists. University of Pittsburgh School of Medicine, Department of Psychiatry. Retrieved 01-10-2017.
Patel, Vikram; Prince, Martin (19 May 2010). “Global mental health: A new global health field comes of age”. Commentary. JAMA. 303 (19): 1976–7. PMC 3432444 Freely accessible. PMID 20483977. doi:10.1001/jama.2010.616.
Mitchell, J.E.; Crosby, R.D.; Wonderlich, S.A.; Adson, D.E. (2000). Elements of Clinical Research in Psychiatry. Washington, DC: American Psychiatric Press. ISBN 978-0-88048-802-0. OCLC 632834662.
Meyendorf, R (1980). “Diagnose und Differentialdiagnose in der Psychiatrie und zur Frage der situationsbezogenen prognostischen Diagnose” [Diagnosis and differential diagnosis in psychiatry and the question of situation referred prognostic diagnosis]. Schweizer Archiv fur Neurologie, Neurochirurgie und Psychiatrie (in German). 126 (1): 121–34. PMID 7414302.
Leigh, Hoyle (1983). Psychiatry in the practice of medicine. Menlo Park, CA: Addison-Wesley. pp. 15,17,67. ISBN 978-0-201-05456-9. OCLC 869194520.
Hampel H, Teipel SJ, Kötter HU, Horwitz B, Pfluger T, Mager T, Möller HJ, Müller-Spahn F (May 1997). “Strukturelle Magnetresonanztomographie in der Diagnose und Erforschung der Demenz vom Alzheimer-Typ” [Structural magnetic resonance imaging in diagnosis and research of Alzheimer’s disease]. Der Nervenarzt (in German). 68 (5): 365–78. PMID 9280846.
Townsend, Brent A.; Petrella, Jeffrey R.; Doraiswamy, P. Murali (July 2002). “The role of neuroimaging in geriatric psychiatry”. Current Opinion in Psychiatry. 15 (4): 427–32. doi:10.1097/00001504-200207000-00014. (Subscription required (help)).
“Neuroimaging and Mental Illness: A Window Into the Brain”. National Institute of Mental Health. U.S. Department of Health and Human Services. 2009. Retrieved 01-10-2017.
Krebs, Marie-Odile (2005). “Future contributions on genetics”. World Journal of Biological Psychiatry. 6 (Sup 2): 49–55. PMID 16166024. doi:10.1080/15622970510030072.
Hensch, Tilman; Herold, Ulf; Brocke, Burkhard (August 2007). “An electrophysiological endophenotype of hypomanic and hyperthymic personality”. Journal of Affective Disorders. 101 (1–3): 13–26. PMID 17207536. doi:10.1016/j.jad.2006.11.018.
Vonk R, van der Schot AC, Kahn RS, Nolen WA, Drexhage HA (15 July 2007). “Is autoimmune thyroiditis part of the genetic vulnerability (or an endophenotype) for bipolar disorder?”. Biological Psychiatry. 62 (2): 135–140. PMID 17141745. doi:10.1016/j.biopsych.2006.08.041.
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Brief psychotic disorder (BPD) according to DSM-5 is the sudden onset of psychotic behavior that lasts less than 1 month followed by complete remission with possible future relapses. It is differentiated from schizophreniform disorder and schizophrenia by the duration of the psychosis. The diagnosis is often anticipatory or retrospective due to the diagnostic requirement of complete remission within 1 month. Brief psychotic disorder is an acute but transient disorder with onset of one or more of the following psychotic symptoms:
At least one of these symptoms must be delusions, hallucinations, or disorganized speech. The symptoms in BPD last between one day to one month, with a complete return to premorbid level of functioning after the disease course in response to antipsychotic medications. The disturbance in behavior cannot be better accounted by schizophrenia, schizoaffective disorder, mood disorder with psychotic features, or be a direct result of a drug, medication, or medical condition like thyrotoxicosis, sarcoidosis, or syphilis.
Although unclear, the underlying etiology of brief psychotic disorder can be a stressful event or trauma. There may be a genetic, neurological, or environmental component to BPD as well. The specific trigger of BPD, if present, must be specified as follows:
Reliable data on the frequency of brief psychotic disorder are not available, mostly because of its low incidence and variation based on the population under study. However, increased frequency of the disorder generally occurs in populations known to be under high stress such as immigrants, refugees, earthquake victims, etc. A study researching the Finnish population found the prevalence of brief psychotic disorder to be 0.05%. Another study in rural Ireland found 10 cases of BPD among 196 first-admission psychosis cases.
Compared to developed countries, reports show a higher incidence of brief psychotic disorder in developing countries. Data drawn from the World Health Organization Determinants of Outcome Study also found that the incidence of BPD in developing countries was ten times as much as that in industrialized countries. BPD is also thought to be more common in women and those with a personality disorder.
The pathophysiology of BPD is not known, especially given the extremely low incidence of the disorder. Its higher prevalence among patients with personality or mood disorders may suggest underlying biological or psychological susceptibility which may some genetic influence.
Three essential elements of the history and physical in an individual with suspected brief psychotic disorder are:
In order to further classify individual cases of brief psychotic disorder, it becomes essential to recognize if the triggering of psychotic symptoms were from a stressful event or if it is postpartum. Common stressors are death, environmental disaster, military activity, recent immigration. Acknowledging patient characteristics such presence of a personality disorder that can limit coping skills will also be crucial to identifying individuals at a greater risk of developing disorders like BPD. It is also important to keep in mind that the presenting symptoms of BPD may occasionally be highly severe and mimic the presentation of delirium as a result.
There are no particular lab studies or psychological testing that are performable to make the diagnosis of a brief psychotic disorder.
The most appropriate tests and imaging to be done would rule out other potential diagnoses or causes for the behavioral disturbances. Hence, it would be apt to do a serum pregnancy test in women to evaluate any underlying triggers for the patient's behavioral disturbances. Other potential tests to consider ordering would be ECG, electrolytes, glucose level, liver function tests, thyroid function tests, and urinalysis. Urine toxicology tests can help exclude any potential drug or medication intoxication or withdrawal. CT and MRI of the brain may also be performed to evaluate for any underlying structural causes for the symptoms.
It is important to first and foremost decide the appropriate level of care and whether the patient should be hospitalized or treated on an outpatient basis. The basis for decisions regarding treatment should be on multiple factors such as the patient's presenting symptoms, socioeconomic stability, the presence of supporting individuals or family, and the presence of homicidal or suicidal ideation. Because of the limited number of clinical trials evaluating the efficacy of specific treatment modalities in patients with brief psychotic disorder, current recommendations for treatment of BPD relies on pharmacological and psychotherapeutic interventions known to be effective in patients with other psychotic disorders.
Pharmacotherapy: Antipsychotics, especially second-generation, are the first-line treatment for brief psychotic disorder. Although BPD characteristically shows complete resolution of symptoms within one month of symptom onset, it is suggested to continue treatment with antipsychotics for one to three months after symptom remission. Although oral formulations are preferable as first-line treatment for BPD, intramuscular formulations may have to be used in patients during immediate assessments and treatment, especially in emergency settings.
Psychotherapy: As expected, a brief yet major psychotic episode can be highly disruptive to the livelihood and functioning of an individual and his/her family and friends. Psychotherapeutic management of BPD would involve medically informing the patient and his/her family about the condition and treatment modalities employed for the particular patient. Along with emphasizing reintegration into the societal milieu, it is essential to focus on managing comorbid disorders or stressors and improving overall coping skills.
During the treatment process, the patient should be monitored on a long-term basis to assess for relapse or presence of residual symptoms that may necessitate referral to a specialist. It is essential to support the patient to maintain medication adherence as a lack of adherence may facilitate symptom relapse. The overall treatment plan for BPD should ideally include both pharmacological and psychosocial interventions. The biological, psychological, and social dimensions of the patient's life should in unison dictate the eventual treatment decisions made.
It is essential to consider other possible etiologies before determining a final diagnosis of the brief psychotic disorder. A diagnosis of brief psychotic disorder can only be made retrospectively after the symptoms have remitted within one month of presentation, as the symptoms of psychosis may otherwise be an early manifestation of another disorder with a psychotic component. Prior to symptomatic remission, a diagnosis of ‘psychotic disorder, not otherwise specified' may be given. Primary differential diagnoses to consider are psychotic affective disorder, schizophrenia-spectrum disorders, personality disorders, delusional disorder, substance use disorder (including withdrawal), substance-induced psychosis, and psychosis secondary to medical conditions.
Psychotic affective disorder is diagnosed in the presence of a major mood component with symptoms of depression or mania. Even with treatment, a patient with affective disorder with psychosis is not expected to return to baseline in 30 days, unlike patients with BPD. Schizophrenia-spectrum disorders such as schizophreniform disorder and schizophrenia are distinguished from BPD based mainly on the presence of symptoms for longer than 30 days. Schizoaffective disorder is diagnosed in a patient who meets the criteria for major depressive disorder or manic disorder who also has psychotic symptoms consistent with schizophrenia concurrently with the mood symptoms and for at least 2 weeks in the absence of mood symptoms. Patients with personality disorder, especially borderline personality disorder, may also have transient episodes of psychosis mostly induced by stress that may only last for 1 day or less. Substance intoxication, substance withdrawal, or medical conditions such as syphilis, neurosarcoidosis, metastasis likely secondary to lung cancer, thyrotoxicosis, and head trauma may occasionally present with symptoms that mimic that of BPD, however, a comprehensive history and physical examination in addition to necessary laboratory testing and imaging will help elucidate the underlying condition.
Given the nature of this condition, the prognosis is considerably well with a complete remission of symptoms within a month per definition based on DSM-5 criteria. However, the symptoms may recur especially in the setting of a stressful psychosocial milieu. Some positive prognostic indicators for the brief psychotic disorder are the absence of genetically-related individuals with schizophrenia or brief psychotic disorder, sudden symptom onset, the presence of stressful triggers, and short duration of symptoms.
Prognosis is notably worse for individuals diagnosed with BPD who have then been able to meet criteria for other disorders characterized by psychosis. A study conducted in Suffolk County, New York in 2000 found that only 2% of the first-admission psychosis patients met the criteria for BPD at the six-month mark. Per the Suffolk County study consisting of 11 patients initially given the diagnosis of brief psychotic disorder, three retained the diagnosis of BPD while the remaining nine received diagnoses of mood disorder, schizophrenia, schizophreniform disorder, and other disorders involving psychosis.
The most significant complication associated with brief psychotic disorder is the sudden onset of symptoms and accompanying loss in functioning. It is crucial to make special note of predisposing stressors and comorbid disorders and manage them appropriately as that may have precipitated this episode and may result in similar manifestations in the future. Although pharmacotherapy may help curb the presenting symptoms of BPD, it is psychotherapy that will empower the patient with the skills and techniques to cope with this disorder during and after the symptoms have remitted.
Patient and family education is an imperative aspect of the psychotherapeutic interventions used to manage brief psychotic disorder. Experiencing one or more psychotic symptoms including delusions, hallucinations, disorganized speech, or grossly disorganized/catatonic behavior can be extremely unsettling to the individual and family likewise. As a result, adequate education about treatment options and psychotherapy are necessary, in addition to facilitating a strong support system for the patient.
As with most other psychiatric pathologies, the diagnosis, treatment, and management of brief psychotic disorder require the coordinated efforts of a strong an interprofessional team that includes the primary care provider, mental health nurse, psychologist, and a psychiatrist. It is paramount to develop and follow a patient-centered approach with a particular focus on psychotherapy and pharmacotherapy, given how disruptive such a disease process can be to the patient and his/her family. Working on the biopsychosocial aspect of well-being will ensure that the patient is well supported all-around and help curtail the overall negative impact of this disorder on the life and functioning of the individual.
|||Regier DA,Kuhl EA,Kupfer DJ, The DSM-5: Classification and criteria changes. World psychiatry : official journal of the World Psychiatric Association (WPA). 2013 Jun [PubMed PMID: 23737408]|
|||Rushing SE,Jean-Baptiste M, Two cases of brief psychotic disorder related to media coverage of the September 11, 2001 events. Journal of psychiatric practice. 2003 Jan; [PubMed PMID: 15985919]|
|||Pfuhlmann B,Stöber G,Franzek E,Beckmann H, Cycloid psychoses predominate in severe postpartum psychiatric disorders. Journal of affective disorders. 1998 Sep; [PubMed PMID: 9858072]|
|||Alexandre J,Ribeiro R,Cardoso G, Ethnic and clinical characteristics of a Portuguese psychiatric inpatient population. Transcultural psychiatry. 2010 Apr; [PubMed PMID: 20603391]|
|||Littlewood R,Lipsedge M, Acute psychotic reactions in Caribbean-born patients. Psychological medicine. 1981 May; [PubMed PMID: 7267872]|
|||Perälä J,Suvisaari J,Saarni SI,Kuoppasalmi K,Isometsä E,Pirkola S,Partonen T,Tuulio-Henriksson A,Hintikka J,Kieseppä T,Härkänen T,Koskinen S,Lönnqvist J, Lifetime prevalence of psychotic and bipolar I disorders in a general population. Archives of general psychiatry. 2007 Jan; [PubMed PMID: 17199051]|
|||Kingston T,Scully PJ,Browne DJ,Baldwin PA,Kinsella A,Russell V,O'Callaghan E,Waddington JL, Diagnostic trajectory, interplay and convergence/divergence across all 12 DSM-IV psychotic diagnoses: 6-year follow-up of the Cavan-Monaghan First Episode Psychosis Study (CAMFEPS). Psychological medicine. 2013 Dec; [PubMed PMID: 23480983]|
|||Susser E,Wanderling J, Epidemiology of nonaffective acute remitting psychosis vs schizophrenia. Sex and sociocultural setting. Archives of general psychiatry. 1994 Apr; [PubMed PMID: 8161289]|
|||Castagnini A,Bertelsen A,Berrios GE, Incidence and diagnostic stability of ICD-10 acute and transient psychotic disorders. Comprehensive psychiatry. 2008 May-Jun; [PubMed PMID: 18396184]|
|||Jørgensen P,Bennedsen B,Christensen J,Hyllested A, Acute and transient psychotic disorder: comorbidity with personality disorder. Acta psychiatrica Scandinavica. 1996 Dec; [PubMed PMID: 9021000]|
|||Beighley PS,Brown GR,Thompson JW Jr, DSM-III-R brief reactive psychosis among Air Force recruits. The Journal of clinical psychiatry. 1992 Aug; [PubMed PMID: 1500405]|
|||Pillmann F,Haring A,Balzuweit S,Blöink R,Marneros A, The concordance of ICD-10 acute and transient psychosis and DSM-IV brief psychotic disorder. Psychological medicine. 2002 Apr; [PubMed PMID: 11989997]|
|||Hultsjö S,Berterö C,Hjelm K, Perceptions of psychiatric care among foreign- and Swedish-born people with psychotic disorders. Journal of advanced nursing. 2007 Nov; [PubMed PMID: 17822426]|
|||Usher K,Foster K,McNamara P, Antipsychotic drugs and pregnant or breastfeeding women: the issues for mental health nurses. Journal of psychiatric and mental health nursing. 2005 Dec; [PubMed PMID: 16336596]|
|||Thomas P,Alptekin K,Gheorghe M,Mauri M,Olivares JM,Riedel M, Management of patients presenting with acute psychotic episodes of schizophrenia. CNS drugs. 2009; [PubMed PMID: 19320529]|
|||Schwartz JE,Fennig S,Tanenberg-Karant M,Carlson G,Craig T,Galambos N,Lavelle J,Bromet EJ, Congruence of diagnoses 2 years after a first-admission diagnosis of psychosis. Archives of general psychiatry. 2000 Jun; [PubMed PMID: 10839338]| | <urn:uuid:51021f68-7a17-460d-8455-2173a5d43b66> | {
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Diabetes type 1, også kalt insulinavhengig diabetes, oppstår i alle aldersgrupper, men oftest hos Alle med diabetes type 1 er avhengig av å tilføre kroppen insulin, og det er du selv som må ta det.. Learn about diabetes mellitus from experts at Cleveland Clinic. Diabetes Mellitus: An Overview. Diabetes prevents your body from properly absorbing energy from the food you eat Diabetes and various types have been discussed in detail as regard for Pg entrance and with various images, tables.. Topics discussed: 1) introduction 2) Learn more about Diabetes. Read all information of Diabetes symptoms, treatments, causes, tests & preventions If you have diabetes - or have to care for someone who has - it's important to be prepared to cope In this article. What happens to my diabetes when I am unwell? What should you do when you are..
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Diabetes mellitus zaznamenáva v posledných desaťročiach nepretržitý systematický nárast a v tejto súvislosti sa čoraz častejšie skloňuje termín pandémia. Ide o ochorenie, ktoré je sprevádzané.. Diabetes and cardiovascular system diseases has been recognized to be closely related to each other for some time now due to the so-called insulin resistance syndrome or metabolic syndrome
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. Learning how to read a lab report helps you take control of your health Последние твиты от Int. Diabetes Fed. (@IntDiabetesFed). The International Diabetes Federation (IDF) is the global advocate for the 463 million people currently living with diabetes and the many.. | <urn:uuid:46afc724-7a55-4a6f-b145-c2e1b4676834> | {
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Asperger syndrome (AS), also known as Asperger's, is a developmental disorder characterized by significant difficulties in social interaction and nonverbal communication, along with restricted and repetitive patterns of behavior and interests. As a milder autism spectrum disorder (ASD), it differs from other ASDs by relatively normal language and intelligence. Although not required for diagnosis, physical clumsiness and unusual use of language are common. Signs usually begin before two years old and typically last for a person's entire life.
The exact cause of Asperger's is unknown. While it is probably partly inherited, the underlying genetics have not been determined conclusively. Environmental factors are also believed to play a role. Brain imaging has not identified a common underlying problem. The diagnosis of Asperger's was removed in the 2013 fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5), and people with these symptoms are now included within the autism spectrum disorder along with autism and pervasive developmental disorder not otherwise specified (PDD-NOS). It remains within the tenth edition of the International Classification of Diseases (ICD-10) as of 2015.
I have been given some useful links below, these are overseas-based websites they do carry ads which may not be available in New Zealand
There is no single treatment, and the effectiveness of particular interventions is supported by only limited data. Treatment is aimed at improving poor communication skills, obsessive or repetitive routines and physical clumsiness. Interventions may include social skills training, cognitive behavioral therapy, physical therapy, speech therapy, parent training and medications for associated problems such as mood or anxiety. Most children improve as they grow up, but social and communication difficulties usually persist. Some researchers and people on the autism spectrum have advocated a shift in attitudes toward the view that autism spectrum disorder is a difference rather than a disease that must be treated or cured.
In 2015, Asperger's was estimated to affect 37.2 million people globally. The syndrome is named after the Austrian pediatrician Hans Asperger, who in 1944 described children in his practice who lacked nonverbal communication, had limited understanding of others' feelings, and were physically clumsy. The modern conception of Asperger syndrome came into existence in 1981 and went through a period of popularization. It became a standardized diagnosis in the early 1990s.
Many questions and controversies remain about aspects of the disorder. There is doubt about whether it is distinct from high-functioning autism (HFA). Partly because of this, the percentage of people affected is not firmly established. | <urn:uuid:068c6725-6fcf-416d-8783-2c907d68f8ae> | {
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Schizophrenia is a psychiatric diagnosis denoting a persistent, often chronic, mental illness variously affecting behavior, thinking, and emotion. The term schizophrenia comes from the Greek words σχίζω (schizo, split or divide) and φρενός (phrenos, mind) and is best translated as "shattered mind". The status of schizophrenia is controversial, largely due to the lack of objective criteria for diagnosis and the subsequent difficulty in adequately researching an inadequately defined condition. Research has suggested however, that both genetic and social influences are important contributing factors. Schizophrenia is commonly, but usually incorrectly, assumed to involve a 'split personality'.
Schizophrenia is most commonly characterized by both 'positive symptoms' (those additional to normal experience and behaviour) and 'negative symptoms' (the lack or decline in normal experience or behaviour). Positive symptoms are grouped under the umbrella term psychosis and typically include delusions, hallucinations, and thought disorder. Negative symptoms may include inappropriate emotional displays or flat emotional affect, poverty of speech, and lack of motivation. Some models of schizophrenia include thought disorder and planning problems in a third grouping, the 'disorganization syndrome'. Additionally, neurocognitive deficits may be present. These take the form of reduction or impairment in basic psychological functions such as memory, attention, problem solving, executive function and social cognition. The onset is typically in late adolescence and early adulthood, with males tending to show symptoms earlier than females.
Psychiatrist Emil Kraepelin was first to make the distinction between what he called dementia praecox and other forms of madness. This classification was later renamed 'schizophrenia' by psychiatrist Eugen Bleuler in 1911 as it became clear Kraepelin's name was not an adequate description of the condition.
The diagnostic approach to schizophrenia has been opposed, most notably by the anti-psychiatry movement, who argue that classifying specific thoughts and behaviours as illness allows social control of people that society finds undesirable but who have committed no crime.
More recently, it has been argued that schizophrenia is just one end of a spectrum of experience and behaviour, and everybody in society may have some such experiences in their life. This is known as the 'continuum model of psychosis' or the 'dimensional approach' and is most notably argued for by psychologist Richard Bentall and psychiatrist Jim van Os .
Although no definite causes of schizophrenia have been identified, most researchers and clinicians currently believe that schizophrenia is primarily a disorder of the brain. It is thought that schizophrenia may result from a mixture of genetic disposition (genetic studies using various techniques have shown relatives of people with schizophrenia are more likely to show signs of schizophrenia themselves) and environmental stress (research suggests that stressful life events may precede a schizophrenic episode).
It is also thought that processes in early neurodevelopment are important, particularly those that occur during pregnancy. In adult life, particular importance has been placed upon the function (or malfunction) of dopamine in the mesolimbic pathway in the brain. This theory, known as the dopamine hypothesis of schizophrenia largely resulted from the accidental finding that a drug group which blocks dopamine function, known as the phenothiazines, reduced psychotic symptoms. These drugs have now been developed further and antipsychotic medication is commonly used as a first line treatment. However, this theory is now thought to be overly simplistic as a complete explanation.
Differences in brain structure have been found between people with schizophrenia and those without. However, these tend only to be reliable on the group level and, due to the significant variability between individuals, may not be reliably present in any particular individual.
Accounts that may relate to symptoms of schizophrenia date back as far as 2000 BC in the Book of Hearts, part of the ancient Ebers papyrus. However, a recent study1 into the ancient Greek and Roman literature showed that whilst the general population probably had an awareness of psychotic disorders, there was no recorded condition that would meet the modern diagnostic criteria for schizophrenia in these societies.
This nonspecific concept of madness has been around for many thousands of years and schizophrenia was only classified as a distinct mental disorder by Kraepelin in 1887. He was the first to make a distinction in the psychotic disorders between what he called dementia praecox (a term first used by psychiatrist Benedict A. Morel) and manic depression. Kraepelin believed that dementia praecox was primarily a disease of the brain2, and particularly a form of dementia. Kraepelin named the disorder 'dementia praecox' (early dementia) to distinguish it from other forms of dementia (such as Alzheimer's disease) which typically occur late in life. He used this term because his studies focused on young adults with dementia.22
The term schizophrenia is derived from the Greek words 'schizo' (split) and 'phrene' (mind) and was coined by Eugene Bleuler to refer to the lack of interaction between thought processes and perception. He was also the first to describe the symptoms as "positive" or "negative."22 Bleuler changed the name to schizophrenia as it was obvious that Krapelin's name was misleading. The word "praecox" implied precocious or early onset, hence premature dementia, as opposed to senile dementia from old age. Bleuler realized the illness was not a dementia (it did not always lead to mental deterioration) and could sometimes occur late as well as early in life and was therefore misnamed.
With the name 'schizophrenia' Bleuler intended the name to capture the separation of function between personality, thinking, memory, and perception, however it is commonly misunderstood to mean that affected persons have a 'split personality' (something akin to the character in Robert Louis Stevenson's The Strange Case of Dr. Jekyll and Mr. Hyde). Schizophrenia is commonly, although incorrectly, confused with multiple personality disorder (now called 'dissociative identity disorder'). Although people diagnosed with schizophrenia may 'hear voices' and may experience the voices as distinct personalities, schizophrenia does not involve a person changing between distinct multiple personalities. The confusion perhaps arises in part due to the meaning of Bleuler's term 'schizophrenia' (literally 'split mind'). Interestingly, the first known misuse of this word schizophrenia to mean 'split personality' (in the Jekyll and Hyde sense) was in an article by the poet T. S. Eliot in 19333.
In the first half of the twentieth century, schizophrenia was considered by many as a "hereditary defect", and people with schizophrenia became the target of the eugenics programs of many countries. Hundreds of thousands were forcibly sterilized, the majority in Germany, the United States, and various Scandinavian countries.
Diagnosis and presentation (signs and symptoms)
Like many mental illnesses, the diagnosis of schizophrenia is based upon the behaviour of the person being assessed. There is a list of diagnostic criteria which must be met for a person to be so diagnosed. These depend on both the presence and duration of certain signs and symptoms.
The most commonly-used criteria for diagnosing schizophrenia are from the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders (DSM) and the World Health Organisation's International Statistical Classification of Diseases and Related Health Problems (ICD). The most recent versions are ICD-10 and DSM-IV-TR.
Below is an abbreviated version of the diagnostic criteria from the DSM-IV-TR, the full version is available here. (DSM cautionary statement)
To be diagnosed as having schizophrenia, a person must display:
- A) Characteristic symptoms: Two or more of the following, each present for a significant portion of time during a one-month period (or less, if successfully treated)
- disorganized speech (e.g., frequent derailment or incoherence). See thought disorder.
- grossly disorganized or catatonic behavior
- negative symptoms, i.e., affective flattening (lack or decline in emotional response), alogia (lack or decline in speech), or avolition (lack or decline in motivation).
- Note: Only one Criterion A symptom is required if delusions are bizarre or hallucinations consist of hearing voices.
- B) Social/occupational dysfunction: For a significant portion of the time since the onset of the disturbance, one or more major areas of functioning such as work, interpersonal relations, or self-care, are markedly below the level achieved prior to the onset.
- C) Duration: Continuous signs of the disturbance persist for at least six months. This six-month period must include at least one month of symptoms (or less, if successfully treated) that meet Criterion A.
Historically, schizophrenia in the West was classified into simple, catatonic, hebephrenic, and paranoid. The DSM now contains five sub-classifications of schizophrenia. These are
- catatonic type (where marked absences or peculiarities of movement are present),
- disorganized type (where thought disorder and flat or inappropriate affect are present together),
- paranoid type (where delusions and hallucinations are present but thought disorder, disorganized behaviour, and affective flattening is absent),
- residual type (where positive symptoms are present at a low intensity only) and
- undifferentiated type (psychotic symptoms are present but the criteria for paranoid, disorganized, or catatonic types has not been met).
Symptoms may also be described as 'positive symptoms' (those additional to normal experience and behaviour) and negative symptoms (the lack or decline in normal experience or behaviour). 'Positive symptoms' describe psychosis and typically include delusions, hallucinations and thought disorder. 'Negative symptoms' describe inappropriate or nonpresent emotion, poverty of speech, and lack of motivation. In three-factor models of schizophrenia, a third symptom grouping, the so called 'disorganisation syndrome' is also given. This considers thought disorder and related disorganized behaviour to be in a separate symptom cluster from delusions and hallucinations.
Some symptoms, such as social isolation, may be caused or appear to be caused by a reaction of the individual to avoid phychosis or other more severe symptoms that are inconvenient or unbearable. The person may place limits on his environment or on his own behaviour intended to avoid or limit whatever he experiences as causes for these symptoms. These limits or the resulting behaviour may appear strange or inappropriate to other people.
It is worth noting that many of the positive or psychotic symptoms may occur in a variety of disorders and not only in schizophrenia. The psychiatrist Kurt Schneider tried to list the particular forms of psychotic symptoms which he thought were particularly useful in distinguishing between schizophrenia and other disorders which could produce psychosis. These are called first rank symptoms or Schneiderian first rank symptoms and include delusions of being controlled by an external force, the belief that thoughts are being inserted or withdrawn from your conscious mind, the belief that your thoughts are being broadcast to other people and hearing hallucinated voices which comment on your thoughts or actions, or may have a conversation with other hallucinated voices. As with other diagnostic methods, the reliability of 'first rank symptoms' has been questioned4, although they remain in use as diagnostic criteria in many countries.
Diagnostic issues and controversies
It has been argued that the diagnostic approach to schizophrenia is flawed, as it relies on an assumption of a clear dividing line between what is considered to be mental illness (fulfilling the diagnostic criteria) and mental health (not fulfilling the criteria). Recently it has been argued, notably by psychiatrist Jim van Os and psychologist Richard Bentall, that this makes little sense, as studies have shown that psychotic symptoms are present in many people who never become 'ill' in the sense of feeling distressed, becoming disabled in some way or needing medical assistance6.
Of particular concern is that the decision as to whether a symptom is present is a subjective decision by the person making the diagnosis or relies on an incoherent definition (for example, see the entries on delusions and thought disorder for a discussion of this issue). More recently, it has been argued that psychotic symptoms are not a good basis for making a diagnosis of schizophrenia as "psychosis is the 'fever' of mental illness — a serious but nonspecific indicator".5
Perhaps because of these factors, studies examining the diagnosis of schizophrenia have typically shown relatively low, or inconsistent levels of diagnostic reliability. Most famously, David Rosenhan's 1972 study, published as On being sane in insane places, demonstrated that the diagnosis of schizophrenia was (at least at the time) often subjective and unreliable. More recent studies have found agreement between any two psychiatrists when diagnosing schizophrenia tends to reach about 65% at best33. This, and the results of earlier studies of diagnostic reliability (which typically reported even lower levels of agreement) have led some critics to argue that the diagnosis of schizophrenia should be abandoned34.
Proponents have argued for a new approach that would use the presence of specific neurocognitive deficits to make a diagnosis. These often accompany schizophrenia and take the form of a reduction or impairment in basic psychological functions such as memory, attention, executive function and problem solving. It is these sorts of difficulties, rather than the psychotic symptoms (which can in many cases be controlled by antipsychotic medication), which seem to be the cause of most disability in schizophrenia. However, this argument is relatively new and it is unlikely that the method of diagnosing schizophrenia will change radically in the near future.
The diagnostic approach to schizophrenia has also been opposed by the anti-psychiatry movement, who argue that classifying specific thoughts and behaviours as an illness allows social control of people that society finds undesirable but who have committed no crime. They argue that this is a way of unjustly classifying a social problem as a medical one to allow the forcible detention and treatment of people displaying these behaviours, which is something which can be done under mental health legislation in most western countries.
An example of this can be seen in the former Soviet Union, where an additional sub-classification of sluggishly progressing schizophrenia was created. Particularly in the RSFSR (Russian Soviet Federated Socialist Republic) this diagnosis was used for the purpose of silencing political dissidents or forcing them to recant their ideas by the use of forcible confinement and treatment. In 2000 similar concerns about the abuse of psychiatry to unjustly silence and detain members of the Falun Gong movement by the Chinese government led the American Psychiatric Association's Committee on the Abuse of Psychiatry and Psychiatrists to pass a resolution to urge the World Psychiatric Association to investigate the situation in China.
Western psychiatric medicine tends to favour a definition of symptoms that depends on form rather than content (an innovation first argued for by psychiatrists Karl Jaspers and Kurt Schneider). Therefore, you should be able to believe anything, however unusual or socially unacceptable, without being diagnosed delusional, unless your belief is judged to be held in a particular way. In principle, this would stop people being forcibly detained or treated simply for what they believe. However, the distinction between form and content is not easy, or always possible, to make in practice (see delusion). This had led to accusations by anti-psychiatry, surrealist and mental health system survivor groups that psychiatric abuses exist to some extent in the West as well.
Genetic and environmental influences
While the reliability of the schizophrenia diagnosis introduces difficulties in measuring the relative effect of genes and environment (for example, symptoms overlap to some extent with severe bipolar disorder or major depression), there is evidence to suggest that a combination of genetic vulnerability and environmental stressors can act in combination to cause schizophrenia.
The extent to which these factors influence the likelihood of being diagnosed with schizophrenia is debated widely, and currently, controversial. Schizophrenia is likely to be a disorder of complex inheritance (analogous to diabetes or high blood pressure). Thus, it is likely that several genes interact to generate risk for schizophrenia. This, combined with disagreements over which research methods are best, or how data from genetic research should be interpreted, has led to differing estimates over genetic contribution.
Some researchers estimate schizophrenia to be highly heritable (some estimates are as high as 70%). However, genetic evidence for the role of the environment comes from the observation that identical twins do not universally develop schizophrenia. A recent review of the genetic evidence has suggested a 28% chance of one identical twin developing schizophrenia if the other already has it7 (see twin study).
However, the estimates of heritablility of schizophrenia from twin studies varies a great deal, with some notable studies3740 showing rates as low as 11.0 - 13.8% among monozygotic twins, and 1.8 - 4.1% among dizygotic twins.
A recent review of linkage studies, listed seven genes as likely to be involved in the inheritance of schizophrenia or the risk of developing schizophrenia26. Evidence comes from research suggesting multiple chromosomal regions are transmitted to people who are later diagnosed as having schizophrenia. Some family association studies have demonstrated a relationship to a gene known as COMT that is involved in encoding the dopamine catabolic enzyme catechol-O-methyl transferase27. This is particularly interesting because of the known link between dopamine function, psychosis, and schizophrenia.
There is also considerable evidence indicating that stress may trigger episodes of schizophrenia. For example, emotionally turbulent families8 and stressful life events9 have been shown to be risk factors for relapses or triggers for episodes of schizophrenia. Other factors such as poverty and discrimination may also be involved. This may explain why minority communities have much higher rates of schizophrenia than when members of the same ethnic groups are resident in their home country.
One particularly stable and replicable finding has been the association between living in an urban environment and risk of developing schizophrenia, even after factors such as drug use, ethnic group and size of social group have been controlled for29. A recent study of 4.4 million men and women in Sweden found a 68–77% increased risk of psychosis for people living in the most urbanized environments, a significant proportion of which is likely to be accounted for by schizophrenia30.
One curious finding is that people diagnosed with schizophrenia are more likely to have been born in winter or spring32 (at least in the northern hemisphere). However, the effect is not large and it is still not clear why this may occur.
It is also thought that processes in early neurodevelopment are important, particularly during pregnancy. For example, women who were pregnant during the Dutch famine of 1944, where many people were close to starvation, had a higher chance of having a child who would later develop schizophrenia10. Similarly, studies of Finnish mothers who were pregnant when they found out that their husbands had been killed during the Winter War of 1939–1940 have shown that their children were much more likely to develop schizophrenia when compared with mothers who found out about their husbands' death after pregnancy11, suggesting that even psychological trauma in the mother may have an effect.
Some researchers have proposed that environmental influences during childhood also interact with neurobiological risk factors to influence the likelihood of developing schizophrenia later in life. The neurological development of children is considered to be sensitive to features of dysfunctional social settings, such as violence, lack of warmth in personal relationships and hostility. These have all been found to be risk factors for the later development of schizophrenia. It is thought that the effects of the childhood environment, favorable or unfavorable, interact with genetics and the processes of neurodevelopment, with long-term consequences for brain function. This is thought to influence the underlying vulnerability for psychosis later in life, particularly during the adult years46.
In adult life, particular importance has been placed upon the function (or malfunction) of dopamine in the mesolimbic pathway in the brain. This theory, known as the dopamine hypothesis of schizophrenia largely resulted from the accidental finding that a drug group which blocks dopamine function, known as the phenothiazines, reduced psychotic symptoms. These drugs have now been developed further and antipsychotic medication is commonly used as a first line treatment.
However, this theory is now thought to be overly simplistic as a complete explanation. Partly as newer antipsychotic medication (called atypical antipsychotic medication) is equally effective as older medication, but also affects serotonin function and may have slightly less of a dopamine blocking effect. Psychiatrist David Healy has also argued that pharmaceutical companies have promoted certain oversimplified biological theories of mental illness to promote their own sales of biological treatments12.
Much recent research has focused on differences in structure or function in certain brain areas in people diagnosed with schizophrenia.
Early evidence for differences in the neural structure came from the discovery of ventricular enlargement in people diagnosed as schizophrenic, for whom negative symptoms were most prominent35. However, this finding has not proved particularly reliable on the level of the individual person, with considerable variation between patients.
More recent studies have shown a large number of differences in brain structure between people with and without diagnoses of schizophrenia36. However, as with earlier studies, many of these differences are only reliably detected when comparing groups of people, and are unlikely to predict any differences in brain structure of an individual person with schizophrenia.
Studies using neuropsychological tests and brain scanning technologies such as fMRI and PET to examine functional differences in brain activity have shown that differences seem to most commonly occur in the frontal lobes, hippocampus, and temporal lobes13. These differences are heavily linked to the neurocognitive deficits which often occur with schizophrenia, particularly in areas of memory, attention, problem solving, executive function and social cognition.
Incidence and prevalence
Schizophrenia is typically diagnosed in late adolescence or early adulthood. It is found approximately equally in men and women, though the onset tends to be later in women, who also tend to have a better course and outcome.
The lifetime prevalence of schizophrenia is commonly given at 1%; however, a recent review of studies from around the world estimated it to be 0.55%14. The same study also found that prevalence may vary greatly from country to country, despite the received wisdom that schizophrenia occurs at the same rate throughout the world. It is worth noting however, that this may be in part due to differences in the way schizophrenia is diagnosed. The incidence of schizophrenia was given as a range of between 7.5 and 16.3 cases per 100,000 of the population.
Schizophrenia is also a major cause of disability. In a recent 14-country study15, active psychosis was ranked the third most disabling condition after quadriplegia and dementia and before paraplegia and blindness.
The first line treatment for schizophrenia is usually the use of antipsychotic medication. The newer atypical antipsychotic medications (such as clozapine, risperidone, olanzapine, quetiapine, ziprasidone and aripiprazole) are preferred over older typical antipsychotic medications (such as chlorpromazine and haloperidol) due to their favorable side-effect profile. Compared to the typical antipsychotics, the atypicals are associated with a lower incident rate of extrapyramidal side-effects (EPS) and tardive dyskinesia (TD). It is still unclear whether newer drugs reduce the chances of developing the rare but potentially life-threatening neuroleptic malignant syndrome (NMS). While the atypical antipsychotics are associated with less EPS and TD than the conventional antipsychotics, some of the agents in this class (especially olanzapine and clozapine) appear to be associated with metabolic side effects such as weight gain, hyperglycemia and hypertriglyceridemia that must be considered when choosing appropriate pharmacotherapy.
Atypical antipsychotics and typical antipsychotics are generally thought to be equivalent for the treatment of the positive symptoms of schizophrenia. It has been suggested by some researchers that the atypicals have some beneficial effects on negative symptoms and cognitive deficits associated with schizophrenia, although the clinical significance of these effects has yet to be established. However, recent reviews have suggested that typical antipsychotics, when dosed conservatively may have similar effects to atypicals47.
The atypical antipsychotics are much more costly as they are still within patent, whereas the older drugs are available in inexpensive generic forms. Aripiprazole a drug from a new class of antipsychotic drugs (variously named 'dopamine system stabilizers' or 'partial dopamine agonists') has recently been developed and early research suggests that it may be a safe and effective treatment for schizophrenia16.
Hospitalisation may occur with severe episodes. This can be voluntary or (if mental health legislation allows it) involuntary (called civil or involuntary commitment). Mental health legislation may also allow a person to be treated against their will. However, in many countries such legislation does not exist, or does not have the power to enforce involuntary hospitalisation or treatment.
Psychotherapy or other forms of talk therapy may be offered, with cognitive behavioural therapy being the most frequently used. This may focus on the direct reduction of the symptoms, or on related aspects, such as issues of self-esteem, social functioning, and insight. There have been some promising results with cognitive behavioural therapy, but the balance of current evidence is inconclusive17.
A relatively new approach has been the use of cognitive remidation therapy , a technique aimed at remediating the neurocognitive deficits sometimes present in schizophrenia. Based on techniques of neuropsychological rehabilitation, early evidence has shown it to be cognitively effective, with some improvements related to measurable changes in brain activation as measured by fMRI 48.
Other support services may also be available such as drop-in centres, visits from members of a 'community mental health team' and patient-led support groups. In recent years the importance of service-user led recovery based movements has grown substantially throughout Europe and America. Groups such as the Hearing Voices Network and more recently, the Paranoia Network , have developed a self-help approach that aims to provide support and assistance outside of the traditional medical model adopted by mainstream psychiatry. By avoiding framing personal experience in terms of criteria for mental illness or mental health, they aim to destigmatise the experience and encourage individual responsibility and a positive self-image.
In many non-Western societies, schizophrenia may be treated with more informal, community-led methods. A particularly sobering thought for Western psychiatry is that the outcome for people diagnosed as schizophrenic in non-Western countries may actually be much better18 than for people in the West. The reasons for this recently discovered fact are still far from clear, although cross-cultural studies are being conducted to find out why. One important factor may be that many non-Western societies (including intact Native American cultures) are collectivist societies, in that they emphasize working together for the good of other society members. This is in contrast to many Western societies, which can be highly individualistic. Collectivist societies tend to stress the importance of the connectedness of extended family, providing a useful support mechanism for the stress that mental illness plays on both the ill and others around them.
Prognosis for any particular individual affected by schizophrenia is particularly hard to judge as treatment and access to treatment is continually changing as new methods become available and medical recommendations change.
However, retrospective studies have shown that about a third of people make a full recovery, about a third show improvement but not a full recovery, and a third remain ill19.
World Health Organization conducted two long-term follow-up studies involving more than 2,000 people labelled schizophrenic in different countries, and discovered these patients have much better long-term outcomes in poor countries (India, Colombia and Nigeria) than in rich countries (USA, England, Ireland, Denmark, Czechoslovakia, Japan, and Russia)39. This result is contrary to the expectations of biopsychiatrists, because patients in poor countries take much less or no neuroleptic drugs. However, according to Robert Whitaker, patients in rich countries fare worse mainly because, in the long run, the brain overcompensates for the effects of prolonged administration of neuroleptic drugs, leading to contrary than expected results.
There is an extremely high suicide rate associated with schizophrenia. A recent study showed that 30% of patients diagnosed with this condition had attempted suicide at least once during their lifetime20. Another study suggested that 10% of persons with schizophrenia die by suicide21.
Schizophrenia and drug use
Schizophrenia can sometimes be triggered by heavy use of stimulant or hallucinogenic drugs, although some claim that a predisposition towards developing schizophrenia is needed for this to occur. There is also some evidence suggesting that people suffering schizophrenia but responding to treatment can have relapse as a result of subsequent drug use.
Drugs such as methamphetamine, ketamine, PCP and LSD have been used to mimic schizophrenia for research purposes, although this has now fallen out of favour with the scientific research community, as the differences between the drug induced states and the typical presentation of schizophrenia have become clear.
Hallucinogenic drugs were also briefly tested as possible treatments for schizophrenia by psychiatrists such as Humphry Osmond and Abram Hoffer in the 1950s. Ironically, it was mainly for this experimental treatment of schizophrenia that LSD administration was legal, briefly before its use as a recreational drug led to its criminalization.
There is now increasing evidence that cannabis use can be a contributing trigger to developing schizophrenia. The most recent studies suggest that cannabis is neither a sufficient nor necessary factor in developing schizophrenia, but that cannabis may significantly increase the risk of developing schizophrenia and may be, among others, a significant causal factor31.
It has been noted that the majority of people with schizophrenia (estimated between between 75% and 90%) smoke tobacco. However, people diagnosed with schizophrenia have a much lower than average chance of getting and dying from lung cancer. While the reason for this is unknown, it may be because of a genetic resistance to the cancer, a side-effect of drugs being taken, or a statistical effect of increased likelihood of dying from causes other than lung cancer22. It is argued that the increased level of smoking in schizophrenia may be due to a desire to self-medicate with nicotine. A recent study of over 50,000 Swedish conscripts found that there was a small but significant protective effect of smoking cigarettes on the risk of developing schizophrenia later in life.28 Whilst the authors of the study stressed that the risks of smoking far outweigh these minor benefits, this study provides further evidence for the 'self-medication' theory of smoking in schizophrenia and may gives clues as to how schizophrenia might develop at the molecular level.
Schizophrenia and violence
Although schizophrenia is sometimes associated with violence in the media, only a minority of people with schizophrenia become violent, and only minority of people who commit criminal violence have been diagnosed with schizophrenia.
Research has suggested that schizophrenia is associated with a slight increase in risk of violence, although this risk is largely due to a small sub-group of individuals for whom violence is associated with concurrent substance abuse, active delusional beliefs of threat or persecution, and ceasing effective treatment for previous violent behaviour41.
For the most serious acts of violence, long-term independent studies of convicted murders in both New Zealand42 and Sweden43 found that only 8.7 - 8.9% had been given a previous diagnosis of schizophrenia.
Furthermore, research has shown that a person diagnosed with schizophrenia is more likely to be a victim of violence than the perpetrator44.
There is some evidence to suggest that in some people, the drugs used to treat schizophrenia may produce an increased risk for violence, largely due to agitation induced by akathisia, a side effect sometimes associated with antipsychotic medication45. Similarly, abuse experienced in childhood may contribute both to a slight increase in risk for violence in adulthood, as well as the development of schizophrenia46.
Alternative approaches to schizophrenia
An approach broadly known as the anti-psychiatry movement, notably most active in the 1960s has opposed the orthodox medical view of schizophrenia as an illness.
Psychiatrist Thomas Szasz has argued that psychiatric patients are not ill but are just individuals with unconventional thoughts and behaviour that make society uncomfortable. He argues that society seeks to unjustly control such individuals by classifying their behaviour as an illness and forcibly treating them as a method of social control. An important but subtle point is that Szasz has never denied the existence of the phenomena that mainstream psychiatry classifies as an illness (such as delusions, hallucinations or mood changes) but simply does not believe that they are a form of illness.
Similarly, psychiatrist R. D. Laing has argued that the symptoms of what we call mental illness are just reasonable (although perhaps not always obviously comprehensible) reactions to impossible demands that society and particularly family life puts on some individuals. Laing was revolutionary in valuing the content of psychotic experience as worthy of interpretation, rather than considering it simply as a secondary but essentially meaningless marker of underlying psychological or neurological distress.
It is worth noting that neither Szasz nor Laing ever considered themselves to be 'anti-psychiatry' in the sense of being against psychiatric treatment, but simply believed that it should be conducted between consenting adults, rather than imposed upon anyone against their will.
In the 1976 book The Origin of Consciousness in the Breakdown of the Bicameral Mind, psychologist Julian Jaynes proposed that until the beginning of historic times, schizophrenia or a similar condition was the normal state of human consciousness. This would take the form of a "bicameral mind" where a normal state of low affect, suitable for routine activities, would be interrupted in moments of crisis by "mysterious voices" giving instructions, which early people characterized as interventions from the gods. This theory was briefly controversial. Continuing research has failed to either further confirm or refute the thesis.
Psychiatrist Tim Crow has argued that schizophrenia may be the evolutionary price we pay for a left brain hemisphere specialisation for language25. Since psychosis is associated with greater levels of right brain hemisphere activation and a reduction in the usual left brain hemisphere dominance, our language abilities may have evolved at the cost of causing schizophrenia when this system breaks down.
Researchers into shamanism have speculated that in some cultures schizophrenia or related conditions may predispose an individual to becoming a shaman24. Certainly the experience of having access to multiple realities is not uncommon in schizophrenia, and is a core experience in many shamanic traditions. Equally, the shaman may have the skill to bring on and direct some of the altered states of consciousness psychiatrists label as illness. (See anti-psychiatry.)
Alternative medicine tends to hold the view that schizophrenia is primarily caused by imbalances in the body's reserves and absorption of dietary minerals, vitamins, fats, and/or the presence of excessive levels of toxic heavy metals. The body's adverse reactions to gluten are also strongly implicated in some alternative theories (see gluten-free, casein-free diet).
Famous people affected by schizophrenia
Bentall, R. (2003) Madness explained: Psychosis and Human Nature. London: Penguin Books Ltd. ISBN 0713992492
- Green, M.F. (2001) Schizophrenia Revealed: From Neurons to Social Interactions. New York: W.W. Norton. ISBN 0393703347
Torey, E.F. (2001) Surviving Schizophrenia: A Manual for Families, Consumers, and Providers (4th Edition). Quill (HarperCollins Publishers) ISBN 0060959193
Vonnegut, M. The Eden Express. ISBN 0553027557. A personal account of schizophrenia.
- Read, J., Mosher, L.R., Bentall, R. (2004) Models of Madness: Psychological, Social and Biological Approaches to Schizophrenia. ISBN 1583919066. A critical approach to biological and genetic theories, and a review of social influences on schizophrenia.
Keen, T. M. (1999) Schizophrenia: orthodoxy and heresies. A review of alternative possibilities. Journal of Psychiatric and Mental Health Nursing, 1999, 6, 415-424. PDF. An article reviewing the dominant (orthodox) and alternative (heretical) theories, hypothesis and beliefs about schizophrenia.
1 Evans, K., McGrath, J., & Milns, R. (2003) Searching for schizophrenia in ancient Greek and Roman literature: a systematic review. Acta Psychiatrica Scandanavica, 107(5), 323–330.
2 Kraepelin, E. (1907) Text book of psychiatry (7th ed) (trans. A.R. Diefendorf). London: Macmillan.
3Turner, T. (1999) 'Schizophrenia'. In G.E. Berrios and R. Porter (eds) A History of Clinical Psychiatry. London: Athlone Press. ISBN 0485242117
4Bertelsen, A. (2002) Schizophrenia and Related Disorders: Experience with Current Diagnostic Systems. Psychopathology, 35, 89–93.
5Tsuang, M. T., Stone, W. S., & Faraone, S. V. (2000) Toward reformulating the diagnosis of schizophrenia. American Journal of Psychiatry, 157(7), 1041–1050.
6Verdoux, H., & van Os, J. (2002) Psychotic symptoms in non-clinical populations and the continuum of psychosis. Schizophr Res, 54(1–2), 59–65.
7Torrey, E.F., Bowler, A.E., Taylor, E.H. & Gottesman, I.I (1994) Schizophrenia and manic depressive disorder. New York: Basic books. ISBN 0465072852
8Bebbington, P., Kuipers, L. (1994) The predictive utility of expressed emotion in schizophrenia: an aggregate analysis. Psychological Medicine, 24 (3),707–18.
9Day R, Nielsen JA, Korten A, Ernberg G, Dube KC, Gebhart J, Jablensky A, Leon C, Marsella A, Olatawura M et al (1987). Stressful life events preceding the acute onset of schizophrenia: a cross-national study from the World Health Organization. Culture, Medicine and Psychiatry, 11 (2), 123–205
10Susser E, Neugebauer R, Hoek HW, Brown AS, Lin S, Labovitz D, Gorman JM (1996) Schizophrenia after prenatal famine. Further evidence. Archives of General Psychiatry, 53(1), 25–31.
11Huttunen MO, Niskanen P. (1978) Prenatal loss of father and psychiatric disorders. Archives of General Psychiatry, 35(4), 429–31.
12Healy, D. (2002) The Creation of Psychopharmacology. Cambridge, MA: Harvard University Press. ISBN 0674006194
13Green, M.F. (2001) Schizophrenia Revealed: From Neurons to Social Interactions. New York: W.W. Norton. ISBN 0393703347
14Goldner EM, Hsu L, Waraich P, Somers JM (2002) Prevalence and incidence studies of schizophrenic disorders: a systematic review of the literature. Canadian Journal of Psychiatry, 47(9), 833–43.
15Üstün TB, Rehm J, Chatterji S, Saxena S, Trotter R, Room R, Bickenbach J, and the WHO/NIH Joint Project CAR Study Group (1999). Multiple-informant ranking of the disabling effects of different health conditions in 14 countries. Lancet, 354(9173), 111–115.
16Potkin SG, Saha AR, Kujawa MJ, Carson WH, Ali M, Stock E, Stringfellow J, Ingenito G, Marder SR (2003) Aripiprazole, an Antipsychotic With a Novel Mechanism of Action, and Risperidone vs Placebo in Patients With Schizophrenia and Schizoaffective Disorder. Archives of General Psychiatry, 60(7), 681–90.
17Cormac I, Jones C, Campbell C. (2002) Cognitive behaviour therapy for schizophrenia. Cochrane Database of Systematic Reviews, (1), CD000524.
18Kulhara P. (1994) Outcome of schizophrenia: some transcultural observations with particular reference to developing countries. European Archives of Psychiatry and Clinical Neuroscience, 244(5), 227–35.
19Harding CM, Brooks GW, Ashikaga T, Strauss JS, Breier A. (1987) The Vermont longitudinal study of persons with severe mental illness, II: Long-term outcome of subjects who retrospectively met DSM-III criteria for schizophrenia. American Journal of Psychiatry, 144(6), 727–35.
20Radomsky ED, Haas GL, Mann JJ, Sweeney JA (1999) Suicidal behavior in patients with schizophrenia and other psychotic disorders. American Journal of Psychiatry, 156(10), 1590–5.
21Caldwell CB, Gottesman II. (1990) Schizophrenics kill themselves too: a review of risk factors for suicide. Schizophrenia Bulletin, 16(4), 571–89.
22"Conditions in Occupational Therapy: effect on occupational performance." ed. Ruth A. Hansen and Ben Atchison (Baltimore: Lippincott Williams & Williams, 2000), 54–74. ISBN 0-683-30417-8
23Psychiatrie. 8. Aufl., Bd. 1: Allgemeine Psychiatrie; Bd. 11: Klinische Psychiatrie, 1. Teil. Barth, Leipzig 1909. Bd. 111, 1913; Bd. IV, 1915. (Translation of section on the disease from the German)
24Polimeni J, Reiss JP. (2002) How shamanism and group selection may reveal the origins of schizophrenia. Medical Hypothesis, 58(3), 244–8.
25Crow, T. J. (1997) Schizophrenia as failure of hemispheric dominance for language. Trends in Neuroscience, 20(8), 339–343.
26Harrison PJ, Owen MJ. (2003) Genes for schizophrenia? Recent findings and their pathophysiological implications. Lancet, 361(9355), 417–9.
27Shifman S, Bronstein M, Sternfeld M, Pisante-Shalom A, Lev-Lehman E, Weizman A, Reznik I, Spivak B, Grisaru N, Karp L, Schiffer R, Kotler M, Strous RD, Swartz-Vanetik M, Knobler HY, Shinar E, Beckmann JS, Yakir B, Risch N, Zak NB, Darvasi A (2002) A highly significant association between a COMT haplotype and schizophrenia. American Journal of Human Genetics, 71(6), 1296–302.
28Zammit S, Allebeck P, Dalman C, Lundberg I, Hemmingsson T, Lewis (2003) Investigating the association between cigarette smoking and schizophrenia in a cohort study. American Journal of Psychiatry, 160 (12), 2216–21.
29Van Os J. (2004) Does the urban environment cause psychosis? British Journal of Psychiatry, 184 (4), 287–288.
30Sundquist K, Frank G, Sundquist J. (2004) Urbanisation and incidence of psychosis and depression: Follow-up study of 4.4 million women and men in Sweden. British Journal of Psychiatry, 184 (4), 293–298.
31Arseneault L, Cannon M, Witton J, Murray RM. (2004) Causal association between cannabis and psychosis: examination of the evidence. British Journal of Psychiatry, 184, 110–7.
32Davies G, Welham J, Chant D, Torrey EF, McGrath J. (2003) A systematic review and meta-analysis of Northern Hemisphere season of birth studies in schizophrenia. Schizophrenia Bulletin, 29 (3), 587–93.
33McGorry PD, Mihalopoulos C, Henry L, Dakis J, Jackson HJ, Flaum M, Harrigan S, McKenzie D, Kulkarni J, Karoly R. (1995) Spurious precision: procedural validity of diagnostic assessment in psychotic disorders. American Journal of Psychiatry, 152 (2), 220–3.
34Read, J. (2004) Does 'schizophrenia' exist ? Reliability and validity. In J. Read, L.R. Mosher, R.P. Bentall (eds) Models of Madness: Psychological, Social and Biological Approaches to Schizophrenia. ISBN 1583919066
35Johnstone EC, Crow TJ, Frith CD, Husband J, Kreel L. (1976) Cerebral ventricular size and cognitive impairment in chronic schizophrenia. Lancet, 30;2 (7992), 924-6.
36Flashman LA, Green MF (2004) Review of cognition and brain structure in schizophrenia: profiles, longitudinal course, and effects of treatment. Psychiatric Clinics of North America, 27 (1), 1-18, vii.
37Koskenvuo M, Langinvainio H, Kaprio J, Lonnqvist J, Tienari P (1984) Psychiatric hospitalization in twins. Acta Genet Med Gemellol (Roma), 33(2),321-32.
38Meyer-Lindenberg A, Miletich RS, Kohn PD, Esposito G, Carson RE, Quarantelli M, Weinberger DR, Berman KF (2002) Reduced prefrontal activity predicts exaggerated striatal dopaminergic function in schizophrenia. Nature Neuroscience, 5, 267-71.
39Whitaker, R. (2001) "Mad in America: Bad Science, Bad Medicine, and the Enduring Mistreatment of the Mentally Ill". Perseus Publishing. ISBN 0738203858.
40Hoeffer A, Pollin W. (1970) Schizophrenia in the NAS-NRC panel of 15,909 veteran twin pairs. Archives of General Psychiatry, 1970 Nov; 23(5):469-77.
41Walsh E, Gilvarry C, Samele C, Harvey K, Manley C, Tattan T, Tyrer P, Creed F, Murray R, Fahy T (2004) Predicting violence in schizophrenia: a prospective study. Schizophrenia Research, 67(2-3), 247-52.
42Simpson AI, McKenna B, Moskowitz A, Skipworth J, Barry-Walsh J. (2004) Homicide and mental illness in New Zealand, 1970-2000. British Journal of Psychiatry, 185, 394-8.
43Fazel S, Grann M. (2004) Psychiatric morbidity among homicide offenders: a Swedish population study. American Journal of Psychiatry, 161(11), 2129-31.
44Fitzgerald PB, de Castella AR, Filia KM, Filia SL, Benitez J, Kulkarni J. (2005) Victimization of patients with schizophrenia and related disorders. Australia and New Zealand Journal of Psychiatry, 39(3), 169-74.
45Leong GB, Silva JA. (2003) Neuroleptic-induced akathisia and violence: a review. Journal of Forensic Science, 48 (1), 187-9.
46 Harriet L. MacMillan, Jan E. Fleming, David L. Streiner, Elizabeth Lin, Michael H. Boyle, Ellen Jamieson, Eric K. Duku, Christine A. Walsh, Maria Y.-Y. Wong, William R. Beardslee. (2001) Childhood Abuse and Lifetime Psychopathology in a Community Sample. American Journal of Psychiatry,158, 1878-83.
47 Leucht S, Wahlbeck K, Hamann J, Kissling W. (2003) New generation antipsychotics versus low-potency conventional antipsychotics: a systematic review and meta-analysis. Lancet, 361(9369), 1581-9.
48 Wykes T, Brammer M, Mellers J, Bray P, Reeder C, Williams C, Corner J. (2002) Effects on the brain of a psychological treatment: cognitive remediation therapy: functional magnetic resonance imaging in schizophrenia. British Journal of Psychiatry, 181, 144-52.
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- ADHD is a clinical diagnosis requiring evaluation of behavior across multiple settings (eg, family, academic, social). There is no laboratory “test” for ADHD.
- ADHD is a chronic condition that may persist into adulthood, extends across developmental phases, and presents different challenges during each phase.
- Clinician interviews and rating scales of parents/caregiver/teachers are the core of ADHD assessment process.
- Therapeutic alliance with patient/parents/caregiver/teachers is crucial to treatment planning/implementation.
- Important role of educational system in patient treatment/monitoring distinguishes ADHD from many other chronic conditions.
- Key to effective long-term management of patient with ADHD is continuity of care with a clinician experienced in treatment of ADHD.
- Treatment plans should:
- Be individualized
- Consider patient strengths and target symptoms identified in assessment process
- Include psychoeducation of parents and patient about ADHD
- Provide periodic, systematized follow-up focused on targeted outcomes and adverse effects based on input from parents, teachers, and patient
- Anticipate long-term therapeutic planning and monitoring
- Treatment goals should be realistic, attainable, and measurable:
- Improved relationships with parents, siblings, teachers, peers
- Decreased disruptive/setting-inappropriate behaviors
- Improved academic performance
- Increased independence by self-monitoring and completion of assigned activities
- Improved self-esteem
- Decision to treat with medication should be based on persistent target symptoms sufficiently severe to cause functional impairment in home, school, work, or peer-related activities, on continuing efficacy of medication, and on family/parent preference.
- Patients treated pharmacologically should have their height and weight monitored throughout treatment.
- Limitations in pharmacologic and behavioral treatments arise from lack of maintenance if treatment discontinued and/or failure in settings where treatment has not been well applied.
- Medication should be reinstituted when target symptoms re-emerge if medication is discontinued and when ratio of therapeutic benefit to side effects is acceptable.
- Psychosocial treatments may be useful for ADHD with comorbid disorders or other problems responsive to such nonmedication treatments.
Diagnosis and Assessment of Disease
Table 1. Five Criteria for ADHD
|2. Some inattention or hyperactivity-impulsivity to be consistent symptoms causing impairment present before age 7|
|3. Some impairment from symptoms present in 2 or more settings (eg, home, school/work, sociala)|
|4. Clear evidence of clinically significant impairment in social, academic, or occupational functioning|
|5. Symptoms do not occur exclusively during course of a pervasive developmental disorder, schizophrenia, or psychotic disorder and are not better accounted for by another mental disorder|
(eg, mood disorder, anxiety disorder, dissociative disorder, personality disorder)
|Types of ADHD|
|ADHD, Combined Type: Criteria for inattention AND hyperactivity-impulsivity met for past 6 mo (DSM-IV code 314.01; ICD-10 code F90.0)|
|ADHD, Predominantly Inattentive Type: Criteria for inattention met but criteria for hyperactivity-impulsivity NOT met for past 6 mo (DSM-IV code 314.00; ICD-10 code F98.8)|
|ADHD, Predominantly Hyperactive-Impulsive Type: Criteria for hyperactivity-impulsivity met but criteria for inattention NOT met for past 6 mo (DSM-IV code 314.01; ICD-10 code F90.0)|
|a Clinical consensus is that severe impairment in one setting can warrant treatment for ADHD (eg, inordinate amount of time after school completing schoolwork not done in class).|
Table 2. Behavior Rating Scales Commonly Used in Assessment of ADHD and Monitoring of Treatment
|Academic Performance Rating Scale (APRS)|
|19-item scale for determining child’s academic productivity and accuracy in grades 1-6 with|
6 scale points, construct, concurrent, and discriminant validity data, as well as norms (n = 247)
|ADHD Rating Scale-IV|
|18-item scale using DSM-IV criteria|
|Brown ADD Rating Scales for Children, Adolescents, and Adults (BADDS)|
|Assess wide range of symptoms of ADHD executive function impairments in children, adolescents, and adults|
|Child Behavior Checklist (CBCL)|
|Parent-completed CBCL and teacher-completed Teacher Report Form (TRF)|
|Conners Parent Rating Scale-Revised (CPRS-R)|
Conners Teacher Rating Scale-Revised (CTRS-R)
Conners Wells Adolescent Self-Report Scale
|Longer form should be used for initial assessment|
Shorter form often used for assessing response to treatment, particularly when repeated administration required
Parent and adolescent self-report versions available
|Home Situations Questionnaire-Revised (HSQ-R)|
School Situations Questionnaire-Revised (SSQ-R)
|14-item scale designed to assess specific problems with attention and concentration across a variety of home and public situations, using a 0-9 scale; has test-retest, internal consistency, construct validity, discriminant validity, concurrent validity, and norms (n = 581)|
|Inattention/Overactivity With Aggression (IOWA)|
Conners Teacher Rating Scale
|10-item scale developed to separate inattention and overactivity ratings from oppositional defiance|
|Swanson, Nolan, and Pelham (SNAP-IV) Scale DSM diagnoses|
|10-item scale (6 deportment and 4 attention items) measuring impairment of functioning at home and at school|
|Swanson, Kotkin, Agler, M/Flynn, and Pelham (SKAMP) Scale|
|26-item scale containing DSM-IV criteria for ADHD and screens for other disorders|
|Vanderbilt ADHD Diagnostic Rating Scale|
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Acute – occurring over a short time, usually minutes to hours.
Acute Effect - an adverse effect on any living organism when severe symptoms develop rapidly. Symptoms often disappear or diminish after exposure stops. The term ‘acute’ may also refer to exposure and toxicity.
Acute Exposure – either one or a series of several short-term exposures (or doses) generally lasting less than 24 hours.
Acute Myocardial Infarction (AMI) - heart attack.
Adverse Birth Outcome(s) - Examples of adverse birth outcomes include pre-term births, low birth weight, congenital abnormalities, miscarriage, or neurodevelopmental defects. Adverse birth outcomes may be the result of harmful environmental exposures to the mother and father, prior to and during the pregnancy, as well as from other sources.
Age-Adjusted Rates - a measure that controls for the effects of age differences on health event rates. When comparing across geographic areas, some method of age-adjusting is typically used to control for the influence that different population age distributions might have on health event rates. Age-adjustment may also be used to control for age effects when comparing across several years of data, as the age distribution of the population changes over time.
Age-Specific Rate - a crude rate limited to a particular age group. The numerator is the number of cases or events in that age group; the denominator is the total number of persons in that age group in the population of interest.
Agency for Toxic Substances and Disease Registry (ATSDR) - a federal public health agency of the U.S. Department of Health and Human Services. For more information, visit the ATSDR web site.
Air Quality Index (AQI) - The Environmental Protection Agency (EPA) designed the AQI for reporting daily air quality with regard to five major air pollutants: ground-level ozone, particulate matter, sulfur dioxide, carbon monoxide and nitrogen dioxide. The AQI reports how clean or polluted the air is and whether air quality at a given time poses a risk to health. For additional information about the AQI, visit the AIRNow web site.
Air Quality System (AQS) - a database which contains ambient air pollution data collected by the U.S. EPA and by state, local, and tribal air pollution control agencies.
Air Toxic (also referred to as hazardous air pollutant or toxic air pollutant) - any air pollutant that is likely to cause serious or irreversible long-term health effects in humans. Air toxics may cause cancer, developmental effects, reproductive problems, neurological disorders, and genetic mutations. They include pollutants for which a national ambient air quality standard does not exist.
Ambient Air - any unconfined portion of the atmosphere: outdoor air.
Analyte – a substance measured in the laboratory. A chemical for which a sample (such as water, air, or blood) is tested in a laboratory.
Aquifers - underground geological formations, or groups of formations, that can store or transmit water. Aquifers are sources of groundwater for wells and springs. Common use of the term normally refers to water-bearing formations capable of yielding enough water to provide a usable supply.
Arithmetic Mean (or simply mean) – an average of all values within a dataset.
Arsenic - a naturally occurring element widely distributed in the earth's crust. In the environment, arsenic is combined with oxygen, chlorine, and sulfur to form inorganic arsenic compounds. Arsenic in animals and plants combines with carbon and hydrogen to form organic arsenic compounds. Inorganic arsenic compounds are mainly used to preserve wood. Organic arsenic compounds are used as pesticides, primarily on cotton plants.
Asthma - a serious, chronic lung disease that causes the airways (bronchial tubes) to become narrow and makes it hard to breathe. Asthma attacks are often caused by environmental triggers, such as molds, dust mites, and tobacco smoke.
Average Annual Count - an average (calculated as the mean), over a multi-year period, of the counts seen each year during that period.
Average Annual Rate – an average (calculated as the mean), over a multi-year period, of the rates or proportions seen each year during that period.
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Background Level – a concentration (of chemicals) that is present in the environment either due to natural occurrence or from man-made sources.
Behavioral Risk Factor Surveillance System (BRFSS) - the largest, continuously conducted, telephone health survey in the world. It enables the Center for Disease Control (CDC), state health departments, and other health agencies to monitor modifiable risk factors for chronic diseases and other leading causes of death. For more information, visit the CDC’s BRFSS web site.
Birth Defects - an abnormal condition that occurs before or at the time of birth. Birth defects include a wide range of abnormalities with varying levels of impact. Examples of birth defects include spina bifida, cleft palate, upper and lower limb deformities.
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Cancer - any one of a group of diseases that occur when cells in the body become abnormal and grow or multiply out of control.
Carbon Monoxide (CO) - a toxic gas that you cannot smell or see. CO is given off whenever fuel or other materials are burned. Breathing high levels of CO can cause severe illness or death in a matter of minutes.
Carbon Monoxide Poisoning - a disease that affects the amount of oxygen getting to the brain and vital organs. As CO gas is inhaled, it readily displaces oxygen in the blood, leading to headache, dizziness, nausea, and at high concentrations, people can become unconscious or die.
Carcinogens - substances, including radionuclides or radiation, that are directly involved in the initiation or promotion of cancer.
Cardiovascular Disease - refers to a group of diseases and conditions affecting the heart and blood vessels, with heart attack and stroke occurring most frequently. Congestive heart failure, hypertension (also known as high blood pressure), and disease of the arteries, veins, and circulatory system are the other diseases and conditions included in the term cardiovascular disease.
Cell Suppression - a statistical method used to report aggregate health data in tables that restricts or suppresses the release of aggregate health data in order to protect the identity and privacy of individuals and to avoid the risk of identification of individuals in small population groups. One type of cell suppression rule is to not release numbers or rates when the number of events (e.g., number of cancer cases among females in a community) is less than 6 and the population (e.g., number of females in the community) is less than 1,200. A cell suppression rule applies only to confidential health data and not data otherwise available to the public, such as air pollution data.
Census - a procedure of systematically acquiring and recording information about the members of a given population. A census of the U.S. population is taken every ten years in order to apportion the number of members of the United States House of Representatives among the several states. Census statistics are also used to apportion federal funding for many social and economic programs. For more information, visit the U.S. Census Bureau web site.
Census Block - the smallest geographic entity for which the U.S. Census Bureau tabulates decennial census data. Many blocks correspond to city blocks bounded by streets, but blocks in rural areas may include several square miles and have some boundaries that are not streets.
Census Block Group - a unit of U.S. census geography that is a combination of census blocks. A block group is the smallest unit for which the U.S. Census Bureau reports a full range of demographic statistics. There are about 700 residents per block group. A block group is a subdivision of a census tract.
Census Tract - a small, statistical subdivision of a county that usually includes approximately 4,000 inhabitants, but which may include from 2,500 to 8,000 inhabitants. A census tract is designed to encompass a population with relatively uniform economic status, living conditions, and some demographic characteristics. Tract boundaries normally follow physical features, but may also follow administrative boundaries or other non-physical features. A census tract is a combination of census block groups.
Center for Health Statistics (CHS) at the New Jersey Department of Health - The Center for Health Statistics (CHS) collects, researches, analyzes and disseminates New Jersey health data and information and serves as a resource to the Department in development of health data policy. For more information, visit the Department’s Center for Health Statistics web site.
Centers for Disease Control and Prevention (CDC) – a federal public health agency, part of Department of Health & Human Services. For more information, visit the the CDC web site.
Childhood Lead Poisoning Prevention Program (CLPPP) - The CLPPP was established for the prevention, screening, diagnosis, and treatment of lead poisoning, including the elimination of sources of poisoning through research and educational, epidemiologic, and clinical activities as may be necessary. CLPPP provides a range of both primary and secondary prevention services to the children of New Jersey, their families and others with an interest in the prevention of lead poisoning.
Chronic Effect - an adverse effect on an organism in which symptoms recur frequently or develop slowly over a long period of time. The term “chronic” can also apply to exposure and toxicity. The term is usually applied to a condition spanning several weeks, months or years.
Community Water System (CWS) – a public water system that serves year-round community residents (at least 25 people or at least 15 service connections).
Concentration - the relative amount of a substance mixed with another substance. Examples are "five parts per million (ppm) of carbon monoxide in air" or "1 milligram per liter (mg/L) of lead in water".
Confidence Interval (CI) - used to account for the difference between a sample from a population and the population itself. They can also be used to account for uncertainty that arises from natural variation. Confidence intervals provide a means of assessing and reporting the precision of a point estimate, such as a hospitalization rate. A CI is a range around a measurement conveying the amount of precision. In general, the wider the range, the less precise the number.
Contaminant – a substance that is either present in an environment where it does not belong or is present at levels that might cause adverse health effects.
Contamination - presence of contaminants in the air, water or soil.
Correlation – a relationship that results when a change in one variable is consistently associated with change in another variable.
Criteria Pollutants - EPA uses six "criteria pollutants" as indicators of air quality, and has established for each of them a maximum concentration above which adverse effects on human health may occur. These six pollutants are: Ozone, Nitrogen Dioxide, Sulfur Dioxide, Particulate Matter (less than 10 microns), Lead, and Carbon Monoxide.
Crude Rate - the number of events (such as deaths) in a specified time period divided by the number of people at risk of these events (typically, a state or county population) in that period. This figure is generally multiplied by a constant such as 1,000 or 100,000 to get a number that is easy to read and compare, and thus, the rate is reported as “per 1,000” or “per 100,000.” A rate per 100 is the same as a percent. Crude rates adjust for differences in population size but not differences in population characteristics, such as age.
Cumulative exposure - the sum of exposures of an organism to a chemical over a period of time.
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Deciliter – one-tenth, , of a liter; (approximately 3 ounces).
Denominator - the lower portion of a fraction used to calculate a rate or ratio.
Detection limit - the lowest concentration of a chemical that can reliably be distinguished from a zero concentration.
Disease Rate – a measure of how frequently a disease occurs in a population.
Disinfection Byproducts (DBP) -Disinfection byproducts, or DBPs, result when disinfectants like chlorine combine with organic matter. Disinfectants are added to drinking water to kill or inactivate harmful organisms that cause various diseases. The most common DBPs formed when chlorine is used are trihalomethanes (THMs), and haloacetic acids (HAAs).
Dose - amount of a substance to which a person is exposed over some time period.
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Emission – pollution discharged into the atmosphere from smokestacks, other vents and surface areas of commercial or industrial facilities, from residential chimneys and from motor vehicle, locomotive, ship or aircraft exhaust.
Environment - air, water, soil, and food and the contaminants found within them
Environmental Contaminant - a pollutant in the environment.
Environmental Hazard - any condition or situation in the environment which poses a threat.
Environmental Justice - the pursuit of equal and fair access to a healthy environment; equal enforcement of environmental regulations; and a movement to protect low-income communities and communities of color from environmental hazards.
Environmental Protection Agency (EPA) – a federal environmental agency. Founded in 1970, EPA's mission is to protect human health and to safeguard the natural environment-air, water, and land-upon which life depends. EPA provides leadership in the nation's environmental science, research, education, and assessment efforts. EPA works closely with other federal agencies, state and local governments, and Indian tribes to develop and enforce regulations under existing environmental laws. EPA is responsible for researching and setting national standards for a variety of environmental programs and delegates to states and tribes responsible for issuing permits and monitoring and enforcing compliance. Where national standards are not met, EPA can issue sanctions and take other steps to assist the states and tribes in reaching the desired levels of environmental quality. The agency also works with industries and all levels of government in a wide variety of voluntary pollution prevention programs and energy conservation efforts. EPA is an active partner in CDC's National Environmental Public Health Tracking Network initiative through the Memorandum of Understanding with the Department of Health and Human Services. For more information about the U.S. EPA, visit the agency web site.
Environmental Public Health Tracking (EPHT) - refers to ongoing collection, integration, analysis, interpretation, and dissemination of data from environmental hazard monitoring and human exposure or health effects surveillance.
Environmental Public Health Tracking Network (EPHTN) - The Centers for Disease Control and Prevention (CDC), in conjunction with grantee states, have developed a national Environmental Public Health Tracking (EPHT) Network. The national network integrates and standardizes data and information from various monitoring and surveillance systems at the federal, state and local levels. For more information, For more information, visit the national EPHT network web site.
Epidemiology - the study of the distribution and determinants of health-related states or events in specified populations, and the application of this study to the control of health problems.
Ethnicity - often used synonymously with ancestry and includes concepts of culture, language, and national origin. Ethnic groups are often multiracial. In terms of health statistics, "ethnicity:" refers to whether or not an individual is Hispanic.
Exposed (exposed group) – often used to connote a group whose members have been in contact with a supposed cause of a disease state or health state of interest.
Exposure – contact of an organism with a chemical or physical agent at a specific concentration for a specific time period.
Exposure Assessment – a measurement or estimation of the magnitude, frequency, duration and route of exposure to a substance for a population of interest.
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Fine Particulate Matter – a reference to particles <2.5 µm in diameter, also denoted as PM2.5
Frequency - the number of times an event occurs within a stated period of time.
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Geographic Information System (GIS) - a mapping system that uses computers to collect, store, manipulate, analyze, and display data. For example, GIS can show the concentration of a contaminant within a community in relation to points of reference such as streets and homes.
Geometric Mean – a measure of central tendency only calculable for positive values. It is calculated by taking the logarithms of all values within a dataset, calculating their arithmetic mean, and then taking the antilogarithm of the resultant.
Groundwater - water beneath the earth's surface in the spaces between soil particles and between rock surfaces
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Haloacetic acids (HAA5) - byproducts resulting from the disinfection of public water supplies. Haloacetic acids (five) is the sum of the concentrations of mono-, di-, and trichloroacetic acids and mono- and dibromoacetic acids.
Health Insurance Portability and Accountability Act (HIPAA) - The Administrative Simplification provisions of the Health Insurance Portability and Accountability Act of 1996 (HIPAA) are intended to reduce the costs and administrative burdens of health care by making possible the standardized, electronic transmission of many administrative and financial transactions that are currently carried out manually on paper. For more information, visit the U.S. Department of Health and Human Services HIPAA web site.
Health Outcome (also known as health effect) - a disease or health condition measured or observed in a population or an individual.
Human Carcinogen – a compound for which sufficient evidence exists in epidemiological studies to support a causal association between exposure and cancer.
Hydrocarbon - a chemical compound consisting only of hydrogen and carbon. Hydrocarbons, which occur naturally in petroleum, natural gas, coal, and wood, are often used as fuels. They are emitted into the air when the fuel does not burn or burns only partially. Hydrocarbons react in the presence of nitrogen oxides and sunlight to form ground-level ozone, a major component of smog. The most commonly tracked hydrocarbons are volatile organic compounds (VOCs).
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ICD-9 - International Classification of Disease, 9th revision; a numbered system for classifying diseases and health conditions that is published by the World Health Organization and used as an international standard for epidemiological and health management purposes.
ICD-10 - International Classification of Disease, 10th revision; published in 1990 as an updated version of ICD-9.
Incidence Rate - the frequency with which new cases of illness occur in a population over a specified period of time. This rate is computed as the number of new cases of a disease occurring in a period of time (numerator) divided by the size of the population at risk of becoming a case during that period of time (denominator). The result is often multiplied by a base number, such as 1,000 or 100,000, so that the resulting rate is the number of new cases of that disease per 100,000 people, which can then be compared.
Incidence Rate, Age Adjusted - an incidence rate that controls for the effects of differences in population age distributions. When comparing across geographic areas, some method of age-adjusting is typically used to control for the influence that different population age distributions might have on health event rates. Direct age-adjustment (or age standardization) is the same as calculating a weighted average. It weights the age-specific rates observed in a population of
interest by the proportion of each age group in a standard population.
Indicator – a factor that identifies and communicates a system's status. An environmental public health indicator (EPHI) provides information about a population's health status with respect to environmental factors. It can be used to assess health or a factor associated with health (i.e., risk factor, intervention) in a specified population through direct or indirect measures.
Indoor Air Pollution - air pollutants that occur within buildings or other enclosed spaces, as opposed to those occurring in outdoor or ambient air. Some examples of indoor air pollutants are nitrogen oxides, smoke, asbestos, formaldehyde, and carbon monoxide.
Infant Mortality - death of a child younger than one year of age. These deaths are often divided into two groupings: neonatal mortality (death of an infant within the first 27 days of life) and postneonatal mortality (death of an infant 28 – 364 days old).
Infant Mortality Rate - the number of children in a population who die before their first birthday divided by the number of live births in that population during the same time period.
Inhalable particles – all dust capable of entering the human respiratory tract.
In situ (cancer) - a tumor that fulfills all microscopic criteria for malignancy but does not invade or penetrate surrounding tissue.
Inspirable Particle – a particle capable of entering the respiratory tract through the nose or mouth and provides a source of absorption into the body.
International Classification of Diseases (ICD) – diagnostic codes; developed and maintained by the World Health Organization (WHO) to classify diseases and signs, symptoms, abnormal findings, complaints, social circumstances and external causes of injury or disease. Usually referred to by version, as in ICD-9 or ICD-10. For more information, visit the U.S. Centers for Disease Control and Prevention web site.
Invasive (cancer) - malignant cancers that have spread from their point of origin when initially diagnosed.
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Lead (elemental symbol Pb) – a metal formed in the earth’s crust, and can be found in all parts of our environment—water, air, and soil.
Leukemia - cancer of the blood or bone marrow, characterized by an abnormal proliferation (production by multiplication) of blood cells, usually white blood cells. Leukemia is a broad term covering a spectrum of diseases.
Low Birth Weight - A baby is born with low birth weight when its weight is less than 2500 grams (approximately 5.5 pounds) at birth.
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Maximum Contaminant Level (MCL) - an enforceable regulation that the EPA considers practically and feasibly attainable. In many cases, such as those regarding water systems, the MCL is equivalent to the MCLG (see below), because the EPA believes that the water system can provide this level of protection. For carcinogenic contaminants, however, the EPA realizes that it is most likely impossible to completely eliminate the contaminant and does not set an MCL at "zero." Rather, the EPA sets a level that can be attained, given available technology and resources.
Maximum Contaminant Level Goal (MCLG) - an MCLG indicates the ideal level of protection that can be provided against any adverse health effects that may be experienced after exposure to a given contaminant through drinking water.
Measure - a quantitative measurement indicating the magnitude of an indicator that can be used for comparison.
Median – the middle value of a distribution above and below which lie an equal number of individual values; a midpoint.
Metadata - data about data that describes the content, quality, and context of a dataset and provides links to additional information such as quality assurance documents and data dictionaries.
mg/L - milligrams per Liter.
Microbiologicals (or microorganisms) - refers to microscopic organisms.
Microenvironments - well-defined surroundings such as the home, office, or kitchen that can be treated as uniform in terms of stressor (contaminant) concentration.
Microgram (µg) - one millionth, , of a gram (about 3.53 x 10-8 ounces).
Micrometer (µm) (also referred to as micron) – one millionth, , of a meter (about 3.94 x 10-5 inches).
Mobile Source – a source of air pollution that moves, such as automobiles, motorcycles, trucks, off-road vehicles, boats and airplanes.
Morbidity - the occurrence of a disease or condition that alters health and quality of life; often measured as incidence or prevalence rates.
Mortality - a fatal outcome; death.
Mortality Rate - the number of deaths in a specific population during a specific period of time divided by the size of the population during that period of time. The result is often multiplied by a base number, such as 1,000 or 100,000.
Multimedia Exposure – exposure to a toxic substance from multiple pathways such as air, water, soil, food, and breast milk.
Myocardial Infarction (MI) – (also termed AMI for acute myocardial infarction, and commonly called heart attack); occurs when blood flow to a section of heart muscle becomes blocked.
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National Ambient Air Quality Standards (NAAQS) – federal air quality standards. The EPA established National Ambient Air Quality standards for six “criteria” pollutants commonly found in outdoor air. EPA calls these pollutants "criteria" air pollutants because it regulates them by developing human health-based and/or environmentally-based criteria (science-based guidelines) for setting permissible levels. For more information about NAAQS, visit the U.S. EPA web site.
National Cancer Institute (NCI) – a federal agency, part of the National Institute of Health (NIH). For more information, visit the NCI web site.
National Center for Environmental Health (NCEH) – a federal environmental public health agency, part of the Centers for Disease Control and Prevention. For more information, visit the NCEH web site.
National Center for Health Statistics (NCHS) – a federal statistical agency for health data, part of the Centers for Disease Control and Prevention. For more information, visit the NCHS web site.
National Institutes of Health (NIH) - a federal agency, part of the Department of Health & Human Services. For more information, visit the NIH web site.
Natural Sources – non-manmade emission sources, including biological and geological sources, wildfires, and windblown dust.
Neonatal Mortality - death in the first 28 days of life. The leading causes of neonatal deaths are birth defects, disorders due to prematurity and low birth weight, and pregnancy complications.
New Jersey State Health Assessment Data (NJ SHAD) System – a website maintained by the New Jersey Department of Health and Senior Service that provides access to non-sensitive public health datasets and information on the health status of New Jerseyans. For more information, visit the Department’s NJ SHAD web site.
Nitrates - compounds of nitrogen and oxygen. The major source is found in food but high levels of nitrates can be found in drinking water due to factors such as septic tanks and fertilizer run-off. Once taken into the body, nitrates are converted into nitrites. High nitrate levels in drinking water can be a risk to infants. Nitrites can pose a risk to children and adults.
Nitric Oxide (NO) – a gas formed by combustion under high temperature and high pressure in an internal combustion engine; it is converted by sunlight and photochemical processes in ambient air to nitrogen oxide. NO is a precursor of ground-level ozone pollution, or smog.
Nitrogen Dioxide (NO2) - the result of nitric oxide combining with oxygen in the atmosphere; major component of photochemical smog.
Nitrogen Oxide (NOx) - the result of photochemical reactions of nitric oxide in ambient air; major component of photochemical smog. Product of combustion from transportation and stationary sources and a major contributor to the formation of acid rain and ozone in the atmosphere. Nitrogen oxides may be harmful to the lungs and aggravate asthmatic symptoms.
Nonattainment area - a geographic area in which the level of a criteria air pollutant persistently exceeds the level allowed by the National Ambient Air Quality Standards (NAAQS).
Non-Hodgkin’s Lymphoma - a diverse group of hematologic cancers which encompass any lymphoma other than Hodgkin lymphoma.
Non-Point Source – a diffuse air pollution source that is not recognized to have a single point of origin.
North American Association of Central Cancer Registries (NAACCR) - a professional organization that develops and promotes uniform data standards for cancer registration and conducts other activities to promote and support high quality cancer surveillance in North America. For more information, visit the NAACR web site.
Numerator - the upper portion of a fraction used to calculate a rate or ratio.
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Occupational Safety and Health Administration (OSHA) – a federal agency, part of the U.S. Department of Labor. Established to ensure safe and healthful working conditions by setting and enforcing standards and by providing training, outreach, education and assistance. For more information, visit the OSHA web site.
Ozone (O3) – usually formed through a chemical reaction between nitrogen oxide and volatile organic compounds (VOCs). Ozone is necessary and important in high levels of the atmosphere, but ground-level ozone is considered “bad” and can be harmful to health. Ozone is one of the six pollutant regulated via the National Ambient Air Quality Standards.
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Part per billion (ppb) – a unit of measurement commonly used to express a contamination ratio, as in establishing the maximum permissible amount of a contaminant in water, land, or air.
Part per million (ppm) – a unit of measurement commonly used to express a contamination ratio, as in establishing the maximum permissible amount of a contaminant in water, land, or air.
Particulates - fine liquid or solid particles such as dust, smoke, mist, fumes, or smog are found in air or emissions. Very small solids suspended in water can vary in size, shape, density and electrical charge and can be gathered together by coagulation and flocculation. See also PM10 and PM2.5.
Pb – lead.
PM - Particulate Matter See PM10 and PM2.5.
PM10 - particulate Matter <10μm in diameter which deposit in upper (larger) air passages in the lungs. PM10 is one of the “criteria” pollutants regulated via the National Ambient Air Quality Standards.
PM2.5 - particulate Matter <2.5μm in diameter which deposit in lower (smaller) air passages in the lungs. PM2.5 is one of the “criteria” pollutants regulated via the National Ambient Air Quality Standards.
Point Source – a discrete object from which pollutants may be discharged (e.g. pipes, conduits, wells, smokestacks).
Possible Human Carcinogen – a compound for which there exists limited evidence from animal studies and inadequate or no data in humans to support a causal association between exposure and cancer.
Post Neonatal Mortality - defined as death from one month of age until the first birthday. The leading causes of post neonatal morality include sudden infant death syndrome (SIDS), birth defects, and injuries.
Preterm Birth - A baby is considered to be preterm when the gestation period is less than 37 weeks.
Prevalence - the proportion of a defined population affected by a disease at a specified point in time. The numerator of the proportion comprises all those who have the disease at that instant, regardless of whether it was diagnosed recently or long ago.
Prevalence Rate - the percent of the population with a particular condition or characteristic. It is calculated as the number of people in a population who have a health condition divided by the total number of people in the population.
Primary standard - a pollution limit set by the EPA for a criteria pollutant and based on health effects.
Private Well Testing Act (PWTA) – a New Jersey consumer information law that requires sellers (or buyers) of property with wells in NJ to test the untreated ground water for a variety of water quality parameters,
including 32 of human health concern, and to review the test results prior to closing of title. For more information, visit the New Jersey Department of Environmental Protection web site.
Probable Human Carcinogen – a compound for which there exists limited evidence in epidemiological studies and/or sufficient evidence from animal studies to support a causal association between exposure and cancer.
Public Water Systems - provide piped water for human consumption to at least 15 service connections or regularly serve 25 individuals. Community water systems are one kind of public system. All public water systems are subject to government regulation for contaminants.
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Query – a search for data.
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Race (or racial group) - usually refers to the categorization of humans into populations or ancestral groups on the basis of various sets of heritable characteristics. In terms of health statistics, race refers to whether a person is American Indian/Alaskan Native, Asian, Black/African American, Native Hawaiian/Other Pacific Islander, and/or White.
Rate - a measure of new events or occurrences in a population. The crude rate is calculated as the number of events per time period divided by the total number of people in the population in the same time period. The crude rate represents the actual burden of disease in the population.
Respirable Particle – a particle <5 micrometers in size that can be deposited into the pulmonary region of the respiratory tract.
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Safe Drinking Water Act (SDWA) – a federal law in the United States that covers drinking water for the public. For more information, visit the U.S. Environmental Protection Agency web site.
Secondary standard – a pollution limit set by the EPA for a criteria pollutant and based on environmental effects such as damage to property, plants, visibility, etc.
Sex Ratio - the ratio of male to female births.
Singleton – a child born from a pregnancy with a single fetus.
Smog – a mixture of air pollutants which includes particulates, nitrogen oxides, ozone, etc. Smog often has a brown haze due to the presence of nitrogen dioxide.
Smoke - created when air combines with the airborne solid and liquid particulates and gases that are emitted when a material undergoes combustion.
Stationary Source – a non-mobile source (e.g. power plant, refinery, manufacturing facility) that emits air pollutants.
Statistically Significant - The difference between two rates is considered statistically significant if the difference would have occurred by chance less than five times out of 100. If a difference is statistically significant, it is not likely due to random chance.
Sulfur Dioxide (SO2) - a pungent, colorless, gas formed primarily by the combustion of fossil fuels; becomes a pollutant when present in large amounts. Sulfur dioxide is one of the six criteria pollutants regulated via the National Ambient Air Quality Standards.
Surveillance - the ongoing, systematic collection, analysis, and interpretation of data (e.g., regarding agent/hazard, risk factor, exposure, health event) essential to the planning, implementation, and evaluation of public health practice, closely integrated with the timely dissemination of these data to those responsible for prevention and control.
Surveillance, Epidemiology and End Results (SEER) – a program of the National Cancer Institute that collects information on cancer incidence, survival, and prevalence from specific geographic areas representing about 25 percent of the US population and compiles reports on all of these plus cancer mortality for the entire US. For more information, visit the SEER web site.
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Toxic Release Inventory (TRI) - EPA’s list of more than 600 designated chemicals that threaten health and the environment. Authorized under the Emergency Planning and Community Right-To-Know Act (EPCRA) of 1986, this system requires manufacturers to report releases of these chemicals to EPA and State governments. EPA compiles the data in an online, publicly accessible national computerized database. For more information, visit the EPA web site.
Toxicity - the degree to which a substance is able to harm a living organism.
Tracking - another word for surveillance and monitoring.
Trihalomethanes (THMs) – a family of disinfection byproducts formed when disinfectants such as chlorine, used to control disease-causing contaminants in drinking water, react with naturally occurring organic matter in the source water. The primary trihalomethanes of concern are chloroform, dibromochloromethane, bromodichloromethane, and bromoform.
Total Trihalomethanes (TTHMs) - the total amount of trihalomethanes allowed by the EPA.
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μg/dL - micrograms per deciliter.
μg/m3 - micrograms per cubic meter of air.
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Very Low Birth Weight - A newborn is considered to be of very low birth weight when its weight is less than 1500 grams (approximately 3 pounds 5 ounces) at birth.
Very Preterm Birth - A newborn is considered to be very preterm when the gestation period is less than 32 weeks.
Volatile organic compounds (VOCs) - substances containing carbon and various proportions of other elements, such as hydrogen, oxygen, fluorine, chlorine, bromine, sulfur, and nitrogen; these substances easily become vapors or gases. VOCs are commonly found in gasoline, solvents (paint thinners, lacquer thinner, degreasers, and dry cleaning fluids), oil-based paints and inks, and consumer products, such as aerosol spray products. VOCs react with nitrogen oxides, sunlight, and heat to form ozone. Many VOCs are considered air toxics.
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Water Contaminant - a potentially harmful substance that is present in water, resulting from either a biological process or from point source or non-point source pollution.
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Acknowledgements: Glossary definitions were compiled from numerous state and federal agencies including: the Centers for Disease Control and Prevention, state EPHT partners, NJ SHAD, U.S. EPA, U.S. Census Bureau and NJDOH resources.
Link to Terms Commonly Encountered in the NJ State Health Assessment Data Query System
Link to NJ SHAD glossary
Link to Terms Commonly Encountered on the National Environmental Public Health Tracking Portal
Link to CDC glossary
Link to Terms Commonly Searched Keywords on the U.S. EPA Website
U.S. EPA Keywords
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Chronic fatigue syndrome (CFS) is the most common name used to designate a significantly debilitating medical disorder or group of disorders generally defined by persistent fatigue accompanied by other specific symptoms for a minimum of six months in adults (and 3 months in children/adolescents), not due to ongoing exertion, not substantially relieved by rest, nor caused by other medical conditions. The disorder may also be referred to as myalgic encephalomyelitis (ME), post-viral fatigue syndrome (PVFS), chronic fatigue immune dysfunction syndrome (CFIDS), or several other terms. Biological, genetic, infectious and psychological mechanisms have been proposed for the development and persistence of symptoms but the etiology of CFS is not understood and may have multiple causes. There is no diagnostic laboratory test or biomarker for CFS.
Symptoms of CFS include post-exertional malaise; unrefreshing sleep; widespread muscle and joint pain; sore throat; headaches of a type not previously experienced; cognitive difficulties; chronic, often severe, mental and physical exhaustion; and other characteristic symptoms in a previously healthy and active person. Persons with CFS may report additional symptoms including muscle weakness, increased sensitivity to light, sounds and smells, orthostatic intolerance, digestive disturbances, depression, and cardiac and respiratory problems. It is unclear if these symptoms represent co-morbid conditions or are produced by an underlying etiology of CFS. CFS symptoms vary from person to person in number, type, and severity.
Fatigue is a common symptom in many illnesses, but CFS is comparatively rare. Estimates of CFS prevalence vary widely, from 7 to 3,000 cases of CFS for every 100,000 adults, but national health organizations have estimated more than 1 million Americans and approximately a quarter of a million people in the UK have CFS. CFS occurs more often in women than men, and is less prevalent among children and adolescents. The quality of life is "particularly and uniquely disrupted" in CFS.
There is agreement on the genuine threat to health, happiness and productivity posed by CFS, but various physicians' groups, researchers and patient advocates promote different nomenclature, diagnostic criteria, etiologic hypotheses and treatments, resulting in controversy about many aspects of the disorder. The name "chronic fatigue syndrome" itself is controversial as many patients and advocacy groups, as well as some experts, believe the name trivializes the medical condition and want the name changed.
Notable definitions include:
- CDC definition (1994)—the most widely used clinical and research description of CFS, it is also called the Fukuda definition and was based on the Holmes or CDC 1988 scoring system. The 1994 criteria require the presence of four or more symptoms beyond fatigue, where the 1988 criteria require six to eight.
- The Oxford criteria (1991)—includes CFS of unknown etiology and a subtype called post-infectious fatigue syndrome (PIFS). Important differences are that the presence of mental fatigue is necessary to fulfill the criteria and symptoms are accepted that may suggest a psychiatric disorder.
- The 2003 Canadian Clinical working definition— states that "A patient with ME/CFS will meet the criteria for fatigue, post-exertional malaise and/or fatigue, sleep dysfunction, and pain; have two or more neurological/cognitive manifestations and one or more symptoms from two of the categories of autonomic, neuroendocrine, and immune manifestations; and [the illness will persist for at least 6 months]".
The different case definitions used to research the illness may influence the types of patients selected for studies, and research also suggests subtypes of patients exist within the heterogeneous illness.
Clinical practice guidelines—with the aim of improving diagnosis, management, and treatment—are generally based on case descriptions. An example is the CFS/ME guideline for the National Health Service in England and Wales, produced in 2007 by the National Institute for Health and Clinical Excellence (NICE).
Chronic fatigue syndrome is the most commonly used designation, but widespread approval of a name is lacking. Different authorities on the illness view CFS as a central nervous system, metabolic, infectious or post-infectious, cardiovascular, immune system or psychiatric disorder, and different symptom profiles may be caused by various disorders.
Over time and in different countries many names have been associated with the condition(s). Aside from CFS, some other names used include Akureyri disease, benign myalgic encephalomyelitis, chronic fatigue immune dysfunction syndrome, chronic infectious mononucleosis, epidemic myalgic encephalomyelitis, epidemic neuromyasthenia, Iceland disease, myalgic encephalomyelitis, myalgic encephalitis, myalgic encephalopathy, post-viral fatigue syndrome, raphe nucleus encephalopathy, Royal Free disease, Tapanui flu and yuppie flu (considered pejorative). Many patients would prefer a different name such as "myalgic encephalomyelitis", believing the name "chronic fatigue syndrome" trivializes the condition, prevents it from being seen as a serious health problem, and discourages research.
A 2001 review referenced myalgic encephalomyelitis symptoms in a 1959 article by Acheson, stating ME could be a distinct syndrome from CFS, but in literature the two terms are generally seen as synonymous. A 1999 review explained the Royal Colleges of Physicians, Psychiatrists, and General Practitioners in 1996 advocated the use of chronic fatigue syndrome instead of myalgic encephalomyelitis or ME which was in wide use in the United Kingdom, "because there is, so far, no recognized pathology in muscles and in the central nervous system as is implied by the term ME." An editorial noted that the 1996 report received some acceptance, but also criticism from those advocating the use of different naming conventions, suggesting the report was biased, dominated by psychiatrists, and that dissenting voices were excluded. In 2002, a Lancet commentary noted the recent report by the "Working Group on CFS/ME" used the compromise name CFS/ME stating, "The fact that both names for the illness were used symbolises respect for different viewpoints whilst acknowledging the continuing lack of consensus on a universally acceptable name."
Signs and symptoms
The majority of CFS cases start suddenly, usually accompanied by a "flu-like illness" while a significant proportion of cases begin within several months of severe adverse stress. An Australian prospective study found that after infection by viral and non-viral pathogens, a sub-set of individuals met the criteria for CFS, with the researchers concluding that "post-infective fatigue syndrome is a valid illness model for investigating one pathophysiological pathway to CFS". However, accurate prevalence and exact roles of infection and stress in the development of CFS are currently unknown.
The most commonly used diagnostic criteria and definition of CFS for research and clinical purposes were published by the United States Centers for Disease Control and Prevention (CDC). The CDC recommends the following three criteria be fulfilled:
- A new onset (not lifelong) of severe fatigue for six consecutive months or greater duration which is unrelated to exertion, is not substantially relieved by rest, and is not a result of other medical conditions.
- The fatigue causes a significant reduction of previous activity levels.
- Four or more of the following symptoms that last six months or longer:
- Impaired memory or concentration
- Post-exertional malaise, where physical or mental exertions bring on "extreme, prolonged exhaustion and sickness"
- Unrefreshing sleep
- Muscle pain (myalgia)
- Pain in multiple joints (arthralgia)
- Headaches of a new kind or greater severity
- Sore throat, frequent or recurring
- Tender lymph nodes (cervical or axillary)
Other common symptoms include:
- Irritable bowel, abdominal pain, nausea, diarrhea or bloating
- Chills and night sweats
- Brain fog
- Chest pain
- Shortness of breath
- Chronic cough
- Visual disturbances (blurring, sensitivity to light, eye pain or dry eyes)
- Allergies or sensitivities to foods, alcohol, odors, chemicals, medications or noise
- Difficulty maintaining upright position (orthostatic instability, irregular heartbeat, dizziness, balance problems or fainting)
- Psychological problems (depression, irritability, mood swings, anxiety, panic attacks)
The CDC proposes that persons with symptoms resembling those of CFS consult a physician to rule out several treatable illnesses: Lyme disease, "sleep disorders, depression, alcohol/substance abuse, diabetes, hypothyroidism, mononucleosis (mono), lupus, multiple sclerosis (MS), chronic hepatitis and various malignancies." Medications can also cause side effects that mimic symptoms of CFS.
People report critical reductions in levels of physical activity and a reduction in the complexity of activity has been observed, with reported impairment comparable to other fatiguing medical conditions including late-stage AIDS, lupus, rheumatoid arthritis, chronic obstructive pulmonary disease (COPD), and end-stage renal disease. CFS affects a person's functional status and well-being more than major medical conditions such as multiple sclerosis, congestive heart failure, or type II diabetes mellitus. The severity of symptoms and disability is the same in both genders with strongly disabling chronic pain, but despite a common diagnosis the functional capacity of individuals with CFS varies greatly. While some lead relatively normal lives, others are totally bed-ridden and unable to care for themselves. Employment rates vary with over half unable to work and nearly two-thirds limited in their work because of their illness. More than half were on disability benefits or temporary sick leave, and less than a fifth worked full-time.
A 2010 meta-analysis concluded cognitive symptoms were principally resultants of decreased attention, memory, and reaction time. The deficits were in the range of 0.5 to 1.0 standard deviations below expected and were judged likely to affect day-to-day activities. Simple and complex information processing speed and functions entailing working memory over long time periods were moderately to extensively impaired. These deficits are generally consistent with those reported by patients. Perceptual abilities, motor speed, language, reasoning, and intelligence did not appear to be significantly altered.
The mechanisms and pathogenesis of chronic fatigue syndrome are unknown. Research studies have examined and hypothesized about the possible biomedical and epidemiological characteristics of the disease, including oxidative stress, genetic predisposition, infection by viruses and pathogenic bacteria, hypothalamic-pituitary-adrenal axis abnormalities, immune dysfunction as well as psychological and psychosocial factors. Although it is unclear which factors are a cause or consequence of CFS, various models are proposed.
There are no characteristic laboratory abnormalities to diagnose CFS, so testing is used to rule out other potential causes for symptoms. When symptoms are attributable to certain other conditions, the diagnosis of CFS is excluded. Important conditions and disorders to exclude are current/active major depression, schizophrenia, eating disorders such as anorexia nervosa, bulimia, bipolar disorder, alcohol abuse or other substance abuse; current morbid obesity, and active medical diseases need to be resolved and excluded before a diagnosis of chronic fatigue syndrome can be made.
Many people do not fully recover from CFS even with treatment. Cognitive behavioural therapy (CBT) and graded exercise therapy (GET) have shown moderate effectiveness for many people in multiple randomized controlled trials. As many of the CBT and GET studies required visits to a clinic, those severely affected may not have been included. Two large surveys of patients indicated that pacing is the most helpful intervention, or is considered useful by 96% of participants. Medication plays a minor role in management. No intervention has been proven effective in restoring the ability to work.
Cognitive behavioral therapy
Cognitive behavioral therapy, a form of psychological therapy often used to treat chronically ill patients, is a moderately effective treatment for CFS that "can be useful in treating some CFS patients." Since the cause or causes of CFS are unknown, CBT tries to help patients understand their individual symptoms and beliefs and develop strategies to improve day-to-day functioning whatever the cause of the symptoms. CBT is also thought to help patients by removing unhelpful illness beliefs which may perpetuate the illness.
A Cochrane Review meta-analysis of 15 randomized, controlled cognitive behavioral therapy trials with 1043 participants concluded that CBT was an effective treatment to reduce the symptom of fatigue. Four reviewed studies showed that CBT resulted in a clinical response for 40% of participants vs 26% of those treated with "usual care". Similarly, in three studies CBT worked better than other types of psychological therapies (48% vs 27%). The effects may diminish after a course of therapy is completed; the reviewers write that "the evidence base at follow-up is limited to a small group of studies with inconsistent findings" and encourage further studies. A 2007 meta-analysis of 5 CBT randomized controlled trials of chronic fatigue and chronic fatigue syndrome reported 33-73% of the patients improved to the point of no longer being clinically fatigued. A 2010 meta-analysis of trials that measured physical activity before and after CBT showed that although CBT effectively reduced fatigue, activity levels were not affected by CBT and changes in physical activity were not related to changes in fatigue. They conclude that the effect of CBT on fatigue is not mediated by a change in physical activity.
CBT has been criticised by patients' organisations because of negative reports from some of their members that have indicated that CBT can sometimes make people worse, a common result across multiple patient surveys.
Graded exercise therapy
Graded exercise therapy is a form of physical therapy. A meta-analysis published in 2004 of five randomized trials found that patients who received exercise therapy were less fatigued after 12 weeks than the control participants, and the authors cautiously conclude that GET shows promise as a treatment. However, after 6 months the benefit became non-significant compared to the control group who did not receive GET, and functional work capacity was not significantly improved after therapy. A systematic review published in 2006 included the same five RCTs, noting that "no severely affected patients were included in the studies of GET". Surveys conducted on behalf of patient organizations commonly report adverse effects.
To avoid detrimental effects from GET, care must be taken to avoid the exacerbation of symptoms while catering the program to individual capabilities and the fluctuating nature of symptoms.
Pacing is an energy management strategy based on the observation that symptoms of the illness tend to increase following minimal exertion. There are two forms: symptom-contingent pacing, where the decision to stop (and rest or change an activity) is determined by an awareness of an exacerbation of symptoms; and time-contingent pacing, which is determined by a set schedule of activities which a patient estimates he or she is able to complete without triggering post-exertional malaise (PEM). Thus the principle behind pacing for CFS is to avoid over-exertion and an exacerbation of symptoms. It is not aimed at treating the illness as a whole. Those whose illness appears stable may gradually increase activity and exercise levels but according to the principle of pacing, must rest if it becomes clear that they have exceeded their limits. Some programmes combine symptom and time-contingent approaches. A trial of one such programme reported limited benefits. A larger, randomised controlled trial found that pacing had statistically better results than relaxation/flexibility therapy. A 2009 survey of 828 Norwegian CFS patients found that pacing was evaluated as useful by 96% of the participants.
Other treatments of CFS have been proposed but their effectiveness has not been confirmed. Medications thought to have promise in alleviating symptoms include antidepressant and immunomodulatory agents. The evidence for antidepressants is mixed, and their use remains controversial. Many CFS patients are sensitive to medications, particularly sedatives, and some patients report chemical and food sensitivities. CFS patients have a low placebo response, especially to psychological-psychiatric interventions, perhaps due to patient expectations.
A systematic review of 14 studies that described improvement and occupational outcomes of people with CFS found that "the median full recovery rate was 5% (range 0–31%) and the median proportion of patients who improved during follow-up was 39.5% (range 8–63%). Return to work at follow-up ranged from 8 to 30% in the three studies that considered this outcome." .... "In five studies, a worsening of symptoms during the period of follow-up was reported in between 5 and 20% of patients." A good outcome was associated with less fatigue severity at baseline, a sense of control over symptoms and not attributing illness to a physical cause. Another review found that children have a better prognosis than adults, with 54–94% having recovered by follow-up compared to less than 10% of adults returning to premorbid levels of functioning.
Two studies were published in 2006 that directly addressed mortality in CFS. A 14 year longitudinal study of persons with CFS reported that all-cause mortality or suicide rates of individuals were not significantly different from standardized mortality rates (SMRs). A smaller retrospective study in individuals with CFS reported the leading causes of death were heart failure, suicide, and cancer. The ages of death for these three conditions were significantly younger than in the general population respectively. Significant limitations of the study were the inability to check the accuracy of the CFS diagnosis of the individuals or causes of death, and the inability to generalize the data to the overall population of patients with CFS due to the data collection methods.
A 2003 review states that studies have reported between 7 and 3,000 cases of CFS for every 100,000 adults. Ranjith reviewed the epidemiological literature on CFS and suggested that the wide variance of the prevalence estimates may be due to the different definitions of CFS in use, the settings in which patients were selected, and the methodology used to exclude study participants with possible alternative diagnoses. The Centers for Disease Control reports that more than 1 million Americans have CFS and approximately 80% of the cases are undiagnosed. Approximately 250,000 people in the UK are affected with the illness according to the National Health Service.
All ethnic and racial groups appear susceptible to the illness, and lower income groups are slightly more likely to develop CFS. A 2009 meta-analysis showed that compared with the White American majority, African Americans and Native Americans have a significantly higher risk of CFS. More women than men get CFS — between 60 and 85% of cases are women; however, there is some indication that the prevalence among men is underreported. The illness is reported to occur more frequently in people between the ages of 40 and 59. CFS is less prevalent among children and adolescents than adults. Blood relatives of people who have CFS appear to be more predisposed. There is no direct evidence that CFS is contagious, though it is seen in members of the same family; this is believed to be a familial or genetic link but more research is required for a definitive answer.
A systematic review in 2008 included 11 primary studies that had assessed various demographic, medical, psychological, social and environmental factors to predict the development of CFS, and found many had reported significant associations to CFS. The reviewers concluded that the lack of generalizability and replication between studies meant that "none of the identified factors appear suitable for the timely identification of patients at risk of developing CFS/ME within clinical practice."
Certain medical conditions can cause chronic fatigue and must be ruled out before a diagnosis of CFS can be given. Hypothyroidism, anemia, diabetes and certain psychiatric disorders are a few of the diseases that must be ruled out if the patient presents with appropriate symptoms.
People with fibromyalgia (FM, or fibromyalgia syndrome, FMS) have muscle pain and sleep disturbances. Fatigue and muscle pain occurs frequently in the initial phase of various hereditary muscle disorders and in several autoimmune, endocrine and metabolic syndromes; and are frequently labelled as CFS or fibromyalgia in the absence of obvious biochemical/metabolic abnormalities and neurological symptoms. Multiple chemical sensitivity, Gulf War syndrome and post-polio syndrome have symptoms similar to those of CFS, and the last is also theorized to have a common pathophysiology.
A 2006 review found that there was a lack of literature to establish the discriminant validity of undifferentiated somatoform disorder from CFS. The author stated that there is a need for proponents of chronic fatigue syndrome to distinguish it from undifferentiated somatoform disorder. The author also mentioned that the experience of fatigue as exclusively physical and not mental is captured by the definition of somatoform disorder but not CFS. Hysterical diagnoses are not merely diagnoses of exclusion but require criteria to be met on the positive grounds of both primary and secondary gain. Depressive symptoms seen in CFS may be differentially diagnosed from primary depression due to the absence of anhedonia and la belle indifference, guilt, and the presence of somatic symptoms such as sore throat, swollen lymph nodes, and exercise intolerance with postexertional exacerbation of symptoms.
Many CFS patients will also have, or appear to have, other medical problems or related diagnoses. Co-morbid fibromyalgia is common, where only patients with fibromyalgia show abnormal pain responses. Fibromyalgia occurs in a large percentage of CFS patients between onset and the second year, and some researchers suggest fibromyalgia and CFS are related. As previously mentioned, many CFS sufferers also experience symptoms of irritable bowel syndrome, temporomandibular joint pain, headache including migraines, and other forms of myalgia. CFS patients have significantly higher rates of current mood disorders than the general population. Feeling depressed is also a commonplace reaction to the losses caused by chronic illness which can in some cases become a comorbid situational depression. Compared with the non-fatigued population, male CFS patients are more likely to experience chronic pelvic pain syndrome (CP/CPPS), and female CFS patients are also more likely to experience chronic pelvic pain. CFS is significantly more common in women with endometriosis compared with women in the general USA population.
In 1934 an outbreak then referred to as atypical poliomyelitis (at the time it was considered a form of polio) occurred at the Los Angeles County Hospital. It strongly resembled what is now called chronic fatigue syndrome and affected a large number of nurses and doctors. In 1955 at the Royal Free Hospital in London, United Kingdom, another outbreak occurred that also affected mostly the hospital staff. Also resembling CFS, it was called both Royal Free disease and benign myalgic encephalomyelitis and formed the basis of descriptions by Acheson, Ramsay, and others. In 1969 benign myalgic encephalomyelitis was first classified into the International Classification of Diseases under Diseases of the nervous system.
The name chronic fatigue syndrome was used in the medical literature in 1987 to describe a condition resembling "chronic active Epstein-Barr virus (EBV) infection" but which presented no evidence of EBV as its cause. The initial case definition of CFS was published in 1988, "Chronic fatigue syndrome: a working case definition", (the Holmes definition), and displaced the name chronic Epstein-Barr virus syndrome. This research case definition was published after US Centers for Disease Control and Prevention epidemiologists examined patients at the Lake Tahoe outbreak. In 2006 the CDC commenced a national program to educate the American public and health care professionals about CFS.
A 2009 study published in the journal "Science", reported an association between a retrovirus xenotropic murine leukemia virus-related virus (XMRV) and CFS. The editors of Science, subsequently attached an "Editorial Expression of Concern" to the report to the effect that the validity of the study "is now seriously in question". and in September 2011, the authors published a "Partial Retraction" of their 2009 findings, this was followed by a full retraction by the magazine’s Editor in Chief after the authors failed to agree on a full retraction statement. Also in September 2011 the Blood XMRV Scientific Research Working Group published a report which concluded "that currently available XMRV/P-MLV assays, including the assays employed by the three participating laboratories that previously reported positive results on samples from CFS patients and controls (2, 4), cannot reproducibly detect direct virus markers (RNA, DNA, or culture) or specific antibodies in blood samples from subjects previously characterized as XMRV/P-MLV positive (all but one with a diagnosis of CFS) or healthy blood donors." In December 2011, the Proceedings of the National Academy of Sciences published a similar retraction for an August 2010 paper.
In November 2006, an unofficial inquiry by an ad hoc group of parliamentarians in the United Kingdom, set up and chaired by former MP, Dr Ian Gibson, called the Group on Scientific Research into ME was informed by a government minister that few good biomedical research proposals have been submitted to the Medical Research Council (MRC) in contrast to those for psychosocial research. They were also told by other scientists of proposals that have been rejected, with claims of bias against support for this type of research.
The MRC confirmed to the Group that, from April 2003 to November 2006, it has turned down 10 biomedical applications relating to CFS/ME and funded five applications relating to CFS/ME, mostly in the psychiatric/psychosocial domain.
In 2008, the MRC set up an expert group to consider how the MRC might encourage new high-quality research into CFS/ME and partnerships between researchers already working on CFS/ME and those in associated areas. It currently lists CFS/ME with a highlight notice, inviting researchers to develop high quality research proposals for funding. In February 2010, the All-Party Parliamentary Group on ME (APPG on ME) produced a legacy paper, which welcomed the recent MRC initiative, but felt that there has been far too much emphasis in the past on psychological research with insufficient attention to biomedical research and that it is vital that further biomedical research be undertaken to help discover a cause and more effective forms of management for this disease.
Society and culture
Reynolds et al. (2004), estimated that the illness caused about $20,000 per person with CFS in lost productivity which totals to $9.1 billion per year in the United States. A 2008 study estimated that the total annual cost burden of ME/CFS to society in the US was approximately $18.7 to $24.0 billion.
A study found that CFS patients report a heavy psychosocial burden. A survey by the Tymes Trust reported that children with CFS often state that they struggle for recognition of their needs and/or they feel bullied by medical and educational professionals. The ambiguity of the status of CFS as a medical condition may cause higher perceived stigma.
A study found that CFS patients in support groups reported no change in negative interactions compared to an improvement in negative interactions reported by those treated with Cognitive Behavioural Therapy. Patients with greater amounts of negative interactions received worse social support on average than disease-free cancer patients or healthy controls which, in turn, led to greater fatigue severity and functional impairment than CBT-treated patients.
May 12 is designated as International Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Awareness Day (ME/CFS). The day is observed so that stakeholders have an occasion to improve the knowledge of "the public, policymakers, and healthcare professionals about the symptoms, diagnosis, and treatment of ME/CFS, as well as the need for a better understanding of this complex illness."
Some in the medical community There has been much disagreement over proposed causes, diagnosis, and treatment of the illness. The context of contested causation may affect the lives of the individuals diagnosed with CFS, affecting the patient-doctor relationship, the doctor's confidence in their ability to diagnose and treat, ability to share issues and control in diagnosis with the patient, and raise problematic issues of reparation, compensation, and blame. Disagreements over how the condition is dealt with by health-care systems have resulted in an expensive and prolonged conflict for all involved.
did not at first recognize CFS as a real condition, nor was there agreement on its prevalence.
A major divide exists over whether funding for research and treatment should focus on physiological, psychological or psychosocial aspects of CFS. This division is especially great between patient groups and psychological and psychosocial treatment advocates in Great Britain. In 2011, it was reported by the BBC this conflict had involved personal vilification and allegations of professional misconduct to professional societies and universities of researchers who were investigating possible psychiatric connections. One of these researchers, Simon Wessely, reported personal death threats, and others noted such vilification would lead researchers to abandon or avoid the area of study entirely, as few would want to undergo this "torrent of abuse." Charles Shepherd from the ME Association condemned the abuse of researchers but emphasised that the underlying frustration stems from government funding of research focusing almost exclusively on psychiatric, rather than biomedical, causes.
Based on the possible link between CFS and XMRV, in 2010 a variety of national blood banks adopted measures to discourage or prohibit individuals diagnosed with CFS from donating blood, and decline donations when aware the potential donor had been diagnosed. Organizations adopting these or similar measures included the Canadian Blood Services, the New Zealand Blood Service, the Australian Red Cross Blood Service and the American Association of Blood Banks, In November 2010 the UK National Blood Service introduced a permanent deferral of donation from CFS patients based on the potential harm to those patients that may result from their giving blood.
Chronic fatigue syndrome is an illness with a long history of controversies. There has been much contention over the etiology, pathophysiology, nomenclature and diagnostic criteria. Controversies still exist over funding for research and treatment of physiological versus psychological and psychosocial aspects of the illness. Historically, many professionals within the medical community were unfamiliar with CFS, or did not recognize it as a real condition, nor was there agreement on its prevalence or seriousness. Contrasting viewpoints among CFS experts became apparent in 1993, when psychiatrists David and Wessely contested the WHO classification of CFS under diseases of the nervous system, arguing that it was a form of neurasthenia to be classified as a psychiatric condition.
- ^ a b c Evangard B, Schacterie R.S., Komaroff A. L. (Nov 1999). "Chronic fatigue syndrome: new insights and old ignorance". Journal of Internal Medicine 246 (5): 455–469. doi:10.1046/j.1365-2796.1999.00513.x. PMID 10583715. http://www3.interscience.wiley.com/cgi-bin/fulltext/119095441/PDFSTART. Retrieved 2009-10-21.
- ^ a b c "Chronic Fatigue Syndrome: Case Definition". CDC. 2006-05-03. http://www.cdc.gov/cfs/case-definition/index.html. Retrieved 2009-01-22.
- ^ Sanders P, Korf J (2008). "Neuroaetiology of chronic fatigue syndrome: an overview". World J. Biol. Psychiatry 9 (3): 165–71. doi:10.1080/15622970701310971. PMID 17853290.
- ^ a b c d Guideline 53: Chronic fatigue syndrome/myalgic encephalomyelitis (or encephalopathy). London: = National Institute for Health and Clinical Excellence. 2007. ISBN 1-84629-453-3. http://guidance.nice.org.uk/CG53.
- ^ a b c d e f g Afari N, Buchwald D (2003). "Chronic fatigue syndrome: a review". Am J Psychiatr 160 (2): 221–36. doi:10.1176/appi.ajp.160.2.221. PMID 12562565. http://ajp.psychiatryonline.org/cgi/content/full/160/2/221.
- ^ "Chronic Fatigue Syndrome Causes". Centers for Disease Control and Prevention. October 15, 2010. http://www.cdc.gov/cfs/causes/index.html. Retrieved 2012-12-20.
- ^ a b c Wyller VB (2007). "The chronic fatigue syndrome--an update". Acta neurologica Scandinavica. Supplementum 187: 7–14. doi:10.1111/j.1600-0404.2007.00840.x. PMID 17419822.
- ^ a b c "Chronic Fatigue Syndrome (CFS), Symptoms". Centers for Disease Control and Prevention. 2012-05-14. http://www.cdc.gov/cfs/symptoms/index.html. Retrieved 2012-09-23.
- ^ a b c Ranjith G (2005). "Epidemiology of chronic fatigue syndrome". Occup Med (Lond) 55 (1): 13–29. doi:10.1093/occmed/kqi012. PMID 15699086.
- ^ a b c d e "Chronic Fatigue Syndrome Basic Facts". Centers for Disease Control and Prevention. May 9, 2006. http://www.cdc.gov/cfs/general/index.html. Retrieved 2008-02-07.
- ^ a b "Chronic fatigue syndrome". The National Health Service. 2009-06-29. http://www.nhs.uk/me/introduction.aspx. Retrieved 2010-05-14.
- ^ a b Gallagher AM, Thomas JM, Hamilton WT, White PD (2004). "Incidence of fatigue symptoms and diagnoses presenting in UK primary care from 1990 to 2001". J R Soc Med 97 (12): 571–5. doi:10.1258/jrsm.97.12.571. PMC 1079668. PMID 15574853. //www.ncbi.nlm.nih.gov/pmc/articles/PMC1079668/.
- ^ a b c "Chronic Fatigue Syndrome Who's at risk?". Centers for Disease Control and Prevention. March 10, 2006. http://www.cdc.gov/cfs/cfscausesHCP.htm. Retrieved 2008-02-07.
- ^ a b Anderson JS, Ferrans CE (June 1997). "The quality of life of persons with chronic fatigue syndrome". J Nerv Ment Dis 185 (6): 359–67. doi:10.1097/00005053-199706000-00001. PMID 9205421.
- ^ a b Ottati, Victor C. (2002). The social psychology of politics. New York: Kluwer Academic/Plenum. pp. 159–160. ISBN 0-306-46723-2. http://books.google.com/?id=OYrErhPFFLwC&dq=+The+social+psychology+of+politics+By+Victor+C.+Ottati&printsec=frontcover&q=name%20change%20survey%20results. Retrieved 2009 08 11.
- ^ a b c Fukuda K, Straus S, Hickie I, Sharpe M, Dobbins J, Komaroff A (15 December 1994). "The chronic fatigue syndrome: a comprehensive approach to its definition and study. International Chronic Fatigue Syndrome Study Group". Ann Intern Med 121 (12): 953–9. doi:10.1059/0003-4819-121-12-199412150-00009. PMID 7978722. http://www.annals.org/cgi/content/full/121/12/953.
- ^ a b Holmes G, Kaplan J, Gantz N, Komaroff A, Schonberger L, Straus S, Jones J, Dubois R, Cunningham-Rundles C, Pahwa S (1988). "Chronic fatigue syndrome: a working case definition,". Ann Intern Med 108 (3): 387–9. PMID 2829679. Details
- ^ Sharpe M, Archard L, Banatvala J, Borysiewicz L, Clare A, David A, Edwards R, Hawton K, Lambert H, Lane R (1991). "A report--chronic fatigue syndrome: guidelines for research". J R Soc Med 84 (2): 118–21. PMC 1293107. PMID 1999813. //www.ncbi.nlm.nih.gov/pmc/articles/PMC1293107/. Synopsis by Oxford criteria for the diagnosis of chronic fatigue syndrome at GPnotebook
- ^ Carruthers BM, Jain AK, De Meirleir KL, Peterson DL, Klimas NG, Lerner AM, Bested AC, Flor-Henry P, Joshi P, Powles ACP, Sherkey JA, van de Sande MI (2003). "Myalgic encephalomyalitis/chronic fatigue syndrome: Clinical working definition, diagnostic and treatment protocols" (PDF). Journal of Chronic Fatigue Syndrome 11 (1): 7–97. doi:10.1300/J092v11n01_02. http://www.cfids-cab.org/cfs-inform/CFS.case.def/carruthers.etal03.pdf.
- ^ a b Reeves WC, Lloyd A, Vernon SD, Klimas N, Jason LA, Bleijenberg G, Evengard B, White PD, Nisenbaum R, Unger ER (2003). "Identification of ambiguities in the 1994 chronic fatigue syndrome research case definition and recommendations for resolution". BMC Health Serv Res 3 (1): 25. doi:10.1186/1472-6963-3-25. PMC 317472. PMID 14702202. //www.ncbi.nlm.nih.gov/pmc/articles/PMC317472/.
- ^ a b c Jason LA, Corradi K, Torres-Harding S, Taylor RR, King C (March 2005). "Chronic fatigue syndrome: the need for subtypes". Neuropsychol Rev 15 (1): 29–58. doi:10.1007/s11065-005-3588-2. PMID 15929497.
- ^ Whistler T, Unger ER, Nisenbaum R, Vernon SD (December 2003). "Integration of gene expression, clinical, and epidemiologic data to characterize Chronic Fatigue Syndrome". J Transl Med 1 (1): 10. doi:10.1186/1479-5876-1-10. PMC 305360. PMID 14641939. //www.ncbi.nlm.nih.gov/pmc/articles/PMC305360/.
- ^ Kennedy G, Abbot NC, Spence V, Underwood C, Belch JJ (February 2004). "The specificity of the CDC-1994 criteria for chronic fatigue syndrome: comparison of health status in three groups of patients who fulfill the criteria". Ann Epidemiol 14 (2): 95–100. doi:10.1016/j.annepidem.2003.10.004. PMID 15018881.
- ^ Aslakson E, Vollmer-Conna U, White PD (April 2006). "The validity of an empirical delineation of heterogeneity in chronic unexplained fatigue". Pharmacogenomics 7 (3): 365–73. doi:10.2217/14622418.104.22.1685. PMID 16610947.
- ^ a b c d Clark C, Buchwald D, MacIntyre A, Sharpe M, Wessely S (January 2002). "Chronic fatigue syndrome: a step towards agreement". Lancet 359 (9301): 97–8. doi:10.1016/S0140-6736(02)07336-1. PMID 11809249. http://linkinghub.elsevier.com/retrieve/pii/S0140673602073361.
- ^ NORD (June 23, 2008). "Chronic Fatigue Syndrome/Myalgic Encephalomyelitis". National Organization for Rare Disorders, Inc.. http://www.rarediseases.org/search/rdbdetail_abstract.html?disname=Chronic%20Fatigue%20Syndrome/Myalgic%20Encephalomyelitis. Retrieved 2008-07-01.
- ^ Donoghue, PJ; Siegel ME (1992). Sick And Tired Of Feeling Sick And Tired: Living with Invisible Chronic Illness. W. W. Norton & Company. p. 15. ISBN 0-393-03408-9. http://books.google.com/?id=8r1dnOxPwdEC&pg=PA15. Retrieved 2008-09-17.
- ^ Sharpe M (2002). "The report of the Chief Medical Officer's CFS/ME working group: what does it say and will it help?". Clin Med 2 (5): 427–9. PMID 12448589.
- ^ Tuller, D. (17 July 2007). "Chronic Fatigue Syndrome No Longer Seen as "Yuppie Flu"". The New York Times. http://www.nytimes.com/2007/07/17/science/17fatigue.html. Retrieved 2008-10-23.
- ^ a b c Whiting P, Bagnall AM, Sowden AJ, Cornell JE, Mulrow CD, Ramirez G (September 2001). "Interventions for the treatment and management of chronic fatigue syndrome: a systematic review". JAMA 286 (11): 1360–8. doi:10.1001/jama.286.11.1360. PMID 11560542. http://jama.ama-assn.org/cgi/content/full/286/11/1360.
- ^ Royal Colleges of Physicians, Psychiatrists and General Practitioners (1996). Chronic fatigue syndrome; Report of a joint working group of the Royal Colleges of Physicians, Psychiatrists and General Practitioners. London, UK: Royal College of Physicians of London. ISBN 1-86016-046-8.
- ^ [No authors listed] (Oct 1996). "Frustrating survey of chronic fatigue.". Lancet 348 (9033): 971. doi:10.1016/S0140-6736(05)64917-3. PMID 8855845. http://www.lancet.com/journals/lancet/article/PIIS0140-6736%2805%2964917-3/fulltext.
- ^ "Report of the Working Party on CSF/ME to the Chief Medical Officer for England and Wales" (PDF). Department of Health. January 2002. Archived from the original on 2003-03-22. http://web.archive.org/web/20030322075848/http://www.doh.gov.uk/cmo/cfsmereport/cfsmereport.pdf. Retrieved 2009-01-25.
- ^ a b Salit IE (1997). "Precipitating factors for the chronic fatigue syndrome". J Psychiatr Res 31 (1): 59–65. doi:10.1016/S0022-3956(96)00050-7. PMID 9201648.
- ^ Hatcher S, House A (2003). "Life events, difficulties and dilemmas in the onset of chronic fatigue syndrome: a case-control study" (PDF). Psychol Med 33 (7): 1185–92. doi:10.1017/S0033291703008274. PMID 14580073. http://eprints.whiterose.ac.uk/1226/1/house3.pdf.
- ^ Theorell T, Blomkvist V, Lindh G, Evengard B (1999). "Critical life events, infections, and symptoms during the year preceding chronic fatigue syndrome (CFS): an examination of CFS patients and subjects with a nonspecific life crisis". Psychosom Med. 61 (3): 304–10. PMID 10367610.
- ^ Hickie I, Davenport T, Wakefield D et al. (2006). "Post-infective and chronic fatigue syndromes precipitated by viral and non-viral pathogens: prospective cohort study". BMJ 333 (7568): 575. doi:10.1136/bmj.38933.585764.AE. PMC 1569956. PMID 16950834. //www.ncbi.nlm.nih.gov/pmc/articles/PMC1569956/.
- ^ a b c "CDC - Chronic Fatigue Syndrome (CFS) - Diagnosis". Cdc.gov. http://www.cdc.gov/cfs/diagnosis/index.html. Retrieved 2012-07-22.
- ^ "CDC, Chronic Fatigue Syndrome (CFS), Making a Diagnosis". Cdc.gov. http://www.cdc.gov/cfs/toolkit/diagnosis.html. Retrieved 2011-01-28.
- ^ McCully KK, Sisto SA, Natelson BH (1996). "Use of exercise for treatment of chronic fatigue syndrome". Sports Med 21 (1): 35–48. doi:10.2165/00007256-199621010-00004. PMID 8771284.
- ^ Burton C, Knoop H, Popovic N, Sharpe M, Bleijenberg G (June 2009). "Reduced complexity of activity patterns in patients with Chronic Fatigue Syndrome: a case control study". Biopsychosoc Med 3 (1): 7. doi:10.1186/1751-0759-3-7. PMC 2697171. PMID 19490619. http://www.bpsmedicine.com/content/3/1/7.
- ^ Solomon L, Nisenbaum R, Reyes M, Papanicolaou DA, Reeves WC (2003). "Functional status of persons with chronic fatigue syndrome in the Wichita, Kansas, population". Health Qual Life Outcomes 1 (1): 48–58. doi:10.1186/1477-7525-1-48. PMC 239865. PMID 14577835. //www.ncbi.nlm.nih.gov/pmc/articles/PMC239865/.
- ^ Mark, Loveless, MD, congressional testimony of, May 12, 1995, as reported in Hillary Johnson. (1996). Osler's Web: Inside the Labyrinth of the Chronic Fatigue Syndrome Epidemic. Crown Publishers, New York. ISBN 0-517-70353-X. pp.364-365
- ^ Komaroff AL, Fagioli LR, Doolittle TH et al. (September 1996). "Health status in patients with chronic fatigue syndrome and in general population and disease comparison groups". Am. J. Med. 101 (3): 281–90. doi:10.1016/S0002-9343(96)00174-X. PMID 8873490.
- ^ Ho-Yen DO, McNamara I (1991). "General practitioners' experience of the chronic fatigue syndrome". Br J Gen Pract 41 (349): 324–6. PMC 1371754. PMID 1777276. //www.ncbi.nlm.nih.gov/pmc/articles/PMC1371754/.
- ^ Meeus M, Nijs J, Meirleir KD (2007). "Chronic musculoskeletal pain in patients with the chronic fatigue syndrome: A systematic review". Eur J Pain 11 (4): 377–386. doi:10.1016/j.ejpain.2006.06.005. PMID 16843021.
- ^ Vanness JM, Snell CR, Strayer DR, Dempsey L 4th, Stevens SR (2003). "Subclassifying chronic fatigue syndrome through exercise testing". Med Sci Sports Exerc 35 (6): 908–13. doi:10.1249/01.MSS.0000069510.58763.E8. PMID 12783037.
- ^ Ross SD, Estok RP, Frame D, Stone LR, Ludensky V, Levine CB (2004). "Disability and chronic fatigue syndrome: a focus on function". Arch Intern Med 164 (10): 1098–107. doi:10.1001/archinte.164.10.1098. PMID 15159267. http://archinte.ama-assn.org/cgi/content/full/164/10/1098.
- ^ Cockshell SJ, Mathias JL (January 2010). "Cognitive functioning in chronic fatigue syndrome: a meta-analysis". Psychol Med 40 (8): 1–15. doi:10.1017/S0033291709992054. PMID 20047703.
- ^ Sanders, Patricia; Korf, Jakob (2008). "Neuroaetiology of chronic fatigue syndrome: an overview". The world journal of biological psychiatry : the official journal of the World Federation of Societies of Biological Psychiatry 9 (3): 165–71. doi:10.1080/15622970701310971. PMID 17853290.
- ^ Patarca-Montero R, Antoni M, Fletcher MA, Klimas NG (2001). "Cytokine and other immunologic markers in chronic fatigue syndrome and their relation to neuropsychological factors". Appl Neuropsychol 8 (1): 51–64. doi:10.1207/S15324826AN0801_7. PMID 11388124.
- ^ Kuratsune H (June 2007). "[Overview of chronic fatigue syndrome focusing on prevalence and diagnostic criteria]" (in Japanese). Nippon Rinsho 65 (6): 983–90. PMID 17561686.
- ^ Vercoulen JH, Swanink CM, Galama JM et al. (1998). "The persistence of fatigue in chronic fatigue syndrome and multiple sclerosis: development of a model". J Psychosom Res 45 (6): 507–17. doi:10.1016/S0022-3999(98)00023-3. PMID 9859853.
- ^ Avellaneda Fernández, A.; Pérez Martín, A.; Izquierdo Martínez, M.; Arruti Bustillo, M.; Barbado Hernández, FJ.; de la Cruz Labrado, J.; Díaz-Delgado Peñas, R.; Gutiérrez Rivas, E. et al. (2009). "Chronic fatigue syndrome: aetiology, diagnosis and treatment.". BMC Psychiatry 9 Suppl 1: S1. doi:10.1186/1471-244X-9-S1-S1. PMID 19857242.
- ^ Rimes KA, Chalder T. (2005). "Treatments for chronic fatigue syndrome". Occupational Medicine 55 (1): 32–39. doi:10.1093/occmed/kqi015. PMID 15699088.
- ^ a b c d e Chambers D, Bagnall AM, Hempel S, Forbes C (2006). "Interventions for the treatment, management and rehabilitation of patients with chronic fatigue syndrome/myalgic encephalomyelitis: an updated systematic review". Journal of the Royal Society of Medicine 99 (10): 506–20. doi:10.1258/jrsm.99.10.506. PMC 1592057. PMID 17021301. //www.ncbi.nlm.nih.gov/pmc/articles/PMC1592057/.
- ^ Raine R, Haines A, Sensky T, Hutchings A, Larkin K, Black N (2002). "Systematic review of mental health interventions for patients with common somatic symptoms: can research evidence from secondary care be extrapolated to primary care?". BMJ 325 (7372): 1082. doi:10.1136/bmj.325.7372.1082. PMC 131187. PMID 12424170. //www.ncbi.nlm.nih.gov/pmc/articles/PMC131187/.
- ^ Reid S, Chalder T, Cleare A, Hotopf M, Wessely S. (2000). "Chronic fatigue syndrome". BMJ 320 (7230): 292–6. doi:10.1136/bmj.320.7230.292. PMC 1117488. PMID 10650029. //www.ncbi.nlm.nih.gov/pmc/articles/PMC1117488/.
- ^ "Survey Summary Report 2008" (PDF). Action for ME. 2008. p. 13. http://www.afme.org.uk/res/img/resources/Survey%20Summary%20Report%202008.pdf. Retrieved 8 March 2010.
- ^ Bjørkum, Torunn; Wang, Catharina E. A.; Waterloo, Knut (June 2009). "Pasienterfaringer med ulike tiltak ved kronisk utmattelsessyndrom [Patients' experience with treatment of chronic fatigue syndrome]" (in Norwegian). Tidsskrift for Den norske legeforening 129 (12): 1214–6. doi:10.4045/tidsskr.09.35791. PMID 19521443.
- ^ Van Houdenhove, B; Pae, CU, Luyten, P (2010 Feb). "Chronic fatigue syndrome: is there a role for non-antidepressant pharmacotherapy?". Expert opinion on pharmacotherapy 11 (2): 215–23. doi:10.1517/14656560903487744. PMID 20088743.
- ^ a b National Center for Infectious Diseases (26 May 2006). "CFS Treatment Options". Centers for Disease Control and Prevention. http://www.cdc.gov/cfs/cfstreatment.htm. Retrieved 24 February 2010.
- ^ Wolfe F; Chalmers A; Littlejohn GO & Salit I (1995). Fibromyalgia, Chronic Fatigue Syndrome, and Repetitive Strain Injury: Current Concepts in Diagnosis, Management, Disability, and Health Economics. New York: Haworth Medical Press. p. 142. ISBN 1-56024-744-4. http://books.google.com/?id=Da0jf7agNvgC&pg=PA142.
- ^ Price JR, Mitchell E, Tidy E, Hunot V (2008). Price, Jonathan R. ed. "Cognitive behaviour therapy for chronic fatigue syndrome in adults". Cochrane Database Syst Rev (3): CD001027. doi:10.1002/14651858.CD001027.pub2. PMID 18646067.
- ^ Malouff JM et al. (June 2008). "Efficacy of cognitive behavioral therapy for chronic fatigue syndrome: a meta-analysis". Clin Psychol Rev 28 (5): 736–45. doi:10.1016/j.cpr.2007.10.004. PMID 18060672.
- ^ Wiborg JF, Knoop H, Stulemeijer M, Prins JB, Bleijenberg G (January 2010). "How does cognitive behaviour therapy reduce fatigue in patients with chronic fatigue syndrome? The role of physical activity". Psychol Med 40 (8): 1–7. doi:10.1017/S0033291709992212. PMID 20047707.
- ^ a b White PD, Sharpe MC, Chalder T, DeCesare JC, Walwyn R (2007). "Protocol for the PACE trial: A randomised controlled trial of adaptive pacing, cognitive behaviour therapy, and graded exercise as supplements to standardised specialist medical care versus standardised specialist medical care alone for patients with the chronic fatigue syndrome/myalgic encephalomyelitis or encephalopathy". BMC Neurol 7: 6. doi:10.1186/1471-2377-7-6. PMC 2147058. PMID 17397525. http://www.biomedcentral.com/1471-2377/7/6.
- ^ Twisk FN, Maes M (August 2009). "A review on cognitive behavorial therapy (CBT) and graded exercise therapy (GET) in myalgic encephalomyelitis (ME) / chronic fatigue syndrome (CFS): CBT/GET is not only ineffective and not evidence-based, but also potentially harmful for many patients with ME/CFS". Neuro Endocrinol Lett 30 (3): 284–299. PMID 19855350. http://node.nel.edu/?node_id=8918.
- ^ Edmonds M, McGuire H, Price J (2004). Price, Jonathan R. ed. "Exercise therapy for chronic fatigue syndrome". Cochrane Database Syst Rev (3): CD003200. doi:10.1002/14651858.CD003200.pub2. PMID 15266475.
- ^ a b Bjørkum T, Wang CE, Waterloo K (June 2009). "[Patients' experience with treatment of chronic fatigue syndrome]". Tidsskr nor Laegeforen 129 (12): 1214–6. doi:10.4045/tidsskr.09.35791. PMID 19521443.
- ^ "Report of the Working Party on CFS/ME to the Chief Medical Officer for England and Wales". Department of Health. January 2002. http://www.dh.gov.uk/en/Publicationsandstatistics/Publications/PublicationsPolicyAndGuidance/DH_4064840. alternative URL:
- ^ a b Nijs J, Paul L, Wallman K (April 2008). "Chronic fatigue syndrome: an approach combining self-management with graded exercise to avoid exacerbations". J Rehabil Med 40 (4): 241–7. doi:10.2340/16501977-0185. PMID 18382818.
- ^ Goudsmit, E; Nijs, J, Jason, LA and Wallman, KE (19). "Pacing as a strategy to improve energy management in myalgic encephalomyelitis/chronic fatigue syndrome: a consensus document". Disability and Rehabilitation Early Online (13): 1–8. doi:10.3109/09638288.2011.635746. PMID 22181560. http://informahealthcare.com/doi/full/10.3109/09638288.2011.635746. Retrieved 21 January 2012.
- ^ Wallman KE, Morton AR, Goodman C, Grove R, Guilfoyle AM (May 2004). "Randomised controlled trial of graded exercise in chronic fatigue syndrome". Med. J. Aust. 180 (9): 444–8. PMID 15115421. http://www.mja.com.au/public/issues/180_09_030504/wal10613_fm.html.
- ^ Nijs J, Meeus M, De Meirleir K. (August 2006). "Chronic musculoskeletal pain in chronic fatigue syndrome: recent developments and therapeutic implications". Man Ther. 11 (3): 187–91. doi:10.1016/j.math.2006.03.008. PMID 16781183.
- ^ Prins JB, van der Meer JW, Bleijenberg G (2006). "Chronic fatigue syndrome". Lancet 367 (9507): 346–55. doi:10.1016/S0140-6736(06)68073-2. PMID 16443043.
- ^ Covelli V, Passeri ME, Leogrande D, Jirillo E, Amati L (2005). "Drug targets in stress-related disorders". Curr. Med. Chem. 12 (15): 1801–9. doi:10.2174/0929867054367202. PMID 16029148.
- ^ Jackson JL, O'Malley PG, Kroenke K (March 200). "Antidepressants and cognitive-behavioral therapy for symptom syndromes". CNS Spectr 11 (3): 212–22. PMID 16575378. http://www.cnsspectrums.com/aspx/articledetail.aspx?articleid=417.
- ^ Pae CU, Marks DM, Patkar AA, Masand PS, Luyten P, Serretti A (July 2009). "Pharmacological treatment of chronic fatigue syndrome: focusing on the role of antidepressants". Expert Opin Pharmacother 10 (10): 1561–70. doi:10.1517/14656560902988510. PMID 19514866.
- ^ National Center for Infectious Diseases (3 May 2006). "Symptoms of CFS". Centers for Disease Control and Prevention. http://www.cdc.gov/cfs/cfssymptoms.htm. Retrieved 24 February 2010.
- ^ Cho HJ, Hotopf M, Wessely S (2005). "The placebo response in the treatment of chronic fatigue syndrome: A systematic review and meta-analysis". Psychosom Med 67 (2): 301–13. doi:10.1097/01.psy.0000156969.76986.e0. PMID 15784798. http://www.psychosomaticmedicine.org/cgi/content/full/67/2/301. Retrieved 2008-12-12.
- ^ Cairns R, Hotopf M (2005). "A systematic review describing the prognosis of chronic fatigue syndrome". Occupational medicine (Oxford, England) 55 (1): 20–31. doi:10.1093/occmed/kqi013. PMID 15699087. http://occmed.oxfordjournals.org/cgi/reprint/55/1/20.
- ^ Joyce J, Hotopf M, Wessely S. (1997). "The prognosis of chronic fatigue and chronic fatigue syndrome: a systematic review". QJM 90 (3): 223–33. doi:10.1093/qjmed/90.3.223. PMID 9093600.
- ^ Smith WR, Noonan C, Buchwald D (2006). "Mortality in a cohort of chronically fatigued patients". Psychological Medicine 36 (9): 1301–6. doi:10.1017/S0033291706007975. PMID 16893495.
- ^ Jason LA, Corradi K, Gress S, Williams S, Torres-Harding S (2006). "Causes of death among patients with chronic fatigue syndrome". Health care for women international 27 (7): 615–26. doi:10.1080/07399330600803766. PMID 16844674.
- ^ Dinos, Sokratis; Khoshaba, Bernadette; Ashby, Deborah; White, Peter D.; Nazroo, James; Wessely, Simon; Bhui, Kamaldeep S. (2009). "A systematic review of chronic fatigue, its syndromes and ethnicity: prevalence, severity, co-morbidity and coping". International Journal of Epidemiology 38 (6): 1554–70. doi:10.1093/ije/dyp147. PMID 19349479.
- ^ Walsh CM, Zainal NZ, Middleton SJ, Paykel ES (2001). "A family history study of chronic fatigue syndrome". Psychiatr Genet 11 (3): 123–8. doi:10.1097/00041444-200109000-00003. PMID 11702053.
- ^ "Chronic Fatigue Syndrome: Who's at Risk?". Centers for Disease Control and Prevention. May 3, 2006. http://www.cdc.gov/cfs/cfsatrisk.htm. Retrieved 2008-12-12.
- ^ a b Hempel S, Chambers D, Bagnall AM, Forbes C (July 2008). "Risk factors for chronic fatigue syndrome/myalgic encephalomyelitis: a systematic scoping review of multiple predictor studies". Psychol Med 38 (7): 915–26. doi:10.1017/S0033291707001602. PMID 17892624.
- ^ a b Craig, T and Kakumanu S (Mar 2002). "Chronic fatigue syndrome: evaluation and treatment". Am Fam Physician. 65 (6): 1083–90. PMID 11925084. http://www.aafp.org/afp/20020315/1083.html.
- ^ Vojdani A, Thrasher J (2004). "Cellular and humoral immune abnormalities in Gulf War veterans". Environ Health Perspect 112 (8): 840–6. doi:10.1289/ehp.6881. PMC 1242010. PMID 15175170. //www.ncbi.nlm.nih.gov/pmc/articles/PMC1242010/.
- ^ a b Bruno RL, Creange SJ, Frick NM (1998). "Parallels between post-polio fatigue and chronic fatigue syndrome: a common pathophysiology?". Am J Med. 105 (3A): 66S–73S. doi:10.1016/S0002-9343(98)00161-2. PMID 9790485.
- ^ van Staden WC (2006). "Conceptual issues in undifferentiated somatoform disorder and chronic fatigue syndrome". Curr Opin Psychiatry 19 (6): 613–8. doi:10.1097/01.yco.0000245753.83502.d9. PMID 17012941.
- ^ Jenkins R, Mowbray J, ed. Post-viral Fatigue Syndrome. 1991 John Wiley & Sons Ltd
- ^ Bradley LA, McKendree-Smith NL, Alarcon GS (2000). "Pain complaints in patients with fibromyalgia versus chronic fatigue syndrome". Curr Rev Pain 4 (2): 148–57. PMID 10998728.
- ^ Friedberg F, Jason LA (2001). "Chronic fatigue syndrome and fibromyalgia: clinical assessment and treatment". J Clin Psychol. 57 (4): 433–55. doi:10.1002/jclp.1040. PMID 11255201.
- ^ Prins J, Bleijenberg G, Rouweler EK, van der Meer J. (2005). "Effect of psychiatric disorders on outcome of cognitive-behavioural therapy for chronic fatigue syndrome". Br J Psychiatry 187 (2): 184–5. doi:10.1192/bjp.187.2.184. PMID 16055833.
- ^ Frank RG, Chaney JM, Clay DL, Shutty MS, Beck NC, Kay DR, Elliott TR, Grambling S (1992). "Dysphoria: a major symptom factor in persons with disability or chronic illness". Psychiatry Res 43 (3): 231–41. doi:10.1016/0165-1781(92)90056-9. PMID 1438622.
- ^ Aaron, Leslie A.; Herrell, Richard; Ashton, Suzanne; Belcourt, Megan; Schmaling, Karen; Goldberg, Jack; Buchwald, Dedra (2001). "Comorbid Clinical Conditions in Chronic Fatigue: A Co-Twin Control Study". Journal of general internal medicine 16 (1): 24–31. doi:10.1111/j.1525-1497.2001.03419.x. PMC 1495162. PMID 11251747. //www.ncbi.nlm.nih.gov/pmc/articles/PMC1495162/.
- ^ Sinaii N, Cleary SD, Ballweg ML, Nieman LK, Stratton P (2002). "High rates of autoimmune and endocrine disorders, fibromyalgia, chronic fatigue syndrome and atopic diseases among women with endometriosis: a survey analysis". Hum Reprod 17 (10): 2715–24. doi:10.1093/humrep/17.10.2715. PMID 12351553. http://humrep.oxfordjournals.org/cgi/content/full/17/10/2715.
- ^ Patarca-Montero R (2004). Medical Etiology, Assessment, and Treatment of Chronic Fatigue and Malaise. Haworth Press. pp. 6–7. ISBN 0-7890-2196-X.
- ^ Acheson, E.D. (1959). "The clinical syndrome variously called benign myalgic encephalomyelitis, Iceland disease and epidemic neuromyasthenia". The American Journal of Medicine 26 (4): 569–95. doi:10.1016/0002-9343(59)90280-3. PMID 13637100.
- ^ International Classification of Diseases. I. World Health Organization. 1969. pp. 158, (vol 2, pp. 173).
- ^ Buchwald, D. (1987). "Frequency of 'chronic active Epstein-Barr virus infection' in a general medical practice". JAMA: the Journal of the American Medical Association 257 (17): 2303–7. doi:10.1001/jama.257.17.2303. PMID 3033338.
- ^ Sharpe M & Campling F (2000). Chronic Fatigue Syndrome (CFS/ME): TheFacts. Oxford: Oxford Press. pp. 14, 15. ISBN 0-19-263049-0. http://books.google.com/?id=_LqAIK616lgC&pg=PA14. Retrieved 2008-04-02.
- ^ Packard RM, Berkelman RL, Brown PJ, Frumkin H (2004). Emerging Illnesses and Society. JHU Press. p. 156. ISBN 0-8018-7942-6. http://books.google.com/?id=EGNFPZrKIKMC&pg=PA156. Retrieved 2008-04-02.
- ^ "Chronic Fatigue Syndrome Mission / Goals". Centers for Disease Control and Prevention. May 11, 2006. http://www.cdc.gov/cfs/mission.htm. Retrieved 2009-08-18.
- ^ Alberts, B. (2011). "Editorial Expression of Concern". Science 333 (6038): 35. doi:10.1126/science.1208542. PMID 21628391.
- ^ Silverman, R. H.; Das Gupta, J.; Lombardi, V. C.; Ruscetti, F. W.; Pfost, M. A.; Hagen, K. S.; Peterson, D. L.; Ruscetti, S. K. et al. (2011). "Partial Retraction". Science 334 (6053): 176. doi:10.1126/science.1212182.
- ^ Alberts, B. (2011). "Retraction". Science 334 (6063): 1636. doi:10.1126/science.334.6063.1636-a. PMID 22194552.
- ^ Simmons, G.; Glynn, S. A.; Komaroff, A. L.; Mikovits, J. A.; Tobler, L. H.; Hackett, J.; Tang, N.; Switzer, W. M. et al. (2011). "Failure to Confirm XMRV/MLVs in the Blood of Patients with Chronic Fatigue Syndrome: A Multi-Laboratory Study". Science 334 (6057): 814–7. doi:10.1126/science.1213841. PMC 3299483. PMID 21940862. //www.ncbi.nlm.nih.gov/pmc/articles/PMC3299483/.
- ^ <Please add first missing authors to populate metadata.> (2011). "Retraction for Lo et al., Detection of MLV-related virus gene sequences in blood of patients with chronic fatigue syndrome and healthy blood donors". Proceedings of the National Academy of Sciences 109 (1): 346. doi:10.1073/pnas.1119641109. PMC 3252929. PMID 22203980. //www.ncbi.nlm.nih.gov/pmc/articles/PMC3252929/.
- ^ "Erythos.com" (PDF). http://www.erythos.com/gibsonenquiry/Docs/ME_Inquiry_Report.pdf. Retrieved 2011-01-28.
- ^ "MRC.ac.uk". MRC.ac.uk. http://www.mrc.ac.uk/Ourresearch/ResearchInitiatives/CFSME/index.htm. Retrieved 2011-01-28.
- ^ "APPGME.org.uk" (PDF). http://appgme.org.uk/Downloads/appg_interim_report_v2.pdf. Retrieved 2011-01-28.
- ^ Reynolds, Kenneth J.; Vernon, Suzanne D.; Bouchery, Ellen; Reeves, William C. (2004). "The economic impact of chronic fatigue syndrome". Cost effectiveness and resource allocation : C/E 2 (1): 4. doi:10.1186/1478-7547-2-4. PMC 449736. PMID 15210053. //www.ncbi.nlm.nih.gov/pmc/articles/PMC449736/.
- ^ Jason LA, Benton MC, Valentine L, Johnson A, Torres-Harding S (2008). "The Economic impact of ME/CFS: Individual and societal costs". Dyn Med 7: 6. doi:10.1186/1476-5918-7-6. PMC 2324078. PMID 18397528. //www.ncbi.nlm.nih.gov/pmc/articles/PMC2324078/.
- ^ Van Houdenhove B, Neerinckx E, Onghena P, Vingerhoets A, Lysens R, Vertommen H (2002). "Daily hassles reported by chronic fatigue syndrome and fibromyalgia patients in tertiary care: a controlled quantitative and qualitative study". Psychother Psychosom 71 (4): 207–13. doi:10.1159/000063646. PMID 12097786.
- ^ Colby J (2007). "Special problems of children with myalgic encephalomyelitis/chronic fatigue syndrome and the enteroviral link". J Clin Pathol 60 (2): 125–8. doi:10.1136/jcp.2006.042606. PMC 1860612. PMID 16935964. 16935964. //www.ncbi.nlm.nih.gov/pmc/articles/PMC1860612/.
- ^ Looper KJ, Kirmayer LJ (2004). "Perceived stigma in functional somatic syndromes and comparable medical conditions". J Psychosom Res 57 (4): 373–8. doi:10.1016/j.jpsychores.2004.03.005. PMID 15518673.
- ^ a b Prins JB, Bos E, Huibers MJ, Servaes P, van der Werf SP, van der Meer JW, Bleijenberg G (2004). "Social support and the persistence of complaints in chronic fatigue syndrome". Psychother Psychosom 73 (3): 174–82. doi:10.1159/000076455. PMID 15031590.
- ^ Lee, Nancy. "Dr. Nancy Lee on International Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Awareness Day". U.S. Department of Health & Human Services. http://www.hhs.gov/advcomcfs/cfsac-cfsa-day.html. Retrieved 2012 05 16.
- ^ a b Wallace, PG; Sharpe, M. (October 1991). "Post-viral fatigue syndrome. Epidemiology: a critical review" (PDF). Br Med Bull. 47 (4): 942–951. PMID 1794092. http://bmb.oxfordjournals.org/content/47/4/942.full.pdf.
- ^ a b c Mounstephen, A.; Sharpe, M. (1997). "Chronic fatigue syndrome and occupational health". Occupational Medicine 47 (4): 217–27. doi:10.1093/occmed/47.4.217. PMID 9231495.
- ^ a b Hooge J (1992). "Chronic fatigue syndrome: cause, controversy and care". Br J Nurs 1 (9): 440–1, 443, 445–6. PMID 1446147.
- ^ a b Sharpe M (1996). "Chronic fatigue syndrome". Psychiatr. Clin. North Am. 19 (3): 549–73. doi:10.1016/S0193-953X(05)70305-1. PMID 8856816.
- ^ Denz-Penhey H, Murdoch JC (1993). "General practitioners acceptance of the validity of chronic fatigue syndrome as a diagnosis". N. Z. Med. J. 106 (953): 122–4. PMID 8474729.
- ^ Greenlee JE, Rose JW (2000). "Controversies in neurological infectious diseases". Semin Neurol 20 (3): 375–86. doi:10.1055/s-2000-9429. PMID 11051301.
- ^ a b Horton-Salway M (2007). "The ME Bandwagon and other labels: constructing the genuine case in talk about a controversial illness". Br J Soc Psychol 46 (Pt 4): 895–914. doi:10.1348/014466607X173456. PMID 17535450.
- ^ Engel CC, Adkins JA, Cowan DN (2002). "Caring for medically unexplained physical symptoms after toxic environmental exposures: effects of contested causation". Environ. Health Perspect. 110 Suppl 4 (Suppl 4): 641–7. PMC 1241219. PMID 12194900. //www.ncbi.nlm.nih.gov/pmc/articles/PMC1241219/.
- ^ Dumit, J. (2005-08-08). "Illnesses you have to fight to get: facts as forces in uncertain, emergent illnesses". Soc Sci Med. Feb;62 (3): 577–90. doi:10.1016/j.socscimed.2005.06.018. PMID 16085344.
- ^ "'Torrent of abuse' hindering ME research". BBC. 2011-07-29. http://www.bbc.co.uk/news/science-environment-14326514. Retrieved 2011-07-31.
- ^ "No blood from chronic fatigue donors: agency". CBC. 2010-04-07. http://www.cbc.ca/health/story/2010/04/07/blood-donations-chronic-fatigue-virus.html. Retrieved 2010-06-25.
- ^ Atkinson, K (2010-04-21). "Chronic Fatigue Set To Disqualify Blood Donors". Voxy.co.nz. http://www.voxy.co.nz/national/chronic-fatigue-set-disqualify-blood-donors/5/45805. Retrieved 2010-06-25.
- ^ "Blood Service updates CFS donor policy". Australian Red Cross Blood Service. 2010-04-23. http://www.donateblood.com.au/news-events/national-news-events/blood-service-updates-cfs-donor-policy. Retrieved 2010-09-27.
- ^ "Recommendation on Chronic Fatigue Syndrome and Blood Donation". American Association of Blood Banks. 2010-06-18. http://www.aabb.org/pressroom/Pages/cfsrecommendation.aspx. Retrieved 2010-06-25.
- ^ NHS Blood and Transplant (2010-11-05). "ME/CFS sufferers permanently deferred from giving blood". http://www.nhsbt.nhs.uk/news/2010/newsrelease071010.html. Retrieved 2011-10-09.
- ^ Tuller, D (2007-07-17). "Chronic Fatigue Syndrome No Longer Seen as ‘Yuppie Flu’". The New York Times. http://health.nytimes.com/ref/health/healthguide/esn-chronicfatigue-ess.html. Retrieved 2009-06-15.
- ^ Couper J (2000). "Chronic fatigue syndrome and Australian psychiatry: lessons from the UK experience". Aust N Z J Psychiatry 34 (5): 762–9. doi:10.1046/j.1440-1614.2000.00810.x. PMID 11037362.
- ^ Jason LA, Richman JA, Friedberg F, Wagner L, Taylor R, Jordan KM (1997). "Politics, science, and the emergence of a new disease. The case of chronic fatigue syndrome". Am Psychol 52 (9): 973–83. doi:10.1037/0003-066X.52.9.973. PMID 9301342.
- ^ David A, Wessely S (1993). "Chronic fatigue, ME, and ICD-10". The Lancet 342 (8881): 1247–8. doi:10.1016/0140-6736(93)92234-K. PMID 7901572. | <urn:uuid:b8f6b607-b8fd-4d07-ae64-31f2283ff3b3> | {
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oPatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.
Synonyms: hyperkinetic disorder, attention deficit disorder (ADD)
Attention deficit hyperactivity disorder (ADHD) is a persistent pattern of inattention and/or hyperactivity and impulsivity that is more frequent and severe than is typically observed in individuals at a comparable level of development. The Tenth Revision of the International Classification of Diseases and Related Health Problems (ICD-10) uses the term hyperkinetic disorder for a more restricted diagnosis. It differs from the Fourth Edition of the Diagnostic and Statistical Manual of Mental Disorders classification in that all three problems of attention, hyperactivity, and impulsiveness must be present. For a diagnosis of ADHD, symptoms of hyperactivity/impulsivity and/or inattention should:
- Meet the diagnostic criteria in DSM-4 (has been updated to DSM-5 since publication of the NICE guideline) or ICD-10 (hyperkinetic disorder); and
- Be associated with at least moderate psychological, social and/or educational or occupational impairment based on interview and/or direct observation in multiple settings; and
- Be pervasive, occurring in two or more important settings, including social, familial, educational and/or occupational settings.
The DSM-5 diagnostic criteria for ADHD
People with ADHD show a persistent pattern of inattention and/or hyperactivity-impulsivity that interferes with functioning or development:
- Inattention: six or more symptoms of inattention for children up to age 16, or five or more for adolescents aged 17 and older and adults; symptoms of inattention have been present for at least six months, and they are inappropriate for developmental level:
- Often fails to give close attention to details or makes careless mistakes in schoolwork, at work, or with other activities.
- Often has trouble holding attention on tasks or play activities.
- Often does not seem to listen when spoken to directly.
- Often does not follow through on instructions and fails to finish schoolwork, chores, or duties in the workplace (eg, loses focus, becomes side-tracked).
- Often has trouble organising tasks and activities.
- Often avoids, dislikes, or is reluctant to do tasks that require mental effort over a long period of time (such as schoolwork or homework).
- Often loses things necessary for tasks and activities (eg, school materials, pencils, books, tools, wallets, keys, paperwork, eyeglasses, mobile telephones).
- Is often easily distracted
- Is often forgetful in daily activities.
- Hyperactivity and impulsivity: six or more symptoms of hyperactivity-impulsivity for children up to age 16, or five or more for adolescents 17 and older and adults; symptoms of hyperactivity-impulsivity have been present for at least six months to an extent that is disruptive and inappropriate for the person’s developmental level:
- Often fidgets with or taps hands or feet, or squirms in seat.
- Often leaves seat in situations when remaining seated is expected.
- Often runs about or climbs in situations where it is not appropriate (adolescents or adults may be limited to feeling restless).
- Often unable to play or take part in leisure activities quietly.
- Is often 'on the go' acting as if 'driven by a motor'.
- Often talks excessively.
- Often blurts out an answer before a question has been completed.
- Often has trouble waiting his/her turn.
- Often interrupts or intrudes on others (eg, butts into conversations or games).
- In addition, the following conditions must be met:
- Several inattentive or hyperactive-impulsive symptoms were present before age 12 years.
- Several symptoms are present in two or more settings, (eg, at home, school or work; with friends or relatives; in other activities).
- There is clear evidence that the symptoms interfere with, or reduce the quality of, social, school, or work functioning.
- The symptoms do not happen only during the course of schizophrenia or another psychotic disorder. The symptoms are not better explained by another mental disorder (eg, mood disorder, anxiety disorder, dissociative disorder, or a personality disorder).
Based on the types of symptoms, three kinds (presentations) of ADHD can occur:
- Combined presentation: if enough symptoms of both criteria inattention and hyperactivity-impulsivity were present for the past six months
- Predominantly inattentive presentation: if enough symptoms of inattention, but not hyperactivity-impulsivity, were present for the past six months
- Predominantly hyperactive-impulsive presentation: if enough symptoms of hyperactivity-impulsivity but not inattention were present for the past six months.
Because symptoms can change over time, the presentation may change over time as well.
- The prevalence of ADHD is estimated to be around 2.4% of children in the UK.
- ADHD is most often diagnosed in children aged 3-7 years, but it may not be recognised until later in life and sometimes not until adulthood.
- ADHD is more commonly diagnosed in boys than in girls.
- ADHD is more common in first-degree relatives of affected children and studies of twins suggest a significant genetic contribution. There are a number of genes that are thought to have a small effect (eg, DRD4 and DRD5) but it is unlikely that any individual genes have a large effect.
- ADHD is more common in learning-disabled children. Other environmental risk factors include obstetric complications and family conflict.
Prevalence and prescribing rates for ADHD have risen steeply over the period of a decade, partly in response to concerns about underdiagnosis and undertreatment. Recent US data showed that 86% of children diagnosed with ADHD are described as having 'mild or moderate' disorder, and some are diagnosed without fulfilling diagnostic criteria for ADHD.
- Young people and adults with ADHD may have associated problems - eg, self-harm, a predisposition to road traffic (and other) accidents, substance misuse, delinquency, anxiety states and academic underachievement.
- ADHD is a part of a spectrum of disorders. 70% also have other conditions such as generalised or specific learning difficulties (eg, dyslexia, language disorders, autistic spectrum disorder), dyspraxia, Gilles de la Tourette's syndrome or tic disorder.
- Oppositional defiant disorder or conduct disorder is present in most children with ADHD; other associated disorders include mood disorder, anxiety disorder and specific developmental disorders such as dyslexia or dyspraxia.
- ADHD should be considered in all age groups. Diagnosis should only be made by a specialist psychiatrist, paediatrician or other healthcare professional with training and expertise in the diagnosis of ADHD. Diagnosis should be based on:
- A full clinical and psychosocial assessment. Discuss behaviour and symptoms in the different domains and settings of the person's everyday life.
- A full developmental and psychiatric history, and observer reports and an assessment of mental state.
- An assessment should include an assessment of the person's needs, co-existing conditions, social, familial and educational or occupational circumstances and physical health. For children and young people there should also be an assessment of their parents' or carers' mental health.
- Determine the severity of behavioural and/or attention problems suggestive of ADHD and how they affect the child or young person and their parents or carers in different domains and settings.
- As part of the diagnostic process, include an assessment of needs, co-existing conditions, social, familial and educational or occupational circumstances and physical health. For children and young people, also include an assessment of the parents' or carer's mental health.
- A number of conditions, such as thyroid disease, anxiety, depression, and substance use disorders, have symptoms similar to those of ADHD.
- Steroids, antihistamines, anticonvulsants, beta-agonists, caffeine, and nicotine can also have adverse effects that mimic ADHD symptoms.
Specialist referral is needed to confirm the diagnosis and to start management. Referral may be to a specialist paediatrician, a child psychiatrist, Child and Adolescent Mental Health Services (CAMHS), or an adult psychiatrist, depending on the age of the person and local service provision. Adults suspected of having ADHD and adults with continuing ADHD from childhood should be referred to a psychiatrist.
Medication should be prescribed for children with severe and persistent symptoms of ADHD, when the diagnosis has been confirmed by a specialist. Children with moderate symptoms of ADHD can be treated with CNS stimulants when psychological interventions have been unsuccessful or are unavailable. Prescribing of CNS stimulants may be continued by general practitioners, under a shared-care arrangement. Treatment of ADHD often needs to be continued into adolescence, and may need to be continued into adulthood.
Drug treatment of ADHD should be part of a comprehensive treatment programme. Pulse, blood pressure, psychiatric symptoms, appetite, weight and height should be recorded at initiation of therapy, following each dose adjustment, and at least every six months thereafter. The need to continue drug treatment for ADHD should be reviewed at least annually and this may involve suspending treatment.
- Parents and affected children need a great deal of explanation and support. There is a great deal of unproven advice available for parents and it is very important that time be taken to explain properly and to discuss the diagnosis and appropriate treatments. Consider providing parents and carers with self-instruction manuals and other materials (such as DVDs) based on positive parenting and behavioural techniques.
- Stress the value of a balanced diet, good nutrition and regular exercise for children and young people with ADHD.
- Eliminating artificial colouring and additives from the diet is not recommended as a generally applicable treatment for ADHD.
- Dietary fatty acid supplements are not recommended for the treatment of ADHD.
- Advise parents or carers to keep a diary if there are foods or drinks that appear to affect behaviour. If the diary supports a link between any foods or drinks and behaviour, offer referral to a dietitian.
- Further management (such as elimination of specific foods) should be jointly undertaken by the dietitian, mental health specialist or paediatrician, and the family.
- If the problems are having an adverse impact on development or family life, consider:
- Watchful waiting for up to ten weeks.
- Offering referral to a parent-training/education programme; this should not wait for a formal diagnosis of ADHD.
- If the problems persist with at least moderate impairment, refer to secondary care, ie paediatrician, child psychiatrist or specialist ADHD CAMHS.
- If the problems are associated with severe impairment, refer directly to secondary care.
- Do not diagnose or start drug treatment for ADHD in children and young people in primary care.
- If a child or young person is currently receiving drug treatment for ADHD and has not yet been assessed in secondary care, refer to a paediatrician, child psychiatrist or to specialist ADHD CAMHS as a clinical priority.
- Drug treatment is usually not recommended for pre-school children with ADHD, for whom parent-training/education programmes for parents or carers are normally first-line treatment.
- For school-age children and young people with ADHD, drug treatment should be reserved for those with severe symptoms and impairment or for those with moderate levels of impairment who have refused non-drug interventions, or whose symptoms have not responded sufficiently to parent-training/education programmes or group psychological treatment.
- Following treatment with a parent-training/education programme, children and young people with ADHD and persisting significant impairment should be offered drug treatment.
- In school-age children and young people with severe ADHD, drug treatment should be offered as the first-line treatment. Parents should also be offered a group-based parent-training/education programme.
- Where drug treatment is considered appropriate, methylphenidate, atomoxetine and dexamfetamine are recommended.
- Drug treatment for children and young people with ADHD should always form part of a comprehensive treatment plan that includes psychological, behavioural and educational advice and interventions.
- Baseline physical assessment before starting drug treatment should include measurement of pulse, blood pressure, weight and height (plotted on centile charts). An ECG should also be considered on an individual basis.
- When a decision has been made to treat children or young people with ADHD with drugs, healthcare professionals should consider:
- Methylphenidate for ADHD without significant comorbidity.
- Methylphenidate for ADHD with comorbid conduct disorder.
- Methylphenidate or atomoxetine when tics, Gilles de la Tourette's syndrome, anxiety disorder, stimulant misuse or risk of stimulant diversion are present.
- Atomoxetine if methylphenidate has been tried and has been ineffective at the maximum tolerated dose, or the child or young person is intolerant to low or moderate doses of methylphenidate.
- Adults with ADHD:
- Drug treatment for adults with ADHD should always form part of a comprehensive treatment programme that addresses psychological, behavioural and educational or occupational needs.
- Following a decision to start drug treatment in adults with ADHD, methylphenidate should normally be tried first.
- Dexamfetamine should be considered when symptoms are unresponsive to a maximum tolerated dose of methylphenidate or atomoxetine.
- If there is no response to methylphenidate, atomoxetine or dexamfetamine, the affected person should be referred to tertiary services. Further treatment may include drugs unlicensed for ADHD (eg, bupropion, clonidine, modafinil and imipramine), or combination treatments (including psychological treatments for the parent or carer and the child or young person).
- Follow-up and monitoring:
- Drug treatment should be reviewed at least once every six months.
- Review should include physical review (height, weight, blood pressure and general health), medication review for efficacy, safety and compliance, and a review of the child's functioning at school, at home, socially and psychologically. Monitoring should include regular feedback from parents, teachers and others in close contact with the child.
- Parents or carers of pre-school children with ADHD should be offered a referral to a parent-training/education programme as the first-line treatment if the parents or carers have not already attended a programme or the programme has had a limited effect.
- Teachers who have received training about ADHD and its management should provide behavioural interventions in the classroom to help children and young people with ADHD.
- If the child or young person with ADHD has moderate levels of impairment, the parents or carers should be offered referral to a group parent-training/education programme, either on its own or together with a group treatment programme (cognitive behavioural therapy (CBT) and/or social skills' training) for the child or young person.
- CBT, behaviour modification and intensive contingency treatment have been used. The latter two treatments are more effective than CBT in improving behaviour and academic performance.
- Family therapy without medication may help to develop structure in the family, help to manage children's behaviour, and may help families cope with distress from the presence of the disorder.
- Underlying learning difficulties will require additional individual or small-group remedial instruction.
- Other allied health professionals may be involved. Occupational therapists can provide specific programmes for handwriting or gross motor difficulties. Speech therapists may be required for language difficulties.
Psychological treatment for adults with ADHD
- Consider group or individual CBT for adults who:
- Are stabilised on medication but have persisting functional impairment associated with ADHD.
- Have partial or no response to drug treatment or who are intolerant to it.
- Have made an informed choice not to have drug treatment.
- Have difficulty accepting the diagnosis of ADHD and accepting and adhering to drug treatment.
- Have remitting symptoms and psychological treatment is considered sufficient to treat mild-to-moderate residual functional impairment.
- Offer group therapy first because it is the most cost-effective.
Many alternative treatments have been promoted and used for ADHD but evidence for their safety and efficacy is limited.
A recent meta-analysis of follow-up studies of children with ADHD found that:
- About 15% continued to have ADHD.
- 65% had persistence of some symptoms and continuing functional impairment, with psychological, social, or educational difficulties.
Further reading & references
- Evidence-based guidelines for management of attention deficit hyperactivity disorder in adolescents in transition to adult services and in adults; British Association for Psychopharmacology (2006)
- Attention deficit hyperactivity disorder: Diagnosis and management of ADHD in children, young people and adults; NICE Clinical Guideline (September 2008)
- Highlights of Changes from DSM-IV-TR to DSM-5; American Psychiatric Association, 2013
- Attention deficit hyperactivity disorder; NICE CKS, August 2013
- Biederman J, Faraone SV; Attention-deficit hyperactivity disorder. Lancet. 2005 Jul 16-22;366(9481):237-48.
- Thomas R, Mitchell GK, Batstra L; Attention-deficit/hyperactivity disorder: are we helping or harming? BMJ. 2013 Nov 5;347:f6172. doi: 10.1136/bmj.f6172.
- Post RE, Kurlansik SL; Diagnosis and management of adult attention-deficit/hyperactivity disorder. Am Fam Physician. 2012 May 1;85(9):890-6.
- British National Formulary
- Attention deficit hyperactivity disorder (ADHD) - methylphenidate, atomoxetine and dexamfetamine; NICE (2006)
- Management of attention deficit and hyperkinetic disorders in children and young people; Scottish Intercollegiate Guidelines Network - SIGN (October 2009)
- Weber W, Newmark S; Complementary and alternative medical therapies for attention-deficit/hyperactivity disorder and autism. Pediatr Clin North Am. 2007 Dec;54(6):983-1006; xii.
- Faraone SV, Biederman J, Mick E; The age-dependent decline of attention deficit hyperactivity disorder: a Psychol Med. 2006 Feb;36(2):159-65.
Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.
Dr Colin Tidy
Dr Colin Tidy
Dr Adrian Bonsall | <urn:uuid:2c20622e-091a-4242-af12-6556d73386dc> | {
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Unraveling autism’s many causes, spread across the genome
By W. Gregory Feero, MD, PhD
Autism and the related autism spectrum disorders are an enigmatic and substantial cause of developmental delay. Affecting up to 0.5-1% of children and recognized as a growing issue in adult populations, autism affects most by the age of 3 and is considerably more common in males than females.
Individuals with autism exhibit complex behavioral abnormalities, including disordered communication, abnormal social interactions and stereotyped repetitive behaviors often associated with cognitive impairment. Autistic spectrum disorders can confer considerable lifelong disability, and no preventive strategies or curative treatments exist.
The causes of autism have been the subject of debate—much of it occurring in the public eye—but it seems likely that the disorder results from a complex interaction of yet-to-be-identified environmental and genetic factors. Despite the 90% heritability of autism, suggesting a very strong genetic component to its etiology, zeroing in on the genetic underpinnings of this disorder has been very challenging.
In the last few years this has begun to change. Mounting evidence suggests that a type of DNA alteration called copy number variation (CNV) plays an important role in the disorder. Copy number variations are regions of DNA that may be duplicated or deleted to change the normal complement of two copies of any given stretch of DNA. This variation in copy number may affect one or many genes. These discoveries open new realms for developing novel diagnostic and therapeutic approaches to autism.
It has long been recognized that features of autism occur in individuals with large scale aberrations in chromosomal structure. The diagnostic workup of patients with features of autism and developmental delay often includes studies that examine the macroscopic structure of chromosomes (so called cytogenetic studies including fluorescent in situ hybridization and more recently comparative genomic hybridization). Macroscopic changes can be detected in about 7% of cases.
However a substantial number of patients have no evident large changes in their DNA. The advent of genome-wide association studies designed to look at the association of single nucleotide polymorphisms in the genome proved disappointing when applied to autism until the technologies evolved to the point where the presence or absence of small copy number variations (variably sized insertions and deletions of the DNA that can be as small as a few base pairs in length) could be reliably measured.
Subsequently, several studies have demonstrated convincing associations between copy number variations and autism at multiple locations throughout the genome. Interestingly these variations have been shown to arise in the setting of apparently sporadic cases (de novo or new mutations) as well as in the setting of more clearly inherited cases. It is now thought that a significant percentage of cases (perhaps as high as 44%) arise from this type of variation in DNA sequence.
Not surprisingly, CNVs in certain regions of the DNA are found in multiple cases. However the situation is complex. Variation in a great variety of regions of DNA can apparently lead to the common phenotype of autism.
The rarity of any one CNV in panels of patients with autism probably reflects not only the complexity of the biology of higher cognitive function, but a principle of population genetics. Unlike late onset conditions such as diabetes and heart disease, there is a high reproductive disadvantage to individuals affected by autism. Consequently, one might reasonably predict that it would be very unlikely that any one gene mutation that confers high disease risk will attain high population prevalence. This fact has implications for making a molecular diagnostic test. Any proposed testing platform will need to be capable of measuring copy number variations across the entire genome. As well, the observation that many genes can contribute to a common clinical picture suggests that the search for therapeutic strategies may be arduous.
Perhaps future studies will be able to identify relationships between seemingly disparate individual regions of CNV, thereby identifying causal pathways that may be amenable to targeted therapeutic development. Finally, large scale studies with longitudinal follow-up to examine genes by environment interactions are imperative if successful preventive strategies are to be developed.
Autism and the autism spectrum of disorders are of tremendous societal importance. Advances in genomic technologies are providing some exciting insights on these disorders and are once again showing that we have much to learn about ourselves.
W. Gregory Feero, MD, PhD, a family physician with a doctorate in human genetics, is senior advisor for genomic medicine in the Office of the Director at the NIH’s National Human Genomic Research Institute.
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|Leprosy (Hansen's disease)|
|Classification and external resources|
A 24-year-old man infected with leprosy.
|eMedicine||med/1281 derm/223 neuro/187|
Leprosy or Hansen's disease (HD), named after Norwegian physician Gerhard Armauer Hansen, is a chronic disease caused by the bacteria Mycobacterium leprae and Mycobacterium lepromatosis. Leprosy is primarily a granulomatous disease of the peripheral nerves and mucosa of the upper respiratory tract; skin lesions are the primary external sign. Left untreated, leprosy can be progressive, causing permanent damage to the skin, nerves, limbs and eyes. Contrary to myth, leprosy does not cause body parts to fall off, although they can become numb and/or diseased as a result of the disease.
Historically, leprosy has affected humanity for over 9,000 years, and was well-recognized in the civilizations of ancient China, Egypt, and India. DNA taken from the shrouded remains of a man discovered in a tomb next to the Old City of Jerusalem shows him to be the first human proven to have suffered from leprosy. In 1995, the World Health Organization (WHO) estimated that between 2 and 3 million people were permanently disabled because of leprosy. In the past 20 years, 15 million people worldwide have been cured of leprosy. Although the forced quarantine or segregation of patients is unnecessary in places where adequate treatments are available, many leper colonies still remain around the world in countries such as India (where there are still more than 1,000 leper colonies), China, Romania, Egypt, Nepal, Somalia, Liberia, Vietnam, and Japan. Leprosy was once believed to be highly contagious and sexually transmitted, and was treated with mercury—all of which applied to syphilis which was first described in 1530. It is now thought that many early cases of leprosy could have been syphilis. Leprosy is in fact neither sexually transmitted nor is it highly infectious after treatment, as approximately 95% of people are naturally immune and sufferers are no longer infectious after as little as 2 weeks of treatment. However, before treatment was developed, leprosy was certainly contagious.
The age-old social stigma, in other words, leprosy stigma associated with the advanced form of leprosy lingers in many areas, and remains a major obstacle to self-reporting and early treatment. Effective treatment for leprosy appeared in the late 1930s with the introduction of dapsone and its derivatives. However, leprosy bacilli resistant to dapsone soon evolved and, due to overuse of dapsone, became widespread. It was not until the introduction of multidrug therapy (MDT) in the early 1980s that the disease could be diagnosed and treated successfully within the community.
MDT for multibacillary leprosy consists of rifampicin, dapsone, and clofazimine taken over 12 months. Dosages adjusted appropriately for children and adults are available in all Primary Health Centres in the form of blister packages. Single dose MDT for single lesion leprosy consists of rifampicin, ofloxacin, and minocycline. The move towards single dose treatment strategies has reduced the prevalence of disease in some regions since prevalence is dependent on duration of treatment.
World Leprosy Day was created to draw awareness to leprosy and its sufferers.
There are several different approaches for classifying leprosy, but parallels exist.
|WHO||Ridley-Jopling||ICD-10||MeSH||Description||Lepromin test||Immune target|
|Paucibacillary||tuberculoid ("TT"), borderline tuberculoid ("BT")||A30.1, A30.2||Tuberculoid||It is characterized by one or more hypopigmented skin macules and anaesthetic patches, where skin sensations are lost because of damaged peripheral nerves that have been attacked by the human host's immune cells.||Positive||bacillus (Th1)|
|Multibacillary||midborderline or borderline ("BB")||A30.3||Borderline||Borderline leprosy is of intermediate severity and is the most common form. Skin lesions resemble tuberculoid leprosy but are more numerous and irregular; large patches may affect a whole limb, and peripheral nerve involvement with weakness and loss of sensation is common. This type is unstable and may become more like lepromatous leprosy or may undergo a reversal reaction, becoming more like the tuberculoid form.|
|Multibacillary||borderline lepromatous ("BL"), and lepromatous ("LL")||A30.4, A30.5||Lepromatous||It is associated with symmetric skin lesions, nodules, plaques, thickened dermis, and frequent involvement of the nasal mucosa resulting in nasal congestion and epistaxis (nose bleeds) but typically detectable nerve damage is late.||Negative||plasmid inside bacillus (Th2)|
There is a difference in immune response to the tuberculoid and lepromatous forms.
Hansen's disease may also be divided into the following types::344-346
Mycobacterium leprae and Mycobacterium lepromatosis are the causative agents of leprosy. M. lepromatosis is a relatively newly idetified mycobacterium which was isolated from a fatal case of diffuse lepromatous leprosy in 2008.
Due to extensive loss of genes necessary for independent growth, M. leprae and M. lepromatosis are unculturable in the laboratory, a factor which leads to difficulty in definitively identifying the organism under a strict interpretation of Koch's postulates. The use of non-culture-based techniques such as molecular genetics has allowed for alternative establishment of causation.
While the causive organisms have to date been impossible to culture in vitro it has been possible to grow them in animals. Charles Shepard, chairman of the United States Leprosy Panel sucessfully grew the organisms in the footpads of mice in 1960. This method was improved with the use of congenitally athymic mice ('nude mice') in 1970 by Joseph Colson and Richard Hilson at St Goeoge's Hospital, London.
A second animal model was developed by Eleanor Storrs at the Gulf South Research Institute. Dr Storrs had worked on the nine banded armadillo for her PhD and reasons that because this animal had a lower body temperature than humans that it might be a suitable animal model. The work started in 1968 with material provided by Waldemar Kirchheimer at the United States Public Health Leprosarium in Carville, Louisiana. These experiments proved unsucessful but additional work in 1970 with material provided by Chapman Binford, medical director of the Leonard's Wood Memorial was sucessful. The papers describing this model lead to a dispute of priority. Further controversy was generated when it was discovered that wild armadillos in Louisana were naturally infected with leprosy.
Several genes have been associated with a susceptibility to leprosy.
The mechanism of transmission of leprosy is prolonged close contact and transmission by nasal droplet. The only animal other than humans that is known to contract leprosy is the nine-banded armadillo. The bacterium can also be grown in the laboratory by injection into the footpads of mice. There is evidence that not all people who are infected with M. leprae develop leprosy, and genetic factors have long been thought to play a role, due to the observation of clustering of leprosy around certain families, and the failure to understand why certain individuals develop lepromatous leprosy while others develop other types of leprosy. It is estimated that due to genetic factors, only 5% of the population is susceptible to leprosy. This is mostly because the body is naturally immune to the bacteria, and those persons who do become infected are experiencing a severe allergic reaction to the disease. However, the role of genetic factors is not entirely clear in determining this clinical expression. In addition, malnutrition and prolonged exposure to infected persons may play a role in development of the overt disease.
The incubation period for the bacteria can last anywhere from two to ten years.
The most widely held belief is that the disease is transmitted by contact between infected persons and healthy persons. In general, closeness of contact is related to the dose of infection, which in turn is related to the occurrence of disease. Of the various situations that promote close contact, contact within the household is the only one that is easily identified, although the actual incidence among contacts and the relative risk for them appear to vary considerably in different studies. In incidence studies, infection rates for contacts of lepromatous leprosy have varied from 6.2 per 1000 per year in Cebu, Philippines to 55.8 per 1000 per year in a part of Southern India.
Two exit routes of M. leprae from the human body often described are the skin and the nasal mucosa, although their relative importance is not clear. It is true that lepromatous cases show large numbers of organisms deep down in the dermis. However, whether they reach the skin surface in sufficient numbers is doubtful. Although there are reports of acid-fast bacilli being found in the desquamating epithelium (sloughing of superficial layer of skin) of the skin, Weddell et al. had reported in 1963 that they could not find any acid-fast bacilli in the epidermis, even after examining a very large number of specimens from patients and contacts. In a recent study, Job et al. found fairly large numbers of M. leprae in the superficial keratin layer of the skin of lepromatous leprosy patients, suggesting that the organism could exit along with the sebaceous secretions.
The importance of the nasal mucosa was recognized as early as 1898 by Schäffer, particularly that of the ulcerated mucosa. The quantity of bacilli from nasal mucosal lesions in lepromatous leprosy was demonstrated by Shepard as large, with counts ranging from 10,000 to 10,000,000. Pedley reported that the majority of lepromatous patients showed leprosy bacilli in their nasal secretions as collected through blowing the nose. Davey and Rees indicated that nasal secretions from lepromatous patients could yield as much as 10 million viable organisms per day.
The entry route of M. leprae into the human body is also not definitively known: the skin and the upper respiratory tract are most likely. While older research dealt with the skin route, recent research has increasingly favored the respiratory route. Rees and McDougall succeeded in the experimental transmission of leprosy through aerosols containing M. leprae in immune-suppressed mice, suggesting a similar possibility in humans. Successful results have also been reported on experiments with nude mice when M. leprae were introduced into the nasal cavity by topical application. In summary, entry through the respiratory route appears the most probable route, although other routes, particularly broken skin, cannot be ruled out. The CDC notes the following assertion about the transmission of the disease: "Although the mode of transmission of Hansen's disease remains uncertain, most investigators think that M. leprae is usually spread from person to person in respiratory droplets."
In leprosy both the reference points for measuring the incubation period and the times of infection and onset of disease are difficult to define; the former because of the lack of adequate immunological tools and the latter because of the disease's slow onset. Even so, several investigators have attempted to measure the incubation period for leprosy. The minimum incubation period reported is as short as a few weeks and this is based on the very occasional occurrence of leprosy among young infants. The maximum incubation period reported is as long as 30 years, or over, as observed among war veterans known to have been exposed for short periods in endemic areas but otherwise living in non-endemic areas. It is generally agreed that the average incubation period is between three and five years.
In a recent trial, a single dose of rifampicin reduced the rate at which contacts acquired leprosy in the two years after contact by 57%; 265 treatments with rifampicin prevented one case of leprosy in this period. A non-randomized study found that rifampicin reduced the number of new cases of leprosy by 75% after three years.
The disease was known in Ancient Greece as elephantiasis (elephantiasis graecorum). The Bible (Mathew 11,5) suggested that leprosy was curable and the practice of laying on of hands or of relics developed from this. Saint Giles, Saint Martin, Saint Maxillian and Saint Roman were associated with this practice. Several monarchs were also associated with this practice: among these were Robert the First of England, Elizabeth the First, Henry the Third and Charlemange.
At various times blood was considered to be a treatment either as a beverage or as a bath. That of virgins or children was considered to be especially potent. This practice seems to have originated with the Ancient Egyptians but was also known in China where people were murdered for their blood. This practice persisted until at least 1790 when the use of dog's blood was mentioned in De Secretis Naturae. Paracelus recommended the use of lamb's blood and even blood from dead bodies was used.
Snakes were also used being mentioned by Pliny, Areteus of Capadocia and Theodorus. Gaucher recommended the use of increase doses of cobra venom. Boinet in 1913 tried increasing doses of bee stings (up to 4000). Scorpions and frogs were used occasionally instead of snakes. The excreta of Anabas (the climbing fish) was even tried.
Alternative treatments included scarification with or without the addition of irritants including arsenic and hellebore. Castration was also practiced in the Middle Ages. Despite its lack of obvious benefit removal of the ovaries or Fallopian tubes in women or vasectomy in men was carried out in the United States for many years.
Hot baths and in particular sulfur springs were tried especially in Japan. After the discovery of the causative organism it was noted that the lesions were largely confined to parts of the body where the temperature was normally below 37 degrees. This lead in the 1930s to the introduction of sauna like treatments similar to those tried earlier. Unsurprisingly the results were no better than before.
Radiotherapy, electric currents and phototherapy were also tried: radiotherapy while providing some analgesic relief did nothing to treat the underlying disease. Various drugs including thymol and strychnine were tried with little effect.
Perhaps the most popular of the pre modern treatments of leprosy was chaulmoogra oil. This agent has been used since ancient times for the treatment of leprosy. One Indian legend relates that Rama acquired leprosy and was cured by eating the fruit of the Kalaw (a species of the genus Hydnocarpus) tree. He went on to cure the princess Piya with the same fruit and the pair returned to Benares to spread the word of their discovery.
The oil has long been used in India as a Ayurvedic medicine for the treatment of leprosy and various skin conditions. It has also been used in China and Burma. It was introduced into the Western formulary by Frederic John Mouat, professor at the Bengal Medical College. He tried out the oil as an oral and as a topical agent in two cases of leprosy and reported significant improvements in 1854 paper in the Indian Annals of Medical Science. He suggested that further work was required before this could be recommended.
This paper caused some confusion. Mouat indicated that the oil was the product of a tree Chaulmoogra odorata which had been described in 1815 by William Roxburgh, a surgeon and naturalist, while he was cataloging the plants in the East India Company’s botanical garden in Calcutta. This tree is also known as Gynocardia odorata. For the rest of the 19th century this tree was thought to be the source of the oil. In 1901 the source was correctly identified by chaulmoogra oil. In 1901 Sir David Prain identified the true chaulmoogra seeds of the Calcutta bazaar and of the Paris and London drugs sellers as coming from Taraktogenos kurzii which is found in Burma and Northeast India. The oil mentioned in the Ayurvedic texts was from the tree Hydnocarpus wightiana known as Tuvakara in Sanskrit and chaulmugra in Hindu and Persian.
The first parental administration was given by the Egyptian doctor Tortoulis Bey, personal physician to the Sultan Hussein Kamel. He had been using subcutaneous injections of creosite for tuberculosis and in 1894 tried out subcutaneous injection of chaulmoogra oil in a 36 year old Egyptian Copt who had been unable to tolerate oral treatment. After 6 years and 584 injection the patient was declared cured.
The first scientific analysis of this oil was carried out by Frederick B. Power in London in 1904. He and his colleagues isolated a new unsaturated fatty acid from the seeds which they named 'chaulmoogric acid'. They also investigated two closely related species species - Hydnocarpus anthelmintica and Hydnocarpus wightiana. From these two trees they isolated both chaulmoogric acid and a closely related compound 'hydnocarpus acid'. They also investigated Gynocardia odorata and found that it produced neither of these acids. Later investigation showed that 'taraktogenos' (Hydnocarpus kurzii) also produced chaulmoogric acid.
The next difficulty with the use of this oil was of administration. Taken orally it is extremely nauseating. Given by enema may cause peri-anal ulcers and fissures. Given by injection the drug caused fever and other local reactions. Despite these difficulties a series of 170 patients were reported in 1916 by Ralph Hopkins, the attending physician at the Louisiana Leper Home in Carville, Louisiana. He divided the patients into two groups - 'incipient' and 'advanced'. In the advanced cases at most a quarter showed any improvement or arrest of their condition. In the incipient cases he reported an improvement or stabilization of the disease in 45%; 4% died and 8% died. The remainder absconded from the Home apparently in improved condition.
Given the apparent usefulness of this agent the search was on for improved formulations. Victor Heiser the Chief Quarantine Officer and Director of Health for Manila and Elidoro Mercado the house physician at the San Lazaro Hospital for lepers in Manila decided to add camphor to a prescription of Chaulmoogra and resorcin which was typically given orally at the suggestion of Merck and Company in Germany to whom Heiser had written. They found that this new compound was readily absorbed without the nausea that had plagued the earlier preparations.
Heiser and Mercado in 1913 then tried the oil by injection out on two patients whom appeared cured of the disease. Since this treatment was administered in conjunction with other materials the results were not clear. A further two patients were treated with the oil by injection without other treatments and again appeared to be cured of the disease. The following year Heiser reported a further 12 patients but the results were much more mixed.
Less toxic injecteble forms of this oil were sought after. Between 1920 and 1922 a series of papers were published describing the esters of these oils. These may have been based on the work of Alice Ball - the record is not clear on this point and Ms Ball died in 1916. Trials of these esters were carried out in 1921 and appeared to give useful results.
These attempts had been preceded by others. Merck of Darmstadt had produced a version of the sodium salts in 1891. They named this sodium gynocardate in the mistaken belief that the origin of the oil was Gynocardia odorata. Bayer in 1908 marketed a commercial version of the esters under the name 'Antileprol'.
To ensure a supply of this agent Joseph Rock, Professor of Systematic Botany at the College of Hawaii was sent to Burma. The local villagers located a grove of trees in seed which he used to establish a plantation in 2,980 trees on the island of Oahu, Hawaii between 1921 and 1922.
The oil remained a popular treatment despite the common side effects until the introduction of sulfones in the 1940s. Debate about its efficacy continued until it was discontinued.
Until the development of promin in the 1940s, there was no effective treatment for leprosy. The efficacy of promin was first discovered by Guy Henry Faget and his co-workers in 1943. Later dapsone was developed. However, it is only weakly bactericidal against M. leprae and it was considered necessary for patients to take the drug indefinitely. Moreover, when dapsone was used alone, the M. leprae population quickly evolved antibiotic resistance; by the 1960s, the world's only known anti-leprosy drug became virtually useless.
The search for more effective anti-leprosy drugs than dapsone led to the use of clofazimine and rifampicin in the 1960s and 1970s. Later, Indian scientist Shantaram Yawalkar and his colleagues formulated a combined therapy using rifampicin and dapsone, intended to mitigate bacterial resistance. Multidrug therapy (MDT) and combining all three drugs was first recommended by a WHO Expert Committee in 1981. These three anti-leprosy drugs are still used in the standard MDT regimens. None of them are used alone because of the risk of developing resistance.
Because this treatment was quite expensive, it was not quickly adopted in most endemic countries. In 1985 leprosy was still considered a public-health problem in 122 countries. The 44th World Health Assembly (WHA), held in Geneva in 1991, passed a resolution to eliminate leprosy as a public-health problem by the year 2000—defined as reducing the global prevalence of the disease to less than 1 case per 10,000. At the Assembly, the World Health Organization (WHO) was given the mandate to develop an elimination strategy by its member states, based on increasing the geographical coverage of MDT and patients’ accessibility to the treatment.
The WHO Study Group's report on the Chemotherapy of Leprosy in 1993 recommended two types of standard MDT regimen be adopted. The first was a 24-month treatment for multibacillary (MB or lepromatous) cases using rifampicin, clofazimine, and dapsone. The second was a six-month treatment for paucibacillary (PB or tuberculoid) cases, using rifampicin and dapsone. At the First International Conference on the Elimination of Leprosy as a Public Health Problem, held in Hanoi the next year, the global strategy was endorsed and funds provided to WHO for the procurement and supply of MDT to all endemic countries.
Between 1995 and 1999, WHO, with the aid of the Nippon Foundation (Chairman Yōhei Sasakawa, World Health Organization Goodwill Ambassador for Leprosy Elimination), supplied all endemic countries with free MDT in blister packs, channelled through Ministries of Health. This free provision was extended in 2000 with a donation by the MDT manufacturer Novartis, which will run until at least the end of 2010. At the national level, non-government organizations (NGOs) affiliated to the national programme will continue to be provided with an appropriate free supply of this WHO supplied MDT by the government.
MDT remains highly effective, and patients are no longer infectious after the first monthly dose. It is safe and easy to use under field conditions due to its presentation in calendar blister packs. Relapse rates remain low, and there is no known resistance to the combined drugs. The Seventh WHO Expert Committee on Leprosy, reporting in 1997, concluded that the MB duration of treatment—then standing at 24 months—could safely be shortened to 12 months "without significantly compromising its efficacy."
Efforts to overcome persistent obstacles to the elimination of the disease include improving detection, educating patients and the population about its cause, and fighting social taboos about a disease whose patients have historically been considered "unclean" or "cursed by God" as outcasts. Where taboos are strong, patients may be forced to hide their condition (and avoid seeking treatment) to avoid discrimination. The lack of awareness about Hansen's disease can lead people to falsely believe that the disease is highly contagious and incurable.
The ALERT hospital and research facility in Ethiopia provides training to medical personnel from around the world in the treatment of leprosy, as well as treating many local patients. Surgical techniques, such as for the restoration of control of movement of thumbs, have been developed.
In 1999, the world incidence of Hansen's disease was estimated to be 640,000. In 2000, 738,284 cases were identified. In 1999, 108 cases occurred in the United States. In 2000, the World Health Organization (WHO) listed 91 countries in which Hansen's disease is endemic. India, Myanmar and Nepal contained 70% of cases. India reports over 50% of the world's leprosy cases. In 2002, 763,917 new cases were detected worldwide, and in that year the WHO listed Brazil, Madagascar, Mozambique, Tanzania and Nepal as having 90% of Hansen's disease cases.
According to recent figures from the WHO, new cases detected worldwide have decreased by approximately 107,000 cases (or 21%) from 2003 to 2004. This decreasing trend has been consistent for the past three years. In addition, the global registered prevalence of HD was 286,063 cases; 407,791 new cases were detected during 2004.
In the United States, Hansen's disease is tracked by the Centers for Disease Control and Prevention (CDC), with a total of 92 cases being reported in 2002. Although the number of cases worldwide continues to fall, pockets of high prevalence continue in certain areas such as Brazil, South Asia (India, Nepal), some parts of Africa (Tanzania, Madagascar, Mozambique) and the western Pacific.
At highest risk are those living in endemic areas with poor conditions such as inadequate bedding, contaminated water and insufficient diet, or other diseases (such as HIV) that compromise immune function. Recent research suggests that there is a defect in cell-mediated immunity that causes susceptibility to the disease. Less than ten percent of the world's population is actually capable of acquiring the disease. The region of DNA responsible for this variability is also involved in Parkinson disease, giving rise to current speculation that the two disorders may be linked in some way at the biochemical level. In addition, men are twice as likely to contract leprosy as women. According to The Leprosy Mission Canada, most people-–about 95 % of the population-–are naturally immune.
Although annual incidence—the number of new leprosy cases occurring each year—is important as a measure of transmission, it is difficult to measure in leprosy due to its long incubation period, delays in diagnosis after onset of the disease and the lack of laboratory tools to detect leprosy in its very early stages. Instead, the registered prevalence is used. Registered prevalence is a useful proxy indicator of the disease burden as it reflects the number of active leprosy cases diagnosed with the disease and receiving treatment with MDT at a given point in time. The prevalence rate is defined as the number of cases registered for MDT treatment among the population in which the cases have occurred, again at a given point in time.
New case detection is another indicator of the disease that is usually reported by countries on an annual basis. It includes cases diagnosed with onset of disease in the year in question (true incidence) and a large proportion of cases with onset in previous years (termed a backlog prevalence of undetected cases). The new case detection rate (NCDR) is defined by the number of newly detected cases, previously untreated, during a year divided by the population in which the cases have occurred.
Endemic countries also report the number of new cases with established disabilities at the time of detection, as an indicator of the backlog prevalence. However, determination of the time of onset of the disease is generally unreliable, is very labor-intensive and is seldom done in recording these statistics.
The Hospital-Colónia Rovisco Pais (the Rovisco Pais Hospital-Colony) was founed in Portugal in 1947 as a national center for the treatment of leprosy. It was renamed in 2007 as the Centro de Medicina de Reabilitação da Região Centro-Rovisco Pais. It still retains a leprosy service in which 25 ex patients live. Between 1988 and 2003 102 patients were treated in Portugal for leprosy.
The Sanitorio de Fontilles (Fontilles Sanatorium) in Spain was founded in 1902 and admitted its first patient in 1909. In 2002 the Sanitorio had 68 in-patients in the Sanatorium, and more than 150 receiving out-patient treatment. A small number of cases continue to be reported
Two indigenous cases were reported from Greece in 2009.
One case was reported in France in 2009
|New case detection during the year|
|Start of 2006||2001||2002||2003||2004||2005|
|South-East Asia||133,422 (0.81)||668,658||520,632||405,147||298,603||201,635|
|Eastern Mediterranean||4,024 (0.09)||4,758||4,665||3,940||3,392||3,133|
|Western Pacific||8,646 (0.05)||7,404||7,154||6,190||6,216||7,137|
|New case detection
|Start of 2004||Start of 2005||Start of 2006||During 2003||During 2004||During 2005|
|Brazil||79,908 (4.6)||30,693 (1.7)||27,313 (1.5)||49,206 (28.6)||49,384 (26.9)||38,410 (20.6)|
|Mozambique||6,810 (3.4)||4,692 (2.4)||4,889 (2.5)||5,907 (29.4)||4,266 (22.0)||5,371 (27.1)|
|Nepal||7,549 (3.1)||4,699 (1.8)||4,921 (1.8)||8,046 (32.9)||6,958 (26.2)||6,150 (22.7)|
|Tanzania||5,420 (1.6)||4,777 (1.3)||4,190 (1.1)||5,279 (15.4)||5,190 (13.8)||4,237 (11.1)|
As reported to WHO by 115 countries and territories in 2006, and published in the Weekly Epidemiological Record the global registered prevalence of leprosy at the beginning of the year was 219,826 cases. New case detection during the previous year (2005 - the last year for which full country information is available) was 296,499. The reason for the annual detection being higher than the prevalence at the end of the year can be explained by the fact that a proportion of new cases complete their treatment within the year and therefore no longer remain on the registers. The global detection of new cases continues to show a sharp decline, falling by 110,000 cases (27%) during 2005 compared with the previous year.
Table 1 shows that global annual detection has been declining since 2001. The African region reported an 8.7% decline in the number of new cases compared with 2004. The comparable figure for the Americas was 20.1%, for South-East Asia 32% and for the Eastern Mediterranean it was 7.6%. The Western Pacific area, however, showed a 14.8% increase during the same period.
Table 2 shows the leprosy situation in the four major countries which have yet to achieve the goal of elimination at the national level. It should be noted that: a) Elimination is defined as a prevalence of less than 1 case per 10,000 population; b) Madagascar reached elimination at the national level in September 2006; c) Nepal detection reported from mid-November 2004 to mid-November 2005; and d) D.R. Congo officially reported to WHO in 2008 that it had reached elimination by the end of 2007, at the national level.
As is the case with much of the rest of the world, People's Republic China also has many leprosy recovered patients who have been isolated from the rest of society. In the '50s the Chinese Communist government created "Recovered Villages" in rural remote mountaintops for the recovered patients. Although leprosy is now curable with the advent of the multi-drug treatment, the villagers remain because they have been stigmatized by the outside world. Health NGOs such as Joy in Action have arisen in China to especially focus on improving the conditions of "Recovered Villages".
The word leprosy comes from ancient Greek λέπρα [léprā], "a disease which makes the skin scaly", in turn a nominal derivation of the verb λέπω [lépō], "to peel, scale off". The word came into the English language via Latin and Old French. The first attested English use is in the Ancrene Wisse, a 13th-century manual for nuns ("Moyseses hond..bisemde o þe spitel uuel & þuhte lepruse." The Middle English Dictionary, s.v., "leprous"). A roughly contemporaneous use is attested in the Anglo-Norman Dialogues of Saint Gregory, "Esmondez i sont li lieprous" (Anglo-Norman Dictionary, s.v., "leprus").
Historically, individuals with Hansen's disease have been known as lepers; however, this term is falling into disuse as a result of the diminishing number of leprosy patients and the pejorative connotations of the term. Because of the stigma to patients, some prefer not to use the word "leprosy," though the term is used by the U.S. Centers for Disease Control and Prevention and the World Health Organization.
Historically, the term Tzaraath from the Hebrew Bible was, erroneously, commonly translated as leprosy, although the symptoms of Tzaraath were not entirely consistent with leprosy and rather referred to a variety of disorders other than Hansen's disease.
In particular, tinea capitis (fungal scalp infection) and related infections on other body parts caused by the dermatophyte fungus Trichophyton violaceum are abundant throughout the Middle East and North Africa today and might also have been common in biblical times. Similarly, the related agent of the disfiguring skin disease favus, Trichophyton schoenleinii, appears to have been common throughout Eurasia and Africa before the advent of modern medicine. Persons with severe favus and similar fungal diseases (and potentially also with severe psoriasis and other diseases not caused by microorganisms) tended to be classed as having leprosy as late as the 17th century in Europe. This is clearly shown in the painting The Regents of the Leper Hospital in Haarlem 1667 by Jan de Bray (Frans Hals Museum, Haarlem, the Netherlands), where a young Dutchman with a vivid scalp infection, almost certainly caused by a fungus, is shown being cared for by three officials of a charitable home intended for leprosy sufferers. The use of the word "leprosy" before the mid-19th century, when microscopic examination of skin for medical diagnosis was first developed, can seldom be correlated reliably with Hansen's disease as we understand it today.
The Oxford Illustrated Companion to Medicine holds that the mention of leprosy, as well as cures for it, were already described in the Hindu religious book Atharva-veda. Writing in the Encyclopedia Britannica 2008, Kearns & Nash state that the first mention of leprosy is in the Indian medical treatise Sushruta Samhita (6th century BC). The Cambridge Encyclopedia of Human Paleopathology (1998) holds that: "The Sushruta Samhita from India describes the condition quite well and even offers therapeutic suggestions as early as about 600 BC" The surgeon Sushruta lived in the Indian city of Kashi by the 6th century BC, and the medical treatise Sushruta Samhita—attributed to him—made its appearance during the 1st millennium BC. The earliest surviving excavated written material which contains the works of Sushruta is the Bower Manuscript—dated to the 4th century AD, almost a millennium after the original work. In 1881, around 120,000 leprosy patients existed in India. The central government passed the Lepers Act of 1898, which provided legal provision for forcible confinement of leprosy sufferers in India. In 2009, a 4,000-year-old skeleton was uncovered in India that was shown to contain traces of leprosy. The discovery was made at a site called Balathal, which is today part of Rajasthan, and is believed to be the oldest case of the disease ever found. This pre-dated the previous earliest recognized case, dating back to 6th-century Egypt, by 1,500 years. It is believed that the excavated skeleton belonged to a male, who was in his late 30s and belonged to the Ahar Chalcolithic culture. Archaeologists have stated that not only does the skeleton represent the oldest case of leprosy ever found, but is also the first such example that dates back to prehistoric India. This finding supports one of the theories regarding the origin of the disease, which is believed to have originated in either India or Africa, before being subsequently spread to Europe by the armies of Alexander the Great.
Regarding ancient China, Katrina C. D. McLeod and Robin D. S. Yates identify the State of Qin's Feng zhen shi 封診式 (Models for sealing and investigating), dated 266-246 BC, as offering the earliest known unambiguous description of the symptoms of low-resistance leprosy, even though it was termed then under li 癘, a general Chinese word for skin disorder. This 3rd century BC Chinese text on bamboo slip, found in an excavation of 1975 at Shuihudi, Yunmeng, Hubei province, not only described the destruction of the "pillar of the nose", but also the "swelling of the eyebrows, loss of hair, absorption of nasal cartilage, affliction of knees and elbows, difficult and hoarse respiration, as well as anesthesia."
Japan has had a unique history of segregation of patients into sanatoriums based on leprosy prevention laws of 1907, 1931 and 1953, and hence, it intensified leprosy stigma. The 1953 law was abrogated in 1996. There are still 2717 ex-patients in 13 national sanatoriums and 2 private hospitals as of 2008. In a document written in 833, leprosy was described as "caused by a parasite which eats five organs of the body. The eyebrows and eyelashes come off, and the nose is deformed. The disease brings hoarseness, and necessitates amputations of the fingers and toes. Do not sleep with the patients, as the disease is transmittable to those nearby." This was the first document concerning infectivity.
In the West, the earliest known description of leprosy there was made by the Roman encyclopedist Aulus Cornelius Celsus (25 BC – 37 AD) in his De Medicina; he called leprosy "elephantiasis". The Roman author Pliny the Elder (23–79 AD) mentioned the same disease. Although "sara't" of Leviticus (Old Testament) is translated as "lepra" in the 5th century AD Vulgate, the original term sara't found in Leviticus was not the elephantiasis described by Celsus and Pliny; in fact, sara't was used to describe a disease which could affect houses and clothing. Katrina C. D. McLeod and Robin D. S. Yates state that sara't "denotes a condition of ritual impurity or a temporary form of skin disease."
Numerous leprosaria, or leper hospitals, sprang up in the Middle Ages; Matthew Paris, a Benedictine Monk, estimated that in the early thirteenth century there were 19,000 across Europe. The first recorded Leper colony was in Harbledown. These institutions were run along monastic lines and, while lepers were encouraged to live in these monastic-type establishments, this was for their own health as well as quarantine. Indeed, some medieval sources indicate belief that those suffering from leprosy were considered to be going through Purgatory on Earth, and for this reason their suffering was considered holier than the ordinary person's. More frequently, lepers were seen to exist in a place between life and death: they were still alive, yet many chose or were forced to ritually separate themselves from mundane existence. The Order of Saint Lazarus was a hospitaller and military order of monks that began as a leper hospital outside Jerusalem in the twelfth century and remained associated with leprosy throughout its history. The first monks in this order were leper knights and they originally had leper grand masters, although these aspects of the order changed over the centuries.
Radegund was noted for washing the feet of lepers. Orderic Vitalis writes of a monk, Ralf, who was so overcome by the plight of lepers that he prayed to catch leprosy himself (which he eventually did). The leper would carry a clapper and bell to warn of his approach, and this was as much to attract attention for charity as to warn people that a diseased person was near.
Leprosy was almost eradicated in most of Europe by 1700 but sometime after 1850 leprosy was re introduced into East Prussia by Lithuanian rural workers immigrating from the Russian empire. The first leprosarium was founded in 1899 in Memel (now Klaipėda in Lithuania). Legislation was introduced in 1900 and 1904 requiring patients to be isolated and not allowed to work with others.
The date of introducton of leprosy into these islands is debated. The most commonly held view is that it was introduced by the Chinese immigrants in the mid 1850s but some historical records suggest that seafarers may have introduced it at an earlier date.
The last known case in Great Britain was acquired in 1798 in the Shetland Islands.
After the end of the 17th century, Norway and Iceland were the only countries in Western Europe where leprosy was a significant problem. During the 1830s, the number of lepers in Norway rose rapidly, causing an increase in medical research into the condition, and the disease became a political issue. Norway appointed a medical superintendent for leprosy in 1854 and established a national register for lepers in 1856, the first national patient register in the world.
He observed a number of non refractile small rods in unstained tissue sections. The rods were not soluble in potassium lye and they were acid and alcohol fast. In 1879 he was able to stain these organisms with Zeihl's method and the similarities with Kock's bacillus (Mycobacterium tuberculosis) were noted. There were three significant differences between these organisms: (1) the rods in the leprosy lesions were extremely numerous (2) they formed characteristic intracellular collections (globii) and (3) the rods had a variety of shapes with branching and swelling. Thse differences suggested that leprosy was caused by an organism related to but distinct from Mycobacterium tuberculosis.
There were cases of leprosy in Atlantic Canada at the end of the 19th century. The patients were first housed on Sheldrake Island in the Miramichi river and later transferred to Tracadie . Catholic nuns (the religieuses hospitalières de Saint-Joseph, RHSJ) came to take care of the sick. They opened the first French-language hospital in New-Brunswick and many more followed. Many hospitals opened by the RHSJ nuns are still in use today. The last hospital to house lepers in Tracadie was demolished in 1991. Its lazaretto section had been closed since 1965. In a century of existence, it had housed not only Acadian victims of the disease, but people from all over Canada as well as sick immigrants from Iceland, Russia and China, among other nations.
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(Heb. tsara'ath, a "smiting," a "stroke," because the disease was regarded as a direct providential infliction). This name is from the Greek lepra, by which the Greek physicians designated the disease from its scaliness. We have the description of the disease, as well as the regulations connected with it, in Lev. 13; 14; Num 12:10-15, etc. There were reckoned six different circumstances under which it might develop itself, (1) without any apparent cause (Lev 13:2-8); (2) its reappearance (9-17); (3) from an inflammation (18-28); (4) on the head or chin (29-37); (5) in white polished spots (38, 39); (6) at the back or in the front of the head (40-44).
Lepers were required to live outside the camp or city (Num 5:1-4; 12:10-15, etc.). This disease was regarded as an awful punishment from the Lord (2Kg 5:7; 2Chr 26:20). (See MIRIAM �T0002562; GEHAZI �T0001452; UZZIAH.)
This disease "begins with specks on the eyelids and on the palms, gradually spreading over the body, bleaching the hair white wherever they appear, crusting the affected parts with white scales, and causing terrible sores and swellings. From the skin the disease eats inward to the bones, rotting the whole body piecemeal." "In Christ's day no leper could live in a walled town, though he might in an open village. But wherever he was he was required to have his outer garment rent as a sign of deep grief, to go bareheaded, and to cover his beard with his mantle, as if in lamentation at his own virtual death. He had further to warn passers-by to keep away from him, by calling out, 'Unclean! unclean!' nor could he speak to any one, or receive or return a salutation, since in the East this involves an embrace."
That the disease was not contagious is evident from the regulations regarding it (Lev 13:12, 13, 36; 2Kg 5:1). Leprosy was "the outward and visible sign of the innermost spiritual corruption; a meet emblem in its small beginnings, its gradual spread, its internal disfigurement, its dissolution little by little of the whole body, of that which corrupts, degrades, and defiles man's inner nature, and renders him unmeet to enter the presence of a pure and holy God" (Maclear's Handbook O.T). Our Lord cured lepers (Mt 8:2, 3; Mk 1:40-42). This divine power so manifested illustrates his gracious dealings with men in curing the leprosy of the soul, the fatal taint of sin.
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Leprosy is an infectious disease. It has been known for a very long time. Today, it is mostly referred to as Hansen's disease, named after the person who discovered the bacterium, Gerhard Armauer Hansen. It is caused by a bacterium, Mycobacterium leprae.
As of 2004, the estimated number of new infections was about 400,000.
Getting the disease is hard, since it requires close contact with someone who has it, over a long period of time. In addition, about 95% of people seem to be naturally immune to it.
Most cases of leprosy occur in India, and other developing countries. There are practically no cases of leprosy in the developed world. This is because there are excellent drugs and people regularly take antibiotics which will kill the leprosy bacteria.
The symptoms of leprosy are irregular spots and patches on the skin. These are either lighter colored than the surrounding skin, or reddish in color. On those patches, hair will fall out, and they will feel numb to the patient. Nerves will form knots there. With the illness progressing the sense of touch will become less and less (until the patient feels completely numb). So called leptomes and ulcers will eat away the skin, the flesh and the organs on the patches.
Usually people do not die of leprosy, but of secondary infections and diseases they get.
For many years there was a leprosy colony on the Hawaiian Island of Molokai called Kalaupapa. Thousands of people from the United States that had the disease were sent there.
Skull deformed by leprosy
Feet deformed by leprosy
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From Wikipedia, the free encyclopedia - View original article
|Reactive attachment disorder|
|Classification and external resources|
Children need sensitive and responsive caregivers to develop secure attachments. RAD arises from a failure to form normal attachments to primary caregivers in early childhood.
|Reactive attachment disorder|
|Classification and external resources|
Children need sensitive and responsive caregivers to develop secure attachments. RAD arises from a failure to form normal attachments to primary caregivers in early childhood.
Reactive attachment disorder (RAD) is described in clinical literature as a severe and relatively uncommon disorder that can affect children. RAD is characterized by markedly disturbed and developmentally inappropriate ways of relating socially in most contexts. It can take the form of a persistent failure to initiate or respond to most social interactions in a developmentally appropriate way—known as the "inhibited form"—or can present itself as indiscriminate sociability, such as excessive familiarity with relative strangers—known as the "disinhibited form". The term is used in both the World Health Organization's International Statistical Classification of Diseases and Related Health Problems (ICD-10) and in the DSM-IV-TR, the revised fourth edition of the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders (DSM). In ICD-10, the inhibited form is called RAD, and the disinhibited form is called "disinhibited attachment disorder", or "DAD". In the DSM, both forms are called RAD; for ease of reference, this article will follow that convention and refer to both forms as reactive attachment disorder.
DSM-V, the fifth revised edition published in 2013, separates RAD into two separate disorders: Reactive Attachment Disorder (previously referred to as the "inhibited" form), and Social Engagement Disorder.
RAD arises from a failure to form normal attachments to primary caregivers in early childhood. Such a failure could result from severe early experiences of neglect, abuse, abrupt separation from caregivers between the ages of six months and three years, frequent change of caregivers, or a lack of caregiver responsiveness to a child's communicative efforts. Not all, or even a majority of such experiences, result in the disorder. It is differentiated from pervasive developmental disorder or developmental delay and from possibly comorbid conditions such as intellectual disability, all of which can affect attachment behavior. The criteria for a diagnosis of a reactive attachment disorder are very different from the criteria used in assessment or categorization of attachment styles such as insecure or disorganized attachment.
Children with RAD are presumed to have grossly disturbed internal working models of relationships which may lead to interpersonal and behavioral difficulties in later life. There are few studies of long-term effects, and there is a lack of clarity about the presentation of the disorder beyond the age of five years. However, the opening of orphanages in Eastern Europe following the end of the Cold War in the early-1990s provided opportunities for research on infants and toddlers brought up in very deprived conditions. Such research broadened the understanding of the prevalence, causes, mechanism and assessment of disorders of attachment and led to efforts from the late-1990s onwards to develop treatment and prevention programs and better methods of assessment. Mainstream theorists in the field have proposed that a broader range of conditions arising from problems with attachment should be defined beyond current classifications.
Mainstream treatment and prevention programs that target RAD and other problematic early attachment behaviors are based on attachment theory and concentrate on increasing the responsiveness and sensitivity of the caregiver, or if that is not possible, placing the child with a different caregiver. Most such strategies are in the process of being evaluated. Mainstream practitioners and theorists have presented significant criticism of the diagnosis and treatment of alleged reactive attachment disorder or attachment disorder within the controversial field commonly known as attachment therapy. Attachment therapy has a scientifically unsupported theoretical base and uses diagnostic criteria or symptom lists unrelated to criteria under ICD-10 or DSM-IV-TR, or to attachment behaviors. A range of treatment approaches are used in attachment therapy, some of which are physically and psychologically coercive, and considered to be antithetical to attachment theory.
Pediatricians are often the first health professionals to assess and raise suspicions of RAD in children with the disorder. The initial presentation varies according to the child's developmental and chronological age, although it always involves a disturbance in social interaction. Infants up to about 18–24 months may present with non-organic failure to thrive and display abnormal responsiveness to stimuli. Laboratory investigations will be unremarkable barring possible findings consistent with malnutrition or dehydration, while serum growth hormone levels will be normal or elevated.
The core feature is severely inappropriate social relating by affected children. This can manifest itself in two ways:
While RAD is likely to occur in relation to neglectful and abusive treatment, automatic diagnoses on this basis alone cannot be made, as children can form stable attachments and social relationships despite marked abuse and neglect.
There is as yet no universally accepted diagnostic protocol for reactive attachment disorder. Often a range of measures is used in research and diagnosis. Recognized assessment methods of attachment styles, difficulties or disorders include the Strange Situation Procedure (devised by developmental psychologist Mary Ainsworth), the separation and reunion procedure and the Preschool Assessment of Attachment, the Observational Record of the Caregiving Environment, the Attachment Q-sort and a variety of narrative techniques using stem stories, puppets or pictures. For older children, actual interviews such as the Child Attachment Interview and the Autobiographical Emotional Events Dialogue can be used. Caregivers may also be assessed using procedures such as the Working Model of the Child Interview.
More recent research also uses the Disturbances of Attachment Interview (DAI) developed by Smyke and Zeanah (1999). The DAI is a semi-structured interview designed to be administered by clinicians to caregivers. It covers 12 items, namely "having a discriminated, preferred adult", "seeking comfort when distressed", "responding to comfort when offered", "social and emotional reciprocity", "emotional regulation", "checking back after venturing away from the care giver", "reticence with unfamiliar adults", "willingness to go off with relative strangers", "self-endangering behavior", "excessive clinging", "vigilance/hypercompliance" and "role reversal". This method is designed to pick up not only RAD but also the proposed new alternative categories of disorders of attachment.
Although increasing numbers of childhood mental health problems are being attributed to genetic defects, reactive attachment disorder is by definition based on a problematic history of care and social relationships. Abuse can occur alongside the required factors, but on its own does not explain attachment disorder. It has been suggested that types of temperament, or constitutional response to the environment, may make some individuals susceptible to the stress of unpredictable or hostile relationships with caregivers in the early years. In the absence of available and responsive caregivers it appears that some children are particularly vulnerable to developing attachment disorders.
There is as yet no explanation for why similar abnormal parenting may produce the two distinct forms of the disorder, inhibited and disinhibited. The issue of temperament and its influence on the development of attachment disorders has yet to be resolved. RAD has never been reported in the absence of serious environmental adversity yet outcomes for children raised in the same environment vary widely.
In discussing the neurobiological basis for attachment and trauma symptoms in a seven-year twin study, it has been suggested that the roots of various forms of psychopathology, including RAD, Borderline Personality Disorder (BPD), and post-traumatic stress disorder (PTSD), can be found in disturbances in affect regulation. The subsequent development of higher-order self-regulation is jeopardized and the formation of internal models is affected. Consequently the "templates" in the mind that drive organized behavior in relationships may be impacted. The potential for "re-regulation" (modulation of emotional responses to within the normal range) in the presence of "corrective" experiences (normative caregiving) seems possible.
RAD is one of the least researched and most poorly understood disorders in the DSM. There is little systematic epidemiologic information on RAD, its course is not well established and it appears difficult to diagnose accurately. There is a lack of clarity about the presentation of attachment disorders over the age of five years and difficulty in distinguishing between aspects of attachment disorders, disorganized attachment or the consequences of maltreatment.
According to the American Academy of Child and Adolescent Psychiatry (AACAP), children who exhibit signs of reactive attachment disorder need a comprehensive psychiatric assessment and individualized treatment plan. The signs or symptoms of RAD may also be found in other psychiatric disorders and AACAP advises against giving a child this label or diagnosis without a comprehensive evaluation. Their practice parameter states that the assessment of reactive attachment disorder requires evidence directly obtained from serial observations of the child interacting with his or her primary caregivers and history (as available) of the child’s patterns of attachment behavior with these caregivers. It also requires observations of the child’s behavior with unfamiliar adults and a comprehensive history of the child’s early caregiving environment including, for example, pediatricians, teachers, or caseworkers. In the US, initial evaluations may be conducted by psychologists, psychiatrists, Licensed Marriage and Family Therapists, Licensed Professional Counselors, specialist Licensed Clinical Social Workers or psychiatric nurses.
In the UK, the British Association for Adoption and Fostering (BAAF) advise that only a psychiatrist can diagnose an attachment disorder and that any assessment must include a comprehensive evaluation of the child’s individual and family history.
According to the AACAP Practice Parameter (2005) the question of whether attachment disorders can reliably be diagnosed in older children and adults has not been resolved. Attachment behaviors used for the diagnosis of RAD change markedly with development and defining analogous behaviors in older children is difficult. There are no substantially validated measures of attachment in middle childhood or early adolescence. Assessments of RAD past school age may not be possible at all as by this time children have developed along individual lines to such an extent that early attachment experiences are only one factor among many that determine emotion and behavior.
ICD-10 describes reactive attachment disorder of childhood, known as RAD, and disinhibited attachment disorder, less well known as DAD. DSM-IV-TR also describes reactive attachment disorder of infancy or early childhood divided into two subtypes, inhibited type and disinhibited type, both known as RAD. The two classifications are similar and both include:
ICD-10 states in relation to the inhibited form only that the syndrome probably occurs as a direct result of severe parental neglect, abuse, or serious mishandling. DSM states in relation to both forms there must be a history of "pathogenic care" defined as persistent disregard of the child's basic emotional or physical needs or repeated changes in primary caregiver that prevents the formation of a discriminatory or selective attachment that is presumed to account for the disorder. For this reason, part of the diagnosis is the child's history of care rather than observation of symptoms.
In DSM-IV-TR the inhibited form is described as persistent failure to initiate or respond in a developmentally appropriate fashion to most social interactions, as manifest by excessively inhibited, hypervigilant, or highly ambivalent and contradictory responses (e.g., the child may respond to caregivers with a mixture of approach, avoidance, and resistance to comforting or may exhibit "frozen watchfulness", hypervigilance while keeping an impassive and still demeanour). Such infants do not seek and accept comfort at times of threat, alarm or distress, thus failing to maintain "proximity", an essential element of attachment behavior. The disinhibited form shows diffuse attachments as manifest by indiscriminate sociability with marked inability to exhibit appropriate selective attachments (e.g., excessive familiarity with relative strangers or lack of selectivity in choice of attachment figures). There is therefore a lack of "specificity" of attachment figure, the second basic element of attachment behavior.
The ICD-10 descriptions are comparable save that ICD-10 includes in its description several elements not included in DSM-IV-TR as follows:
The first of these is somewhat controversial, being a commission rather than omission and because abuse of itself does not lead to attachment disorder.
The inhibited form has a greater tendency to ameliorate with an appropriate caregiver, while the disinhibited form is more enduring. ICD-10 states the disinhibited form "tends to persist despite marked changes in environmental circumstances". Disinhibited and inhibited are not opposites in terms of attachment disorder and can coexist in the same child. The question of whether there are two subtypes has been raised. The World Health Organization acknowledges that there is uncertainty regarding the diagnostic criteria and the appropriate subdivision. One reviewer has commented on the difficulty of clarifying the core characteristics of and differences between atypical attachment styles and ways of categorizing more severe disorders of attachment.
As of 2010, the American Psychiatric Association has proposed to redefine RAD into two distinct disorders in the DSM-V. Corresponding with the inhibited type, one disorder will be reclassified as Reactive Attachment Disorder of Infancy and Early Childhood.
In regards to pathogenic care, or the type of care in which these behaviors are present, a new criterion for Disinhibited Social Engagement Disorder now includes chronically harsh punishment or other types of severely inept caregiving. Relating to pathogenic care for both proposed disorders, a new criterion is rearing in atypical environments such as institutions with high child/caregiver ratios that cut down on opportunities to form attachments with a caregiver.
The diagnostic complexities of RAD mean that careful diagnostic evaluation by a trained mental health expert with particular expertise in differential diagnosis is considered essential. Several other disorders, such as conduct disorders, oppositional defiant disorder, anxiety disorders, post traumatic stress disorder and social phobia share many symptoms and are often comorbid with or confused with RAD, leading to over and under diagnosis. RAD can also be confused with neuropsychiatric disorders such as autism spectrum disorders, pervasive developmental disorder, childhood schizophrenia and some genetic syndromes. Infants with this disorder can be distinguished from those with organic illness by their rapid physical improvement after hospitalization. Children with an autistic disorder are likely to be of normal size and weight and often exhibit a degree of intellectual disability. They are unlikely to improve upon being removed from the home.
In the absence of a standardized diagnosis system, many popular, informal classification systems or checklists, outside the DSM and ICD, were created out of clinical and parental experience within the field known as attachment therapy. These lists are unvalidated and critics state they are inaccurate, too broadly defined or applied by unqualified persons. Many are found on the websites of attachment therapists. Common elements of these lists such as lying, lack of remorse or conscience and cruelty do not form part of the diagnostic criteria under either DSM-IV-TR or ICD-10. Many children are being diagnosed with RAD because of behavioral problems that are outside the criteria. There is an emphasis within attachment therapy on aggressive behavior as a symptom of what they describe as attachment disorder whereas mainstream theorists view these behaviors as comorbid, externalizing behaviors requiring appropriate assessment and treatment rather than attachment disorders. However, knowledge of attachment relationships can contribute to the etiology, maintenance and treatment of externalizing disorders.
The Randolph Attachment Disorder Questionnaire or RADQ is one of the better known of these checklists and is used by attachment therapists and others. The checklist includes 93 discrete behaviours, many of which either overlap with other disorders, like conduct disorder and oppositional defiant disorder, or are not related to attachment difficulties. Critics assert that it is unvalidated and lacks specificity.
Assessing the child's safety is an essential first step that determines whether future intervention can take place in the family unit or whether the child should be removed to a safe situation. Interventions may include psychosocial support services for the family unit (including financial or domestic aid, housing and social work support), psychotherapeutic interventions (including treating parents for mental illness, family therapy, individual therapy), education (including training in basic parenting skills and child development), and monitoring of the child's safety within the family environment
In 2005 the American Academy of Child and Adolescent Psychiatry laid down guidelines (devised by N.W. Boris and C.H. Zeanah) based on its published parameters for the diagnosis and treatment of RAD. Recommendations in the guidelines include the following:
Mainstream prevention programs and treatment approaches for attachment difficulties or disorders for infants and younger children are based on attachment theory and concentrate on increasing the responsiveness and sensitivity of the caregiver, or if that is not possible, placing the child with a different caregiver. These approaches are mostly in the process of being evaluated. The programs invariably include a detailed assessment of the attachment status or caregiving responses of the adult caregiver as attachment is a two-way process involving attachment behavior and caregiver response. Some of these treatment or prevention programs are specifically aimed at foster carers rather than parents, as the attachment behaviors of infants or children with attachment difficulties often do not elicit appropriate caregiver responses. Approaches include "Watch, wait and wonder," manipulation of sensitive responsiveness, modified "Interaction Guidance", "Clinician-Assisted Videofeedback Exposure Sessions (CAVES)", "Preschool Parent Psychotherapy", "Circle of Security", "Attachment and Biobehavioral Catch-up" (ABC), the New Orleans Intervention, and parent–child psychotherapy. Other treatment methods include Developmental, Individual-difference, and Relationship-based therapy (DIR, also referred to as Floor Time) by Stanley Greenspan, although DIR is primarily directed to treatment of pervasive developmental disorders.
The relevance of these approaches to intervention with fostered and adopted children with RAD or older children with significant histories of maltreatment is unclear.
Outside the mainstream programs is a form of treatment generally known as attachment therapy, a subset of techniques (and accompanying diagnosis) for supposed attachment disorders including RAD. In general, these therapies are aimed at adopted or fostered children with a view to creating attachment in these children to their new caregivers. The theoretical base is broadly a combination of regression and catharsis, accompanied by parenting methods which emphasize obedience and parental control. There is considerable criticism of this form of treatment and diagnosis as it is largely unvalidated and has developed outside the scientific mainstream. There is little or no evidence base and techniques vary from non-coercive therapeutic work to more extreme forms of physical, confrontational and coercive techniques, of which the best known are holding therapy, rebirthing, rage-reduction and the Evergreen model. These forms of the therapy may well involve physical restraint, the deliberate provocation of rage and anger in the child by physical and verbal means including deep tissue massage, aversive tickling, enforced eye contact and verbal confrontation, and being pushed to revisit earlier trauma. Critics maintain that these therapies are not within the attachment paradigm, are potentially abusive, and are antithetical to attachment theory. The APSAC Taskforce Report of 2006 notes that many of these therapies concentrate on changing the child rather than the caregiver. Children may be described as "RADs", "Radkids" or "Radishes" and dire predictions may be made as to their supposedly violent futures if they are not treated with attachment therapy. The Mayo Clinic, a well known U.S. non-profit medical practice and medical research group, cautions against consulting with mental health providers who promote these types of methods and offer evidence to support their techniques; to date, this evidence base is not published within reputable medical or mental health journals.
The AACAP guidelines state that children with reactive attachment disorder are presumed to have grossly disturbed internal models for relating to others. However, the course of RAD is not well studied and there have been few efforts to examine symptom patterns over time. The few existing longitudinal studies (dealing with developmental change with age over a period of time) involve only children from poorly run Eastern European institutions.
Findings from the studies of children from Eastern European orphanages indicate that persistence of the inhibited pattern of RAD is rare in children adopted out of institutions into normative care-giving environments. However, there is a close association between duration of deprivation and severity of attachment disorder behaviors. The quality of attachments that these children form with subsequent care-givers may be compromised, but they probably no longer meet criteria for inhibited RAD. The same group of studies suggests that a minority of adopted, institutionalized children exhibit persistent indiscriminate sociability even after more normative caregiving environments are provided. Indiscriminate sociability may persist for years, even among children who subsequently exhibit preferred attachment to their new caregivers. Some exhibit hyperactivity and attention problems as well as difficulties in peer relationships. In the only longitudinal study that has followed children with indiscriminate behavior into adolescence, these children were significantly more likely to exhibit poor peer relationships.
Studies of children who were reared in institutions have suggested that they are inattentive and overactive, no matter what quality of care they received. In one investigation, some institution-reared boys were reported to be inattentive, overactive, and markedly unselective in their social relationships, while girls, foster-reared children, and some institution-reared children were not. It is not yet clear whether these behaviors should be considered as part of disordered attachment.
There is one case study on maltreated twins published in 1999 with a follow-up in 2006. This study assessed the twins between the ages of 19 and 36 months, during which time they suffered multiple moves and placements. The paper explores the similarities, differences and comorbidity of RAD, disorganized attachment and post traumatic stress disorder. The girl showed signs of the inhibited form of RAD while the boy showed signs of the indiscriminate form. It was noted that the diagnosis of RAD ameliorated with better care but symptoms of post traumatic stress disorder and signs of disorganized attachment came and went as the infants progressed through multiple placement changes. At age three, some lasting relationship disturbance was evident.
In the follow-up case study when the twins were aged three and eight years, the lack of longitudinal research on maltreated as opposed to institutionalized children was again highlighted. The girl's symptoms of disorganized attachment had developed into controlling behaviors—a well-documented outcome. The boy still exhibited self-endangering behaviors, not within RAD criteria but possibly within "secure base distortion", (where the child has a preferred familiar caregiver, but the relationship is such that the child cannot use the adult for safety while gradually exploring the environment). At age eight the children were assessed with a variety of measures including those designed to access representational systems, or the child's "internal working models". The twins' symptoms were indicative of different trajectories. The girl showed externalizing symptoms (particularly deceit), contradictory reports of current functioning, chaotic personal narratives, struggles with friendships, and emotional disengagement with her caregiver, resulting in a clinical picture described as "quite concerning". The boy still evidenced self-endangering behaviors as well as avoidance in relationships and emotional expression, separation anxiety and impulsivity and attention difficulties. It was apparent that life stressors had impacted each child differently. The narrative measures used were considered helpful in tracking how early attachment disruption is associated with later expectations about relationships.
One paper using questionnaires found that children aged three to six, diagnosed with RAD, scored lower on empathy but higher on self-monitoring (regulating your behavior to "look good"). These differences were especially pronounced based on ratings by parents, and suggested that children with RAD may systematically report their personality traits in overly positive ways. Their scores also indicated considerably more behavioral problems than scores of the control children.
Epidemiological data are limited, but reactive attachment disorder appears to be very uncommon. The prevalence of RAD is unclear but it is probably quite rare, other than in populations of children being reared in the most extreme, deprived settings such as some orphanages. There is little systematically gathered epidemiologic information on RAD. A cohort study of 211 Copenhagen children to the age of 18 months found a prevalence of 0.9%.
Attachment disorders tend to occur in a definable set of contexts such as within some types of institutions, in the presence of repeated changes of primary caregiver or of extremely neglectful identifiable primary caregivers who show persistent disregard for the child's basic attachment needs, but not all children raised in these conditions develop an attachment disorder. Studies undertaken on children from Eastern European orphanages from the mid-1990s showed significantly higher levels of both forms of RAD and of insecure patterns of attachment in the institutionalized children, regardless of how long they had been there. It would appear that children in institutions like these are unable to form selective attachments to their caregivers. The difference between the institutionalized children and the control group had lessened in the follow-up study three years later, although the institutionalized children continued to show significantly higher levels of indiscriminate friendliness. However, even among children raised in the most deprived institutional conditions the majority did not show symptoms of this disorder.
A 2002 study of children in residential nurseries in Bucharest, in which the DAI was used, challenged the current DSM and ICD conceptualizations of disordered attachment and showed that inhibited and disinhibited disorders could coexist in the same child.
There are two studies on the incidence of RAD relating to high risk and maltreated children in the U.S. Both used ICD, DSM and the DAI. The first, in 2004, reported that children from the maltreatment sample were significantly more likely to meet criteria for one or more attachment disorders than children from the other groups, however this was mainly the proposed new classification of disrupted attachment disorder rather than the DSM or ICD classified RAD or DAD. The second study, also in 2004, attempted to ascertain the prevalence of RAD and whether it could be reliably identified in maltreated rather than neglected toddlers. Of the 94 maltreated toddlers in foster care, 35% were identified as having ICD RAD and 22% as having ICD DAD, and 38% fulfilled the DSM criteria for RAD. This study found that RAD could be reliably identified and also that the inhibited and disinhibited forms were not independent. However, there are some methodological concerns with this study. A number of the children identified as fulfilling the criteria for RAD did in fact have a preferred attachment figure.
It has been suggested by some within the field of attachment therapy that RAD may be quite prevalent because severe child maltreatment, which is known to increase risk for RAD, is prevalent and because children who are severely abused may exhibit behaviors similar to RAD behaviors. The APSAC Taskforce consider this inference to be flawed and questionable. Severely abused children may exhibit similar behaviors to RAD behaviors but there are several far more common and demonstrably treatable diagnoses which may better account for these difficulties. Further, many children experience severe maltreatment and do not develop clinical disorders. Resilience is a common and normal human characteristic. RAD does not underlie all or even most of the behavioral and emotional problems seen in foster children, adoptive children, or children who are maltreated and rates of child abuse and/or neglect or problem behaviors are not a benchmark for estimates of RAD.
There are few data on comorbid conditions, but there are some conditions that arise in the same circumstances in which RAD arises, such as institutionalization or maltreatment. These are principally developmental delays and language disorders associated with neglect. Conduct disorders, oppositional defiant disorder, anxiety disorders, post-traumatic stress disorder and social phobia share many symptoms and are often comorbid with or confused with RAD. Attachment disorder behaviors amongst institutionalized children are correlated with attentional and conduct problems and cognitive levels but nonetheless appear to index a distinct set of symptoms and behaviors.
Reactive attachment disorder first made its appearance in standard nosologies of psychological disorders in DSM-III, 1980, following an accumulation of evidence on institutionalized children. The criteria included a requirement of onset before the age of 8 months and was equated with failure to thrive. Both these features were dropped in DSM-III-R, 1987. Instead, onset was changed to being within the first 5 years of life and the disorder itself was divided into two subcategories, inhibited and disinhibited. These changes resulted from further research on maltreated and institutionalized children and remain in the current version, DSM-IV, 1994, and its 2000 text revision, DSM-IV-TR, as well as in ICD-10, 1992. Both nosologies focus on young children who are not merely at increased risk for subsequent disorders but are already exhibiting clinical disturbance.
The broad theoretical framework for current versions of RAD is attachment theory, based on work conducted from the 1940s to the 1980s by John Bowlby, Mary Ainsworth and René Spitz. Attachment theory is a framework that employs psychological, ethological and evolutionary concepts to explain social behaviors typical of young children. Attachment theory focuses on the tendency of infants or children to seek proximity to a particular attachment figure (familiar caregiver), in situations of alarm or distress, behavior which appears to have survival value. This is known as a discriminatory or selective attachment. Subsequently, the child begins to use the caregiver as a base of security from which to explore the environment, returning periodically to the familiar person. Attachment is not the same as love and/or affection although they are often associated. Attachment and attachment behaviors tend to develop between the ages of six months and three years. Infants become attached to adults who are sensitive and responsive in social interactions with the infant, and who remain as consistent caregivers for some time. Caregiver responses lead to the development of patterns of attachment, that in turn lead to internal working models which will guide the individual's feelings, thoughts, and expectations in later relationships. For a diagnosis of reactive attachment disorder, the child's history and atypical social behavior must suggest the absence of formation of a discriminatory or selective attachment.
The pathological absence of a discriminatory or selective attachment needs to be differentiated from the existence of attachments with either typical or somewhat atypical behavior patterns, known as styles or patterns. There are four attachment styles ascertained and used within developmental attachment research. These are known as secure, anxious-ambivalent, anxious-avoidant, (all organized) and disorganized. The latter three are characterised as insecure. These are assessed using the Strange Situation Procedure, designed to assess the quality of attachments rather than whether an attachment exists at all.
A securely attached toddler will explore freely while the caregiver is present, engage with strangers, be visibly upset when the caregiver departs, and happy to see the caregiver return. The anxious-ambivalent toddler is anxious of exploration, extremely distressed when the caregiver departs but ambivalent when the caregiver returns. The anxious-avoidant toddler will not explore much, avoid or ignore the parent—showing little emotion when the parent departs or returns—and treat strangers much the same as caregivers with little emotional range shown. The disorganized/disoriented toddler shows a lack of a coherent style or pattern for coping. Evidence suggests this occurs when the caregiving figure is also an object of fear, thus putting the child in an irresolvable situation regarding approach and avoidance. On reunion with the caregiver, these children can look dazed or frightened, freezing in place, backing toward the caregiver or approaching with head sharply averted, or showing other behaviors implying fear of the person who is being sought. It is thought to represent a breakdown of an inchoate attachment strategy and it appears to affect the capacity to regulate emotions.
Although there are a wide range of attachment difficulties within the styles which may result in emotional disturbance and increase the risk of later psychopathologies, particularly the disorganized style, none of the styles constitute a disorder in themselves and none equate to criteria for RAD as such. A disorder in the clinical sense is a condition requiring treatment, as opposed to risk factors for subsequent disorders. Reactive attachment disorder denotes a lack of typical attachment behaviors rather than an attachment style, however problematic that style may be, in that there is an unusual lack of discrimination between familiar and unfamiliar people in both forms of the disorder. Such discrimination does exist as a feature of the social behavior of children with atypical attachment styles. Both DSM-IV and ICD-10 depict the disorder in terms of socially aberrant behavior in general rather than focusing more specifically on attachment behaviors as such. DSM-IV emphasizes a failure to initiate or respond to social interactions across a range of relationships and ICD-10 similarly focuses on contradictory or ambivalent social responses that extend across social situations. The relationship between patterns of attachment in the Strange Situation and RAD is not yet clear.
There is a lack of consensus about the precise meaning of the term "attachment disorder". The term is frequently used both as an alternative to reactive attachment disorder and in discussions about different proposed classifications for disorders of attachment beyond the limitations of the ICD and DSM classifications. It is also used within the field of attachment therapy, as is the term reactive attachment disorder, to describe a range of problematic behaviors not within the ICD or DSM criteria or not related directly to attachment styles or difficulties at all.
Research from the late 1990s indicated there were disorders of attachment not captured by DSM or ICD and showed that RAD could be diagnosed reliably without evidence of pathogenic care, thus illustrating some of the conceptual difficulties with the rigid structure of the current definition of RAD. Research published in 2004 showed that the disinhibited form can endure alongside structured attachment behavior (of any style) towards the child's permanent caregivers.
Some authors have proposed a broader continuum of definitions of attachment disorders ranging from RAD through various attachment difficulties to the more problematic attachment styles. There is as yet no consensus, on this issue but a new set of practice parameters containing three categories of attachment disorder has been proposed by C.H. Zeanah and N. Boris. The first of these is disorder of attachment, in which a young child has no preferred adult caregiver. The proposed category of disordered attachment is parallel to RAD in its inhibited and disinhibited forms, as defined in DSM and ICD. The second category is secure base distortion, where the child has a preferred familiar caregiver, but the relationship is such that the child cannot use the adult for safety while gradually exploring the environment. Such children may endanger themselves, cling to the adult, be excessively compliant, or show role reversals in which they care for or punish the adult. The third type is disrupted attachment. Disrupted attachment is not covered under ICD-10 and DSM criteria, and results from an abrupt separation or loss of a familiar caregiver to whom attachment has developed. This form of categorisation may demonstrate more clinical accuracy overall than the current DSM-IV-TR classification, but further research is required. The practice parameters would also provide the framework for a diagnostic protocol. Most recently, Daniel Schechter and Erica Willheim have shown a relationship between some maternal violence-related posttraumatic stress disorder and secure base distortion (see above) which is characterized by child recklessness, separation anxiety, hypervigilance, and role-reversal.
Some research indicates there may be a significant overlap between behaviors of the inhibited form of RAD or DAD and aspects of disorganized attachment where there is an identified attachment figure.
An ongoing question is whether RAD should be thought of as a disorder of the child's personality or a distortion of the relationship between the child and a specific other person. It has been noted that as attachment disorders are by their very nature relational disorders, they do not fit comfortably into noslogies that characterize the disorder as centered on the person. Work by C.H. Zeanah indicates that atypical attachment-related behaviors may occur with one caregiver but not with another. This is similar to the situation reported for attachment styles, in which a particular parent's frightened expression has been considered as possibly responsible for disorganized/disoriented reunion behavior during the Strange Situation Procedure.
The draft of the proposed DSM-V suggests dividing RAD into two disorders, Reactive Attachment Disorder for the current inhibited form of RAD, and Disinhibited Social Engagement Disorder for what is currently the disinhibited form of RAD, with some alterations in the proposed DSM definition. | <urn:uuid:a3d71a22-22b4-410b-8173-abdde3ecde54> | {
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Writing a Research Abstract
The written abstract is used in making selections for presentations at scientific meetings. Writing a good abstract is a formidable undertaking and many novice researchers wonder how it is possible to condense months of work into 300 to 400 words. Nevertheless, creating a well-written abstract is a skill that can be learned and mastering the skill will increase the probability that your research will be selected for presentation.
The first rule of writing abstracts is to know the rules. Organizers of scientific meetings set explicit limits on the length abstracts.
Authors must pay close attention to the published details of the meeting including deadlines and suggested format. Since reviewers have many abstracts to read and rank; those that don't conform to the stated rules are simply discarded.
The scientific abstract is usually divided into five unique sections: Title and Author Information, Introduction, Methods, Results, and Conclusions. The following paragraphs summarize what is expected in each of these sections.
Title and Author Information: The title should summarize the abstract and convince the reviewers that the topic is important, relevant, and innovative. To create a winning title, write out 6 to 10 key words found in the abstract and string them into various sentences. Once you have a sentence that adequately conveys the meaning of the work, try to condense the title yet still convey the essential message. Some organizations require a special format for the title, such as all uppercase letters, all bolded, or in italics. Be sure to check the instructions.
Following the title, the names of all authors and their institutional affiliations are listed. It is assumed the first author listed will make the oral presentation. Determine if the first author needs to meet any eligibility requirements to make the presentation. For example, the first author may need to be a member of the professional society sponsoring the research meeting. This information is always included with the abstract instructions.
Introduction: This usually consists of several sentences outlining the question addressed by the research. Make the first sentence of the introduction as interesting and dramatic as possible. For example, "100,000 people each year die of…" is more interesting than "An important cause of mortality is…" If space permits, provide a concise review of what is known about the problem addressed by the research, what remains unknown, and how your research project fills the knowledge gaps. The final sentence of the introduction describes the purpose of the study or the study's a priori hypothesis.
Methods: This is the most difficult section of the abstract to write. It must be scaled down sufficiently to allow the entire abstract to fit into the box, but at the same time it must be detailed enough to judge the validity of the work. For most clinical research abstracts, the following areas are specifically mentioned: research design; research setting; number of patients enrolled in the study and how they were selected; a description of the intervention (if appropriate); and a listing of the outcome variables and how they were measured. Finally, the statistical methods used to analyze the data are described.
Results: This section begins with a description of the subjects that were included and excluded from the study. For those excluded, provide the reason for their exclusion. Next, list the frequencies of the most important outcome variables. If possible, present comparisons of the outcome variables between various subgroups within the study (treated vs. untreated, young vs. old, male vs. female, and so forth). This type of data can be efficiently presented in a table, which is an excellent use of space. But before doing this, check the rules to see if tables can be used in the abstract. Numerical results should include standard deviations or 95% confidence limits and the level of statistical significance. If the results are not statistically significant, present the power of your study (beta-error rate) to detect a difference.
Conclusion: State concisely what can be concluded and its implications. The conclusions must be supported by the data presented in the abstract; never present unsubstantiated personal opinion. If there is room, address the generalizability of the results to populations other than that studied and the weaknesses of the study.
Research literature has a special language that concisely and precisely communicates meaning to other researches. Abstracts should contain this special language and be used appropriately. See The Glossary of commonly used research terms.
Avoid the use of medical jargon and excessive reliance on abbreviations. Limit abbreviations to no more than three and favor commonly used abbreviations. Always spell out the abbreviations the first time they are mentioned unless they are commonly recognized (e.g., CBC).
Although short in length, a good abstract typically takes several days to write. Take this into account when budgeting your time. Seek the help of an experienced mentor. Share the abstract with your mentor and make revisions based upon the feedback. Allow others to read your draft for clarity and to check for spelling and grammatical mistakes. Reading the abstract orally is an excellent way to catch grammatical errors and word omissions. Use the Scientific Abstract Checklist to assist your completion of the task. Finally, an example of an abstract previously accepted for presentation at the ACP Resident Research Competition is attached for your review.
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Making the Most of Your ICD-10 Transition
To help you and your practice make a smooth and successful transition to ICD-10 coding, ACP and ICD-10 content developers have created multiple resources available at discounted rates for ACP members. | <urn:uuid:e977bbe1-a3d7-4c82-bf61-4f9c676a292d> | {
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High-functioning autism and Asperger syndrome are both part of the 'autism spectrum'. The main difference between the two is thought to be in language development: people with Asperger syndrome, typically, will not have had delayed language development when younger.
Signs of high-functioning autism and Asperger syndrome
Gillberg and Ehlers (1998) identify four main areas where controversy over the difference in diagnosis still exists.
Level of cognitive functioning
The view that Asperger syndrome is autism without any additional learning disability is helpful from the diagnostic point of view as it is fairly easy to make a distinction in these circumstances. However, Asperger himself said that there might be unusual circumstances where a person could present the symptoms of Asperger syndrome with additional learning disability. It is widely recognised that high-functioning autism cannot occur in someone with an IQ below 65-70.
In recent years the view that Asperger syndrome can only occur when there are additional difficulties with motor skills has become more prominent. Certainly Asperger himself was well aware of the prevalence of motor skill problems in the group of people he tried to describe. It seems likely that most children with Asperger syndrome experience poor co-ordination and difficulties with fine motor control. However, many children with higher functioning autism will also have difficulties in these areas.
This is the area that probably causes the greatest controversy. Both ICD-10 and DSM-IV1 state that for a diagnosis of Asperger syndrome, spoken language development must be normal. Children with high-functioning autism may have had significant language delay. However, Asperger's original descriptions of the condition stated that speech and language peculiarities are a key feature of Asperger syndrome. Often diagnoses of Asperger syndrome are made when a child is quite old and they or their parents may have difficulty remembering the details of their language development.
Age of onset
A diagnosis of high-functioning autism and one of Asperger syndrome can be made in the same individual at different stages of development. Occasionally a child has been diagnosed with high-functioning autism in early childhood and this diagnosis has been changed to Asperger syndrome when they started school. Some diagnosticians are clearly of the view that Asperger syndrome cannot be diagnosed before a child starts school. However this is largely because areas such as social skills deficits may not become apparent until a child spends a lot of time in social settings.
- Both people with high-functioning autism and Asperger syndrome are affected by the 'triad of impairments' common to all people with autism.
- Both groups are likely to be of average or above average intelligence.
- The debate as to whether we need two diagnostic terms is ongoing.
- However, there may be features such as age of onset and motor skill deficits which differentiate the two conditions.
Although it is frustrating to be given a diagnosis which has yet to be clearly defined it is worth remembering that the fundamental presentation of the two conditions is largely the same. This means that treatments, therapies and educational approaches should also be largely similar. At the same time, all people with autism or Asperger syndrome are unique and have their own special skills and abilities. These deserve as much recognition as the areas they have difficulty in.
If you or your son or daughter has recently been given a diagnosis of either high-functioning autism or Asperger syndrome then it is worth checking what criteria the diagnostician was using.
Read about the history of the terms 'high-functioning autism' and Asperger syndrome on the next page.
The history of the term 'autism' and Asperger syndrome
The controversy over the differences between high-functioning autism and Asperger syndrome goes back a long way: here we examine some of the literature available and the reasoning behind the existence of the two separate terms.
The term 'autism' has an unusual history. It was originally coined by a psychiatrist Eugen Bleuler in 1911 to describe what he perceived as one of the key symptoms of schizophrenia, that of social withdrawal. Autism, literally meaning 'selfism', seemed to him to describe the active detachment which affected many of his patients.
Leo Kanner and Hans Asperger
In the 1940s when Leo Kanner in America and Hans Asperger in Austria were both beginning to identify the existence of autism they separately stumbled on this term which they felt described what they were witnessing in the children they were treating.
Kanner started from the premise that these children were experiencing childhood schizophrenia. In time he became aware that they were not exhibiting all the symptoms of schizophrenia and used the phrase 'infantile autism' to describe their condition.
Asperger identified a personality disorder affecting some of the children referred to his child psychiatry clinic which he felt was described, albeit imperfectly, by the term autism. His acute identification of autism was extraordinarily ahead of its time considering he was among the first people to chart it. Unlike schizophrenic patients, children with autism do not show a disintegration of personality. They are not psychotic; instead they show a greater or lesser degree of autism.
Kanner, an American, was writing in English. His paper was published in the UK where it gained a lot of attention. The term 'infantile autism' became increasingly widely used in the 1950s and 60s, more and more children were diagnosed with the condition. In the English-speaking world the work of Hans Asperger went largely ignored. However, in Europe he continued to conduct research and have an influence over child psychiatry.
Judith Gould and Lorna Wing's research
We don't know if Kanner was ever aware of the work of Asperger but we do know that Asperger in later years read about the work of Leo Kanner. He argued, albeit unconvincingly, that they had identified separate syndromes with a great overlap. Other academics began to argue that Asperger's and Kanner's autism were the same syndrome. Most notably Judith Gould and Lorna Wing in their ground-breaking study in Camberwell in the late 1970s came to the conclusion that autism existed on a continuum. In 1981, Lorna Wing used the phrase 'Asperger syndrome' in a research paper to describe a distinct sub-group of patients that she had been seeing. The term became much more widely used in the English-speaking world as a result. Some professionals have felt that Asperger syndrome is a more acceptable diagnosis from the point of view of parents. They argue that there is a social stigma attached to autism which is not attached to the term Asperger syndrome.
In the case of Asperger syndrome its recognition has resulted in its placement among developmental disorders in general and autistic spectrum disorders in particular. It may well be proved to have no independent existence but this does not detract from Asperger's achievement in discerning something very special in the children he described."
Uta Frith, 1998
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False memory syndrome
||It has been suggested that this article be merged into False memory. (Discuss) Proposed since July 2014.|
False memory syndrome (FMS) describes a condition in which a person's identity and relationships are affected by memories that are factually incorrect but that they strongly believe. Peter J. Freyd originated the term, which the False Memory Syndrome Foundation (FMSF) subsequently popularized. The term is not recognized as a mental disorder in any of the medical manuals, such as the ICD-10 or the DSM-5; however, the principle that memories can be altered by outside influences is overwhelmingly accepted by scientists.
False memories may be the result of recovered memory therapy, a term also defined by the FMSF in the early 1990s, which describes a range of therapy methods that are prone to creating confabulations. Some of the influential figures in the genesis of the theory are forensic psychologist Ralph Underwager, psychologist Elizabeth Loftus and sociologist Richard Ofshe.
False memory syndrome is a condition in which a person's identity and interpersonal relationships center around a memory of a traumatic experience that is objectively false but that the person strongly believes. Note that the syndrome is not characterized by false memories as such. We all have inaccurate memories. Rather, the syndrome is diagnosed when the memory is so deeply ingrained that it orients the individual's entire personality and lifestyle—disrupting other adaptive behavior. False memory syndrome is destructive because the person assiduously avoids confronting evidence that challenges the memory. Thus it takes on a life of its own; the memory becomes encapsulated and resistant to correction. Subjects may focus so strongly on the memory that it effectively distracts them from coping with real problems in their life.
The FMS concept is controversial, and the Diagnostic and Statistical Manual of Mental Disorders does not include it. Paul R. McHugh, member of the FMSF, stated that the term was not adopted into the fourth version of the manual due to the pertinent committee being headed by believers in recovered memory.
Recovered memory therapy
Recovered memory therapy is used to describe the therapeutic processes and methods that are believed to create false memories and false memory syndrome. These methods include hypnosis, sedatives and probing questions where the therapist believes repressed memories of traumatic events are the cause of their client's problems. The term is not listed in DSM-IV or used by any mainstream formal psychotherapy modality.
Memory consolidation becomes a critical element of false memory and recovered memory syndromes. Once stored in the hippocampus, the memory may last for years or even for life, regardless that the memorized event never actually took place. Obsession to a particular false memory, planted memory, or indoctrinated memory can shape a person's actions or even result in delusional disorder.
Mainstream psychiatric and psychological professional associations now harbor strong skepticism towards the notion of recovered memories of trauma. They argue that self-help books, and recovered memory therapists can influence adults to develop false memories. According to this theory, psychologists and psychiatrists may accidentally implant these false memories. The American Psychiatric Association and American Medical Association condemn such practices, whether they are formally called "Recovered Memory Therapy" or simply a collection of techniques that fit the description. In 1998, the Royal College of Psychiatrists Working Group on Reported Recovered Memories of Sexual Abuse wrote:
No evidence exists for the repression and recovery of verified, severely traumatic events, and their role in symptom formation has yet to be proved. There is also striking absence in the literature of well-corroborated cases of such repressed memories recovered through psychotherapy. Given the prevalence of childhood sexual abuse, even if only a small proportion are repressed and only some of them are subsequently recovered, there should be a significant number of corroborated cases. In fact there are none.
That such techniques have been used in the past is undeniable. Their continued use is cause for malpractice litigation worldwide. An Australian psychologist was de-registered for engaging in them.
Evidence for false memories
Human memory is created and highly suggestible, and can create a wide variety of innocuous, embarrassing, and frightening memories through different techniques—including guided imagery, hypnosis, and suggestion by others. Though not all individuals exposed to these techniques develop memories, experiments suggest a significant number of people do, and will actively defend the existence of the events, even if told they were false and deliberately implanted. Questions about the possibility of false memories created an explosion of interest in suggestibility of human memory and resulted in an enormous increase in the knowledge about how memories are encoded, stored and recalled, producing pioneering experiments such as the lost in the mall technique. In Roediger and McDermott's (1995) experiment, subjects were presented with a list of related items (such as candy, sugar, honey) to study. When asked to recall the list, participants were just as, if not more, likely to recall semantically related words (such as sweet) than items that were actually studied, thus creating false memories. This experiment, though widely replicated, remains controversial due to debate considering that people may store semantically related items from a word list conceptually rather than as language, which could account for errors in recollection of words without the creation of false memories. Susan Clancy discovered that people claiming to have been victims of alien abductions are more likely to recall semantically related words than a control group in such an experiment.
The lost in the mall technique is a research method designed to implant a false memory of being lost in a shopping mall as a child to test whether discussing a false event could produce a "memory" of an event that did not happen. In her initial study, Elizabeth Loftus found that 25% of subjects came to develop a "memory" for the event which had never actually taken place. Extensions and variations of the lost in the mall technique found that an average of one third of experimental subjects could become convinced that they experienced things in childhood that had never really occurred—even highly traumatic, and impossible events.
Sexual abuse cases
The question of the accuracy and dependability of a repressed memory that someone has later recalled has contributed to some investigations and court cases, including cases of alleged sexual abuse or child sexual abuse (CSA). while others have been deemed confabulations or "false memories" that were not legally admissible. The research of Elizabeth Loftus has been used to counter claims of recovered memory in court and it has resulted in stricter requirements for the use of recovered memories being used in trials, as well as a greater requirement for corroborating evidence. In addition, some states no longer allow prosecution based on recovered memory testimony. Insurance companies have become reluctant to insure therapists against malpractice suits relating to recovered memories.
Supporters of recovered memories believe that there is "overwhelming evidence that the mind is capable of repressing traumatic memories of child sexual abuse." Whitfield states that the "false memory" defense is "seemingly sophisticated, but mostly contrived and often erroneous." He states that this defense has been created by "accused, convicted and self-confessed child molesters and their advocates" to try to "negate their abusive, criminal behavior." Brown states that when pro-false memory expert witnesses and attorneys state there is no causal connection between CSA and adult psychopathology, that CSA doesn't cause specific trauma-related problems like borderline and dissociative identity disorder, that other variables than CSA can explain the variance of adult psychopathology and that the long-term effects of CSA are non-specific and general, that this testimony is inaccurate and has the potential of misleading juries.
During the late 1990s, there were multiple lawsuits in the United States in which psychiatrists and psychologists were successfully sued, or settled out of court, on the charge of propagating iatrogenic memories of childhood sexual abuse, incest and satanic ritual abuse.
Some of these suits were brought by individuals who later declare that their recovered memories of incest or satanic ritual abuse had been false. The False Memory Syndrome Foundation uses the term retractors to describe these individuals, and have shared their stories publicly. There is debate regarding the total number of retractions as compared to the total number of allegations, and the reasons for retractions.
- False allegation of child sexual abuse
- Alien abduction
- Lost in the mall technique
- McMartin preschool trial
- Memory bias
- Memory conformity
- McHugh, PR (2008). Try to remember: Psychiatry's clash over meaning, memory and mind. Dana Press. pp. 66–7. ISBN 1-932594-39-6.
- McHugh 2008, p. 55.
- Rix, Rebecca (2000). Sexual abuse litigation: a practical resource for attorneys, clinicians, and advocates. Routledge. p. 33. ISBN 0-7890-1174-3.
- "icd 10 codes: psychiatry". Priory Lodge Education Ltd. Retrieved 21 October 2013.
- American Psychiatric Association (2013). Diagnostic and Statistical Manual of Mental Disorders (Fifth ed.). Arlington, VA: American Psychiatric Publishing. ISBN 978-0-89042-555-8.
- Paterson, H. M., Kemp, R. I., & Forgas, J. P. (2010). "Co-witnesses, confederates, and conformity: The effects of discussion and delay on eyewitness memory.," Psychiatry, Psychology and Law.
- Loftus, Elizabeth F. Memory: Surprising New Insights Into How We Remember and Why We Forget (Reading, Mass.: Addison-Wesley Pub. Co., 1980).
- Schacter, Daniel L. The Seven Sins of Memory : How the Mind Forgets and Remembers (Houghton Mifflin Co., 2001).
- Association for Psychological Science (2008, August 20). "False Memories Affect Behavior."
- Whitfield, Charles L.; Joyanna L. Silberg; Paul Jay Fink (2001). Misinformation Concerning Child Sexual Abuse and Adult Survivors. Haworth Press. p. 56. ISBN 0-7890-1901-9.
- McHugh 2008, pp. 67–68.
- Dallam, S. (2002). "Crisis or Creation: A systematic examination of false memory claims". Journal of Child Sexual Abuse 9 (3/4): 9–36. doi:10.1300/J070v09n03_02. PMID 17521989. Retrieved 2008-06-27.
- Dalenberg, C (2006). "Recovered memory and the Daubert criteria: recovered memory as professionally tested, peer reviewed, and accepted in the relevant scientific community". Trauma Violence Abuse 7 (4): 274–310. doi:10.1177/1524838006294572. PMID 17065548.
- McHugh 2008, p. 63.
- Brandon S, Boakes J, Glaser D & Green R (1998). "Recovered memories of childhood sexual abuse: implications for clinical practice". British Journal of Psychiatry 172: 296–307. doi:10.1192/bjp.172.4.296. PMID 9722329.
- "Malpractice Suit Against Dr. Bennett Braun". Fortea.us. Retrieved 2010-12-12.
- "HEALTH CARE COMPLAINTS COMMISSION v TYNAN NSWPST 1". Austlii.edu.au. 10 February 2010. Retrieved 2010-12-12.
- Schacter, DL (2002). The Seven Sins of Memory: How the Mind Forgets and Remembers. Houghton Mifflin Harcourt. pp. 123–30. ISBN 0-618-21919-6.
- Roediger, Henry L.; Kathleen B. McDermott (July 1995). "Creating False Memories: Remembering Words Not Presented in Lists". Journal of Experimental Psychology: Learning, Memory, and Cognition. 4 21: 803–814. doi:10.1037/0278-73126.96.36.1993.
- "Starship memories". Harvard Gazette. October 31, 2002. Retrieved 2014-02-23.
- Wilson, A (2002-11-03). "War & remembrance: Controversy is a constant for memory researcher Elizabeth Loftus, newly installed at UCI". The Orange County Register. Retrieved 2009-01-19.
- Strange, D; Clifasefi S & Garry M (2007). "False memories.". In Garry M & Hayne H. Do Justice and Let the Sky Fall: Elizabeth F. Loftus and Her Contributions to Science, Law, and Academic Freedom. Mahwah, NJ: Lawrence Erlbaum Associates. pp. 137–68. ISBN 0805852328.
- Ramirez, S., et al., (2013). Creating a False Memory in the Hippocampus Science 26 July 2013: Vol. 341 no. 6144 pp. 387-391 doi:10.1126/science.1239073
- Jha, Alok (25 July 2013). "False memory planted in mouse's brain". The Guardian.
- "Are Recovered Memories Reliable?". Religioustolerance.org. Retrieved 2010-12-12.
- Colleen Born. "Elizabeth Loftus". Muskingum.edu. Retrieved 2010-12-12.
- "The Recovered Memory Project". Brown.edu. 1993-05-03. Retrieved 2010-12-12.
- Neimark, J. (1996). The diva of disclosure, memory researcher Elizabeth Loftus. Psychology Today, 29, 48-53,80.
- Saletan, W (2010-06-04). "The memory doctor: the future of false memories". Slate. Retrieved 2012-05-08.
- Murphy, W. "Debunking 'false memory'myths in sexual abuse cases". Archived from the original on 2008-01-07. Retrieved 2008-01-10.
- Whitfield, C. (March 2002). "The "False Memory" Defense Using Disinformation and Junk Science In and Out of Court". Journal of Child Sexual Abuse 9 (3/4): 53–78. doi:10.1300/J070v09n03_04. Retrieved 2008-01-11.
- Brown, D. (2001). "(Mis)representation of the Long-Term Effects of Childhood Sexual Abuse in the Courts". Journal of Child Sexual Abuse 9 (3/4): 79–107. doi:10.1300/J070v09n03_05. PMID 17521992. Retrieved 2008-01-28.
- "Recovered Memory Lawsuit Sparks Litigation". Psychiatrictimes.com. Retrieved 2010-12-12.
- Macdonald, Gail (1999). "Women Against Women". Making of an Illness: My Experience With Multiple Personality Disorder. Sudbury, Ontario: Laurentian University Press. p. 111. ISBN 0-88667-045-4. Retrieved 31 July 2013.
- Summit, R. (1983). "The child sexual abuse accommodation syndrome". Child Abuse & Neglect 7 (2): 177–193. doi:10.1016/0145-2134(83)90070-4. PMID 6605796.
- False memory syndrome at DMOZ
- Memory controversies at DMOZ
- is a website with information from all sides of the issue. Primary resources include an extensive bibliography / abstract database and pre-print archive. Also available are sections for criminal investigation, criminal defense and many other useful resources.
- False Memory Syndrome, Child & Woman Abuse Study Unit, London Metropolitan Hospital. Argues that "false memories" are real memories. | <urn:uuid:5f7be681-78c0-458f-8c47-5ec8c7e63201> | {
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Fetal alcohol syndrome
|Fetal alcohol syndrome|
Baby with fetal alcohol syndrome.
|Classification and external resources|
|Patient UK||Fetal alcohol syndrome|
Fetal alcohol syndrome (FAS) or foetal alcohol syndrome is a pattern of physical and mental defects that can develop in a fetus in association with high levels of alcohol consumption during pregnancy. Alcohol crosses the placental barrier and can stunt fetal growth or weight, create distinctive facial stigmata, damage neurons and brain structures, which can result in intellectual disability and other psychological or behavioral problems, and also cause other physical damage. The main effect of FAS is permanent central nervous system damage, especially to the brain. Developing brain cells and structures can be malformed or have development interrupted by prenatal alcohol exposure; this can create an array of primary cognitive and functional disabilities (including poor memory, attention deficits, impulsive behavior, and poor cause-effect reasoning) as well as secondary disabilities (for example, predispositions to mental health problems and drug addiction). Alcohol exposure presents a risk of fetal brain damage at any point during a pregnancy, since brain development is ongoing throughout pregnancy.
As of 1987, fetal alcohol exposure was the leading known cause of intellectual disability in the Western world. In the United States and Europe, the FAS prevalence rate is estimated to be between 0.2–2 in every 1000 live births. FAS should not be confused with Fetal Alcohol Spectrum Disorders (FASD), a condition which describes a continuum of permanent birth defects caused by maternal consumption of alcohol during pregnancy, which includes FAS, as well as other disorders, and which affects about 1% of live births in the US (i.e., about 10 cases per 1000 live births). The lifetime medical and social costs of FAS are estimated to be as high as US$800,000 per child born with the disorder. Surveys found that in the United States, 10–15% of pregnant women report having recently drunk alcohol, and up to 30% drink alcohol at some point during pregnancy. The current recommendation of the Surgeon General of the United States, the British Department of Health and the Australian Government National Health and Medical Research Council is to drink no alcohol at all during pregnancy.
- 1 Signs and symptoms
- 2 Causes
- 3 Diagnosis
- 4 Prevention
- 5 Treatment
- 6 Prognosis
- 7 History
- 8 References
- 9 Further reading
- 10 External links
Signs and symptoms
Growth deficiency is defined as below average height, weight or both due to prenatal alcohol exposure, and can be assessed at any point in the lifespan. Growth measurements must be adjusted for parental height, gestational age (for a premature infant), and other postnatal insults (e.g., poor nutrition), although birth height and weight are the preferred measurements. Deficiencies are documented H191 when height or weight falls at or below the 10th percentile of standardized growth charts appropriate to the patient's population.
The CDC and Canadian guidelines use the 10th percentile as a cut-off to determine growth deficiency. The "4-Digit Diagnostic Code" (4-DDC), allows for mid-range gradations in growth deficiency (between the 3rd and 10th percentiles) and severe growth deficiency at or below the 3rd percentile. Growth deficiency (at severe, moderate, or mild levels) contributes to diagnoses of FAS and PFAS (Partial Fetal Alcohol Syndrome), but not ARND (Alcohol-Related Neurodevelopmental Disorder) or static encephalopathy.
Growth deficiency is ranked as follows by the 4-DDC:
- Severe — Height and weight at or below the 3rd percentile.
- Moderate — Either height or weight at or below the 3rd percentile, but not both.
- Mild — Both height and weight between the 3rd and 10th percentiles.
- None — Height and weight both above the 10th percentile.
Several characteristic craniofacial abnormalities are often visible in individuals with FAS. The presence of FAS facial features indicates brain damage, though brain damage may also exist in their absence. FAS facial features (and most other visible, but non-diagnostic, deformities) are believed to be caused mainly during the 10th and 20th week of gestation.
Refinements in diagnostic criteria since 1975 have yielded three distinctive and diagnostically significant facial features known to result from prenatal alcohol exposure and distinguishes FAS from other disorders with partially overlapping characteristics. The three FAS facial features are:
- A smooth philtrum — The divot or groove between the nose and upper lip flattens with increased prenatal alcohol exposure.
- Thin vermilion — The upper lip thins with increased prenatal alcohol exposure.
- Small palpebral fissures — Eye width decreases with increased prenatal alcohol exposure.
Measurement of FAS facial features uses criteria developed by the University of Washington. The lip and philtrum are measured by a trained physician with the Lip-Philtrum Guide, a 5-point Likert Scale with representative photographs of lip and philtrum combinations ranging from normal (ranked 1) to severe (ranked 5). Palpebral fissure length (PFL) is measured in millimeters with either calipers or a clear ruler and then compared to a PFL growth chart, also developed by the University of Washington.
- Severe — All three facial features ranked independently as severe (lip ranked at 4 or 5, philtrum ranked at 4 or 5, and PFL two or more standard deviations below average).
- Moderate — Two facial features ranked as severe and one feature ranked as moderate (lip or philtrum ranked at 3, or PFL between one and two standard deviations below average).
- Mild — A mild ranking of FAS facial features covers a broad range of facial feature combinations:
- Two facial features ranked severe and one ranked within normal limits,
- One facial feature ranked severe and two ranked moderate, or
- One facial feature ranked severe, one ranked moderate and one ranked within normal limits.
- None — All three facial features ranked within normal limits.
These distinctive facial features in a patient do strongly correlate to brain damage. Sterling Clarren of the University of Washington's Fetal Alcohol and Drug Unit told a conference in 2002:
“I have never seen anybody with this whole face who doesn't have some brain damage. In fact in studies, as the face is more FAS-like, the brain is more likely to be abnormal. The only face that you would want to counsel people or predict the future about is the full FAS face. But the risk of brain damage increases as the eyes get smaller, as the philtrum gets flatter, and the lip gets thinner. The risk goes up but not the diagnosis.”
“At one-month gestation, the top end of your body is a brain, and at the very front end of that early brain, there is tissue that has been brain tissue. It stops being brain and gets ready to be your face ... Your eyeball is also brain tissue. It's an extension of the second part of the brain. It started as brain and "popped out." So if you are going to look at parts of the brain from alcohol damage, or any kind of damage during pregnancy, eye malformations and midline facial malformations are going to be very actively related to the brain across syndromes ... and they certainly are with FAS.”
Central nervous system
Central nervous system (CNS) damage is the primary feature of any Fetal Alcohol Spectrum Disorder (FASD) diagnosis. Prenatal exposure to alcohol — which is classified as a teratogen — can damage the brain across a continuum of gross to subtle impairments, depending on the amount, timing, and frequency of the exposure as well as genetic predispositions of the fetus and mother. While functional abnormalities are the behavioral and cognitive expressions of the FAS disability, CNS damage can be assessed in three areas: structural, neurological, and functional impairments.
All four diagnostic systems allow for assessment of CNS damage in these areas, but criteria vary. The IOM system requires structural or neurological impairment for a diagnosis of FAS. The 4-DDC and CDC guidelines state that functional anomalies must measure at two standard deviations or worse in three or more functional domains for a diagnosis of FAS. The 4-DDC further elaborates the degree of CNS damage according to four ranks:
- Definite — Structural impairments or neurological impairments for FAS or static encephalopathy.
- Probable — Significant dysfunction of two standard deviations or worse in three or more functional domains.
- Possible — Mild to moderate dysfunction of two standard deviations or worse in one or two functional domains or by judgment of the clinical evaluation team that CNS damage cannot be dismissed.
- Unlikely — No evidence of CNS damage.
Structural abnormalities of the brain are observable, physical damage to the brain or brain structures caused by prenatal alcohol exposure. Structural impairments may include microcephaly (small head size) of two or more standard deviations below the average, or other abnormalities in brain structure (e.g., agenesis of the corpus callosum, cerebellar hypoplasia).
Microcephaly is determined by comparing head circumference (often called occipitofrontal circumference, or OFC) to appropriate OFC growth charts. Other structural impairments must be observed through medical imaging techniques by a trained physician. Because imaging procedures are expensive and relatively inaccessible to most patients, diagnosis of FAS is not frequently made via structural impairments, except for microcephaly.
During the first trimester of pregnancy, alcohol interferes with the migration and organization of brain cells, which can create structural deformities or deficits within the brain. During the third trimester, damage can be caused to the hippocampus, which plays a role in memory, learning, emotion, and encoding visual and auditory information, all of which can create neurological and functional CNS impairments as well.
As of 2002, there were 25 reports of autopsies on infants known to have FAS. The first was in 1973, on an infant who died shortly after birth. The examination revealed extensive brain damage, including microcephaly, migration anomalies, callosal dysgenesis, and a massive neuroglial, leptomeningeal heterotopia covering the left hemisphere.
In 1977, Dr. Clarren described a second infant whose mother was a binge drinker. The infant died ten days after birth. The autopsy showed severe hydrocephalus, abnormal neuronal migration, and a small corpus callosum (which connects the two brain hemispheres) and cerebellum. FAS has also been linked to brainstem and cerebellar changes, agenesis of the corpus callosum and anterior commissure, neuronal migration errors, absent olfactory bulbs, meningomyelocele, and porencephaly.
When structural impairments are not observable or do not exist, neurological impairments are assessed. In the context of FAS, neurological impairments are caused by prenatal alcohol exposure which causes general neurological damage to the central nervous system (CNS) and the peripheral nervous system (PNS). A determination of a neurological problem must be made by a trained physician, and must not be due to a postnatal insult, such as a high fever, concussion, traumatic brain injury, etc.
All four diagnostic systems show virtual agreement on their criteria for CNS damage at the neurological level, and evidence of a CNS neurological impairment due to prenatal alcohol exposure will result in a diagnosis of FAS, and functional impairments are highly likely.
Neurological problems are expressed as either hard signs, or diagnosable disorders, such as epilepsy or other seizure disorders, or soft signs. Soft signs are broader, nonspecific neurological impairments, or symptoms, such as impaired fine motor skills, neurosensory hearing loss, poor gait, clumsiness, poor eye-hand coordination. Many soft signs have norm-referenced criteria, while others are determined through clinical judgment. "Clinical judgment" is only as good as the clinician, and soft signs should be assessed by either a pediatric neurologist, a pediatric neuropsychologist, or both. Those affected have mild retardation.
When structural or neurological impairments are not observed, all four diagnostic systems allow CNS damage due to prenatal alcohol exposure to be assessed in terms of functional impairments. Functional impairments are deficits, problems, delays, or abnormalities due to prenatal alcohol exposure (rather than hereditary causes or postnatal insults) in observable and measurable domains related to daily functioning, often referred to as developmental disabilities. There is no consensus on a specific pattern of functional impairments due to prenatal alcohol exposure and only CDC guidelines label developmental delays as such, so criteria vary somewhat across diagnostic systems.
The four diagnostic systems list various CNS domains that can qualify for functional impairment that can determine an FAS diagnosis:
- Evidence of a complex pattern of behavior or cognitive abnormalities inconsistent with developmental level in the following CNS domains — sufficient for a PFAS (partial fetal alcohol syndrome) or ARND (alcohol-related neurodevelopmental disorder) diagnosis using IOM guidelines
- Performance at two or more standard deviations on standardized testing in three or more of the following CNS domains — sufficient for a FAS, PFAS or static encephalopathy diagnosis using the 4-DDC.
- General cognitive deficits (e.g., IQ) at or below the 3rd percentile on standardized testing — sufficient for an FAS diagnosis using CDC guidelines
- Performance at or below the 16th percentile on standardized testing in three or more of the following CNS domains — sufficient for an FAS diagnosis using CDC guidelines
- Performance at two or more standard deviations on standardized testing in three or more of the following CNS domains — sufficient for an FAS diagnosis using Canadian guidelines
Other conditions may commonly co-occur with FAS, stemming from prenatal alcohol exposure. However, these conditions are considered Alcohol-Related Birth Defects and not diagnostic criteria for FAS.
- Cardiac — A heart murmur that frequently disappears by one year of age. Ventricular septal defect most commonly seen, followed by an atrial septal defect.
- Skeletal — Joint anomalies including abnormal position and function, altered palmar crease patterns, small distal phalanges, and small fifth fingernails.
- Renal — Horseshoe, aplastic, dysplastic, or hypoplastic kidneys.
- Ocular — Strabismus, optic nerve hypoplasia (which may cause light sensitivity, decreased visual acuity, or involuntary eye movements).
- Occasional abnormalities — ptosis of the eyelid, microophthalmia, cleft lip with or without a cleft palate, webbed neck, short neck, tetralogy of Fallot, coarctation of the aorta, spina bifida, and hydrocephalus.
Prenatal alcohol exposure is the cause of fetal alcohol syndrome. A study of over 400,000 American women, all of whom had consumed alcohol during pregnancy, concluded that consumption of 15 drinks or more per week was associated with a reduction in birth weight. Though consumption of less than 15 drinks per week was not proven to cause FAS-related effects, the study authors recommend limiting consumption to no more than one standard drink per day. Also, threshold values are based upon group averages, and it is not appropriate to conclude that exposure below this threshold is necessarily ‘safe’ because of the significant individual variations in alcohol pharmacokinetics.
An analysis of seven medical research studies involving over 130,000 pregnancies found that consuming 2 to 14 drinks per week did not significantly increase the risk of giving birth to a child with either malformations or fetal alcohol syndrome. Pregnant women who consume approximately 144 grams of pure alcohol per day have a 30–33% chance of having a baby with FAS.
A number of studies have shown that light drinking (1–2 drinks/week) during pregnancy does not appear to pose a risk to the fetus. A study of pregnancies in eight European countries found that consuming no more than one drink per day did not appear to have any effect on fetal growth.
A follow-up of children at 18 months of age found that those from women who drank during pregnancy, even two drinks per day, scored higher in several areas of development, though in a different study, as little as one drink per day resulted in poorer spelling and reading abilities at age 6 and a linear dose-response relationship was seen between prenatal alcohol exposure and poorer arithmetic scores at the same age.
Despite intense research efforts, it has not been possible to identify a single clear-cut mechanism for development of FAS or FASD. On the contrary, clinical and animal studies have identified a broad spectrum of pathways through which maternal alcohol can negatively affect the outcome of a pregnancy. Clear conclusions with universal validity are difficult to draw, since different ethnic groups show considerable genetic polymorphism for the hepatic enzymes responsible for ethanol detoxification.
- The placenta allows free entry of ethanol and toxic metabolites like acetaldehyde into the fetal compartment. The so-called placental barrier is no barrier with respect to ethanol.
- The developing fetal nervous system appears particularly sensitive to ethanol toxicity. The latter impacts negatively on proliferation, differentiation, neuronal migration, axonic outgrowth, integration and fine tuning of the synaptic network. In short, all major processes in the developing central nervous system appear compromised.
- Fetal tissues are quite different from adult tissues in function and purpose. For example, the main detoxicating organ in adults is the liver, whereas fetal liver is incapable of detoxicating ethanol as the ADH and ALDH enzymes have not yet been brought to expression at this early stage. Up to term, fetal tissues do not have significant capacity for the detoxification of ethanol, and the fetus remains exposed to ethanol in the amniotic fluid for periods far longer than the decay time of ethanol in the maternal circulation.
Generally, fetal tissues have far less antioxidant protection than adult tissues as they express no significant quantities ADH or ALDH, and far less antioxidant enzymes like SOD, glutathion transferases or glutathion peroxidases.
Several diagnostic systems have been developed in North America:
- The Institute of Medicine's guidelines for FAS, the first system to standardize diagnoses of individuals with prenatal alcohol exposure,
- The University of Washington's 4-DDC, which ranks the four key features of FASD on a Likert scale of one to four and yields 256 descriptive codes that can be categorized into 22 distinct clinical categories, ranging from FAS to no findings.
- The Centers for Disease Control's "Fetal Alcohol Syndrome: Guidelines for Referral and Diagnosis," which established general consensus on the diagnosis FAS in the U.S. but deferred addressing other FASD conditions, and
- Canadian guidelines for FASD diagnosis, which established criteria for diagnosing FASD in Canada and harmonized most differences between the IOM and University of Washington's systems.
Fetal alcohol syndrome is the only expression of FASD that has garnered consensus among experts to become an official ICD-9 and ICD-10 diagnosis. To make this diagnosis (or determine any FASD condition), a multi-disciplinary evaluation is necessary to assess each of the four key features for assessment. Generally, a trained physician will determine growth deficiency and FAS facial features. While a qualified physician may also assess central nervous system structural abnormalities and/or neurological problems, usually central nervous system damage is determined through psychological assessment. A pediatric neuropsychologist may assess all areas of functioning, including intellectual, language processing, and sensorimotor. Prenatal alcohol exposure risk may be assessed by a qualified physician or psychologist.
- Growth deficiency — Prenatal or postnatal height or weight (or both) at or below the 10th percentile
- FAS facial features — All three FAS facial features present
- Central nervous system damage — Clinically significant structural neurological, or functional impairment
- Prenatal alcohol exposure — Confirmed or Unknown prenatal alcohol exposure
Alcohol intake is determined by interview of the biological mother or other family members knowledgeable of the mother's alcohol use during the pregnancy, prenatal health records, and review of available birth records, court records, chemical dependency treatment records, or other reliable sources. Exposure level is assessed as Confirmed Exposure, Unknown Exposure, and Confirmed Absence of Exposure by the IOM, CDC and Canadian diagnostic systems. The 4-DDC further distinguishes confirmed exposure as High Risk and Some Risk:
- High Risk — Confirmed use of alcohol during pregnancy known to be at high blood alcohol levels (100 mg/dL or greater) delivered at least weekly in early pregnancy.
- Some Risk — Confirmed use of alcohol during pregnancy with use less than High Risk or unknown usage patterns.
- Unknown Risk — Unknown use of alcohol during pregnancy.
- No Risk — Confirmed absence of prenatal alcohol exposure, which rules out an FAS diagnosis.
Amount, frequency, and timing of prenatal alcohol use can dramatically impact the other three key features of FAS. While consensus exists that alcohol is a teratogen, there is no clear consensus as to what level of exposure is toxic. The CDC guidelines are silent on these elements diagnostically. The IOM and Canadian guidelines explore this further, acknowledging the importance of significant alcohol exposure from regular or heavy episodic alcohol consumption in determining, but offer no standard for diagnosis. Canadian guidelines discuss this lack of clarity and parenthetically point out that "heavy alcohol use" is defined by the National Institute on Alcohol Abuse and Alcoholism as five or more drinks per episode on five or more days during a 30 day period.
The 4-DDC ranking system distinguishes between levels of prenatal alcohol exposure as High Risk and Some Risk. It operationalizes high risk exposure as a blood alcohol concentration (BAC) greater than 100 mg/dL delivered at least weekly in early pregnancy. This BAC level is typically reached by a 55 kg (121 lb) woman drinking six to eight beers in one sitting.
For many adopted or adult patients and children in foster care, records or other reliable sources may not be available for review. Reporting alcohol use during pregnancy can also be stigmatizing to birth mothers, especially if alcohol use is ongoing. In these cases, all diagnostic systems use an unknown prenatal alcohol exposure designation. A diagnosis of FAS is still possible with an unknown exposure level if other key features of FASD are present at clinical levels.
The CDC reviewed nine syndromes that have overlapping features with FAS; however, none of these syndromes include all three FAS facial features, and none are the result of prenatal alcohol exposure:
- Aarskog syndrome
- Williams syndrome
- Noonan syndrome
- Dubowitz syndrome
- Brachman-DeLange syndrome
- Toluene syndrome
- Fetal hydantoin syndrome
- Fetal valproate syndrome
- Maternal PKU fetal effects
The only certain way to prevent FAS is to simply avoid drinking alcohol during pregnancy. In the United States, the Surgeon General recommended in 1981, and again in 2005, that women abstain from alcohol use while pregnant or while planning a pregnancy, the latter to avoid damage even in the earliest stages (even weeks) of a pregnancy, as the woman may not be aware that she has conceived. In the United States, federal legislation has required that warning labels be placed on all alcoholic beverage containers since 1988 under the Alcoholic Beverage Labeling Act.
There is some controversy surrounding the "zero-tolerance" approach taken by many countries when it comes to alcohol consumption during pregnancy. The assertion that moderate drinking causes FAS is said to lack strong evidence and, in fact, the practice of equating a responsible level of drinking with potential harm to the fetus may have negative social, legal, and health impacts. In addition, special care should be taken when considering statistics on this disease, as prevalence and causation is often linked with FASD, which is more common and causes less harm, as opposed to FAS.
There is no cure for FAS, because the CNS damage creates a permanent disability, but treatment is possible. Because CNS damage, symptoms, secondary disabilities, and needs vary widely by individual, there is no one treatment type that works for everyone.
Traditional behavioral interventions are predicated on learning theory, which is the basis for many parenting and professional strategies and interventions. Along with ordinary parenting styles, such strategies are frequently used by default for treating those with FAS, as the diagnoses Oppositional Defiance Disorder (ODD), Conduct Disorder, Reactive Attachment Disorder (RAD), etc. often overlap with FAS (along with ADHD), and these are sometimes thought to benefit from behavioral interventions. Frequently, a patient's poor academic achievement results in special education services, which also utilizes principles of learning theory, behavior modification, and outcome-based education.
Because the "learning system" of a patient with FAS is damaged, however, behavioral interventions are not always successful, or not successful in the long run, especially because overlapping disorders frequently stem from or are exacerbated by FAS. Kohn (1999) suggests that a rewards-punishment system in general may work somewhat in the short term but is unsuccessful in the long term because that approach fails to consider content (i.e., things "worth" learning), community (i.e., safe, cooperative learning environments), and choice (i.e., making choices versus following directions). While these elements are important to consider when working with FAS and have some usefulness in treatment, they are not alone sufficient to promote better outcomes. Kohn's minority challenge to behavioral interventions does illustrate the importance of factors beyond learning theory when trying to promote improved outcomes for FAS, and supports a more multi-model approach that can be found in varying degrees within the advocacy model and neurobehavioral approach.
Many books and handouts on FAS recommend a developmental approach, based on developmental psychology, even though most do not specify it as such and provide little theoretical background. Optimal human development generally occurs in identifiable stages (e.g., Jean Piaget's theory of cognitive development, Erik Erikson's stages of psychosocial development, John Bowlby's attachment framework, and other developmental stage theories). FAS interferes with normal development, which may cause stages to be delayed, skipped, or immaturely developed. Over time, an unaffected child can negotiate the increasing demands of life by progressing through stages of development normally, but not so for a child with FAS.
By knowing what developmental stages and tasks children follow, treatment and interventions for FAS can be tailored to helping a patient meet developmental tasks and demands successfully. If a patient is delayed in the adaptive behavior domain, for instance, then interventions would be recommended to target specific delays through additional education and practice (e.g., practiced instruction on tying shoelaces), giving reminders, or making accommodations (e.g., using slip-on shoes) to support the desired functioning level. This approach is an advance over behavioral interventions, because it takes the patient's developmental context into account while developing interventions.
The advocacy model takes the point of view that someone is needed to actively mediate between the environment and the person with FAS. Advocacy activities are conducted by an advocate (for example, a family member, friend, or case manager) and fall into three basic categories. An advocate for FAS: (1) interprets FAS and the disabilities that arise from it and explains it to the environment in which the patient operates, (2) engenders change or accommodation on behalf of the patient, and (3) assists the patient in developing and reaching attainable goals.
An understanding of the developmental framework would presumably inform and enhance the advocacy model, but advocacy also implies interventions at a systems level as well, such as educating schools, social workers, and so forth on best practices for FAS. However, several organizations devoted to FAS also use the advocacy model at a community practice level as well.
The neurobehavioral approach focuses on the neurological underpinnings from which behaviors and cognitive processes arise. It is an integrative perspective that acknowledges and encourages a multi-modal array of treatment interventions that draw from all FAS treatment approaches. The neurobehavioral approach is a serious attempt at shifting single-perspective treatment approaches into a new, coherent paradigm that addresses the complexities of problem behaviors and cognitions emanating from the CNS damage of FAS.
The neurobehavioral approach's main proponent is Diane Malbin, MSW, a recognized speaker and trainer in the FASD field, who first articulated the approach with respect to FASD and characterizes it as "Trying differently rather than trying harder." The idea to try differently refers to trying different perspectives and intervention options based on effects of the CNS damage and particular needs of the patient, rather than trying harder at implementing behavioral-based interventions that have consistently failed over time to produce improved outcomes for a patient. This approach also encourages more strength-based interventions, which allow a patient to develop positive outcomes by promoting success linked to the patient's strengths and interests.
Public health and policy
Treating FAS at the public health and public policy levels promotes FAS prevention and diversion of public resources to assist those with FAS. It is related to the advocacy model but promoted at a systems level (rather than with the individual or family), such as developing community education and supports, state or province level prevention efforts (e.g., screening for maternal alcohol use during OB/GYN or prenatal medical care visits), or national awareness programs. Several organizations and state agencies in the U.S. are dedicated to this type of intervention.
The primary disabilities of FAS are the functional difficulties with which the child is born as a result of CNS damage due to prenatal alcohol exposure. Often, primary disabilities are mistaken as behavior problems, but the underlying CNS damage is the originating source of a functional difficulty, rather than a mental health condition, which is considered a secondary disability.
The exact mechanisms for functional problems of primary disabilities are not always fully understood, but animal studies have begun to shed light on some correlates between functional problems and brain structures damaged by prenatal alcohol exposure. Representative examples include:
- Learning impairments are associated with impaired dendrites of the hippocampus
- Impaired motor development and functioning are associated with reduced size of the cerebellum
- Hyperactivity is associated with decreased size of the corpus callosum
Functional difficulties may result from CNS damage in more than one domain, but common functional difficulties by domain include: Note that this is not an exhaustive list of difficulties.
- Achievement — Learning disabilities
- Adaptive behavior — Poor impulse control, poor personal boundaries, poor anger management, stubbornness, intrusive behavior, too friendly with strangers, poor daily living skills, developmental delays
- Attention — Attention-Deficit/Hyperactivity Disorder (ADHD), poor attention or concentration, distractible
- Cognition — Intellectual disability, confusion under pressure, poor abstract skills, difficulty distinguishing between fantasy and reality, slower cognitive processing
- Executive functioning — Poor judgment, Information-processing disorder, poor at perceiving patterns, poor cause and effect reasoning, inconsistent at linking words to actions, poor generalization ability
- Language — Expressive or receptive language disorders, grasp parts but not whole concepts, lack understanding of metaphor, idioms, or sarcasm
- Memory — Poor short-term memory, inconsistent memory and knowledge base
- Motor skills — Poor handwriting, poor fine motor skills, poor gross motor skills, delayed motor skill development (e.g., riding a bicycle at appropriate age)
- Sensory processing and soft neurological problems — sensory processing disorder, sensory defensiveness, undersensitivity to stimulation
- Social communication — Intrude into conversations, inability to read nonverbal or social cues, "chatty" but without substance
The secondary disabilities of FAS are those that arise later in life secondary to CNS damage. These disabilities often emerge over time due to a mismatch between the primary disabilities and environmental expectations; secondary disabilities can be ameliorated with early interventions and appropriate supportive services.
Six main secondary disabilities were identified in a University of Washington research study of 473 subjects diagnosed with FAS, PFAS (partial fetal alcohol syndrome), and ARND (alcohol-related neurodevelopmental disorder):
- Mental health problems — Diagnosed with ADHD, Clinical Depression, or other mental illness, experienced by over 90% of the subjects
- Disrupted school experience — Suspended or expelled from school or dropped out of school, experienced by 60% of the subjects (age 12 and older)
- Trouble with the law — Charged or convicted with a crime, experienced by 60% of the subjects (age 12 and older)
- Confinement — For inpatient psychiatric care, inpatient chemical dependency care, or incarcerated for a crime, experienced by about 50% of the subjects (age 12 and older)
- Inappropriate sexual behavior — Sexual advances, sexual touching, or promiscuity, experienced by about 50% of the subjects (age 12 and older)
- Alcohol and drug problems — Abuse or dependency, experienced by 35% of the subjects (age 12 and older)
- Dependent living — Group home, living with family or friends, or some sort of assisted living, experienced by 80% of the subjects (age 21 and older)
- Problems with employment — Required ongoing job training or coaching, could not keep a job, unemployed, experienced by 80% of the subjects (age 21 and older)
Protective factors and strengths
- Living in a stable and nurturing home for over 73% of life
- Being diagnosed with FAS before age six
- Never having experienced violence
- Remaining in each living situation for at least 2.8 years
- Experiencing a "good quality home" (meeting 10 or more defined qualities) from age 8 to 12 years old
- Having been found eligible for developmental disability (DD) services
- Having basic needs met for at least 13% of life
- Having a diagnosis of FAS (rather than another FASD condition)
Malbin (2002) has identified the following areas of interests and talents as strengths that often stand out for those with FASD and should be utilized, like any strength, in treatment planning:
- Music, playing instruments, composing, singing, art, spelling, reading, computers, mechanics, woodworking, skilled vocations (welding, electrician, etc.), writing, poetry
- Participation in non-impact sport or physical fitness activities
Anecdotal accounts of prohibitions against maternal alcohol use from Biblical, ancient Greek, and ancient Roman sources imply a historical awareness of links between maternal alcohol use and negative child outcomes. In Gaelic Scotland, the mother and nurse were not allowed to consume ale during pregnancy and breastfeeding (Martin Martin).
The earliest recorded observation of possible links between maternal alcohol use and fetal damage was made in 1899 by Dr. William Sullivan, a Liverpool prison physician who noted higher rates of stillbirth for 120 alcoholic female prisoners than their sober female relatives; he suggested the causal agent to be alcohol use. This contradicted the predominating belief at the time that heredity caused intellectual disability, poverty, and criminal behavior, which contemporary studies on the subjects usually concluded. A case study by Henry H. Goddard of the Kallikak family — popular in the early 1900s — represents this earlier perspective, though later researchers have suggested that the Kallikaks almost certainly had FAS. General studies and discussions on alcoholism throughout the mid-1900s were typically based on a heredity argument.
Prior to fetal alcohol syndrome being specifically identified and named in 1973, a few studies had noted differences between the children of mothers who used alcohol during pregnancy or breast-feeding and those who did not, but identified alcohol use as a possible contributing factor rather than heredity.
Recognition as a syndrome
Fetal Alcohol Syndrome was named in 1973 by two dysmorphologists, Drs. Kenneth Lyons Jones and David Weyhe Smith of the University of Washington Medical School in Seattle, United States. They identified a pattern of "craniofacial, limb, and cardiovascular defects associated with prenatal onset growth deficiency and developmental delay" in eight unrelated children of three ethnic groups, all born to mothers who were alcoholics. The pattern of malformations indicated that the damage was prenatal. News of the discovery shocked some, while others were skeptical of the findings.
Dr. Paul Lemoine of Nantes, France had already published a study in a French medical journal in 1968 about children with distinctive features whose mothers were alcoholics, and in the U.S., Christy Ulleland and colleagues at the University of Washington Medical School had conducted an 18-month study in 1968–1969 documenting the risk of maternal alcohol consumption among the offspring of 11 alcoholic mothers. The Washington and Nantes findings were confirmed by a research group in Gothenburg, Sweden in 1979. Researchers in France, Sweden, and the United States were struck by how similar these children looked, though they were not related, and how they behaved in the same unfocused and hyperactive manner.
Within nine years of the Washington discovery, animal studies, including non-human monkey studies carried out at the University of Washington Primate Center by Dr. Sterling Clarren, had confirmed that alcohol was a teratogen. By 1978, 245 cases of FAS had been reported by medical researchers, and the syndrome began to be described as the most frequent known cause of intellectual disability.
While many syndromes are eponymous, i.e. named after the physician first reporting the association of symptoms, Dr. Smith named FAS after the causal agent of the symptoms. He reasoned that doing so would encourage prevention, believing that if people knew maternal alcohol consumption caused the syndrome, then abstinence during pregnancy would follow from patient education and public awareness. Nobody was aware of the full range of possible birth defects from FAS or its prevalence rate at that time, but admission of alcohol use during pregnancy can feel stigmatizing to birth mothers and complicate diagnostic efforts of a syndrome with its preventable cause in the name.
Over time, as subsequent research and clinical experience suggested that a range of effects (including physical, behavioral, and cognitive) could arise from prenatal alcohol exposure, the term Fetal Alcohol Spectrum Disorder (FASD) was developed to include FAS as well as other conditions resulting from prenatal alcohol exposure. Currently, FAS is the only expression of prenatal alcohol exposure defined by the International Statistical Classification of Diseases and Related Health Problems and assigned ICD-9 and diagnoses.
- Ulleland, C.N. (1972). The offspring of alcoholic mothers. Annals New York Academy of Sciences, 197, 167–169. doi:10.1111/j.1749-6632.1972.tb28142.x PMID 4504588
- Lemoine, P., Harousseau, H., Borteyru, J.B., & Menuet, J.C. (1968). Les enfants de parents alcooliques. Anomalies observées, à propos de 127 cas. Quest Medical, 21, 476–482. PMID 12657907
- Streissguth, A. (1997). Fetal Alcohol Syndrome: A Guide for Families and Communities. Baltimore: Brookes Publishing. ISBN 1-55766-283-5.
- Ethen MK; Ramadhani TA; Scheuerle AE et al. (March 2008). "Alcohol Consumption by Women Before and During Pregnancy". Maternal and child health journal 13 (2): 274–85. doi:10.1007/s10995-008-0328-2. PMID 18317893.
- Streissguth, A.P., Barr, H.M., Kogan, J., & Bookstein, F.L. (1996). Understanding the occurrence of secondary disabilities in clients with fetal alcohol syndrome (FAS) and fetal alcohol effects (FAE): Final report to the Centers for Disease Control and Prevention on Grant No. RO4/CCR008515 (Tech. Report No. 96-06). Seattle: University of Washington, Fetal Alcohol and Drug Unit.
- Guerri, C. (2002). Mechanisms involved in central nervous system dysfunctions induced by prenatal ethanol exposure. Neurotoxicity Research, 4 (4), 327–335. PMID 12829422
- Abel, E.L., & Sokol, R.J. (1987). Incidence of fetal alcohol syndrome and economic impact of FAS-related anomalies: Drug alcohol syndrome and economic impact of FAS-related anomalies. Drug and Alcohol Dependency, 19 (1), 51–70. doi:10.1016/0376-8716(87)90087-1 PMID 3545731
- Lancet. 1986 Nov 22;2(8517):1222. PMID 2877359
- Vaux, Keith K. "Fetal Alcohol Syndrome". Medscape Reference. Retrieved 28 March 2012.
- Sampson et al. (1997), Teratology, Volume 56, Issue 5, November 1997, Pages 317–326
- Astley, S.J. (2004). Diagnostic Guide for Fetal Alcohol Spectrum Disorders: The 4-Digit Diagnostic Code. Seattle: University of Washington. PDF available at FAS Diagnostic and Prevention Network. Retrieved on 2007-04-11
- May, PA.; Gossage, JP. (2001). "Estimating the prevalence of fetal alcohol syndrome. A summary". Alcohol Res Health 25 (3): 159–67. PMID 11810953.
- Ratey, J.J. (2001). A User's Guide to the Brain: Perception, Attention, and the Four Theaters of the Brain. New York: Vintage Books. ISBN 0-375-70107-9.
- Bloss, G. (1994). "The economic cost of FAS". Alcohol Health & Research World 18 (1): 53–54.
- Havens JR, Simmons LA, Shannon LM, Hansen WF (September 2008). "Factors associated with substance use during pregnancy: Results from a national sample". Drug and alcohol dependence 99 (1–3): 89–95. doi:10.1016/j.drugalcdep.2008.07.010. PMID 18778900.
- Ebrahim SH, Gfroerer J (February 2003). "Pregnancy-related substance use in the United States during 1996–1998". Obstetrics and gynecology 101 (2): 374–9. doi:10.1016/S0029-7844(02)02588-7. PMID 12576263. Archived from the original on 2013-01-25.
- Advisory on Alcohol Use in Pregnancy. US Surgeon General and CDC. Press release (February 21, 2005). Retrieved on 2014-06-20
- Can I drink alcohol if I’m pregnant? Retrieved on 2009-10-14
- Institute of Medicine (IOM), Stratton, K.R., Howe, C.J., & Battaglia, F.C. (1996). Fetal Alcohol Syndrome: Diagnosis, Epidemiology, Prevention, and Treatment. Washington, DC: National Academy Press. ISBN 0-309-05292-0
- "Australian Government National Health and Medical Research Council". Retrieved 4 November 2012.
- Clinical growth charts. National Center for Growth Statistics. Retrieved on 2007-04-10
- Fetal Alcohol Syndrome: Guidelines for Referral and Diagnosis (PDF). CDC (July 2004). Retrieved on 2007-04-11 Archived September 26, 2007 at the Wayback Machine
- Chudley A; Conry J; Cook J et al. (2005). "Fetal alcohol spectrum disorder: Canadian guidelines for diagnosis". CMAJ 172 (5 Suppl): S1–S21. doi:10.1503/cmaj.1040302. PMC 557121. PMID 15738468. Retrieved 2007-04-10.
- Jones K, Smith D (1975). "The fetal alcohol syndrome". Teratology 12 (1): 1–10. doi:10.1002/tera.1420120102. PMID 1162620.
- Renwick J, Asker R (1983). "Ethanol-sensitive times for the human conceptus". Early Hum Dev 8 (2): 99–111. doi:10.1016/0378-3782(83)90065-8. PMID 6884260.
- Astley SJ, Clarren SK (1996). Most FAS children have a smaller brain then other children "A case definition and photographic screening tool for the facial phenotype of fetal alcohol syndrome". Journal of Pediatrics, 129(1), 33–41. PMID 8757560
- Astley SJ, Stachowiak J, Clarren SK, Clausen C. (2002). "Application of the fetal alcohol syndrome facial photographic screening tool in a foster care population". Journal of Pediatrics, 141(5), 712–717. PMID 12410204
- Lip-philtrum guides. FAS Diagnostic and Prevention Network, University of Washington. Retrieved on 2007-04-10.
- FAS facial features. FAS Diagnostic and Prevention Network, University of Washington. Retrieved on 2007-04-10
- Astley, Susan. Backside of Lip-Philtrum Guides (2004) (PDF). University of Washington, Fetal Alcohol Syndrome Diagnostic and Prevention Network. Retrieved on 2007-04-11
- Dr Sterling Clarren's Keynote Address to the Yukon 2002 Prairie Northern Conference on Fetal Alcohol Syndrome. Retrieved on 2007-04-10
- West, J.R. (Ed.) (1986). Alcohol and Brain Development. New York: Oxford University Press.
- Clarren S, Alvord E, Sumi S, Streissguth A, Smith D (1978). "Brain malformations related to prenatal exposure to ethanol". J Pediatr 92 (1): 64–7. doi:10.1016/S0022-3476(78)80072-9. PMID 619080.
- Coles C, Brown R, Smith I, Platzman K, Erickson S, Falek A (1991). "Effects of prenatal alcohol exposure at school age. I. Physical and cognitive development". Neurotoxicol Teratol 13 (4): 357–67. doi:10.1016/0892-0362(91)90084-A. PMID 1921915.
- Jones, K.L., & Smith, D.W. (1973). Recognition of the fetal alcohol syndrome in early infancy. Lancet, 2, 999–1001. PMID 4127281
- Mattson, S.N., & Riley, E.P. (2002). "Neurobehavioral and Neuroanatomical Effects of Heavy Prenatal Exposure to Alcohol," in Streissguth and Kantor. (2002). p. 10.
- Strömland K, Pinazo-Durán M (2002). "Ophthalmic involvement in the fetal alcohol syndrome: clinical and animal model studies". Alcohol Alcohol 37 (1): 2–8. doi:10.1093/alcalc/37.1.2. PMID 11825849.
- Guerri, C; Riley, E; Strömland, K (July–August 1999). "Commentary on the recommendations of the Royal College of Obstetricians and Gynaecologists concerning alcohol consumption in pregnancy". Alcohol and alcoholism (Oxford, Oxfordshire) 34 (4): 497–501. doi:10.1093/alcalc/34.4.497. PMID 10456576.
- Polygenis, D. (1998). "Moderate alcohol consumption during pregnancy and the incidence of fetal malformations: a meta-analysis". Neurotoxicol Teralol 20: 61–67. doi:10.1016/s0892-0362(97)00073-1. PMID 9511170.
- Kelly Y, Sacker A, Gray R, Kelly J, Wolke D, Quigley MA (February 2009). "Light drinking in pregnancy, a risk for behavioural problems and cognitive deficits at 3 years of age?". Int J Epidemiol 38 (1): 129–40. doi:10.1093/ije/dyn230. PMID 18974425.
- * Day NL (1992). "The effects of prenatal exposure to alcohol." Alcohol Health and Research World, 16(2), 328–244.
- Streissguth AP, et al. (1994). "Prenatal alcohol and offspring development: the first fourteen years". Drug and Alcohol Dependence, 36(2), 89–99. doi:10.1016/0376-8716(94)90090-6 PMID 7851285
- Forrest, F., and du Florey, C. Reported social alcohol consumption during pregnancy and infants' development at 18 months. British Medical Journal, 1991, 303, 22–26
- du Florey, D., et al. A European concerted action: maternal alcohol consumption and its relation to the outcome of pregnancy and development at 18 months. International Journal of Epidemiology, 1992, 21 (Supplement #1)
- Goldschmidt, L; Richardson, GA; Stoffer, DS; Geva, D; Day, NL (1996). "Prenatal alcohol exposure and academic achievement at age six: A nonlinear fit". Alcoholism, clinical and experimental research 20 (4): 763–70. doi:10.1111/j.1530-0277.1996.tb01684.x. PMID 8800397.
- K. Warren and T-K Li, Birth Defect Res A 73 (2005) 195–203.
- J. Brien et al, Am J Obstet Gynecol 146 (1983) 181–186.
- A. Nava-Ocampo et al, Reproduct Toxicol 18 (20004) 613–617
- U.S. Department of Health and Human Services. (2000). National Institute on Alcohol Abuse and Alcoholism. Tenth special report to the U.S> Congress on alcohol and health: Highlights frfom current research. Washington, DC: The Institute.
- Buxton, B. (2005). Damaged Angels: An Adoptive Mother Discovers the Tragic Toll of Alcohol in Pregnancy. New York: Carroll & Graf. ISBN 0-7867-1550-2.
- Malbin, D. (2002). Fetal Alcohol Spectrum Disorders: Trying Differently Rather Than Harder. Portland, OR: FASCETS, Inc. ISBN 0-9729532-0-5.
- Kohn, A. (1999). Punished by Rewards: The Trouble with Gold Stars, Incentive Plans, A's, Praise, and Other Bribes. Boston: Houghton Mifflin. ISBN 0-618-00181-6.
- McCreight, B. (1997). Recognizing and Managing Children with Fetal Alcohol Syndrome/Fetal Alcohol Effects: A Guidebook. Washington, DC: CWLA. ISBN 0-87868-607-X.
- National Organization on Fetal Alcohol Syndrome, Minnesota Organization on Fetal Alcohol Syndrome. Retrieved on 2007-04-11
- Understanding FASD (Fetal Alcohol Spectrum Disorders. Fetal Alcohol Syndrome Consultation, Education and Training Services, Inc., Retrieved on 2007-04-11
- Malbin, D. (1993). Fetal Alcohol Syndrome, Fetal Alcohol Effects: Strategies for Professionals. Center City, MN: Hazelden. ISBN 0-89486-951-5
- Abel EL, Jacobson S, Sherwin BT (1983). "In utero alcohol exposure: Functional and structural brain damage". Neurobehavioral Toxicology and Teratology, 5, 363–366. PMID 6877477
- Meyer L, Kotch L, Riley E (1990). "Neonatal ethanol exposure: functional alterations associated with cerebellar growth retardation". Neurotoxicol Teratol 12 (1): 15–22. doi:10.1016/0892-0362(90)90107-N. PMID 2314357.
- Zimmerberg B, Mickus LA (1990). "Sex differences in corpus callosum: Influence of prenatal alcohol exposure and maternal undernutrition". Brain Research, 537, 115–122. PMID 2085766
- Sullivan, W.C. (1899). A note on the influence of maternal inebriety on the offspring. Journal of Mental Science, 45, 489–503.
- Goddard, H.H. (1912). The Kallikak Family: A Study in the Heredity of Feeble-Mindedness. New York: Macmillan.
- Karp, R.J., Qazi, Q.H., Moller, K.A., Angelo, W.A., & Davis, J.M. (1995). Fetal alcohol syndrome at the turn of the century: An unexpected explanation of the Kallikak family. Archives of Pediatrics and Adolescent Medicine, 149(1), 45–48. PMID 7827659
- Haggard, H.W., & Jellinek, E.M. (1942). Alcohol Explored. New York: Doubleday.
- Jones, K.L., Smith, D.W, Ulleland, C.N., Streissguth, A.P. (1973). Pattern of malformation in offspring of chronic alcoholic mothers. Lancet, 1, 1267–1271. PMID 4126070
- Streissguth, A.P. (2002). In A. Streissguth, & J. Kanter (Eds.), The Challenge in Fetal Alcohol Syndrome: Overcoming Secondary Disabilities. Seattle: University of WA Press. ISBN 0-295-97650-0.
- Olegard, R., Sabel, K.G., Aronsson, M. Sandin, B., Johannsson, P.R., Carlsson, C., Kyllerman, M., Iversen, K. & Hrbek, A. (1979). Effects on the child of alcohol abuse during pregnancy. Acta Paediatrica Scandinavica, 275, 112–121. PMID 291283
- Clarren, S.K. (2005). A thirty year journey from tragedy to hope. Foreword to Buxton, B. (2005). Damaged Angels: An Adoptive Mother Discovers the Tragic Toll of Alcohol in Pregnancy. New York: Carroll & Graf. ISBN 0-7867-1550-2.
- Clarren, S.K., & Smith, D.W. (1978). Fetal alcohol syndrome. New England Journal of Medicine, 298, 1063–1067. PMID 347295
- Ernst van Faassen and Onni Niemelä: Biochemistry of prenatal alcohol exposure. NOVA Biomedical Books, New York 2011. ISBN 978-1-61122-511-2: A mongraph with a global overview over the recent scientific literature, in which the various mechanisms and biochemical pathways of FAS and FASD are discussed and compared.
- Ed. Joshua Hoffmann: Pregnancy and Alcohol Consumption. NOVA Science publishers, New York 2011. ISBN 978-1-61761-122-3: A collection of many different aspects of the effects of parental alcohol consumption on fertility and fetal health.
|Wikimedia Commons has media related to Fetal alcohol syndrome.|
- CDC’s National Center on Birth Defects and Developmental Disabilities
- Canadian FASD resource — Motherisk | <urn:uuid:94c8d5b0-0f11-4e62-95e5-09f1b43be6d3> | {
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|Classification and external resources|
Hyperkinetic disorder is a psychiatric syndrome emerging in early childhood that features an enduring pattern of severe, developmentally inappropriate inattention, hyperactivity and impulsivity across different settings (e.g., home and school) that significantly impair academic, social and work performance.
Hyperkinetic children display disorganized, poorly controlled and excessive activity; they lack perseverance in tasks involving thought and attention, and tend to move from one activity to the next without completing any. They are frequently accident-prone, reckless and impulsive, and may thoughtlessly (rather than defiantly) break rules. While they are commonly incautious and unreserved with adults, they may be isolated and unpopular with other children. Cognitive impairment and delayed language and motor development are more common in this group than in the general population; and they may experience low self-esteem and engage in dissocial behavior as a consequence of the disorder.
Though the American Psychiatric Association's criteria for attention deficit hyperactivity disorder (ADHD), and the World Health Organization's criteria for hyperkinetic disorder each list a very similar set of 18 symptoms, the differing rules governing diagnosis mean that hyperkinetic disorder features greater impairment and more impulse-control difficulties than typical ADHD, and it most resembles a severe case of ADHD combined type.
Unlike ADHD, a diagnosis of hyperkinetic disorder requires that the clinician directly observes the symptoms (rather than relying only on parent and teacher reports); that onset must be by age 6 not 7; and that at least six inattention, three hyperactivity and one impulsivity symptom be present in two or more settings. While ADHD may exist comorbid with (in the presence of) mania or a depressive or anxiety disorder, the presence of one of these rules out a diagnosis of hyperkinetic disorder. Most cases of hyperkinetic disorder appear to meet the broader criteria of ADHD.
The prevalence in school age children is thought to be about 1.5%, compared with an estimated 5.3% for ADHD.
Once the patient and family have been educated about the nature, management and treatment of the disorder and a decision has been made to treat, the European ADHD Guidelines group recommends medication rather than behavioral training as the first treatment approach; and the UK's National Institute for Health and Clinical Excellence recommends medication as first line treatment for those with severe ADHD, and the provision of group parent-training in all cases of ADHD.
- Banaschewski, Tobias; Rohde, Louis (2009). "Phenomenology". In Banaschewski, Tobias; Coghill, David; Danckaerts, Marina. Attention Deficit Hyperactivity Disorder and Hyperkinetic Disorder. Oxford, UK: OUP. pp. 3—18. ISBN 9780191576010.
- "International Statistical Classification of Diseases and Related Health Problems 10th Revision (ICD-10) Version for 2010". World Health Organisation. 2010. Retrieved 2014-01-17.
- Professor Michael Fitzgerald; Dr. Mark Bellgrove; Michael Gill (30 April 2007). Handbook of Attention Deficit Hyperactivity Disorder. John Wiley & Sons. p. 270. ISBN 978-0-470-03215-2.
- Santosh, Paramala J; Henry, Amy; Varley, Christopher K (24 January 2008). "ADHD and hyperkinetic disorder". In Peter Tyrer; Kenneth R. Silk. Cambridge Textbook of Effective Treatments in Psychiatry. Cambridge University Press. p. 782. ISBN 978-1-139-46757-5.
- Banaschewski T, Coghill D, Santosh P, et al. (March 2008). "[Long-acting medications for the treatment of hyperkinetic disorders - a systematic review and European treatment guideline. Part 1: overview and recommendations]". Z Kinder Jugendpsychiatr Psychother (in German) 36 (2): 81–94; quiz 94–5. doi:10.1024/1422-49220.127.116.11. PMID 18622938.
- Coghill, David; Danckaerts, Marina (2009). "Organizing and Delivering Treatment". In Banaschewski, Tobias; Coghill, David; Danckaerts, Marina. Attention Deficit Hyperactivity Disorder and Hyperkinetic Disorder. Oxford, UK: OUP. pp. 91—106. ISBN 9780191576010. | <urn:uuid:285933f3-13f7-4102-9c8c-c27edf9a0b19> | {
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|Behavior Disorder Home | Child Behavior | Teen Behavior | Adult Behavior ||
Disruptive Behavior Disorders
Disruptive Behavior Disorders are often diagnosed during early childhood and associated with Attention Deficit Hyperactivity Disorder. This article defines disruptive behavior disorders such as ADHD, Oppositional Defiant Disorder (ODD), and conduct disorders. Get information on treatment of these disorders as well.
What Is a Disruptive Behavior Disorder?
Disruptive Behavior Disorder is a technical term that refers to a specific portion of the Diagnostic and Statistical Manual of Mental Disorders, 4th Edition, Text Revision, abbreviated as DSM-IV-TR. The section is a subset of the Disorders Usually First Diagnosed in Infancy, Childhood, or Adolescence, with the subcategory name of Attention-Deficit and Disruptive Behavior Disorders.
The diagnoses that are left in this category when the Attention Deficit Hyperactivity Disorder is excluded are:
It is reported that the Disruptive Behavior Disorders occur in between 4% and 9% of children, making them the most frequently found psychiatric disorder of children. It is found 3 to 4 times more often in children with an IQ that is below average than in those children who have a normal IQ. It is not unusual to find it coexisting with other disorders, including ADHD, mood disorders (such as depression), and substance abuse. In fact, estimates suggest that about 2/3 of children with ADHD will have a comorbid Disruptive Behavior Disorder diagnosis.
The DSM-IV-TR characterizes the child with ODD as negative, hostile, and defiant more than is expected for his or her age and over a period of at least 6 months. At least four behaviors from a list of 8 must be present. These include being annoying or being annoyed, losing his/her temper, arguing with adults and resisting their requests or rules, blaming others, showing anger, resentfulness, spite, or vindictiveness. Oppositional Defiant Disorder is characterized as involving less aggression or violence than is found in Conduct Disorder.
The DSM-IV-TR characterizes the child with Conduct Disorder as violating norms, rules, and the rights of others in a persistent and repetitive way, with 3 of 4 criteria evident over 12 months and at least 1 in the past 6 months, those criteria being: aggression towards people and animals, property destruction, theft or deception, and serious rule-breaking.
The ICD-10 does not have a category called "Disruptive Behavior Disorder," but it does have subcategories of Conduct Disorder that refer to problems that are restricted entirely or almost entirely to the family situation (i.e., the child's behavior outside the home—at school, for instance—does not show the characteristics of Conduct Disorder) and to a social form in which the characteristic behavior occur in a group of peers who act out together.
Both these Disruptive Behavior Disorders cause impaired functioning in the educational, occupational, and/or social realm, and for a diagnosis, the behaviors must not be limited to times during which a mood disorder or psychotic disorder is present.
Treatment of Disruptive Behavior Disorders
Treatment will depend on the age of the child and whether there are comorbid issues. Treatments may include medication and therapy and may often involve family members as well.
Related Article: Behavior Modification >> | <urn:uuid:ac78a197-aa3f-4613-a0d0-6c31022c8000> | {
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|Classification and external resources|
Drug addiction, also called substance dependence or dependence syndrome, is a condition where a person feels a strong need to take a drug. Addiction also involves other behaviours. These include finding it difficult to control the need to use the drug and feeling the use of the drug to be more important than more normal things such as family or work. When the person does not use the drug for an amount of time, they may suffer from withdrawal.
When a person is addicted, they are usually addicted to a class (a specific kind) of drug. For example: Heroin is a drug that is in the Opiate class. Which means that a person addicted to Heroin may also be seen to have an addiction to other opiates such as Morphine.
A person who may easily become addicted to drugs is said to have an addictive personality. The Diagnostic and Statistical Manual of Mental Disorders defines drug addiction as a mental disorder. Drug addiction is often linked with other mental disorders.
References[change | change source]
- International Classification of Diseases (ICD-10) [Code F10.2]
- National Institutes of Health website: "Drug dependence means that a person needs a drug to function normally. Abruptly stopping the drug leads to withdrawal symptoms. Drug addiction is the compulsive use of a substance, despite its negative or dangerous effects." http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0002490/ | <urn:uuid:3849098d-6841-4878-9618-c1dfbb8b32bc> | {
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In this article
Although they seem similar, there are some significant differences between the two terms electronic medical record (EMR) and electronic health record (HER). The term EMR came first; the word “medical” relates mostly to treatment or diagnosis by physicians. On the other hand, the word “health” refers to the general status of the body. In short, “health” covers more territory than “medical.”
Electronic Medical Record (EMR)
The EMR concerns everything related to the medical history of the patient, including diagnoses, immunization dates, allergies, and medications. EMR is therefore limited to the territory of medical practitioners. It may sometimes be necessary to print and send it to another health provider to evaluate previous medical history.
Electronic Health Record (EHR)
The EHR is a digital version of health information that contains more than patient medical information. It may include diagnoses, progress notes, medications, immunization dates, past medical history, vital signs, allergies, imaging reports, and lab data. Additionally, an EHR can have other relevant patient information, such as demographic and insurance data, as well as information taken from personal wellness instruments.
EHR not only helps in storing the data but also in sharing the information among authorized providers (various health organizations) with ease. This helps immensely in coordinating and making the right clinical decisions.
EHR also aids in improved patient care by supporting the Medicaid and Medicare programs. This helps in avoiding penalties during reimbursements of Medicaid and Medicare program to the eligible providers, as EHR makes health information accessible instantly.
EHR can be regarded as the future of healthcare because the records provide critical patient information, thus helping with clinical decisions as well as coordinating care between different healthcare providers.
Main Differences between EMR and EHR
An electronic medical record is simply the digitized version of the earlier paper charts used in the physician’s office. Itcontains the patient’s treatment and medical history. The advantages of EMR over paper records are:
- Easily track patient information over time.
- Identify patients requiring checkups or preventive screenings with ease.
- Readily check patient outcomes and how they are doing on against certain parameters (vaccinations or readings of blood pressure).
- Monitor the overall care quality within the practice for improvement
The problem with EMR is that it does not travel well outside during the sharing of health information among providers. The records often have to be printed in order to send to different physicians and specialists. Thus, in this regard, EMR can be treated much as paper records.
Electronic health records do all the same things and some more. The focus of an EHR is on the patient’s total health, reaching beyond collecting standard clinical data on the patients in the clinician’s office. It includes a broader perspective of patient care. EHR is built to share clinical data of patients across different health care providers, including various specialists and laboratories. Therefore, EHR contains information from all the physicians involved in the care of the patient. An EHR can be made, consulted, and managed by authorized physicians and health workers across different healthcare organizations.
The information usually travels to the physicians from the patients along with the healthcare organizations (hospitals, nursing homes) present, even across different countries. EHR makes the sharing of medical information across different stakeholders easy. It is designed to be viewed even by the patients themselves.
EHR makes a difference, as information becomes more powerful when shared securely. Healthcare does not depend only on individual efforts. Rather, it is a team endeavor that requires sharing of key patient information. Effective communication and sharing of patient information among different clinicians helps in achieving the desired result in health care. After all, the ability to engage the various parties in interactive communication with shared information is the key to success in healthcare.
Therefore, while “medical records” implies mainly clinical data derived from diagnosis and treatment of patients, “health records” can be regarded as a broader term that relates to the overall health condition of the patient.
The Advantages and Disadvantages of Using EHR and EMR
EHR or EMR records are advantageous over paper-based record systems in many ways. Digitized information can have information management tools to aid health workers in providing better patient care through more efficiently interpreting, organizing, and reacting to patient records.
EHR software can give alerts for clinical reminders, connect specialists regarding critical health care decisions, and analyze health records for future research as well as for care management.
The interactive EHR systems prompt providers for additional information that helps to get more information and enhances data completeness.
With its provision of critical data that help care coordination between health providers and informs clinical decisions, EHR systems are the future of healthcare. The focus of EHR systems is on the overall patient’s health and it is designed to extend beyond the reach of healthcare organizations originally collecting and compiling patient health data. EHR is developed to share patient data with different health care providers, including specialists and clinical laboratories. The intent is to have all the patient information from different clinicians involved in the care of the patient.
The patient data moves along across the healthcare organization, the patient, the specialist, even the next state or outside the country. All the people involved in the patient care can access the EHR system, including the patients themselves for better care delivery to the patients.
However, the EHR and EMR systems for managing patient information have some disadvantages. Maintaining such software systems is relatively expensive initially because are investments are required for proper hardware, installation, training of the health workers, and managing support from IT organizations. The software also comes with a cost (free versions are available, though with less functionality). There are chances of malfunction and loss of all patient data if the software is not built properly.
Security of electronic patient information from the cybercriminals is also a serious concern, as the handling of cases involving data breaches is very expensive.
The Benefits of EHR over EMR
In short, an EHR system manages the following attributes in a healthcare organization, helping in critical clinical decisions and has advantages over EMR:
- EHR holds all the healthcare information and data, including lists of problems, test results, a list of medications and ICD-10.
- Helps in results management by allowing electronic storage of various lab result sand X-ray images, and ensures that there is no duplication of tests.
- Automated order entry via secured e-prescribing technology.
- Easy access to various clinicians and specialists, offering exclusive decision support. The EHR system can even warn clinicians about possible drug interactions, help in the diagnosis process, and provide evidence-based guidelines during evaluation of treatment options.
- EHR allows electronic connectivity and communication facility where the physicians or medical assistants in a different places even can securely talk to the patients in cyberspace.
- EHR makes it possible to share educational material with the patients through home monitoring devices and online questionnaires.
- The administrative processes take less time when using an EHR, thus minimizing delays in treatment. Scheduling of appointments can be done by the patients themselves. They can also check for insurance eligibility.
- EHR also prides a searchable database that allows the user to have important information regarding patient demographics, the types of disease that are predominating, and so on (for example, the number of diabetic patients treated in 2015).
The Security of EMR and EHR
With coordinated and improved care, EHR also brings additional security concerns. Previously, it was difficult to steal healthcare data stored on paper because it is bulky. The electronic system now makes it easier for hackers to steal this valuable information (as they are stored in smaller devices such as USB drives) and sell at a good price. So, with EHR come concerns about the security and privacy of patient information. Does using EHR compromise patient data safety? What are the safety measures that should be employed to ensure patient data safety?
Health information of patients is protected by the Health Insurance Portability and Accountability Act (HIPAA), which accounts for the privacy and security of the health information. Although, with EHR the health providers can use patient information more effectively, thereby improving the efficiency and quality of care, it does not change the existing obligations of the health care providers to keep patient health data private and secure.
The Security Rule of HIPAA requires that healthcare organizations set up specific security measures to safeguard patient information stored in the EHR. These security measures include physical, technical, and administrative protection of the health information stored in an EHR system. The safety measures to be built into EHR system are:
- Implementing access controls by introducing PIN numbers and passwords. This will limit access to patient health information to authorized personnel only.
- Encryption of stored information to ensure that these data cannot be read or understood by unauthorized users. Encrypted data can be read only after its correct decryption, using a special key available to authorized users only. Encrypted data have often been safe even after getting lost or stolen.
- Audit trail of stored information to record who is accessing the information, as well as what and when changes are made to them.
As per HIPAA Privacy Rule, patients have the rights over their own health data, irrespective of its form (in paper or electronic). The patients have the right:
- To see and receive a copy of their medical record.
- To request that any mistakes be corrected.
- To receive a notice whenever health information of patients is shared, stolen or used.
- To state where and how the patient wants to be contacted by the health care provider.
- To file a complaint whenever the patient feels that the above rights are not recognized.
In cases where the patient information falls to someone who should not have it or see it, federal law requires the respective healthcare organizations or providers notify the patient about the breach and the providers will be accountable (often the resultant fines are costly to the healthcare providers).
Table: Reviews and ratings of the leading electronic medical record (EMR) and electronic health record (EHR) systems.
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It is also important to note that administration of different medications of ADHD achieves treatment results differently for different patients. Medication for ADHD Children Attention Deficit Hyperactivity Disorder is a neurobehavioral condition that is common among children. The behavior can be regarded as an inappropriate developmental behavior with impairing degrees of hyperactivity and inattentitiveness. ADHD disorder is often accompanied by a significant co-morbidity. However, parents have hope since there are various methods of treating children with Attention Deficit Hyperactivity Disorder. Treatment includes a variety of stimulants that are used to reduce hyperactivity and inattentiveness. These medications have sustained release of newer versions for improvement over previous disadvantages (Tobaiqy, et al., 2011, p.212). However, children with ADHD have been given medications that only help contain the situation and not to treat the disorder for a permanent solution with respect to medication. Research claims have brought about controversial issues with regards to whether ADHD is wholly a biological illness causes a structural defect of the brain. ADHD medications that are being currently used to suppress and treat the individuals with disorder predominantly base its opinion on the fact that the disorder is a mixture of genetic disorder and environmental aspects. It is clear that medications focus on the brain since there are clear-cut evidence through differences of brains of non-ADHD patients and those with the disorder. This brings forth the medications focusing on the brain though there is no clear-cut evidence on how these brain differences result in ADHD. Medications being given to children with attention deficit disorder such as stimulants, antidepressants and even therapy can surely help treat the situation considering the prove of the disorder being a biological illness. However, medications for attention deficit hyperactivity disorder needs rethinking and advancement considering the fact that those patients with the disorder are biologically fit and normal. Dynamics are paramount given the fact that despite biological aspects contributing widely to hyperactivity, impulsivity and lack of attention, the patients found to have manifestations of these behavior are proved not to have any deficiencies biologically. It is important that these children receive better treatment since attention deficit disorder is a core issue of concern since these patients cannot work on or perform duties that are essential in the society. Despite ADHD patients non-performance they have the tendency of being attentive and performing tasks that are interesting and therefore cannot be left out in normal education. Governments have placed children with ADHD into consideration by giving them budgetary and policy priority to assist their education through improvement of the system of education in their favor. The principle of inclusive education has enabled children with ADHD to receive quality education despite shortcomings. Governments have encouraged participation of organizations, parents, and communities to facilitate inclusive education for these children. There are many stimulants for treating ADHD and each child may respond differently to the different stimulants. Some medications that work for one child may not work for
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Running head: Medication for ADHD Children Medication for ADHD Children Insert Name Insert Insert 29 October 2011 Abstract Medication of children with Attention Deficit Hyperactivity Disorder generally helps to reduce inattentiveness and hyperactivity among children and adults with the disorder…
The study will be conducted with administration of pre and post tests to a group of 60 randomly selected fourth grade students from Ludlow Elementary School, a small urban school of 500 students in Philadelphia, Pennsylvania. The students will be randomly assigned to two groups of 30 students in either an experimental group in which students will have the experimental ADHD medication, or control group in which students will follow a traditional schedule.
Attention Deficit Hyperactivity Disorder (ADHD)" Introduction Attention Deficit Hyperactivity Disorder popularly called as ADHD, is a developmental, neurobiological state characterized by the existence of strict and persistent signs of inattentiveness, hyperactivity and impetuosity (American Psychiatric Association (APA), 1994).
The ICD-10 and the DSM-IV stress that the fundamental features of ADHD are “inattentiveness, hyperactivity and impulsiveness” (Steinhausen 393). Although health professionals have recognized the veracity of ADHD and its prevalence, other scholars have criticized the validity of ADHD as a real disorder (Steinhausen; Tait).
ADHD Author Institution ADHD Introduction The paper pursues to review evidence on the effectiveness or efficacy of cognitive behavioural therapies in addressing ADHD. According to Dobson & Dobson (2009), attention deficit hyperactivity disorder (ADHD) can be regarded as one of the prevalent childhood disorders that can continue throughout adolescence to adulthood.
These children also experience impulsivity, as well as hyperactivity, resulting in difficulty in controlling their actions in both home and school. One of the hallmark features of ADHD is the impairment of a child's cognitive, as well as psychosocial, capacity.
It tends to be more common in boys than in girls, as current estimates show it exists three times as much in boys than in girls (Shut, 2009). It is considered to be a chronic disorder, due to the fact that
Two, hyperactivity; such as constantly fidgeting while sitting at their desk and three, acting out without considering the consequences. Children diagnosed with ADHD can often be heard speaking loudly, seen overreacting in a given situation and not
Emily and John have a son, who for confidentiality sake will be called, “Carl.” Carl is a 7 year-old boy who was diagnosed six months ago with having ADHD. Emily and John said that their son Carl is a fun and active child. They said that | <urn:uuid:c2f685e0-ffcd-4179-8889-411b1f5747ed> | {
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Pedophilia, also spelled paedophilia, also called pedophilic disorder, psychosexual disorder, generally affecting adults, characterized by sexual fantasies about or attempts to engage in sexual acts with a prepubescent child of the same or opposite sex.
In the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5; 2013), pedophilia (pedophilic disorder) is classified as a type of paraphilia—a category of recognized disorders defined by unusual fantasies, urges, or behaviours that are recurrent and sexually arousing. According to the DSM-5, in order for pedophilia to be diagnosed clinically, such thoughts and behaviours must cause distress or interpersonal hardship to the affected individual or cause distress, injury, or death to persons who are unwilling or unable to consent to sexual behaviours. The World Health Organization’s ICD-10 Classification of Mental and Behavioural Disorders (1993) uses a similar definition. According to both publications, the thoughts or behaviours in question must be present for at least six months for clinical diagnosis, and the affected individual must be at least 16 years of age and at least 5 years older than the child (or children) at the centre of the individual’s sexual fantasies.
Pedophilia may be distinguished from hebephilia (sexual preference for individuals who typically are between ages 11 and 14) and ephebophilia (sexual preference for late-stage adolescents, typically ages 15 and 16). In many countries an individual who is convicted in a court of law for child sexual abuse (see child abuse), which involves sexual abuse of a prepubescent or postpubescent individual up to age 18, is known as a sex offender; some of those individuals are also later clinically diagnosed with pedophilia.
The typical pedophile is unable to find satisfaction in an adult sexual relationship and may have low self-esteem. Sexual attraction toward children dominates the pedophile’s life, often causing the individual to live in fear of the attraction and in some cases causing the person to act on his or her urges. If a pedophile attempts a sexual encounter, the encounter frequently stops short of intercourse, with the pedophile obtaining sexual gratification through fondling the child and sometimes through genital display alone. Reactions of the child victim can range from fright—particularly if force or violence (or the threat of force or violence) is involved—to bewilderment or passive enjoyment. Although some children seem more upset by previous parental warnings than by an actual encounter, the sexual encounter can often be quite traumatic to them, especially if there is associated violence. There is also evidence that children who have been sexually victimized are more likely to be troubled adults.
The underlying cause of pedophilia is unclear. Although biological abnormalities such as hormone imbalance may contribute to the disorder in some individuals, biological factors have not been proved as causes. In many cases pedophilic behaviour appears to be associated with sexual abuse or neglect experienced during childhood and with atypical emotional or psychological development. Research also has indicated that boys who were sexually abused are more likely to become pedophiles or sex offenders. Girls who were sexually abused more frequently respond by engaging in self-destructive behaviours, such as substance abuse or prostitution. Most pedophiles are men; the condition is rare in women.
When a person with pedophilia acts on his or her urges and causes a child to suffer, it generally is considered a serious sexual offense. Patients who are diagnosed with the disorder are expected to participate in treatment programs. Among effective forms of treatment for pedophilia are cognitive and behavioral therapies (see cognitive behaviour therapy) that employ empathy training and restructuring of distorted and deviant thought patterns. Empathy training teaches the patient to view his or her behaviour from the perspective of the victim. Cognitive distortion therapy attempts to restructure a patient’s deviant notions—for example, by reinforcing the fact that coercion of children into sexual activities is an inappropriate behaviour. In some cases medications such as cyproterone that suppress the activity of testosterone in men can be effective in reducing aggressive behaviour and sex drive. | <urn:uuid:58491c5f-7d6e-436b-ac96-a46a4e5523ee> | {
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The term Pervasive Developmental Disorder (PDD) was once used to refer to a category of developmental delays that included autism and four similar disorders, and was defined as the umbrella that these five disorders fell under:
- Asperger syndrome
- Rett syndrome
- Childhood disintegrative disorder
- Pervasive developmental disorder not otherwise specified (PDD-NOS)
In 2013, the 5th edition of the Diagnostic and Statistical Manual (DSM) of Mental Disorders – the primary diagnostic criteria resource psychiatric professionals use – was released. In the DSM-5 the old definitions for Pervasive Developmental Disorder (PDD) became obsolete.
In the DSM-5, all five of the separate categories were grouped into the new definition for autism spectrum disorder. As a practical matter, this eliminated the need for the term “pervasive developmental disorder” to describe them—now, autism spectrum disorder means the same thing.
This is part of the reason why the term PDD has become a source of some confusion – and the reason it has largely fallen out of use.
Still, you may hear autism spectrum disorder (ASD) referred to as part of a larger class of developmental delays called pervasive developmental disorders. You may also hear of people diagnosed with pervasive developmental disorders not otherwise specified (PDD-NOS) … an entirely different class of diagnoses once considered separate from ASD. But the term PDD-NOS has become obsolete too as it now falls under autism spectrum disorder.
Not surprisingly, there is a considerable amount of confusion around the term PDD.
The problem is that clinicians still sometimes use the term PDD, but they don’t always use it consistently. Some still stick to the DSM-4 definition while others use the term more or less interchangeably with “ASD,“ in line with how the DSM-5 defines it.
Pervasive Developmental Disorder Is Still Widely Used Despite Being Unofficial
Not all clinicians have immediately adopted the DSM-5 definitions, because they believe that the DSM-4 categories were more descriptive. Others use the DSM-5 criteria clinically, but continue to use some of the old nomenclature from DSM-4 out of habit or as shorthand for categories that DSM-5 does not explicitly define.
Making matters even more complicated, medical professionals and many insurers use the International Statistical Classification of Diseases and Related Health Problems, or ICD-10, for diagnoses. The ICD-10 continues to include a classification for pervasive developmental disorder, unspecified, although it does not contain detailed criteria for providing a diagnosis.
That is in keeping with the original use of PDD-NOS, however, which was essentially a catch-all diagnosis for individuals who exhibited some autistic symptoms but did not meet the previously more stringent criteria for a definitive autism diagnosis. Additionally, because of the sometimes gradual onset of autism symptoms in toddlers, clinicians sometimes preferred to makes a diagnosis of PDD-NOS in cases where there remained some question as to whether or not full-blown autism would manifest in younger patients.
So, although PDD and PDD-NOS were (and still are, by some professionals) sometimes used interchangeably, they did not refer to the same thing. Today, both are essentially absorbed into the broader definition of autism spectrum disorder. | <urn:uuid:a8f8272d-6daf-4eeb-bb63-33e15b7fca5f> | {
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Auditory processing disorder Auditory processing disorder (APD), also known as central auditory processing disorder (CAPD), is an umbrella term for a variety of disorders that affect the way the brain processes
Auditory processing disorder
auditory information. Individuals with APD usually have normal structure and function of the outer, middle and inner ear (peripheral hearing). However, they cannot process the information they hear in the same way as others do, which leads to difficulties in recognizing and interpreting sounds, especially the sounds composing speech. It is thought that these
Classification and external resources
difficulties arise from dysfunction in the central nervous system. The American Academy of Audiology notes that APD is diagnosed by difficulties in one or more auditory processes known to reflect the function of the central auditory nervous system.
Specialty Psychiatry ICD-10
H93.2 (http://apps.who.i nt/classifications/icd10/b rowse/2016/en#/H93.2)
388.45 (http://www.icd9 data.com/getICD9Code. ashx?icd9=388.45) 388.40 (http://www.icd9 data.com/getICD9Code. ashx?icd9=388.40)
D001308 (http://www.nl m.nih.gov/cgi/mesh/201 8/MB_cgi?field=uid&ter m=D001308)
APD can affect both children and adults, although the actual prevalence is currently unknown. It has been suggested that males are twice as likely to be affected by the disorder as females, but there are no good epidemiological studies.
Contents Presentation in adults Definitions Causes Acquired auditory processing disorder Hereditary and genetic characteristics of central auditory processing disorder Developmental auditory processing disorder Diagnosis Types of testing Modality-specificity and controversies Characteristics Relation to specific language impairment and developmental dyslexia Relation to attention deficit hyperactivity disorder Remediation and training History See also References External links
Presentation in adults CAPD can continue into adulthood. Cooper and Gates (1991) estimated the prevalence of adult APD to be 10 to 20%. Many people experience problems with learning and day-to-day tasks with difficulties over time. Adults with this disorder talk louder than necessary have trouble remembering a list or sequence often need words or sentences repeated have poor ability to memorize information learned by listening interpret words too literally need assistance hearing clearly in noisy environments rely on accommodation and modification strategies find or request a quiet work space away from others request written material when attending oral presentations ask for directions to be given one step at a time
Definitions The American Speech-Language-Hearing Association (ASHA) published "(Central) Auditory Processing Disorders" in January 2005 as an update to the "Central Auditory Processing: Current Status of Research and Implications for Clinical Practice (ASHA, 1996)". The American Academy of Audiology has released more current practice guidelines related to the disorder. ASHA formally defines APA as "a difficulty in the efficiency and effectiveness by which the central nervous system (CNS) utilizes auditory information." In 2011, the British Society of Audiology published 'best practice guidelines'. Auditory processing disorder can be developmental or acquired. It may result from ear infections, head injuries or neurodevelopmental delays that affect processing of auditory information. This can include problems with: "...sound localization and lateralization (see also binaural fusion); auditory discrimination; auditory pattern recognition; temporal aspects of audition, including temporal integration, temporal discrimination (e.g., temporal gap detection), temporal ordering, and temporal masking; auditory performance in competing acoustic signals (including dichotic listening); and auditory performance with degraded acoustic signals". The Committee of UK Medical Professionals Steering the UK Auditory Processing Disorder Research Program have developed the following working definition of Auditory Processing Disorder: "APD results from impaired neural function and is characterized by poor recognition, discrimination, separation, grouping, localization, or ordering of speech sounds. It does not solely result from a deficit in general attention, language or other cognitive processes."
Causes Acquired auditory processing disorder Acquired APD can be caused by any damage to or dysfunction of the central auditory nervous system and can cause auditory processing problems. For an overview of neurological aspects of APD, see Griffiths.
Hereditary and genetic characteristics of central auditory processing disorder The ability to listen to and comprehend multiple messages at the same time is a trait that is heavily influenced by our genes say federal researchers. These "short circuits in the wiring" sometimes run in families or result from a difficult birth, just like any learning disability. Auditory processing disorder can be associated with conditions affected by genetic traits, such as various developmental disorders. Inheritance of Auditory Processing Disorder refers to whether the condition is inherited from your parents or "runs" in families. Central auditory processing disorder may be hereditary neurological traits from the mother or the father.
Developmental auditory processing disorder In the majority of cases of developmental APD, the cause is unknown. An exception is acquired epileptic aphasia or Landau-Kleffner syndrome, where a child's development regresses, with language comprehension severely affected. The child is often thought to be deaf, but normal peripheral hearing is found. In other cases, suspected or known causes of APD in children include delay in myelin maturation, ectopic (misplaced) cells in the auditory cortical areas, or genetic predisposition. In a family with autosomal dominant epilepsy, seizures which affected the left temporal lobe seemed to cause problems with auditory processing. In another extended family with a high rate of APD, genetic analysis showed a haplotype in chromosome 12 that fully co-segregated with language impairment. Hearing begins in utero, but the central auditory system continues to develop for at least the first decade. There is considerable interest in the idea that disruption to hearing during a sensitive period may have long-term consequences for auditory development. One study showed thalamocortical connectivity in vitro was associated with a time sensitive developmental window and required a specific cell adhesion molecule (lcam5) for proper brain plasticity to occur. This points to connectivity between the thalamus and cortex shortly after being able to hear (in vitro) as at least one critical period for auditory processing. Another study showed that rats reared in a single tone environment during critical periods of development had permanently impaired auditory processing. ‘Bad’ auditory experiences, such as temporary deafness by cochlear removal in rats leads to neuron shrinkage. In a study looking at attention in APD patients, children with one ear blocked developed a strong right-ear advantage but were not able to modulate that advantage during directed-attention tasks. In the 1980s and 1990s, there was considerable interest in the role of chronic Otitis media (middle ear disease or 'glue ear') in causing APD and related language and literacy problems. Otitis media with effusion is a very common childhood disease that causes a fluctuating conductive hearing loss, and there was concern this may disrupt auditory development if it occurred during a sensitive period. Consistent with this, in a sample of young children with chronic ear infections recruited from a hospital otolargyngology department, increased rates of auditory difficulties were found later in childhood. However, this kind of study will suffer from sampling bias because children with otitis media will be more likely to be referred to hospital departments if they are experiencing developmental difficulties. Compared with hospital studies, epidemiological studies, which assesses a whole population for otitis media and then evaluate outcomes, have found much weaker evidence for long-term impacts of otitis media on language outcomes.
Diagnosis APD is a difficult disorder to detect and diagnose. The subjective symptoms that lead to an evaluation for APD include an intermittent inability to process verbal information, leading the person to guess to fill in the processing gaps. There may also be disproportionate problems with decoding speech in noisy environments. APD has been defined anatomically in terms of the integrity of the auditory areas of the nervous system. However, children with symptoms of APD typically have no evidence of neurological disease and the diagnosis is made on the basis of performance on behavioral auditory tests. Auditory processing is "what we do with what we hear", and in APD there is a mismatch between peripheral hearing ability (which is typically normal) and ability to interpret or discriminate sounds. Thus in those with no signs of neurological impairment, APD is diagnosed on the basis of auditory tests. There is, however, no consensus as to which tests should be used for diagnosis, as evidenced by the succession of task force reports that have appeared in recent years. The first of these occurred in 1996. This was followed by a conference organized by the American Academy of Audiology. Experts attempting to define diagnostic criteria have to grapple with the problem that a child may do poorly on an auditory test for reasons other than poor auditory perception: for instance, failure could be due to inattention, difficulty in coping with task demands, or limited language ability. In an attempt to rule out at least some of these factors, the American Academy of Audiology conference explicitly advocated that for APD to be diagnosed, the child must have a modality-specific problem, i.e. affecting auditory but not visual processing. However, an ASHA committee subsequently rejected modality-specificity as a defining characteristic of auditory processing disorders.
Types of testing 1. SCAN is the most common tool for diagnosing APD, and it also standardized. It is composed for four subsets: discrimination of monaurally presented single words against background noise, acoustically degraded single words, dichotically presented single words, sentence stimuli. Different versions of the test are used depending on the age of the patient. 2. Random Gap Detection Test (RGDT) is also a standardized test. It assesses an individual’s gap detection threshold of tones and white noise. The exam includes stimuli at four different frequencies (500, 1000, 2000, and 4000 Hz) and white noise clicks of 50 ms duration. It is a useful test because it provides an index of auditory temporal resolution. In children, an overall gap detection threshold greater than 20 ms means they have failed. 3. Gaps in Noise Test (GIN) also measures temporal resolution by testing the patient's gap detection threshold in white noise. 4. Pitch Patterns Sequence Test (PPT) and Duration Patterns Sequence Test (DPT) measure auditory pattern identification. The PPS has s series of three tones presented at either of two pitches (high or low). Meanwhile, the DPS has a series of three tones that vary in duration rather than pitch (long or short). Patients are then asked to describe the pattern of pitches presented.
Modality-specificity and controversies The issue of modality-specificity has led to considerable debate among experts in this field. Cacace and McFarland have argued that APD should be defined as a modality-specific perceptual dysfunction that is not due to peripheral hearing loss. They criticise more inclusive conceptualizations of APD as lacking diagnostic specificity. A requirement for modality-specificity could potentially avoid including children whose poor auditory performance is due to general factors such as poor attention or memory. Others, however, have argued that a modality-specific approach is too narrow, and that it would miss children who had genuine perceptual problems affecting both visual and auditory processing. It is also impractical, as audiologists do not have access to standardized tests that are visual analogs of auditory tests. The debate over this issue remains unresolved. It is clear, however, that a modalityspecific approach will diagnose fewer children with APD than a modality-general one, and that the latter approach runs a risk of including children who fail auditory tests for reasons other than poor auditory processing. Although modality-specific testing has been advocated for well over a decade, to date no tests have been published which would allow audiologists to perform a modality-specific evaluation (i.e., no clinical versions of visual analogs to auditory processing tests exist). Another controversy concerns the fact that most traditional tests of APD use verbal materials. The British Society of Audiology has embraced Moore's (2006) recommendation that tests for APD should assess processing of nonspeech sounds. The concern is that if verbal materials are used to test for APD, then children may fail because of limited language ability. An analogy may be drawn with trying to listen to sounds in a foreign language. It is much harder to distinguish between sounds or to remember a sequence of words in a language you do not know well: the problem is not an auditory one, but rather due to lack of expertise in the language. In recent years there have been additional criticisms of some popular tests for diagnosis of APD. Tests that use tape-recorded American English have been shown to over-identify APD in speakers of other forms of English. Performance on a battery of non-verbal auditory tests devised by the Medical Research Council's Institute of Hearing Research was found to be heavily influenced by non-sensory task demands, and indices of APD had low reliability when this was controlled for. This research undermines the validity of APD as a distinct entity in its own right and suggests that the use of the term "disorder" itself is unwarranted. In a recent review of such diagnostic issues, it was recommended that children with suspected auditory processing impairments receive a holistic psychometric assessment including general intellectual ability, auditory memory, and attention, phonological processing, language, and literacy. The authors state that "a clearer understanding of the relative contributions of perceptual and non-sensory, unimodal and supramodal factors to performance on psychoacoustic tests may well be the key to unravelling the clinical presentation of these individuals." Depending on how it is defined, APD may share common symptoms with ADD/ADHD, specific language impairment, Asperger syndrome and other forms of autism. A review showed substantial evidence for atypical processing of auditory information in children with autism. Dawes and Bishop noted how specialists in audiology and speech-language pathology often adopted different approaches to child assessment, and they concluded their review as follows: "We regard it as crucial that these different professional groups work together in carrying out assessment, treatment and management of children and undertaking cross-disciplinary research." In practice, this seems rare. To ensure that APD is correctly diagnosed, the examiners must differentiate APD from other disorders with similar symptoms. Factors that should be taken into account during the diagnosis are: attention, auditory neuropathy, fatigue, hearing and sensitivity, intellectual and developmental age, medications, motivation, motor skills, native language and language experience, response strategies and decision-making style, and visual acuity. It should also be noted that children under the age of seven cannot be evaluated correctly because their language and auditory processes are still developing. In addition, the presence of APD cannot be evaluated when a child's primary language is not English.
Characteristics The National Institute on Deafness and Other Communication Disorders state that children with Auditory Processing Disorder often: have trouble paying attention to and remembering information presented orally, and may cope better with visually acquired information have problems carrying out multi-step directions given orally; need to hear only one direction at a time have poor listening skills need more time to process information have low academic performance have behavior problems have language difficulties (e.g., they confuse syllable sequences and have problems developing vocabulary and understanding language) have difficulty with reading, comprehension, spelling, and vocabulary APD can manifest as problems determining the direction of sounds, difficulty perceiving differences between speech sounds and the sequencing of these sounds into meaningful words, confusing similar sounds such as "hat" with "bat", "there" with "where", etc. Fewer words may be perceived than were actually said, as there can be problems detecting the gaps between words, creating the sense that someone is speaking unfamiliar or nonsense words. In addition, it is common for APD to cause speech errors involving the distortion and substitution of consonant sounds. Those suffering from APD may have problems relating what has been said with its meaning, despite obvious recognition that a word has been said, as well as repetition of the word. Background noise, such as the sound of a radio, television or a noisy bar can make it difficult to impossible to understand speech, since spoken words may sound distorted either into irrelevant words or words that don't exist, depending on the severity of the auditory processing disorder. Using a telephone can be problematic for someone with auditory processing disorder, in comparison with someone with normal auditory processing, due to low quality audio, poor signal, intermittent sounds and the chopping of words. Many who have auditory processing disorder subconsciously develop visual coping strategies, such as lip reading, reading body language, and eye contact, to compensate for their auditory deficit, and these coping strategies are not available when using a telephone. As noted above, the status of APD as a distinct disorder has been queried, especially by speech-language pathologists and psychologists, who note the overlap between clinical profiles of children diagnosed with APD and those with other forms of specific learning disability. Many audiologists, however, would dispute that APD is just an alternative label for dyslexia, SLI, or ADHD, noting that although it often co-occurs with these conditions, it can be found in isolation.
Relation to specific language impairment and developmental dyslexia There has been considerable debate over the relationship between APD and Specific language impairment (SLI). SLI is diagnosed when a child has difficulties with understanding or producing spoken language for no obvious cause. The problems cannot be explained in terms of peripheral hearing loss. The child is typically late in starting to talk, and may have problems in producing speech sounds clearly, and in producing or understanding complex sentences. Some theoretical accounts of SLI regard it as the result of auditory processing problems. However, this view of SLI is not universally accepted, and others regard the main difficulties in SLI as stemming from problems with higher-level aspects of language processing. Where a child has both auditory and language problems, it can be hard to sort out cause-and-effect. Similarly with developmental dyslexia, there has been considerable interest in the idea that for some children reading problems are downstream consequences of difficulties in rapid auditory processing. Again, cause and effect can be hard to unravel. This is one reason why experts such as Moore have recommended using non-verbal auditory tests to diagnose APD. Specifically regarding the neurological factors of dyslexia, the disorder has been linked to polymicrogyria which causes cell migrational problems. This relates to APD because children that have polymicrogyri almost always present deficits on APD testing. It has also been suggested that APD may be related to cluttering, a fluency disorder marked by word and phrase repetitions. It has been found that a higher than expected proportion of individuals diagnosed with SLI and dyslexia on the basis of language and reading tests also perform poorly on tests in which APD is tested. APD can be assessed using tests that involve identifying, repeating or discriminating speech, and a child may do poorly because of primary language problems. In a study comparing children with a diagnosis of dyslexia and those with a diagnosis of APD, they found the two groups could not be distinguished. obtained similar findings in studies comparing children diagnosed with SLI or APD. The two groups had very similar profiles. This raises the worrying possibility that the diagnosis that a child receives may be largely a function of the specialist they see: the same child who would be diagnosed with APD by an audiologist may be diagnosed with SLI by a speech-language therapist or with dyslexia by a psychologist.
Relation to attention deficit hyperactivity disorder It has been discovered that APD and ADHD present overlapping symptoms. Below is a ranked order of behavioral symptoms that are most frequently observed in each disorder. Professionals evaluated the overlap of symptoms between the two disorders. The order below is of symptoms that are almost always observed. This chart proves that although the symptoms listed are different, it is easy to get confused between many of them. ADHD
1. Difficult hearing in background noise
2. Difficulty following oral instructions
3. Poor listening skills
4. Fidgety or restless
4. Academic difficulties
5. Hasty or impulsive
5. Poor auditory association skills
6. Interrupts or intrudes
6. Distracted 7. Inattentive
There is a high rate of co-occurrence between AD/HD and CAPD. Research shows that 84% of children with APD have confirmed or suspected ADHD. Co-occurrence between ADHD and APD is 41% for children with confirmed diagnosis of ADHD, and 43% for children suspected of having ADHD.
Remediation and training Treatment of APD typically focuses on three primary areas: changing learning environment, developing higher-order skills to compensate for the disorder, and remediation of the auditory deficit itself. However, there is a lack of well-conducted evaluations of intervention using randomized controlled trial methodology. Most evidence for effectiveness adopts weaker standards of evidence, such as showing that performance improves after training. This does not control for possible influences of practice, maturation, or placebo effects. Recent research has shown that practice with basic auditory processing tasks (i.e. auditory training) may improve performance on auditory processing measures and phonemic awareness measures. Changes after auditory training have also been recorded at the physiological level. Many of these tasks are incorporated into computer-based auditory training programs such as Earobics and Fast ForWord, an adaptive software available at home and in clinics worldwide, but overall, evidence for effectiveness of these computerised interventions in improving language and literacy is not impressive. One small-scale uncontrolled study reported successful outcomes for children with APD using auditory training software. Treating additional issues related to APD can result in success. For example, treatment for phonological disorders (difficulty in speech) can result in success in terms of both the phonological disorder as well as APD. In one study, speech therapy improved auditory evoked potentials (a measure of brain activity in the auditory portions of the brain). While there is evidence that language training is effective for improving APD, there is no current research supporting the following APD treatments: Auditory Integration Training typically involves a child attending two 30-minute sessions per day for ten days. Lindamood-Bell Learning Processes (particularly, the Visualizing and Verbalizing program) Physical activities that require frequent crossing of the midline (e.g., occupational therapy) Sound Field Amplification Neuro-Sensory Educational Therapy Neurofeedback However, use of a FM transmitter has been shown to produce significant improvements over time with children.
History The first research into APD began in 1954 with Helmer Myklebust's study, "Auditory Disorders in Children". Myklebust's work suggested auditory processing disorder was separate from language learning difficulties. His work sparked interest in auditory deficits after acquired brain lesions affecting the temporal lobes and led to additional work looking at the physiological basis of auditory processing, but it was not until the late seventies and early eighties that research began on APD in depth. In 1977, the first conference on the topic of APD was organized by Robert W. Keith, Ph.D. at the University of Cincinnati. The proceedings of that conference was published by Grune and Stratton under the title "Central Auditory Dysfunction" (Keith RW Ed.) That conference started a new series of studies focusing on APD in children. Virtually all tests currently used to diagnose APD originate from this work. These early researchers also invented many of the auditory training approaches, including interhemispheric transfer training and interaural intensity difference training. This period gave us a rough understanding of the causes and possible treatment options for APD. Much of the work in the late nineties and 2000s has been looking to refining testing, developing more sophisticated treatment options, and looking for genetic risk factors for APD. Scientists have worked on improving behavioral tests of auditory function, neuroimaging, electroacoustic, and electrophysiologic testing. Working with new technology has led to a number of software programs for auditory training. With global awareness of mental disorders and increasing understanding of neuroscience, auditory processing is more in the public and academic consciousness than ever before.
See also Amblyaudia Auditory verbal agnosia Cortical deafness Echoic memory King-Kopetzky syndrome (part of UK medical definition of APD) Language processing Spatial hearing loss Music-specific disorders
References 1. American Academy of Audiology. "Clinical Practice Guidelines: Diagnosis, Treatment and Management of Children and Adults with Central Auditory" (http://audiology-web.s3.amazonaws.com/migrated/CAPD%20 Guidelines%208-2010.pdf_539952af956c79.73897613.pdf) (PDF). Retrieved 16 January 2017. 2. La Trobe University. "(C)APD" (http://www.latrobe.edu.au/hcs/resources/capd/capd/index.html). Retrieved 14 November 2010. 3. Musiek, Frank; Gail, Chermak (2007). Handbook of central auditory processing disorder [auditory neuroscience and diagnosis]. Plural Publishing. p. 448. ISBN 1-59756-056-1. 4. (Cooper JC Jr., Gates GA. Hearing in the elderly – the Framingham cohort, 1983–1985: Part II. Prevalence of central auditory processing disorders. Ear Hear. 1991;12(5):304–311) 5. National Center for Learning Disabilities | NCLD.org – NCLD. National Center for Learning Disabilities | NCLD.org – NCLD. N.p., n.d. Web. 19 Nov. 2014. 6. "Central Auditory Processing: Current Status of Research and Implications for Clinical Practice. Technical Report, (1996)" (http://www.asha.org/docs/html/TR1996-00241.html). Working Group on Auditory Processing Disorders. American Speech-Language-Hearing Association. 7. Paul, Rhea (25 August 2007). "Auditory Processing Disorder". Journal of Autism and Developmental Disorders. 38 (1): 208–209. doi:10.1007/s10803-007-0437-6 (http://doi.org/10.1007%2Fs10803-007-0437-6). 8. British Society of Audiology (2011). "British Society of Audiology Best Practice Guidelines" (http://thebsa.org.uk/images/stories/docs/BSA_APD_Management_1Aug11_FINAL_amended17Oct11.pdf) (PDF). 9. "(Central) Auditory Processing Disorders. Technical Report, (2005)" (http://www.asha.org/docs/html/TR2005-00043.html). Working Group on Auditory Processing Disorders. American Speech-Language-Hearing Association. 10. "The British Society of Audiology and the UK APD Steering Group" (http://www.thebsa.org.uk/index.php?option=com_content&view=category&layout=blog&id=21&Itemid=29). 11. Musiek FE, Chermak GD, Weihing J, Zappulla M, Nagle S (June 2011). "Diagnostic accuracy of established central auditory processing test batteries in patients with documented brain lesions". J Am Acad Audiol. 22 (6): 342–58. doi:10.3766/jaaa.22.6.4 (http://doi.org/10.3766%2Fjaaa.22.6.4). PMID 21864472 (http://www.ncbi.nlm.nih.gov/pubmed/21864472). 12. Lew HL, Weihing J, Myers PJ, Pogoda TK, Goodrich GL (2010). "Dual sensory impairment (DSI) in traumatic brain injury (TBI)--An emerging interdisciplinary challenge". NeuroRehabilitation. 26 (3): 213–22. doi:10.3233/NRE-2010-0557 (http://doi.org/10.3233%2FNRE-2010-0557). PMID 20448311 (http://www.ncbi.nlm.nih.gov/pubmed/20448311). 13. Griffiths, T. D. (2002). "Central auditory pathologies". British Medical Bulletin. 63 (1): 107–120. doi:10.1093/bmb/63.1.107 (http://doi.org/10.1093%2Fbmb%2F63.1.107). 14. ("Genetics Influence Auditory Processing." Psych Central.com. N.p., n.d. Web. 02 Dec. 2014.) 15. (NCLD.org – NCLD." National Center for Learning Disabilities | NCLD.org.) 16. ("Inheritance and Genetics of Auditory Processing Disorder." – RightDiagnosis.com. N.p., n.d. Web. 02 Dec. 2014.) 17. Fandiño M, Connolly M, Usher L, Palm S, Kozak FK (January 2011). "Landau-Kleffner syndrome: a rare auditory processing disorder series of cases and review of the literature". Int. J. Pediatr. Otorhinolaryngol. 75 (1): 33–8. doi:10.1016/j.ijporl.2010.10.001 (http://doi.org/10.1016%2Fj.ijporl.2010.10.001). PMID 21074868 (http://www.ncbi.nlm.nih.gov/pubmed/21074868). 18. Weihing, Jeff; Musiek, Frank (2007). "15 Dichotic Interaural Intensity Difference (DIID)". In Ross-Swain, Deborah; Geffner, Donna S;. Auditory Processing Disorders: Assessment, Management and Treatment. Plural Publishing Inc. ISBN 1-59756-107-X. OCLC 255602759 (http://www.worldcat.org/oclc/255602759). 19. Boscariol M, Garcia VL, Guimarães CA, et al. (April 2010). "Auditory processing disorder in perisylvian syndrome". Brain Dev. 32 (4): 299–304. doi:10.1016/j.braindev.2009.04.002 (http://doi.org/10.1016%2Fj.brai ndev.2009.04.002). PMID 19410403 (http://www.ncbi.nlm.nih.gov/pubmed/19410403). 20. Bamiou DE, Campbell NG, Musiek FE, et al. (April 2007). "Auditory and verbal working memory deficits in a child with congenital aniridia due to a PAX6 mutation". Int J Audiol. 46 (4): 196–202. doi:10.1080/14992020601175952 (http://doi.org/10.1080%2F14992020601175952). PMID 17454233 (http://www.ncbi.nlm.nih.gov/pubmed/17454233). 21. Pisano T, Marini C, Brovedani P, Brizzolara D, Pruna D, Mei D, Moro F, Cianchetti C, Guerrini R (January 2005). "Abnormal phonologic processing in familial lateral temporal lobe epilepsy due to a new LGI1 mutation". Epilepsia. 46 (1): 118–23. doi:10.1111/j.0013-9580.2005.26304.x (http://doi.org/10.1111%2Fj.0013-9580.2005.26304.x). PMID 15660777 (http://www.ncbi.nlm.nih.gov/pubmed/15660777). 22. Addis L, Friederici AD, Kotz SA, Sabisch B, Barry J, Richter N, Ludwig AA, Rübsamen R, Albert FW, Pääbo S, Newbury DF, Monaco AP (August 2010). "A locus for an auditory processing deficit and language impairment in an extended pedigree maps to 12p13.31-q14.3" (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2948670). Genes, Brain, and Behavior. 9 (6): 545–61. doi:10.1111/j.1601-183X.2010.00583.x (http:// doi.org/10.1111%2Fj.1601-183X.2010.00583.x). PMC 2948670 (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2948670) . PMID 20345892 (http://www.ncbi.nlm.nih.gov/pubmed/20345892). 23. Moore DR (2002). "Auditory development and the role of experience" (http://bmb.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=12324392). British Medical Bulletin. 63: 171–81. doi:10.1093/bmb/63.1.171 (htt ps://doi.org/10.1093%2Fbmb%2F63.1.171). PMID 12324392 (http://www.ncbi.nlm.nih.gov/pubmed/12324392). 24. Thai-Van H, Veuillet E, Norena A, Guiraud J, Collet L (March 2010). "Plasticity of tonotopic maps in humans: influence of hearing loss, hearing aids and cochlear implants". Acta Otolaryngol. 130 (3): 333–7. doi:10.3109/00016480903258024 (http://doi.org/10.3109%2F00016480903258024). PMID 19845491 (http://www.ncbi.nlm.nih.gov/pubmed/19845491). 25. Barkat TR, Polley DB, Hensch TK (September 2011). "A critical period for auditory thalamocortical connectivity" (http://dx.doi.org/10.1038/nn.2882). Nature Neuroscience. 14 (9): 1189–94. doi:10.1038/nn.2882 (h ttps://doi.org/10.1038%2Fnn.2882). PMC 3419581 (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3419581) . PMID 21804538 (http://www.ncbi.nlm.nih.gov/pubmed/21804538). 26. Han YK, Köver H, Insanally MN, Semerdjian JH, Bao S (September 2007). "Early experience impairs perceptual discrimination" (http://dx.doi.org/10.1038/nn1941). Nature Neuroscience. 10 (9): 1191–7. doi:10.1038/nn1941 (http://doi.org/10.1038%2Fnn1941). PMID 17660815 (http://www.ncbi.nlm.nih.gov/pubmed/17660815). 27. Asbjørnsen A, Holmefjord A, Reisaeter S, Møller P, Klausen O, Prytz B, Boliek C, Obrzut JE (July 2000). "Lasting auditory attention impairment after persistent middle ear infections: a dichotic listening study" (ht tp://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0012-1622&date=2000&volume=42&issue=7&spage=481). Developmental Medicine and Child Neurology. 42 (7): 481–6. doi:10.1111/j.1469-8749.2000.tb00352.x (http://doi.org/10.1111%2Fj.1469-8749.2000.tb00352.x). PMID 10972421 (http://www.ncbi.nlm.nih.gov/pubmed/10972421). 28. Whitton JP, Polley DB (October 2011). "Evaluating the perceptual and pathophysiological consequences of auditory deprivation in early postnatal life: a comparison of basic and clinical studies" (http://www.ncbi. nlm.nih.gov/pmc/articles/PMC3173557). J. Assoc. Res. Otolaryngol. 12 (5): 535–47. doi:10.1007/s10162-011-0271-6 (http://doi.org/10.1007%2Fs10162-011-0271-6). PMC 3173557 (http://www.ncbi.nlm.nih.gov/p mc/articles/PMC3173557) . PMID 21607783 (http://www.ncbi.nlm.nih.gov/pubmed/21607783). 29. Hartley DE, Moore DR (June 2005). "Effects of otitis media with effusion on auditory temporal resolution". International Journal of Pediatric Otorhinolaryngology. 69 (6): 757–69. doi:10.1016/j.ijporl.2005.01.009 (htt ps://doi.org/10.1016%2Fj.ijporl.2005.01.009). PMID 15885328 (http://www.ncbi.nlm.nih.gov/pubmed/15885328). 30. Feldman, H.M.; et al. (2003). "Parent-reported language skills in relation to otitis media during the first 3 years of life". Journal of Speech, Language and Hearing Research. 46: 273–287. doi:10.1044/10924388(2003/022) (http://doi.org/10.1044%2F1092-4388%282003%2F022%29). 31. Rintelmann, W.F. (1985). "Monaural speech tests in the detection of central auditory disorders.". In Marilyn L Pinheiro and Frank E Musiek. Assessment of central auditory dysfunction : foundations and clinical correlates. Baltimore: Williams & Wilkins. pp. 173–200. ISBN 978-0-683-06887-0. OCLC 11497885 (http://www.worldcat.org/oclc/11497885). 32. Katz, Jack (1992). "Classification of auditory processing disorders". In Jack Katz and Nancy Austin Stecker and Donald Henderson. Central auditory processing : a transdisciplinary view. St. Louis: Mosby Year Book. pp. 81–92. ISBN 978-1-55664-372-9. OCLC 25877287 (http://www.worldcat.org/oclc/25877287). 33. Jerger J, Musiek F (October 2000). "Report of the Consensus Conference on the Diagnosis of Auditory Processing Disorders in School-Aged Children" (http://www.taracentar.hr/download/diagnosis_apd_school.pdf ) (pdf). J Am Acad Audiol. 11 (9): 467–74. PMID 11057730 (http://www.ncbi.nlm.nih.gov/pubmed/11057730). 34. Keith, Robert W. (2000). "SCAN-C Test for Auditory Processing Dis- orders in Children". Revised, Psychological Corporation. 35. Keith, Robert W. (2011). "Random gap detection test". 36. Musiek, Frank E.; Shinn, Jennifer B.; Jirsa, Robert; Bamiou, Doris-Eva; Baran, Jane A.; Zaida, Elena (December 2005). "GIN (Gaps-In-Noise) Test Performance in Subjects with Confirmed Central Auditory Nervous System Involvement". Ear and Hearing. 26 (6): 608–618. doi:10.1097/01.aud.0000188069.80699.41 (http://doi.org/10.1097%2F01.aud.0000188069.80699.41). 37. Musiek, Frank (1994). "Frequency (Pitch) and Duration Pattern Tests". Journal of the American Academy of Audiology: 265-268. 38. Cacace, Anthony T.; Dennis J. McFarland (July 1995). "Opening Pandora's Box: The Reliability of CAPD Tests" (http://aja.asha.org/cgi/content/citation/4/2/61). American Journal of Audiology. 4 (2): 61–62. Retrieved 2010-08-31. 39. Cacace, Anthony T.; Dennis J. McFarland (December 2005). "The Importance of Modality Specificity in Diagnosing Central Auditory Processing Disorder" (http://aja.asha.org/cgi/content/short/14/2/112). American Journal of Audiology. 14 (2): 112–123. doi:10.1044/1059-0889(2005/012) (http://doi.org/10.1044%2F1059-0889%282005%2F012%29). PMID 16489868 (http://www.ncbi.nlm.nih.gov/pubmed/16489868). Retrieved 2010-08-31. 40. Cacace, Anthony T.; Dennis J. McFarland (April 1998). "Central Auditory Processing Disorder in School-Aged Children A Critical Review" (http://jslhr.asha.org/cgi/content/abstract/41/2/355). Journal of Speech, Language, and Hearing Research. 41 (2): 355–373. PMID 9570588 (http://www.ncbi.nlm.nih.gov/pubmed/9570588). Retrieved 2010-08-31. 41. Moore, David R. (2006). "Auditory processing disorder (APD): Definition, diagnosis, neural basis, and intervention". Audiological Medicine. 4 (1): 4–11. doi:10.1080/16513860600568573 (http://doi.org/10.1080%2F 16513860600568573). 42. Dawes, P; Bishop, D.V. M. (2007). "The SCAN-C in testing for auditory processing disorder in a sample of British children". International Journal of Audiology. 46: 780–786. doi:10.1080/14992020701545906 (http: //doi.org/10.1080%2F14992020701545906). 43. Moore, D.R.; Ferguson, M.A.; Edmondson-Jones, A.M.; Ratib, S; Riley, A (2010). "Nature of auditory processing disorder in children". Pediatrics. 126 (2): e382–390. doi:10.1542/peds.2009-2826 (http://doi.org/10 .1542%2Fpeds.2009-2826). 44. Moore, D.R.; Cowan, J.A.; Riley, A; Edmondson-Jones, A.M.; Ferguson, M.A. (2011). "Development of auditory processing in 6-11 year old children". Ear and Hearing. 32 (3): 269–285. doi:10.1097/AUD.0b013e318201c468 (http://doi.org/10.1097%2FAUD.0b013e318201c468). 45. Cowan J, Rosen S, Moore DR (2009). "Putting the Auditory Processing Back into Auditory Processing Disorder in Children". In Cacace AT, McFarland DJ. Controversies in central auditory processing disorder. San Diego, Calif.; Abingdon: Plural. pp. 187–197. ISBN 978-159-756260-7. 46. O'Connor K (December 2011). "Auditory processing in autism spectrum disorder: A review". Neurosci Biobehav Rev. 36 (2): 836–54. doi:10.1016/j.neubiorev.2011.11.008 (http://doi.org/10.1016%2Fj.neubiorev.20 11.11.008). PMID 22155284 (http://www.ncbi.nlm.nih.gov/pubmed/22155284). 47. Dawes P, Bishop D (2009). "Auditory processing disorder in relation to developmental disorders of language, communication and attention: a review and critique". Int J Lang Commun Disord. 44 (4): 440–65. doi:10.1080/13682820902929073 (http://doi.org/10.1080%2F13682820902929073). PMID 19925352 (http://www.ncbi.nlm.nih.gov/pubmed/19925352). 48. Jerger, James; Musick, Frank (2000). "Report of the Consensus Conference on the Diagnosis of Auditory Processing Disorders in School-Aged Children". Journal of the American Academy of Audiology. 11 (9): 467–474. 49. Brandstaetter, Patt; Hunter, Lisa; Kalweit, Linda; Kloos, Eric; Landrud, Sherry; Larson, Nancy; Packer, Amy; Wall, Deb (2003). "Introduction to Auditory Processing Disorders". Minnesota Department of Education Total Special Education System. 50. "Auditory Processing Disorder in Children [NIDCD Health Information]" (http://www.nidcd.nih.gov/health/voice/auditory.html). 51. DeVore, Brooke; Nagao, Kyoko; Pereira, Olivia; Nemith, Julianne; Sklar, Rachele; Deeves, Emily; Kish, Emily; Welsh, Kelsey; Morlet, Thierry (2016). "Speech errors among children with auditory processing disorder". Proceedings of Meetings on Acoustics. 29 (1): 6. doi:10.1121/2.0000440 (http://doi.org/10.1121%2F2.0000440). 52. Anderson S, Kraus N (October 2010). "Sensory-cognitive interaction in the neural encoding of speech in noise: a review" (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3075209). J Am Acad Audiol. 21 (9): 575– 85. doi:10.3766/jaaa.21.9.3 (http://doi.org/10.3766%2Fjaaa.21.9.3). PMC 3075209 (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3075209) . PMID 21241645 (http://www.ncbi.nlm.nih.gov/pubmed/21241645). 53. Kamhi, A.G. (2011). "What speech-language pathologists need to know about Auditory Processing Disorder". Language Speech and Hearing Services in Schools. 42 (3): 265–272. doi:10.1044/0161-1461(2010/100004) (http://doi.org/10.1044%2F0161-1461%282010%2F10-0004%29). 54. Lovett, B.J. (2011). "Auditory processing disorder: School psychologist beware?". Psychology in the Schools. 48: 855–867. doi:10.1002/pits.20595 (http://doi.org/10.1002%2Fpits.20595). 55. Chermak, Gail D (2001). "Auditory processing disorder: An overview for the clinician". Hearing Journal. 54 (7): 10–25. doi:10.1097/01.HJ.0000294109.14504.d8 (http://doi.org/10.1097%2F01.HJ.0000294109.14504 .d8). 56. Miller, C. A. (2011). "Auditory processing theories of language disorders: Past, present, and future". Language Speech and Hearing Services in Schools. 42 (3): 309–319. doi:10.1044/0161-1461(2011/10-0040) (htt ps://doi.org/10.1044%2F0161-1461%282011%2F10-0040%29). 57. Ferguson, M. A.; Hall, R. L.; Riley, A; Moore, D. R. (2011). "Communication, listening, cognitive and speech perception skills in children with auditory processing disorder (APD) or specific language impairment (SLI)". Journal of Speech Language and Hearing Research. 54 (1): 211–227. doi:10.1044/1092-4388(2010/09-0167) (http://doi.org/10.1044%2F1092-4388%282010%2F09-0167%29). 58. Chermak, Gail; Musiek, Frank (2014). Handbook of central auditory processing disorder. comprehensive intervention (2 ed.). San Diego, CA: Plural Publishing. ISBN 978-1-59756-562-2. 59. Pindzola, Rebekah H.; Haynes, William O.; Moran, Michael J. (2006). Communication disorders in the classroom: an introduction for professionals in school setting. Boston: Jones and Bartlett Publishers. p. 251. ISBN 0-7637-2743-1. OCLC 59401841 (http://www.worldcat.org/oclc/59401841). 60. Moore, David R. (July 2007). "Auditory processing disorders: Acquisition and treatment". Journal of Communication Disorders. 40 (4): 295–304. doi:10.1016/j.jcomdis.2007.03.005 (http://doi.org/10.1016%2Fj.jco mdis.2007.03.005). 61. Dawes, P; Bishop, D (2010). "Psychometric profile of children with auditory processing disorder (APD) and children with dyslexia" (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3576918). Archives of Disease in Childhood. 95: 432–436. doi:10.1136/adc.2009.170118 (http://doi.org/10.1136%2Fadc.2009.170118). PMC 3576918 (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3576918) . PMID 20501538 (http://www.ncbi. nlm.nih.gov/pubmed/20501538). 62. Miller, C.A.; Wagstaff, D.A. (2011). "Behavioral profiles associated with auditory processing disorder and specific language impairment". Journal of Communication Disorders. 44 (6): 745–763. doi:10.1016/j.jcomdis.2011.04.001 (http://doi.org/10.1016%2Fj.jcomdis.2011.04.001). 63. Corriveau K, Pasquini E, Goswami U (June 2007). "Basic auditory processing skills and specific language impairment: a new look at an old hypothesis". J. Speech Lang. Hear. Res. 50 (3): 647–66. doi:10.1044/1092-4388(2007/046) (http://doi.org/10.1044%2F1092-4388%282007%2F046%29). PMID 17538107 (http://www.ncbi.nlm.nih.gov/pubmed/17538107). 64. Dlouha O, Novak A, Vokral J (June 2007). "Central auditory processing disorder (CAPD) in children with specific language impairment (SLI). Central auditory tests". Int. J. Pediatr. Otorhinolaryngol. 71 (6): 903–7. doi:10.1016/j.ijporl.2007.02.012 (http://doi.org/10.1016%2Fj.ijporl.2007.02.012). PMID 17382411 (http://www.ncbi.nlm.nih.gov/pubmed/17382411). 65. Chermak, Gail D.; Somers, Erin K.; Seikel, J. Anthony (1998). "Behavioral signs of central auditory processing disorder and attention deficit hyperactivity disorder". Journal of American Academy of Audiology: 7884. 66. RICCIO, CYNTHIA A.; HYND, GEORGE W.; COHEN, MORRIS J.; HALL, JOSH; MOLT, LAWRENCE (July 1994). "Comorbidity of Central Auditory Processing Disorder and Attention-Deficit Hyperactivity Disorder". Journal of the American Academy of Child & Adolescent Psychiatry. 33 (6): 849–857. doi:10.1097/00004583-199407000-00011 (http://doi.org/10.1097%2F00004583-199407000-00011). 67. Bellis, Teri James. "Auditory Processing Disorders (APD) in Children" (http://www.asha.org/public/hearing/Understanding-Auditory-Processing-Disorders-in-Children/). www.asha.org. ASHA. 68. Chermak GD, Silva ME, Nye J, Hasbrouck J, Musiek FE (May 2007). "An update on professional education and clinical practices in central auditory processing". J Am Acad Audiol. 18 (5): 428–52; quiz 455. doi:10.3766/jaaa.18.5.7 (http://doi.org/10.3766%2Fjaaa.18.5.7). PMID 17715652 (http://www.ncbi.nlm.nih.gov/pubmed/17715652). 69. Moore DR (2007). "Auditory processing disorders: acquisition and treatment". J Commun Disord. 40 (4): 295–304. doi:10.1016/j.jcomdis.2007.03.005 (http://doi.org/10.1016%2Fj.jcomdis.2007.03.005). PMID 17467002 (http://www.ncbi.nlm.nih.gov/pubmed/17467002). 70. Moore DR, Rosenberg JF, Coleman JS (July 2005). "Discrimination training of phonemic contrasts enhances phonological processing in mainstream school children". Brain Lang. 94 (1): 72–85. doi:10.1016/j.bandl.2004.11.009 (http://doi.org/10.1016%2Fj.bandl.2004.11.009). PMID 15896385 (http://www.ncbi.nlm.nih.gov/pubmed/15896385). 71. Russo NM, Nicol TG, Zecker SG, Hayes EA, Kraus N (January 2005). "Auditory training improves neural timing in the human brainstem". Behav. Brain Res. 156 (1): 95–103. doi:10.1016/j.bbr.2004.05.012 (http:// doi.org/10.1016%2Fj.bbr.2004.05.012). PMID 15474654 (http://www.ncbi.nlm.nih.gov/pubmed/15474654). 72. Alonso R, Schochat E (2009). "The efficacy of formal auditory training in children with (central) auditory processing disorder: behavioral and electrophysiological evaluation". Braz J Otorhinolaryngol. 75 (5): 726– 32. doi:10.1590/S1808-86942009000500019 (http://doi.org/10.1590%2FS1808-86942009000500019). PMID 19893943 (http://www.ncbi.nlm.nih.gov/pubmed/19893943). 73. Loo, J.H.Y.; Bamiou, D.-E.; Campbell, N.; Luxon, L.M. (2010). "Computer-based auditory training (CBAT): benefits for children with language- and reading-related learning difficulties". Developmental Medicine and Child Neurology. 52 (8): 708–717. doi:10.1111/j.1469-8749.2010.03654.x (http://doi.org/10.1111%2Fj.1469-8749.2010.03654.x). 74. Cameron S, Dillon H (November 2011). "Development and Evaluation of the LiSN & Learn Auditory Training Software for Deficit-Specific Remediation of Binaural Processing Deficits in Children: Preliminary Findings". Journal of the American Academy of Audiology. 22 (10): 678–96. doi:10.3766/jaaa.22.10.6 (http://doi.org/10.3766%2Fjaaa.22.10.6). PMID 22212767 (http://www.ncbi.nlm.nih.gov/pubmed/22212767). 75. Leite RA, Wertzner HF, Matas CG (2010). "Long latency auditory evoked potentials in children with phonological disorder" (http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0104-56872010000400034&lng= en&nrm=iso&tlng=en). Pró-fono : Revista De Atualização Científica. 22 (4): 561–6. doi:10.1590/s0104-56872010000400034 (http://doi.org/10.1590%2Fs0104-56872010000400034). PMID 21271117 (http://www.n cbi.nlm.nih.gov/pubmed/21271117). 76. Mudford OC, Cullen C (2004). "Auditory integration training: a critical review". In Jacobson JW, Foxx RM, Mulick JA. Controversial Therapies for Developmental Disabilities. Routledge. pp. 351–62. ISBN 0-80584192-X. 77. Myklebust, H. (1954). Auditory disorders in children. New York: Grune & Stratton. 78. Bocca E, Calearo C, Cassinari V (1954). "A new method for testing hearing in temporal lobe tumours; preliminary report". Acta Oto-laryngologica. 44 (3): 219–21. doi:10.3109/00016485409128700 (http://doi.org/1 0.3109%2F00016485409128700). PMID 13197002 (http://www.ncbi.nlm.nih.gov/pubmed/13197002). 79. Bocca E, Calearo C, Cassinari V, Migliavacca F (1955). "Testing "cortical" hearing in temporal lobe tumours". Acta Oto-laryngologica. 45 (4): 289–304. doi:10.3109/00016485509124282 (http://doi.org/10.3109%2 F00016485509124282). PMID 13275293 (http://www.ncbi.nlm.nih.gov/pubmed/13275293). 80. Kimura, Doreen (1961). "Cerebral dominance and the perception of verbal stimuli". Canadian Journal of Psychology. 15 (3): 166–171. doi:10.1037/h0083219 (http://doi.org/10.1037%2Fh0083219). ISSN 0008-4255 (http://www.worldcat.org/issn/0008-4255). 81. Katz, J., & Illmer, R. (1972). Auditory perception in children with learning disabilities. In J. Katz (Ed.), Handbook of clinical audiology (pp. 540–563). Baltimore: Williams & Wilkins. 82. Keith, Robert W. (1977). Central auditory dysfunction: University of Cincinnati Medical Center Division of Audiology and Speech Pathology symposium. New York: Grune & Stratton. ISBN 0-8089-1061-2. OCLC 3203948 (http://www.worldcat.org/oclc/3203948). 83. Sweetow RW, Reddell RC (1978). "The use of masking level differences in the identification of children with perceptual problems". J Am Audiol Soc. 4 (2): 52–6. PMID 738915 (http://www.ncbi.nlm.nih.gov/pubme d/738915). 84. Manning WH, Johnston KL, Beasley DS (February 1977). "The performance of children with auditory perceptual disorders on a time-compressed speech discrimination measure". J Speech Hear Disord. 42 (1): 77– 84. doi:10.1044/jshd.4201.77 (http://doi.org/10.1044%2Fjshd.4201.77). PMID 839757 (http://www.ncbi.nlm.nih.gov/pubmed/839757). 85. Willeford, J. A. (1977). "Assessing central auditory behavior in children A test battery approach". In Keith, Robert W. Central auditory dysfunction. New York: Grune & Stratton. pp. 43–72. ISBN 0-8089-1061-2. OCLC 3203948 (http://www.worldcat.org/oclc/3203948). 86. Jerger J, Thibodeau L, Martin J, et al. (September 2002). "Behavioral and electrophysiologic evidence of auditory processing disorder: a twin study". J Am Acad Audiol. 13 (8): 438–60. PMID 12371661 (http://ww w.ncbi.nlm.nih.gov/pubmed/12371661). 87. Estes RI, Jerger J, Jacobson G (February 2002). "Reversal of hemispheric asymmetry on auditory tasks in children who are poor listeners". J Am Acad Audiol. 13 (2): 59–71. PMID 11895008 (http://www.ncbi.nl m.nih.gov/pubmed/11895008). 88. Chermak GD, Musiek FE (2002). "Auditory training: Principles and approaches for remediation and managing auditory processing disorders". Seminars in Hearing. 23 (4): 287–295. doi:10.1055/s-2002-35878 (https ://doi.org/10.1055%2Fs-2002-35878). ISSN 0734-0451 (http://www.worldcat.org/issn/0734-0451). 89. Musiek F (June 1999). "Habilitation and management of auditory processing disorders: overview of selected procedures". J Am Acad Audiol. 10 (6): 329–42. PMID 10385875 (http://www.ncbi.nlm.nih.gov/pubmed /10385875). 90. Task Force on Central Auditory Processing Consensus Development (1996). "Central auditory processing: Current status of research and implications for clinical practice [Technical Report]" (http://www.asha.org/ docs/html/TR1996-00241.html). American Journal of Audiology. 5: 41–54. doi:10.1044/policy.TR1996-00241 (http://doi.org/10.1044%2Fpolicy.TR1996-00241). 91. Jerger J, Musiek F (October 2000). "Report of the Consensus Conference on the Diagnosis of Auditory Processing Disorders in School-Aged Children" (http://www.bsnpta.org/geeklog/public_html/filemgmt/filemgm t_data/files/Auditory_Processing_Disorders_in_Children.pdf) (pdf). J Am Acad Audiol. 11 (9): 467–74. PMID 11057730 (http://www.ncbi.nlm.nih.gov/pubmed/11057730). 92. Keith, Robert W. (1981). Central auditory and language disorders in children. San Diego, CA: College-Hill Press. ISBN 0-933014-74-0. OCLC 9258682 (http://www.worldcat.org/oclc/9258682). 93. Katz, Jack; Henderson, Donald; Stecker, Nancy Austin (1992). Central auditory processing: a transdisciplinary view. St. Louis, MO: Mosby Year Book. ISBN 1-55664-372-1. OCLC 2587728 (http://www.worldcat. org/oclc/2587728). 94. Katz, Jack; Stecker, Nancy Austin (1998). Central auditory processing disorders: mostly management. Boston: Allyn and Bacon. ISBN 0-205-27361-0. OCLC 246378171 (http://www.worldcat.org/oclc/246378171).
External links Auditory processing disorder: An overview for the clinician (http://journals.lww.com/thehearingjournal/Fulltext/2001/07000/Auditory_processing_disorder__An_overview_for_the.3.aspx) American Speech-Language-Hearing Association (ASHA) (http://search.asha.org/default.aspx?q=auditory+processing+disorder) UK Medical Research Council Institute of Hearing Research) (http://www.ihr.mrc.ac.uk/research/apd.php/) Auditory Processing Disorder in the UK (APDUK) (http://www.apduk.org.uk/) Support community for CAPD (http://www.capdsupport.org) Retrieved from "http://en.wikipedia.org/w/index.php?title=Auditory_processing_disorder&oldid=834033969" | <urn:uuid:b6102c69-6634-4a55-9bc7-59c71b81042f> | {
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During the 1970s and 1980s the only available tool for diagnosing Fragile X syndrome (FXS) was the chromosome (“cytogenetic”) test. While it was helpful, it was not always accurate. In the 1990s, scientists identified the FMR1 gene that causes FXS, and accurate DNA testing became available. The “FMR1 DNA Test” (sometimes called the “Fragile X DNA Test”) thus replaced chromosome testing, and became the “standard of care” for determining the presence of Fragile X. DNA testing detects more than 99 percent of individuals (both males and females) with FXS, as well as Fragile X carriers.
Who Should Have Fragile X Testing?
There are three general circumstances in which Fragile X testing should be considered:
- Clinical symptoms that suggest Fragile X Syndrome, FXTAS or infertility/FXPOI.
- A family history of Fragile X syndrome, FXTAS, intellectual or learning disabilities or autism of unknown cause, or infertility.
- Family or personal history of a Fragile X Genetics and Inheritance (carrier).
Specific indications for testing include:
- Any male or female with intellectual disabilities, developmental delay, speech and language delay, autism or learning disabilities of unknown cause.
- Any female with infertility, elevated FSH levels, premature ovarian failure, primary ovarian insufficiency or irregular menses.
- Any adult over 50 with features of FXTAS, including intention tremors, ataxia, memory loss, cognitive decline, personality change, especially in combination with a positive family history of Fragile X.
- Any preconception or pregnant woman who expresses interest in or requests Fragile X carrier testing.
Lab Tests for Fragile X
The FMR1 DNA Test can be administered with two different lab procedures.
- The Southern blot analysis test determines if the gene has a full mutation, its approximate size, whether the gene has been “methylated” and if there is mosaicism of the gene (a mixture of different cell types).
- The polymerase chain reaction (PCR) analysis can determine the actual number of “CGG repeats” (a pattern of DNA) that are present in the Fragile X gene. For various technical reasons, PCR has been not the test of choice to diagnose a full mutation, but is quite accurate in determining premutation and normal gene repeat numbers. However, PCR is less expensive and quicker than Southern blot, and recent advances in technology have increased its ability to identify Fragile X full mutations. PCR may thus be the only test used in the near future.
Testing Cost and Reporting Time
The blood test usually ranges from $300-$600, and results are usually available in 2-4 weeks.
How Are Testing Arrangements Made?
The test must be ordered by a genetic counselor or physician. A genetic counselor often will facilitate the testing, and make certain that the correct drawing, shipping and processing of the sample occurs. The genetic counselor is trained and experienced in the interpretation and explaining of the test results. She/he can coordinate any follow-up appointments and work with your physician to make referrals to resources in your area. You can locate a genetic counselor in your area by logging on to the “Find a counselor” feature on the National Society of Genetic Counselors website or by contacting the NFXF at firstname.lastname@example.org or (800) 688-8765 for a referral to a counselor in your area.
In most cases you will be directed to go to a blood drawing station for a blood drawing procedure. Although this facility is often referred to as a “lab,” it is not the actual lab doing the DNA test. After the blood is drawn it is sent to a specific genetics or “reference” lab for the genetic test.
If your insurance company (or state/public insurance such as Medicaid) is paying for the testing, it is likely that the sample will go to the laboratory with which they are contracted. If you are paying for the test yourself, your physician or genetic counselor can locate a genetics lab in your area or one with which they have a relationship. The National Fragile X Foundation can assist your provider in locating a laboratory as well. For providers only, there is also a listing of laboratories that provide genetic testing; log onto GeneTests for information.
CPT and ICD-10 Codes for Fragile X Testing
When ordering the FMR1 DNA test, if the CPT codes are needed, check with the lab where the test will be performed. However, here is a list of the CPT codes most commonly associated with FMR1 DNA testing:
Pertinent ICD-10 codes:
- Fragile X Syndrome: Q99.2
- Testing of male for genetic disease carrier status: Z31.440
- Testing for genetic disease carrier status of female: Z31.430
What Do Test Results Report?
The test will determine the number of CGG repeats that are present in the area of the Fragile X gene that is studied. If Southern blot is ordered, the test will also tell you the methylation pattern of the Fragile X gene. If the testing is performed on a female, two numbers will be provided—one for each X chromosome. In males, only one result will be provided, though that number might be a range, such as 200-400, because the gene often expands in an unpredictable manner.
Who Receives Test Results?
Test results go to the provider who ordered the test, such as the genetic counselor or physician. Other recipients may include a pediatrician, obstetrician, or other health care provider involved in the patient’s or family’s care.
Other Tests for Children With Developmental Delay
Physicians and other providers ordering Fragile X testing often arrange for other genetic testing to provide more information on a child’s condition. Depending on the child’s presenting features or symptoms, this might include chromosome analysis, chromosome microarray (CGH), FISH testing (for other single gene conditions such as Velo-cardio-facial syndrome) and metabolic/ biochemical tests. Other types of medical evaluations might be recommended as well, including magnetic resonance imaging (MRI), electroencephalography (EEG), computer tomography (CT scan) or X-rays.
Chromosomal Microarray Analysis and the DNA Test for Fragile X
Chromosomal microarray analysis is a powerful test for detecting certain genetic causes of developmental disabilities; however, it is not able to detect Fragile X mutations of any kind.
For this reason, the diagnostic work-up of children with autism, global developmental delay, or intellectual disabilities should include both a microarray analysis and a separate Fragile X DNA analysis. If your child just had the microarray analysis but not the specific DNA test for Fragile X, then he has not been checked for Fragile X. | <urn:uuid:6332f85d-c5bf-46b5-b6b7-4999ee5f6139> | {
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The World Health Organization is planning to add “gaming disorder” – excessive addiction to video games – to its list of recognised mental disorders. In a draft of the next revision of its International Classification of Diseases, the WHO described the condition as a “pattern of persistent or recurrent gaming behaviour”.
The International Classification of Diseases’ newest version, ICD-11, is scheduled for release in 2018. The last version, ICD-10, was published in 1990, and is used by 117 member nations to report health statistics.
The draft describes gaming disorder as the condition in which one loses control over the activity, begins to give it more priority over other life interests, and continues to indulge in it even after negative consequences show up.
The behaviour pattern as a result can “result in significant impairment in personal, family, social, educational, occupational or other important areas of functioning”, the draft said.
Diagnosis can be done if the condition remains evident for at least a year, the draft said.
Here is the full text of the draft’s description of “gaming disorder”:
Gaming disorder is characterised by a pattern of persistent or recurrent gaming behaviour (“digital gaming” or “video-gaming”), which may be online or offline, manifested by:
- impaired control over gaming (e.g., onset, frequency, intensity, duration, termination, context),
- increasing priority given to gaming to the extent that gaming takes precedence over other life interests and daily activities,
- continuation or escalation of gaming despite the occurrence of negative consequences.
The behaviour pattern is of sufficient severity to result in significant impairment in personal, family, social, educational, occupational or other important areas of functioning. The pattern of gaming behaviour may be continuous or episodic and recurrent. The gaming behaviour and other features are normally evident over a period of at least 12 months in order for a diagnosis to be assigned, although the required duration may be shortened if all diagnostic requirements are met and symptoms are severe. | <urn:uuid:8da8f4f3-afc8-489f-bfe4-482a03351129> | {
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In placental mammals, the umbilical cord (also called the navel string, birth cord or funiculus umbilicalis) is a conduit between the developing embryo or fetus and the placenta. During prenatal development, the umbilical cord is physiologically and genetically part of the fetus and (in humans) normally contains two arteries (the umbilical arteries) and one vein (the umbilical vein), buried within Wharton's jelly. The umbilical vein supplies the fetus with oxygenated, nutrient-rich blood from the placenta. Conversely, the fetal heart pumps deoxygenated, nutrient-depleted blood through the umbilical arteries back to the placenta.
Umbilical cord of a three-minute-old baby. A medical clamp has been applied.
Structure and developmentEdit
The umbilical cord develops from and contains remnants of the yolk sac and allantois. It forms by the fifth week of development, replacing the yolk sac as the source of nutrients for the embryo. The cord is not directly connected to the mother's circulatory system, but instead joins the placenta, which transfers materials to and from the maternal blood without allowing direct mixing. The length of the umbilical cord is approximately equal to the crown-rump length of the fetus throughout pregnancy. The umbilical cord in a full term neonate is usually about 50 centimeters (20 in) long and about 2 centimeters (0.75 in) in diameter. This diameter decreases rapidly within the placenta. The fully patent umbilical artery has two main layers: an outer layer consisting of circularly arranged smooth muscle cells and an inner layer which shows rather irregularly and loosely arranged cells embedded in abundant ground substance staining metachromatic. The smooth muscle cells of the layer are rather poorly differentiated, contain only a few tiny myofilaments and are thereby unlikely to contribute actively to the process of post-natal closure.
The umbilical cord contains Wharton's jelly, a gelatinous substance made largely from mucopolysaccharides which protects the blood vessels inside. It contains one vein, which carries oxygenated, nutrient-rich blood to the fetus, and two arteries that carry deoxygenated, nutrient-depleted blood away. Occasionally, only two vessels (one vein and one artery) are present in the umbilical cord. This is sometimes related to fetal abnormalities, but it may also occur without accompanying problems.
It is unusual for a vein to carry oxygenated blood and for arteries to carry deoxygenated blood (the only other examples being the pulmonary veins and arteries, connecting the lungs to the heart). However, this naming convention reflects the fact that the umbilical vein carries blood towards the fetus's heart, while the umbilical arteries carry blood away.
The blood flow through the umbilical cord is approximately 35 ml / min at 20 weeks, and 240 ml / min at 40 weeks of gestation. Adapted to the weight of the fetus, this corresponds to 115 ml / min / kg at 20 weeks and 64 ml / min / kg at 40 weeks.
Connection to fetal circulatory systemEdit
The umbilical cord enters the fetus via the abdomen, at the point which (after separation) will become the umbilicus (or navel). Within the fetus, the umbilical vein continues towards the transverse fissure of the liver, where it splits into two. One of these branches joins with the hepatic portal vein (connecting to its left branch), which carries blood into the liver. The second branch (known as the ductus venosus) bypasses the liver and flows into the inferior vena cava, which carries blood towards the heart. The two umbilical arteries branch from the internal iliac arteries, and pass on either side of the urinary bladder into the umbilical cord, completing the circuit back to the placenta.
Changes after birthEdit
In absence of external interventions, the umbilical cord occludes physiologically shortly after birth, explained both by a swelling and collapse of Wharton's jelly in response to a reduction in temperature and by vasoconstriction of the blood vessels by smooth muscle contraction. In effect, a natural clamp is created, halting the flow of blood. In air at 18 °C, this physiological clamping will take three minutes or less. In water birth, where the water temperature is close to body temperature, normal pulsation can be 5 minutes and longer.
Closure of the umbilical artery by vasoconstriction consists of multiple constrictions which increase in number and degree with time. There are segments of dilatations with trapped uncoagulated blood between the constrictions before complete occlusion. Both the partial constrictions and the ultimate closure are mainly produced by muscle cells of the outer circular layer. In contrast, the inner layer seems to serve mainly as a plastic tissue which can easily be shifted in an axial direction and then folded into the narrowing lumen to complete the closure. The vasoconstrictive occlusion appears to be mainly mediated by serotonin and thromboxane A2. The artery in cords of preterm infants contracts more to angiotensin II and arachidonic acid and is more sensitive to oxytocin than in term ones. In contrast to the contribution of Wharton's jelly, cooling causes only temporary vasoconstriction.
Within the child, the umbilical vein and ductus venosus close up, and degenerate into fibrous remnants known as the round ligament of the liver and the ligamentum venosum respectively. Part of each umbilical artery closes up (degenerating into what are known as the medial umbilical ligaments), while the remaining sections are retained as part of the circulatory system.
Problems and abnormalitiesEdit
A number of abnormalities can affect the umbilical cord, which can cause problems that affect both mother and child:
- Umbilical cord compression can result from, for example, entanglement of the cord, a knot in the cord, or a nuchal cord, (which is the wrapping of the umbilical cord around the fetal neck) but these conditions do not always cause obstruction of fetal circulation.
- Velamentous cord insertion
- Single umbilical artery
- Umbilical cord prolapse
- Vasa praevia
Clamping and cuttingEdit
The cord can be clamped at different times; however delaying the clamping of the umbilical cord until one minute after birth improves outcomes as long as there is the ability to treat jaundice if it occurs. Clamping is followed by cutting of the cord, which is painless due to the absence of nerves. The cord is extremely tough, like thick sinew, and so cutting it requires a suitably sharp instrument. While umbilical severance may be delayed until after the cord has stopped pulsing (5–20 minutes after birth), there is ordinarily no significant loss of either venous or arterial blood while cutting the cord. Current evidence neither supports, nor refutes, delayed cutting of the cord, according to the American Congress of Obstetricians and Gynecologists (ACOG) guidelines.
There are umbilical cord clamps which incorporate a knife. These clamps are safer and faster, allowing one to first apply the cord clamp and then cut the umbilical cord. After the cord is clamped and cut, the newborn wears a plastic clip on the navel area until the compressed region of the cord has dried and sealed sufficiently.
The length of umbilical left attached to the newborn varies by practice; in most hospital settings the length of cord left attached after clamping and cutting is minimal. In the United States, however, where the birth occurred outside of the hospital and an emergency medical technician (EMT) clamps and cuts the cord, a longer segment up to 18 cm (7 in) in length is left attached to the newborn.
The remaining umbilical stub remains for up to 10 days as it dries and then falls off.
Early versus delayed clampingEdit
A Cochrane review in 2013 came to the conclusion that delayed cord clamping (between one and three minutes after birth) is "likely to be beneficial as long as access to treatment for jaundice requiring phototherapy is available". In this review delayed clamping, as contrasted to early, resulted in no difference in risk of severe maternal postpartum hemorrhage or neonatal mortality, low Apgar score. On the other hand, delayed clamping resulted in an increased birth weight of on average about 100 g, and an increased hemoglobin concentration of on average 1.5 g/dL with half the risk of being iron deficient at three and six months, but an increased risk of jaundice requiring phototherapy.
In 2012, the American College of Obstetricians and Gynecologists officially endorsed delaying clamping of the umbilical cord for 30–60 seconds with the newborn held below the level of the placenta in all cases of preterm delivery based largely on evidence that it reduces the risk of intraventricular hemorrhage in these children by 50%.[obsolete source] In the same committee statement, ACOG also recognize several other likely benefits for preterm infants, including "improved transitional circulation, better establishment of red blood cell volume, and decreased need for blood transfusion". In January 2017, a revised Committee Opinion extended the recommendation to term infants, citing data that term infants benefit from increased hemoglobin levels in the newborn period and improved iron stores in the first months of life, which may result in improved developmental outcomes. ACOG recognized a small increase in the incidence of jaundice in term infants with delayed cord clamping, and recommended policies be in place to monitor for and treat neonatal jaundice. ACOG also noted that delayed cord clamping is not associated with increased risk of postpartum hemorrhage.
Several studies have shown benefits of delayed cord clamping: A meta-analysis showed that delaying clamping of the umbilical cord in full-term neonates for a minimum of 2 minutes following birth is beneficial to the newborn in giving improved hematocrit, iron status as measured by ferritin concentration and stored iron, as well as a reduction in the risk of anemia (relative risk, 0.53; 95% CI, 0.40-0.70). A decrease was also found in a study from 2008. Although there is higher hemoglobin level at 2 months, this effect did not persist beyond 6 months of age. Not clamping the cord for three minutes following the birth of a baby improved outcomes at four years of age. A delay of three minutes or more in umbilical cord clamping after birth reduce the prevalence of anemia in infants.
Negative effects of delayed cord clamping include an increased risk of polycythemia. Still, this condition appeared to be benign in studies. Infants whose cord clamping occurred later than 60 seconds after birth had a higher rate of neonatal jaundice requiring phototherapy.
Delayed clamping is not recommended as a response to cases where the newborn is not breathing well and needs resuscitation. Rather, the recommendation is instead to immediately clamp and cut the cord and perform cardiopulmonary resuscitation. The umbilical cord pulsating is not a guarantee that the baby is receiving enough oxygen.
Some parents choose to omit cord severance entirely, a practice called "lotus birth" or umbilical nonseverance. The entire intact umbilical cord is allowed to dry and separates on its own (typically on the 3rd day after birth), falling off and leaving a healed umbilicus.
Umbilical cord catheterizationEdit
As the umbilical vein is directly connected to the central circulation, it can be used as a route for placement of a venous catheter for infusion and medication. The umbilical vein catheter is a reliable alternative to percutaneous peripheral or central venous catheters or intraosseous canulas and may be employed in resuscitation or intensive care of the newborn.
From 24 to 34 weeks of gestation, when the fetus is typically viable, blood can be taken from the cord in order to test for abnormalities (particularly for hereditary conditions). This diagnostic genetic test procedure is known as percutaneous umbilical cord blood sampling.
Storage of cord bloodEdit
The blood within the umbilical cord, known as cord blood, is a rich and readily available source of primitive, undifferentiated stem cells (of type CD34-positive and CD38-negative). These cord blood cells can be used for bone marrow transplant.
Some parents choose to have this blood diverted from the baby's umbilical blood transfer through early cord clamping and cutting, to freeze for long-term storage at a cord blood bank should the child ever require the cord blood stem cells (for example, to replace bone marrow destroyed when treating leukemia). This practice is controversial, with critics asserting that early cord blood withdrawal at the time of birth actually increases the likelihood of childhood disease, due to the high volume of blood taken (an average of 108ml) in relation to the baby's total supply (typically 300ml). The Royal College of Obstetricians and Gynaecologists stated in 2006 that "there is still insufficient evidence to recommend directed commercial cord blood collection and stem-cell storage in low-risk families".
The American Academy of Pediatrics has stated that cord blood banking for self-use should be discouraged (as most conditions requiring the use of stem cells will already exist in the cord blood), while banking for general use should be encouraged. In the future, cord blood-derived embryonic-like stem cells (CBEs) may be banked and matched with other patients, much like blood and transplanted tissues. The use of CBEs could potentially eliminate the ethical difficulties associated with embryonic stem cells (ESCs).
While the American Academy of Pediatrics discourages private banking except in the case of existing medical need, it also says that information about the potential benefits and limitations of cord blood banking and transplantation should be provided so that parents can make an informed decision.
In the United States, cord blood education has been supported by legislators at the federal and state levels. In 2005, the National Academy of Sciences published an Institute of Medicine (IoM) report which recommended that expectant parents be given a balanced perspective on their options for cord blood banking. In response to their constituents, state legislators across the country are introducing legislation intended to help inform physicians and expectant parents on the options for donating, discarding or banking lifesaving newborn stem cells. Currently 17 states, representing two-thirds of U.S. births, have enacted legislation recommended by the IoM guidelines.
The use of cord blood stem cells in treating conditions such as brain injury and Type 1 Diabetes is already being studied in humans, and earlier stage research is being conducted for treatments of stroke, and hearing loss.
Cord blood stored with private banks is typically reserved for use of the donor child only. In contrast, cord blood stored in public banks is accessible to anyone with a closely matching tissue type and demonstrated need. The use of cord blood from public banks is increasing. Currently it is used in place of a bone marrow transplant in the treatment of blood disorders such as leukemia, with donations released for transplant through one registry, Netcord.org, passing 1,000,000 as of January 2013. Cord blood is used when the patient cannot find a matching bone marrow donor; this "extension" of the donor pool has driven the expansion of public banks.
The umbilical cord in other animalsEdit
The umbilical cord in some mammals, including cows and sheep, contains two distinct umbilical veins. There is only one umbilical vein in the human umbilical cord.
In some animals, the mother will gnaw through the cord, thus separating the placenta from the offspring. The cord along with the placenta is often eaten by the mother, to provide nourishment and to dispose of tissues that would otherwise attract scavengers or predators. In chimpanzees, the mother leaves the cord in place and nurses her young with the cord and placenta attached until the cord dries out and separates naturally, within a day of birth, at which time the cord is discarded. (This was first documented by zoologists in the wild in 1974.)
Animals that lay eggs seem to have a false umbilical-cord that attaches the embryo and yolk together in much the same way.
Other uses for the term "umbilical cord"Edit
The term "umbilical cord" or just "umbilical" has also come to be used for other cords with similar functions, such as the hose connecting surface-supplied divers to their surface supply of air and/or heating, or space-suited astronauts to their spacecraft. Engineers sometimes use the term to describe a complex or critical cable connecting a component, especially when composed of bundles of conductors of different colors, thickness and types, terminating in a single multi-contact disconnect.
Cancer-causing toxicants in human umbilical cordsEdit
In multiple American and international studies, cancer-causing chemicals have been found in the blood of umbilical cords. These originate from certain plastics, computer circuit boards, fumes and synthetic fragrances among others. Over 300 chemical toxicants have been found, including bisphenol A (BPA), tetrabromobisphenol A (TBBPA), Teflon-related perfluorooctanoic acid, galaxolide and synthetic musks among others. The studies in America showed higher levels in African Americans, Hispanic Americans and Asian Americans due, it is thought, to living in areas of higher pollution.
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- "Umbilical - Search Online Etymology Dictionary". www.etymonline.com. Retrieved 27 March 2018.
- "The Umbilical Cord". yale.edu. Retrieved 27 March 2018.
- Meyer WW, Rumpelt HJ, Yao AC, Lind J (July 1978). "Structure and closure mechanism of the human umbilical artery". Eur. J. Pediatr. 128 (4): 247–59. doi:10.1007/BF00445610. PMID 668732.
- "Fetal Circulation". www.heart.org. Retrieved 27 March 2018.
- Kiserud, T.; Acharya, G. (2004). "The fetal circulation". Prenatal Diagnosis. 24 (13): 1049–1059. doi:10.1002/pd.1062. PMID 15614842.
- "Peculiarities in the Vascular System in the Fetus - Gray's Anatomy of the Human Body - Yahoo! Education". Archived from the original on January 23, 2012.
- Cohain, J. S. (2010). "A Proposed Protocol for Third Stage Management - Judy's 3,4,5,10 minute method". Birth. 37 (1): 84–85. doi:10.1111/j.1523-536x.2009.00385_2.x.
- Yao AC, Lind J, Lu T (1977). "Closure of the human umbilical artery: a physiological demonstration of Burton's theory". Eur. J. Obstet. Gynecol. Reprod. Biol. 7 (6): 365–8. doi:10.1016/0028-2243(77)90064-8. PMID 264063.
- Quan A, Leung SW, Lao TT, Man RY (December 2003). "5-hydroxytryptamine and thromboxane A2 as physiologic mediators of human umbilical artery closure". J. Soc. Gynecol. Investig. 10 (8): 490–5. doi:10.1016/S1071-5576(03)00149-7. PMID 14662162.
- White RP (January 1989). "Pharmacodynamic study of maturation and closure of human umbilical arteries". Am. J. Obstet. Gynecol. 160 (1): 229–37. doi:10.1016/0002-9378(89)90127-0. PMID 2912087.
- "Umbilical Cord Complications: eMedicine Obstetrics and Gynecology". Retrieved 2010-01-24.
- P02.5 Fetus and newborn affected by other compression of umbilical cord in ICD-10, the International Statistical Classification of Diseases
- "Fetus or Newborn Problems: Labor and Delivery Complications: Merck Manual Home Edition". Retrieved 2010-03-27.
- McDonald, SJ; Middleton, P; Dowswell, T; Morris, PS (Jul 11, 2013). "Effect of timing of umbilical cord clamping of term infants on maternal and neonatal outcomes". The Cochrane Database of Systematic Reviews. 7: CD004074. doi:10.1002/14651858.CD004074.pub3. PMID 23843134.
- Stiegler, Paul M., M.D. (May 2007). "EMT-BASIC \ EMT BASIC INTERMEDIATE TECHNICIAN PROTOCOLS" (PDF). Dane County Emergency Medical Services. Retrieved December 17, 2011.
- Meersman, Jack. "EMT-B: Obstetrics, Infants and Children". Wild Iris Medical Education. Retrieved December 17, 2011.
- McDonald, S. J.; Middleton, P.; Dowswell, T.; Morris, P. S. (2013). McDonald, Susan J, ed. "Effect of timing of umbilical cord clamping of term infants on maternal and neonatal outcomes". The Cochrane Library. 7: CD004074. doi:10.1002/14651858.CD004074.pub3. PMID 23843134.
- Committee on Obstetric Practice, American College of Obstetricians and, Gynecologists (December 2012). "Committee Opinion No.543: Timing of umbilical cord clamping after birth". Obstetrics and gynecology. 120 (6): 1522–6. doi:10.1097/01.aog.0000423817.47165.48. PMID 23168790.
- "Committee Opinion No. 684". Obstetrics & Gynecology. 129 (1): e5–e10. 2017-01-01. doi:10.1097/aog.0000000000001860. ISSN 1873-233X.
- Hutton EK, Hassan ES (March 2007). "Late vs early clamping of the umbilical cord in full-term neonates: systematic review and meta-analysis of controlled trials". JAMA. 297 (11): 1241–52. doi:10.1001/jama.297.11.1241. PMID 17374818.
- Examination of the Newborn & Neonatal Health: A Multidimensional Approach, p. 116-117
- "Effect of timing of umbilical cord clamping of term infants on maternal and neonatal outcomes." Cochrane Database Syst Rev. 2008; (2):CD004074
- Andersson, O; Lindquist, B; Lindgren, M; Stjernqvist, K; Domellöf, M; Hellström-Westas, L (1 July 2015). "Effect of Delayed Cord Clamping on Neurodevelopment at 4 Years of Age: A Randomized Clinical Trial". JAMA Pediatrics. 169 (7): 631–8. doi:10.1001/jamapediatrics.2015.0358. PMID 26010418.
- "Can delayed umbilical cord clamping reduce infant anemia at age 8, 12 months?". medicalxpress.com. Retrieved 27 March 2018.
- Military Obstetrics & Gynecology – Delivery of the Baby The Brookside Associates Medical Education Division. Retrieved Jan 10, 2009
- Waterbirth International – Waterbirth FAQ Retrieved Jan 10, 2009
- Crowther, S (2006). "Lotus birth: leaving the cord alone". The Practising Midwife. 9 (6): 12–14. PMID 16830839.
- "Human Reproduction, Lectures: Clinical Genetics". Retrieved 2010-02-11.
- American Academy of Pediatrics. "Cord Blood Banking for Potential Future Transplantation".
- "Cord blood yields 'ethical' embryonic stem cells.", Coghlin A. New Scientist, August 18, 2005. Accessed June 25, 2007.
- Cord Blood for Neonatal Hypoxic-Ischemic Encephalopathy, Autologous Cord Blood Cells for Hypoxic Ischemic Encephalopathy Study 1. Phase I Study of Feasibility and Safety
- Haller MJ; Viener, HL; Wasserfall, C; Brusko, T; Atkinson, MA; Schatz, DA; et al. (2008). "Autologous Umbilical Cord Blood Infusion for Type 1 Diabetes". Exp. Hematol. 36 (6): 710–715. doi:10.1016/j.exphem.2008.01.009. PMC . PMID 18358588.
- Vendrame M, et al. (2006). "Cord blood rescues stroke-induced changes in splenocyte phenotype and function". Exp. Neurol. 199 (1): 191–200. doi:10.1016/j.expneurol.2006.03.017. PMID 16713598.
- Vendrame M, et al. (2005). "Anti-inflammatory effects of human cord blood cells in a rat model of stroke". Stem Cells Dev. 14 (5): 595–604. doi:10.1089/scd.2005.14.595. PMID 16305344.
- Revoltella RP, et al. (2008). "Cochlear repair by transplantation of human cord blood CD133+ cells to nod-scid mice made deaf with kanamycin and noise". Cell Transplant. 17 (6): 665–678. doi:10.3727/096368908786092685. PMID 18819255.
- Meat Hygiene y J. F. Gracey, D. S. Collins, Robert J. Huey. Page 32.
- See In the Shadow of Man, by Jane Goodall.
- "Sharks (Chondrichthyes)". FAO. Retrieved 2009-09-14.
- Chen, Mei-Huei; Ha, Eun-Hee; Wen, Ting-Wen; Su, Yi-Ning; Lien, Guang-Wen; Chen, Chia-Yang; Chen, Pau-Chung; Hsieh, Wu-Shiun (3 August 2012). "Perfluorinated Compounds in Umbilical Cord Blood and Adverse Birth Outcomes". PLOS ONE. 7 (8): e42474. doi:10.1371/journal.pone.0042474. Retrieved 27 March 2018 – via PLoS Journals.
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Causes, Symptoms, Prevention, icd 10 Code For Thrombocytopenia
There are little pieces of cells in blood which function is to stop bleeding by clumping and clotting blood vessel injuries. These cells called platelets or some people also called it as thrombocytes. Normal human platelet count ranges from 150.000 to 450.000 per micro liter of blood. Having too many or too few platelets may harm your health. One common problem of people is having too few platelets. This kind of disease called as thrombocytopenia. Keep reading to know more about this.
ICD-10 Code for Thrombocytopenia
A system that is full of codes to diagnose some diseases in medical term is called as ICD. ICD stands for International Classification of Diseases which is used internationally. This system is expending by year and year. From the first version, ICD is arrived in its tenth revision (ICD-10). ICD-10 code for thrombocytopenia is D69.6. It is a valid ICD-10 diagnosis code that you can find on Chapter 3 in section D65-D69. The icd 10 code for thrombocytopenia can be found on category D69.
Causes of Thrombocytopenia
In general, your body may not produce enough platelets if you have a:
- Cancer, for example leukemia or lymphoma
- Blood disorders called aplastic anemia.
- Virus such as chickenpox, mumps, HIV, rubella or Epstein-Barr.
- Platelet-lowering disease that runs in your family.
- Rare diseases that make blood clots form in the body.
Besides such diseases, you platelets can also be damaged by some condition:
- Medicines (antibiotics, antiseizure drugs)
Symptoms of Thrombocytopenia
Some people do not have any symptoms from thrombocytopenia. The bleeding can happen inside or outside your body and it can be heavy and hard to stop. The common symptoms that you may experience when your platelet is very low are:
- Heavy menstrual periods
- Purple or red bruises called purpura
- Blood in your urine or bowel movement
- Tiny red or may be purple spots on your skin (petechiae)
Prevention of Thrombocytopenia
Prevention is always better than healing or treatment. Some things that u can simply do to prevent this kind of diseases include:
- Since we know that this diseases forms by certain medicines. You can avoid medicines that decreased your platelet.
- Avoid heavy drinking.
- Avoid contact with toxic chemicals such as pesticides, arsenic and benzene.
- Do not be lazy to talk with your doctor about getting vaccinated for viruses that can affect your platelets. | <urn:uuid:e854caa4-0d9e-4f3c-91b1-48ce7a26d7fe> | {
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Listening leads to superlative nursing care
Thursday, March 16, 2017
It's been said that we have two ears and one mouth so that we'll listen twice as much as we talk. As nurses, we work with patients at their most vulnerable and frightened. So, are we listening enough or talking too much?
When a nurse wants to know how a patient's lungs are doing, she uses her stethoscope to listen to the patient's breath sounds. If the nurse tries to talk with the patient while auscultating the lungs, the usefulness of the lung assessment is compromised.
Similarly, if a nurse asks a patient how he feels and then busies herself with tasks or note-taking as the patient speaks, the nurse loses the opportunity to truly listen and hear the patient's concerns.
When we ask a question, we need to actually listen to the answer. This is increasingly difficult in this age of information saturation and constant distraction.
During nurse-patient interactions, try to decrease distractions in the interest of speaking and listening with total attention. Here are some factors to bear in mind during patient care:
- In a hospital setting, is it possible to close the door for privacy and noise reduction?
- Can televisions and radios be turned off during conversations?
- During home care visits, can pets and children be removed from the room where patient care is performed?
- In any care setting, can the nurse silence all mobile devices in order to be fully present?
- Can pens, paper, clipboards and computers be set aside for certain portions of the visit? Can the nurse listen without taking notes?
We may feel we're present while taking notes, but this can be a distracting factor during nurse-patient communication. If the nurse needs to take notes, perhaps she can put down her pen or laptop during portions of the conversation, then verbally reassure the patient that when she needs to write something down, she'll resume eye contact as soon as possible.
Open listening can be nurtured and practiced with relatively simple techniques. Eye contact was already mentioned above, and here are several additional suggestions for creating an environment where the patient will feel both seen and heard.
- Crossed arms and legs are perceived as "closed" postures. Uncross your limbs and maintain an open posture.
- Lean forward slightly rather than leaning back. This shows interest and engagement.
- Nod while looking in the patient's eyes to show that you hear what is being said.
- Paraphrase and empathize in relation to what the patient has shared. You can say, "Mr. Smith, I hear that you're feeling frustrated with your pain level. Let me talk to the surgeon and see what we can do to make you more comfortable."
If you approach patient conversations with the idea that you should listen twice as much as you speak, you can powerfully change the nurse-patient dynamic. Patients want to feel heard; they also want to feel your empathy, even if you're not able to offer an immediate solution.
Listen with open ears and an open mind, and use your words to communicate empathy, understanding of the patient's point of view and a willingness to truly listen. This is a powerful tool in the nurse's communication toolbox.
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Beta thalassemia is a blood disorder that reduces the production of hemoglobin. Hemoglobin is the iron-containing protein in red blood cells that carries oxygen to cells throughout the body. In people with beta thalassemia, low levels of hemoglobin lead to a lack of oxygen in many parts of the body. Affected individuals present with anemia, pale skin, weakness, fatigue, and more serious complications. People with beta thalassemia are at an increased risk of developing abnormal blood clots. Thalassemia has been classified into two types: major and intermedia.
Mutations in the HBB gene cause beta thalassemia. The HBB gene provides instructions for making a protein called beta-globin. Beta-globin is a component of hemoglobin. Hemoglobin consists of four protein subunits, typically two subunits of beta-globin and two subunits of another protein called alpha-globin. Some mutations in the HBB gene prevent the production of any beta-globin. The absence of beta-globin is referred to as beta-zero (B0) thalassemia. Other HBB gene mutations allow some beta-globin to be produced but in reduced amounts. A reduced amount of beta-globin is called beta-plus (B+) thalassemia. Having either B0 or B+ thalassemia does not necessarily predict disease severity, however; people with both types have been diagnosed with thalassemia major and thalassemia intermedia.
Thalassemia major and thalassemia intermedia are inherited in an autosomal recessive pattern, which means both copies of the HBB gene in each cell have mutations. The parents of an individual with an autosomal recessive condition each carry one copy of the mutated gene, but they typically do not show signs and symptoms of the condition. Sometimes, however, people with only one HBB gene mutation in each cell develop mild anemia. These mildly affected people are said to have thalassemia minor.
|Thalassemia major, also known as Cooley's anemia
||Symptoms appear within the first 2 years of life. Life-threatening anemia, failure to thrive, yellowing of the skin and whites of the eyes, enlarged spleen, liver, and heart, and bones may be misshapen. Some adolescents with thalassemia may experience delayed puberty. Many people with thalassemia major have such severe symptoms that they need frequent blood transfusions to replenish their red blood cell supply. Over time, an influx of iron-containing hemoglobin from chronic blood transfusions can lead to a buildup of iron in the body, resulting in liver, heart, and hormone problems.
||Milder form, signs and symptoms of thalassemia intermedia appear in early childhood or later in life. Affected individuals have mild to moderate anemia and may also have slow growth and bone abnormalities.
Methodology: Sequencing of entire coding region
Purpose: Confirmation of Clinical Diagnosis
ICD-10 Code D56.1
Test Requisition: Sequencing Requisition
CPT Codes: 81364 Cost: $530.00
Turn-around-time: 3-4 weeks
1. Olivieri NF. The beta-thalassemias. N Engl J Med. 1999 Jul 8;341(2):99-109. Review. Erratum in: N Engl J Med 1999 Oct 28;341(18):1407.
2. Panigrahi I, Agarwal S. Thromboembolic complications in beta-thalassemia: Beyond the horizon. Thromb Res. 2007;120(6):783-9. Epub 2007 Mar 7. Review.
3. Rund D, Rachmilewitz E. Beta-thalassemia. N Engl J Med. 2005 Sep 15;353(11):1135-46. Review.
4. Taher A, Isma'eel H, Cappellini MD. Thalassemia intermedia: revisited. Blood Cells Mol Dis. 2006 Jul-Aug;37(1):12-20. Epub 2006 Jun 5. Review.
5. Thein SL. Genetic insights into the clinical diversity of beta thalassaemia. Br J Haematol. 2004 Feb;124(3):264-74. Review. | <urn:uuid:914edcb6-a507-4656-a28d-674727bd406b> | {
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SLEEP BRUXISM (SB):
During sleep it is common for the lower jaw to move around. This is termed Rhythmic Masticatory Muscle Activity or RMMA. This consists of two forms of muscle activity: a series of repetitive contractions or an isolated sustained contraction of jaw clenching. These muscle contractions, when extreme, produce the tooth grinding sounds during sleep and are referred to as Sleep Bruxism (SB). It is often reported by a spouse that the sound of the teeth is disturbing and waking them. The patient is usually unaware that they are doing this as it occurs once they are asleep. It is often their bed partner that alerts them to this.
The World Health Organization (WHO) have created an international classification of diseases with a specific code being given to every disease known. They break the diseases down into categories or systems. The following flow chart summarizes this (click to enlarge):
This classification from WHO differentiates awake bruxism and sleep bruxism. Sleep bruxism is a disease of the nervous system, or neurogenic, whereas awake bruxism is classified under mental and behavioral disorders. They are diagnosed and treated very differently and cannot be considered related. It should be noted that both disorders can and do occur together in the same patient.
The Center for Disease Control (CDC) in the USA also use the WHO classification except that they add “clinical modifications” to it. This is designated as CM following the WHO coding (for example, sleep bruxism would be ICD-10 G47.63 CM under the CDC classification). The clinical modification for sleep bruxism is that it excludes awake bruxism and awake bruxism (ICD-10 F48.3 CM) excludes sleep bruxism.
As sleep bruxism is a central mediated disorder (the brain triggers the event) there is a cascade of events that occurs:
- there is an increase in heart rate and blood pressure
- there is an increase in EEG (brain electrical) activity
- the muscles above the hyoid (Adam’s apple) bone activate
- the masseter and temporalis jaw muscles contract
- often finishes with a swallow reflex
This sequence of events occurs with every Sleep Bruxism event and can occur hundreds of times each night.
Rhythmic movements such as chewing and bruxing are controlled by central pattern generators (CPG) within the brain. Mastication (and sleep bruxism) are driven by the hypoglossal nucleus, which is controlled by the dorsal medullary reticular column (DMRC) and the nucleus of the tractus solitaries (NTS). It has been recently found that patients suffering from sleep bruxism have a genetic mutation of gene HTR2A rs2770304, which is involved in the release of serotonin (a neurotransmitter in the brain and gut) occurs in multiple copies (polymorphism) resulting in too much serotonin being released into the brain. This results in suppression of the neurons that prevent the jaw muscles from contracting too hard and inactivation of the masseter inhibitory reflex. The result is increased frequency and intensity of contraction of the masseter and temporalis muscles resulting in damage to the teeth, jaws, muscles and TMJ. Serotonin acts on the inhibitory neurons in another way. There is a connection from these neurons to the dorsal motor neuron of cranial nerve 10, the vagus nerve. This nerve controls heart rate (as well as a number of important functions) resulting in stimulation of the heart and an increase in heart rate with each bruxism event. This combination of serotonin suppressing the inhibitory neurons (allowing 100% muscle contraction) and stimulation of the dorsal motor neuron of the vagus nerve, explains the mechanism behind sleep bruxism. Because the cause is polymorphism of the HTR2A rs2770304 gene, sleep bruxism cannot be cured at this time, only controlled.
Recently, restless leg syndrome was linked to cardiovascular disease, due to the increase in heart rate and blood pressure associated with restless leg syndrome. To date, there have not been any studies of sleep bruxism, with its associated increase of heart rate and blood pressure but is likely only a matter of time before this relationship is also confirmed.
Those who suffer from sleep bruxism demonstrate an interesting finding: when they lightly touch their incisors together (as in biting a piece of thread), the lower jaw will begin to shake or tremor. This finding is a positive sign of active sleep bruxism.
The forces generated by sleep bruxism are much greater than when awake:
- Chewing meat = 25 psi (pounds per square inch)
- Chewing a hard carrot = 28 psi
- Biting as hard as you can when awake = ~30
- Sleep Bruxism can exceed 100-150 psi in some individuals
This is due to a reflex of the jaw muscles, the masseter inhibition reflex (MIR) being suppressed by sleep bruxism. The MIR normally restricts how hard the masseter muscle contracts, limiting it to safe levels. During sleep bruxism, this reflex is effectively turned off and the masseter contracts with 100% of its force. The forward bite of the Luco Hybrid OSA Appliance re-establishes this reflex during sleep, preventing over-contraction of the masseter, allowing it, and the other associated muscles to relax and heal. This is the primary mechanism in which this advanced device reduces significantly or completely eliminates sleep bruxism events and their duration during sleep.
The following screen shot of a sleep study of a sleep bruxism patient demonstrates the elimination of sleep bruxism events, stabilization of the patients respiration and stabilization of the heart rate (which was being affected by the sleep bruxism).
As you can see, the forces generated during sleep bruxism are substantial and can potentially cause very serious damage. Left untreated, this condition can cause progressive irreversible damage to the teeth, surrounding bone, jaw bones, musculature, and TMJ. Sleep bruxism is a significant cause of TMJ problems due to the considerable pressure placed on the TMJ during sleep bruxism events (it only takes about 15 psi to cause damage to the TMJ).
80% of the time, Sleep Bruxism occurs together with sleep apnea, as they are both sleep disorders. If is estimated that 8% of the population suffer from Sleep Bruxism and about 16% from sleep apnea. Sleep Bruxism occurs in over 30% of OSA cases! In 20%, Sleep Bruxism occurs independently of sleep apnea on its own.
Sleep Bruxism occurs in different forms:
- Tonic or clenching type
- Phasic or grinding type
- Mixed or a combination of both types
Sleep related bruxism is usually diagnosed by either the patient (with changes to their teeth or jaws or pain symptoms), the dentist (with clinical signs such as premature failure of fillings, abfraction lesions etc.) or by a sleep specialist during a sleep study.
It has been proposed for a sub-classified into three subtypes:
- Possible: patient reported symptoms without clinical signs
- Probable: patient reported symptoms with clinical signs
- Definite: patient reported symptoms, clinical signs and an overnight sleep study with muscle recording (supported by a microphone or video recording).
Dental radiographs can identify the effects on the jaws from sleep bruxism. The following image shows a panorex (orthopantomograph) of a normal patient. The second shows the effects of sleep bruxism. The first demonstrates calcified stylomandibular ligaments (ligaments that restrict the range of motion of the lower jaw to normal movements) and antigonial notching or a bend in the lower jaw caused by tonic sleep bruxism (clenching type) involving the masseter and medial pterygoid muscles. The lower border of the mandible should be straight and not bent as seen. The ligaments are soft tissue and should not show on a radiograph. This is termed Eagle’s Syndrome. They should not be seen on a radiograph.
The second panorex demonstrates coronoid elongation or stretching of the coronoid process (attachment of the temporalis muscle) caused by tonic sleep bruxism involving the temporalis muscles. The orange dotted line marks the highest point of the coronoid process. In a normal individual, this line should pass through the yellow dots on the condyles (balls) of the TMJ.
SB does not require a sleep study for diagnosis and treatment, a dentist can diagnose this and treat it in their office from the signs and symptoms observed. If the dentist suspects a concurrent sleep disorder, they are obliged to refer the patient for a sleep study to ensure all the sleep problems are being addressed. There are medical conditions that have bruxism as a symptom ( such as faciomandibular myoclonus, SRBD, RBD, abnormal swallowing, gastro-esophageal reflux, night terrors, confusional arousals, dyskinetic jaw movements persisting in sleep (dystonia, tremor, chorea, dyskinesia), and, rarely, in sleep related epilepsy). If the dentist is unsure, a sleep study is the always the best course of action.
Sleep studies can accurately record sleep bruxism if equipped to record this. The following tracings are an actual patient’s recordings using a 12 channel Type 3 sleep monitor (Medibyte Event) with electromyographic (EMG) muscle recording module. The first is a tracing of normal sleep and the second demonstrates numerous sleep bruxism bursts (click to enlarge).
In the second tracing above, the amplitude or amount of force being generated is in the range of 10-14 x the normal maximum bite when awake. These bruxism events or bursts can occur hundreds of times per night, disturbing the patient’s sleep. The Epworth Sleepiness Scale is used to screen patients for excessive sleepiness. With OSA it is >10. With only Sleep Bruxism patients score in the 6-9 range for sleepiness.
SB can be destructive to the teeth, the supporting bone and gum tissues, the TMJ complex including the neck, and the musculature. The effects often result in hypersensitivity of the teeth to temperatures, headaches (particularly in the temple region upon waking), repeated damage to the teeth and sleep disruption. SB can jam cranial sutures affecting normal CSF flow (from the ventricles of the brain through the spinal cord). These excessive forces cause shifting of the teeth and can relapse orthodontic treatment.
This condition is usually diagnosed when a patient brings the symptoms up to the attention of their dentist or doctor. In younger healthy patients with SB, there is less sleep disruption. Often jaw muscle pain affecting the massater (main cheek muscle) and temporalis (the muscle on the side of the head) muscles are reported with associated morning headaches. Fatigue in the muscles and limitation is opening upon waking are common with SB.
SB can shorten the life of an OSA appliance. Acrylic appliances can break under the increased force of SB. This is a concern as small pieces of broken appliance may be swallowed or aspirated into the lungs during sleep. The Luco Hybrid OSA Appliance is designed to withstand this and breakage is extremely rare (less than 3 cases in 3000). Because of this, this appliance can last in excess of 4 years with some lasting much longer.
There are a number of signs and symptoms related to SB. It should be noted however, that some people with SB have very few symptoms and only experience disturbances in sleep. The following table outlines the signs and symptoms of SRB commonly seen:
|Unpleasant tooth and muscle sensations||Flattening or excessive wear of the teeth|
|Limitations of jaw movement, TMJ pain||Fractured teeth and fillings, vertical cracks in teeth|
|Orofacial Pain (pain around the face region)||Waking with the jaw locked, unable to open wide for a few minutes.|
|Temporal/tension headaches on waking or later in the day||Abfraction lesions (painful notching of the roots at the gum line|
SB varies considerably between individuals regarding intensity and duration. In most cases it occurs hundreds of times a night. There is no direct link, however, between the severity of SB and the symptoms a patient will present to their dentist or doctor with. SB is indexed by the number of SB events per hour. Interestingly, patients with RMMAs of 2-4 per hour are much more likely to report muscle pain than more severe cases of > 4 RMMA/hour. The normal range of sleep bruxism events is <5 per hour or a bruxism index of <5.
Psychological factors may also be linked to SB. Currently there is a weak correlation between SB and psychological stress in both adults and children. Healthy patients with SB tend to have higher scores regarding stress, anxiety and psychiatric scales compared to patients without SB.
There are two subtypes of SB: Primary SB which occurs without any clear cause and Secondary SB which often occurs in children with medical diseases such as Cerebral Palsy, and other forms of mental retardation. Myoclonus is a muscular disorder (either oro-mandibular or facio-mandibular) that is associated with SB in adults. Sleep related breathing disorders (OSA and UARS) commonly occur with secondary SB.
The research has shown that SB is highest in children at about 14-17%. In teenagers and young adults, it has been reported to drop to about 12%. It drops to 8% in young to middle age patients and down to around 3% in elderly patients. In elderly, the significant drop may actually be due to decreased reporting and may actually be higher. Because of the overlap of symptoms of other conditions such as migraine syndrome (headaches in the same regions) and the variability in symptoms (some patients have no symptoms and would therefore not be included in these stats). Clinically however, most dentists see the results of SB much more often and more research is needed regarding epidemiology of this disease.
As well, severe SB in childhood may persist as severe throughout the lifetime of the patient. In these patients, the symptoms do not follow the normal progression of decreasing with age. There is also a relationship between SB in children and Attention Deficit Disorder Syndrome (ADHD), parasomnias (such as confusion arousals, sleep-walking, sleep talking, head banging and sleep relating eating disorder), sleep related breathing disorders, snoring, and many psychological and medical conditions. Variability is high resulting in many patients not being diagnosed. SB occurring in childhood persists into adulthood in more than 65% of the cases!
Genetic patterns in SB are possible as this tends to be seen in families with approximately 20-25% of affected patients having a close family member with a history of sleep related bruxism. To date, no gene mutations have been linked to primary SB in genetic testing, but in the future genetic testing may identify genes and could be used to screen patients for this disorder.
Interestingly, SB can start at any age. It is very difficult to study as the symptoms are so variable they are not reported by the patients to their doctors until the symptoms are affecting them significantly. The condition could have been present for years before being reported. Often the symptoms are not related to sleeping and treated (sometimes inappropriately) as other conditions, leaving the condition untreated and allowing it to persist.
It should be noted as well that RMMA occurs in everyone. In normal sleep RMMA is observed at about 1 episode per hour of sleep. However, with SRB the contractions are not only more often, but with much greater intensity (in the range of 10-14X normal chewing pressure). SRB also can vary considerably night to night. Sleep studies can miss this at a rate of up to 25% of the time due this nightly variability in some cases.
Electroencephalogram (EEG) tracings have found differences between men who suffer from sleep bruxism. Women affected by sleep bruxism show a significantly lower Theta and Alpha EEG activity during sleep compared with normal subjects. This was found to be true regardless of level of associated pain reported. When muscle recording is included in the EEG tracing, a significant increase in activity of the masseter and temporalis muscles is seen. This is associated with an increase in heart rate and blood pressure.
Abnormal wear of the teeth and dental damage are the most common signs of SB. It is important though to differential SB and tooth wear from an abrasive diet which can look similar. Disorders of the TMJ are common (pain and clicking in the TMJ, closed locking).
Hypertrophy or enlargement of the jaw muscles can occur in some people, primarily in the massater and temporalis muscles. The following sections will outline the types of dental problems that are commonly seen with SB. The following image demonstrates hypertrophy or bulking up of the masseter muscle as is seen with severe sleep bruxism.
Fractured Roots: Although rare, root fractures are very painful and require urgent dental care (removal). Root fractures are caused by excessive lateral or side-to-side pressure on the teeth such as occurs in sleep-related bruxism.
Cracked Teeth: These are common and also are very painful requiring urgent dental care (removal). Cracked teeth are caused by excessive vertical pressure or downward pressure on a tooth causing it to split through the roots. This can be caused by the pressure of sleep-related bruxism over time. Initially, the tooth will be hypersensitive to hot and cold as well as biting on hard foods. As it progresses, the symptoms worsen until the tooth cracks in two.
Cracked Fillings: Fillings are not as strong as teeth and the effects of sleep-related bruxism accelerates wearing of the filling. The life span of fillings in the presence of sleep bruxism is dramatically reduced.
Abfraction Lesions: Painful notches at the neck of the tooth used to be blamed on aggressive tooth brushing. It is now known that this is a direct result of excessive lateral side-to-side pressure on teeth as is seen in sleep bruxism. The enamel at the gum line chips off and the exposed dentin, which is softer, wears away very quickly leading to the characteristic notches seen in abfraction lesions. These are challenging to manage as fillings do not hold well in these areas unless the source of the problem, the sleep bruxism, is treated. Gum recession in the area of the abfraction lesion is common and can lead to bone loss between the teeth and loosening of the teeth.
Excessive Tooth Wear
Tooth wear is a normal part of aging. It becomes a concern when it occurs at an accelerated rate. With sleep bruxism, this occurs often disfiguring of the teeth or shortening them so far that root canals become necessary due to exposure of the nerves. Sometimes the teeth are so badly worn they can only be removed. If this occurs in primary teeth in children, this can affect the position of the erupting permanent teeth as the permanent teeth only erupt to the height established by the primary teeth.
Other Dental Problems that Can Occur:
- loosening of teeth due to excessive pressure during grinding, bone loss around the tooth, and/or stretching of the ligaments that attach the teeth to the jaw bone
- acceleration of periodontal bone loss due to excessive loading of the teeth during sleep
- fractured cusps of teeth (corners of the teeth breaking off)
- hypersensitivity to hot, cold and sweet
- healthy teeth requiring root canal therapy for unknown reason (due to the teeth being compressed into their sockets restricting blood flow into the tooth and tooth nerve death).
Chronic Myofascial Pain (CMP)
Myofascial pain refers to pain originating in the muscles and fascia covering of the muscles that refers pain to adjacent regions or structures. The hallmark of myofascial pain is the development of trigger points, which are painful spasms inside a larger muscle group that feel like a knot or lump in the muscle. These muscle spasms can persist for months and even years and cause a myriad of symptoms. A primary trigger point can spread into other muscle groups and form secondary trigger points. in this way, the condition can spread and cause widespread pain symptoms. There is some evidence that CMP has a genetic basis and is activated by a trauma. In the case of sleep-related bruxism, the trauma is obvious: the overloading of the muscles.
When a trigger point develops in the muscles of the head and neck regions, the referred pain is interpreted as a headache. Depending upon which muscle is affected will determine where the headache occurs. It should be noted that hypoxia or low oxygen levels while sleeping also causes headaches (sleep apnea, UARS) from the low oxygen levels. There are a series of muscles of the jaws that are involved in opening, closing, retracting, advancing and moving the jaw laterally side-to-side. The closing muscles are the chewing muscles however there are a series of neck muscles also involved that support the mandible, support the skull and support the neck when chewing. Sleep-related bruxism and UARS are both associated with chronic myofascial pain and the development of trigger points in these muscle groups. The following images show the most common areas in these muscles where trigger points commonly develop (x) and the expected referral patterns (headaches) from the trigger points (in red).
The Masseter Muscle
The Medial Pterygoid Muscle
The Temporalis Muscle
The Digastric Muscles
The Sternocleidomastoid Muscle
Jaw Problems: TMD (Temporomandibular Dysfunction)
Temporomandibular Dysfunction refers to disorders involving the TMJ or jaw joints. Excessive pressure exerted by the chewing muscles may cause a compression of the TMJ. This can trigger capsulitis of the back joint compartment of the TMJ resulting in severe pain when biting. This pain is caused by inflammation of the TMJ and, as it is encapsulated or in a capsule, the posterior or back joint compartment swells painfully forcing the entire mandible forward. This alters the bite resulting in difficulty closing the back teeth together and the front teeth hitting harder than normal. This is usually self-limiting and heals in a few weeks. It should be noted that patients with deep overbites can have this last much longer as their lower jaws naturally sit too far back. The back area of the TMJ is where all of the nerves and blood vessels reside. The American Academy of Sleep Medicine recognizes that patients with severe Sleep Related Bruxism can experience TMD problems and locking of the jaw upon waking is a common symptom in severe SRB.
Normal TMJ Function: The disk (yellow in animation) stays between the bones at all times preventing bone wear and arthritis. The loading or pressure of the bite is directed through the disk at all times protecting the bones from damaging wear. There is never any pressure on the back portion of the joint and the nerves and blood vessels. (click to see animation)
Clicking TMJ: When the upper jaw does not develop to a normal size (as seen in many SB and OSA patients), the lower jaw can become too long for the upper. When biting, this excessive length of the lower jaw is expressed back towards the ear canals. The disk in the joint slips forward and, when the patient is biting, the TMJ becomes dislocated. On opening, the disk must re-seat into normal position with the characteristic click or popping sound. With this type of misalignment, the lower jaw is positioned too far back in the joint compressing the nerves and blood vessels of this region. Patients with clicking jaw are at much higher risk of capsulitis (pain and swelling of the TMJ) due to this positioning. Many chronic ear conditions can be attributed to capsulitis of the TMJ. This can also result in abnormal function of the Eustachian tubes resulting in difficulty in equalizing pressure in the inner ear.
The timing of the click in the opening cycle determines the prognosis for the TMJ. An early click, meaning the disk pops back into alignment quickly, indicates a relatively healthy disk. If the click is later, nearer to wide opening, the prognosis is not as good as the disk is dislocated for more of the opening cycle. If the ligaments that attach the disk to the jaw bone (condyle) stretch so much that they tear, a closed lock occurs. The symptoms of a closed lock are very restricted opening and side to side movement, severe muscle pain in the jaw and neck muscles, and disturbed sleep patterns (due to the pain).
Non-Reducing Closed Lock: This occurs when the disk tears free of the jaw bone sliding forward (and usually inward) blocking the normal movement of the jaw. This is often a very sudden and painful occurrence requiring urgent dental attention. If acute, the jaw will be restricted to about 28mm and accompanied by severe muscle spasms on the affected side. If left untreated, it will stretch out to 32-34 mm but the muscles usually develop painful trigger points. A normal opening is 45-52 mm or three fingers wide, and about 10 mm left, right and forward. With a closed lock, the jaw movement is blocked on the locked side so the jaw cannot move forward or to the side. Typically, the jaw would deviate to the affected side as the healthy joint would move and the locked joint would not. If both joints are involved, there would be no movement to either side, and no movement forward possible.
Patients with chronic closed locks eventually stretch their ligaments and can open up to 38-40mm with 4-5 mm side to side and 5-6 mm forward. This restriction is functional but almost always accompanied by painful headaches due to numerous trigger points.
Before a diagnosis of sleep bruxism can be made, there are other medical conditions with similar symptoms that must be ruled out. TMD or Temporomandibular Dysfunction is fairly common disorder of the jaw joints and chewing muscles that can have similar symptomology. It is not uncommon for TMD sufferers to have disturbed sleep patterns due to chronic pain. Limitation in opening is common due to myopathy, as are waking with headaches and headaches lasting into the day. Clenching is more common than grinding (tonic awake bruxism) in this group and damage to teeth such as excessive wear and abfraction lesions are also common (phasic awake bruxism). There is usually cervical (neck) involvement of the pain in TMD and often a precipitating event (such as a whiplash injury, jaw injury, blow to the face etc.). It should be noted however, that SB and TMD can and do often occur in the same patients, as TMD patients may also have OSA or UARS predating the TMD. These are, by far, the most difficult patients to treat but also the most rewarding when treatment succeeds in treating both conditions. The Luco Hybrid OSA Appliance was designed specifically for these patients. It effectively treats TMD, Chronic Myofascial Pain, Sleep Bruxism and Sleep Apnea simultaneously. With thousands of patients treated, this appliance is clinically proven and very effective.
As discussed earlier, there are some medical conditions that overlap symptoms with SB as well. Some of these include oro-mandibular myoclonus, facio-mandibular myoclonus, SRBD, RBD, abnormal swallowing, GERD, night terrors, confusional disorders, dyskinetic jaw movements persisting into sleep (dystonia, tremor, chorea and dyskinesia) and rarely, sleep related epilepsy. SRB is much more common than any of these disorders but they still must be considered before initiating treatment for SRB as they may require other medical treatments to manage.
Oro-mandibular or Facio-mandibular Monoclonus occurs in a fairly high number of SRB patients (10%). It is also seen in patients with excessive RMMA events during sleep. Facio-mandibular Monoclonus is much different than SRB. It consists of very short bursts of muscle activity of very short duration as opposed to longer sessions of grinding and clenching associated with SRB. This can only be diagnosed with a sleep study recording the muscle activity.
With partial complex or generalized seizure disorder, rhythmic jaw movements are also seen. Because of this, these disorders should always be considered in the differential diagnosis of SRB and a medical consultation is always prudent before treatment.
Until recently there were no recognized treatments of Sleep Bruxism. The Luco Hybrid OSA Appliance is now the first and only recognized treatment of sleep bruxism making this device truly unique and separates it from all other OSA appliances.
The Luco Hybrid OSA Appliance is the only sleep apnea appliance that is FDA cleared for the treatment of patients suffering from sleep apnea and sleep bruxism. These two diseases occur in over 30% of sleep apnea cases! | <urn:uuid:416a6fb7-0ddd-4e56-a4b5-2eca507b8a4f> | {
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Mood Disorders: Safe, Effective, and Natural Solutions
Vis Medicatrix Naturae
Todd A. Born, ND, CNS
Mood disorders are mental health issues that primarily impact a person’s emotional state; an affected person may experience periods of extreme happiness, extreme sadness, or both, that last at least several weeks.1 In the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition(DSM-5), the list of mood disorders and their diagnostic criteria is lengthy; however, the most common mood disorders include major depression; dysthymia; bipolar disorder; major depressive disorder with seasonal pattern [ie, seasonal affective disorder, or SAD]; and depression related to an illness, substance abuse, or medication.2 For simplicity in this article, I will refer to these issues collectively as mood disorders unless otherwise indicated.
The 2001 to 2003 National Comorbidity Survey Replication shows an estimated 9.7% of US adults (anyone over 18) having any mood disorder within the past year, with a higher prevalence among females (11.6%) than males (7.7%); the report also estimated that 21.4% of US adults will experience a mood disorder at some point during their lives.3 (Please note that these figures are a combination of mood disorders; frequently updated individual statistics may be found on the website of the National Institute of Mental Health.4)
Depression, alone, affects almost 300 million people worldwide.5 Bipolar disorder affects around 45 million worldwide.5 SAD is estimated to affect about 5% of the US population, depending on geographical location.6 The direct and indirect costs of these health issues are immense. For example, in 2008 the World Health Organization (WHO) found major depression to be the third leading cause of disease burden in high-income countries worldwide, and predicted that major depression will rank as first by the year 2030.7 In 2015, it was estimated that the total global cost of treatment for Bipolar I Disorder (BDI) was $202.1 billion, an average of $81 559 USD per affected individual.8
Sadly, the aforementioned numbers of afflicted individuals, as well as cost burden, are likely underestimates because many of the individuals that struggle with mood disorders go undiagnosed. At times, they may be reluctant to seek help due to the social stigma associated with these conditions. Due to the variety of patient presentations, the unpredictable course and prognosis of mood disorders, and the inconsistent responses to treatment, clinicians are also challenged in terms of diagnosis and management.9,10
Alternatives are Needed
There is an urgent need for safer and more efficacious alternatives to pharmaceuticals. Medications certainly have their role in mood disorders, but they must be used judiciously. For example, it has been well established that in mild-to-moderate depression, medications are probably no more effective than placebo.11 In manic and depressive states of bipolar disorder, the data is mixed on how efficacious medications really are.12
The extensive laundry list of side effects of mood disorder medications is so vast, it makes one’s head spin. In clinical practice, many patients find the side effects intolerable enough that they would rather suffer from their illness than deal with the negative consequences of the medications. Antidepressants, anxiolytics, stimulants, antipsychotics, and mood stabilizers are the medications typically used in mood disorders. A full discussion of their efficacy and potential side effects is beyond the scope of this article.
To better understand mood disorders and provide more effective treatment interventions, it is beneficial to look at underlying etiologies, risk factors, and genetics (encompassing family history). Each particular mood disorder has its own unique set of etiologies; however, commonalities among all of them include brain structural changes (not yet well understood) compared to those without mood disorders, neurotransmitter alterations, and hormonal imbalances. Risk factors include low self-esteem, a high degree of self-criticism, history of traumatic and stressful events (eg, physical or sexual abuse or loss of a loved one), comorbid mental disorders (eg, schizophrenia or anxiety disorders), alcohol and recreational drug abuse, and chronic illness and side effects of certain medications (eg, sleeping pills or anti-hypertensive drugs).13
An enormous risk factor is one’s genetics,14 and even epigenetics.15 Research into the role that single nucleotide polymorphisms (SNPs) play in mood disorders has exploded within the last 15 years or so, and offers promise in helping to improve people’s lives through nutritional and botanical interventions.16,17 Indeed, even pharmacogenetic testing is finally becoming more mainstream in clinical practice, offering safer, more specific, and personalized pharmaceutical options.18-20
A comprehensive, integrative approach to mood disorders works very well in clinical practice.21 This may include all or most of the following: lifestyle and dietary modifications, constitutional homeopathy, botanical medicines, nutraceutical support, psychotherapy, and, occasionally, pharmaceutical interventions.
Studies consistently indicate that up to half of all individuals diagnosed with a mood disorder use 1 or more complementary and alternative medicine (CAM) therapies.22,23 It has been shown that a healthy diet,24 exercise,25 sleep, a strong supportive social network, and a low-stress environment reduce relapses in individuals with mood disorders.26 Even targeting the proverbial “gut microbiome” can have a tremendous positive impact!27,28 Given space limitations, this article will focus on evidence-based botanical and nutraceutical interventions.
Given all of the aforementioned information, it is clear that there is a dire need for safe and effective alternatives. But are there really any nutraceutical and/or botanical interventions that work? The answer is: yes, definitely.
Vitamins & Minerals
Vitamin B12 (cobalamin) is involved in DNA synthesis, red blood cell (RBC) formation, homocysteine metabolism, and synthesis of S-adenosylmethionine (SAMe). B12 is also heavily involved in the proper functioning of the nervous and immune systems.29 Observational studies have shown that as many as 30% of patients hospitalized with depression are deficient in this vitamin.30 Depression can be induced by B12 deficiency, even with normal hematological and blood parameters,31 which has led to the recommendation of a therapeutic intervention of 1000 µg (1 mg) of oral B12 daily.32 The forms of B12 in these studies have varied.
It has been shown that individuals with various neuropsychiatric conditions have impaired transport of vitamin B12 across the blood-brain barrier and/or an accelerated catabolism of the vitamin, hence the need for increased requirements.29 Some studies have demonstrated clinical improvements in such patients when treated with B12.31
Folate is a generic term that refers to natural folates in food as well as folic acid (the synthetic form of folate used in many fortified foods and supplements). Folate is critical for the synthesis of DNA and RNA, several amino acids, methylation reactions, homocysteine, and B12 metabolism, and it assists in the proper functioning of the central nervous and immune systems.33
Like B12, low RBC folate levels have been found in 15-38% of adults diagnosed with depression.34 Efficacious doses of folic acid, given along with medication(s), have ranged from 500 µg to 3 mg, depending on the study and the mood disorder.35,36 Note that most trials have been conducted on folic acid, not its biologically active forms, ie, 5-methyltetrahydrofolate (5-MTHF, the major circulating form of folate in the body) and 5,10-methylenetetrahydrofolate. In individuals with methylenetetrahydrofolate reductase (MTHFR) SNPs and/or who are on medications that inhibit dihydrofolate reductase (by reducing interactions), as well as in individuals having compromised gastrointestinal function, folinic acid and 5-MTHF may be the preferred forms.37,38
Vitamin B6 (pyridoxine, pyridoxal, and pyridoxamine) and its coenzyme form, pyridoxal 5′-phosphate (P5P), are essential to over 50 enzymes that are involved in the metabolism of lipids, amino acids, and carbohydrates; B6 is also involved in steroid hormone action.29 B6 cannot be synthesized in the body, so must be obtained from the diet. In the brain, P5P is necessary to metabolize serotonin from tryptophan, and dopamine from L-3,4-dihydroxyphenylalanine (L-Dopa). Other neurotransmitters and amino acids that are P5P-dependent include glycine, D-serine, glutamate, histamine, and gamma-aminobutyric acid (GABA).39 P5P also plays a role in the metabolism of homocysteine. Dosing of pyridoxine commonly ranges from 10 to 200 mg per day, though anyone taking more than 200 mg/day should be monitored for neurotoxic symptoms.29
Vitamin D3 (cholecalciferol) is a fat-soluble vitamin that functions as a hormone precursor. It is biologically inactive and must first be hydroxylated in the liver to 25-hydroxyvitamin D (25[OH]D), with further hydroxylation in the kidneys to its active form, 1,25-dihydroxyvitamin D – the form that acts as a steroid. In this form, it suppresses prostaglandin action; inhibits p38 stress kinase signaling, tumor angiogenesis, invasion and metastasis; and inhibits nuclear factor-kappa B (NF-κB) signaling.40
Many studies have demonstrated a correlation between low serum concentrations of 25(OH)D and mood disorders.41 While the exact mechanism(s) of action haven’t been fully elucidated, vitamin D supplementation has been shown to improve mood in both depression and SAD.42,43 It should be noted that the Endocrine Society has suggested that “optimal” serum levels of 25(OH)D are at least 30 ng/mL.44
Magnesium insufficiency and frank deficiency are both rampant in the United States and most industrialized nations. Almost half of the US population (ages ≥4 years) is considered to be underconsuming this vital mineral.45 Medications, chronic diseases, diminishing magnesium content of food crops, and the plethora of refined and processed foods46 have all contributed to this epidemic.
Next to potassium, magnesium is the second most abundant cation in soft tissues, and is a cofactor for at least 300 enzymes. It plays a role in adenosine triphosphate (ATP) production, neuronal activity, cardiac function, and electrical properties of cell membranes47; it also has antispasmodic effects and assists in glutathione synthesis.48 In addition to all of these accolades, magnesium has anxiolytic properties, increases stress tolerance, and has been shown in human and animal studies to be an effective antidepressant.49,50 The recommended daily allowance (RDA) varies by age and gender, ranging from 360 to 420 mg per day of elemental magnesium.
Zinc, well known for its immune properties, also plays an important role in mood, as it is essential for over 300 enzyme-dependent reactions.51 The RDA for individuals 19 years and older is 11 mg daily for males and 8 mg daily for females. Therapeutically, trials have shown efficacy at much higher doses, although this depends on the condition being addressed. A meta-analysis of 9 studies found an inverse association between risk of depression and zinc and iron intake.52 In many of the clinical trials conducted, a dose of 25 mg daily of elemental zinc has been utilized.53 Excessive zinc intake can have toxic effects and can also deplete copper; as a result, the US Food and Nutrition Board has set the tolerable upper limit for those 19 years or older at 40 mg/day.54
Omega-3 Fatty Acids
Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are well known for their anti-inflammatory effects,55 which are mediated by suppression of NF-κB, cyclooxygenase-2 (COX-2), tumor necrosis factor-alpha (TNFα), and interleukin-beta (IL-1β).56 These fatty acids also have a solid reputation for assisting those afflicted with mood disorders. Doses of 500 mg to 10 g of EPA and DHA (common dose of 1-2 g/day in clinical trials) have been shown to be effective in prevention and treatment of depressive disorders.57-59 According to a meta-analysis, EPA appears to be more efficacious than DHA.60 In bipolar disorders, there is strong evidence that omega-3 fatty acids are helpful for attenuating depression but not mania.61
SAMe is produced in vivo from homocysteine and 5-MTHF, and is also available as a supplement. It is the body’s major methyl-group donor and is vital for membrane function and neurotransmission.62 Depending on the study, total daily doses of SAMe ranging from 150 to 1600 mg have been shown to be as effective as tricyclic antidepressants, and with a lower side-effect profile.63 SAMe has also been shown to have a beneficial adjunctive effect in depressed individuals for whom medication was not fully resolving their symptoms.64 Note that SAMe should be used with caution in bipolar disorder, as it can trigger mania.65
5-Hydroxytryptophan (5-HTP) is the rate-limiting intermediary in the synthesis of serotonin from L-tryptophan. It is probably for this reason that the amino acid has been found to be superior to placebo for the treatment of depression in several studies,66 as well as an effective adjuvant to prescription antidepressant therapy.67 When used as a supplement, the dosage of 5-HTP depends on the condition being treated. In studies of mood disorders, dosages have frequently been 150 mg/day or higher.68,69 Commonly, 5-HTP is dosed at 50-100 mg, 1-3 times daily, with the some of the best evidence at this dose seen in anxiety disorders.68,70 For depression, several clinical trials have used 150-400 mg per day in divided doses.71,72 Caution is advised for those on selective serotonin reuptake inhibitors (SSRIs), since 5-HTP supplementation will increase serotonin levels.
N-acetylcysteine (NAC) is a derivative of L-cysteine, but is more stable than the latter. NAC is well known for its function as an antioxidant and precursor to glutathione73; it also acts as a mucolytic,74 has anti-inflammatory properties,75 and is the treatment of choice for acetaminophen-induced hepatic necrosis.76,77 In dose ranges of 1200-3600 mg daily, this sulfhydryl molecule has also exhibited efficacy in numerous neuropsychiatric conditions.78-80 It appears to increase the uptake of cysteine, which activates a reverse transport of glutamate into the extracellular space.81 Restoring glutamate to the extracellular space inhibits more glutamate release, thereby improving some compulsive behaviors.
Taurine can be synthesized in vivofrom cysteine. It stabilizes cell membranes, is an osmoregulator, assists in bile acid conjugation, contributes to cardiac contractility, inhibits platelet aggregation, is an anti-arrhythmic and anticonvulsant, and, last but not least, also functions as a neurotransmitter.82,83 While direct clinical trials of taurine on mood disorders may not exist, taurine has been shown to inhibit the release of excitatory neurons like glutamate, act as a GABA agonist, inhibit TNFα, and increase ATP production.83,84
Hypericum perforatum (St John’s wort), is a highly revered botanical medicine with antibacterial, antiviral, anticancer (in vitro), antioxidant, neuroprotective, anti-inflammatory, and vulnerary (wound-healing) properties.85 It is probably most well known for its antidepressant effects and minimal side effects, often showing equal efficacy to tricyclic antidepressants and SSRIs but with higher tolerability.86-88 Animal studies suggest that St John’s wort’s constituents, hyperforin and adhyperforin, appear to modulate the effects of serotonin, dopamine, and norepinephrine, as well as inhibit reuptake of these neurotransmitters.89,90 Many studies examining St John’s wort have shown clinical improvements in depression, anxiety, and SAD using a dosage of 300 mg 3 times daily.91,92 Caution should be used in individuals on medications that can induce certain cytochrome P450 enzymes (eg, CYP1A2, 2C9, 2C19, and 3A4), monoamine oxidase inhibitors (MAOIs), P-glycoprotein inducers, photosensitizers, and serotonergic agents.93
What doesn’t Curcuma longa (turmeric) do? Its benefits are endless, but one that you may not be aware of is its efficacy in depressive disorders. Studies have shown that just 1000 mg of the herb taken daily is as effective as 20 mg of fluoxetine, and when used in combination with the medication, response rates for those with major depression have been shown to rise from 65% to 78%.94 A 2017 meta-analysis also showed its efficacy in depression.95 In addition, it has been shown to reduce anxiety.95,96 It is postulated that turmeric inhibits the activity of both MAO-A and MAO-B, increases the levels of neurotrophic factors (particularly brain-derived neurotrophic factor [BDNF]), and modulates serotonin and dopamine neurotransmission in the brain.97
Rhodiola rosea (rhodiola) is a wonderful plant that thrives in cold regions and high altitudes and is notorious for its ability to increase resistance to physical, chemical, and biological stressors.98 In-vitro and animal studies have shown the constituents rhodioloside, salidroside, and tyrosol to regulate the activity of serotonin, dopamine, and norepinephrine as well as inhibit MAO-A.99-101 In depressed individuals, 340 mg taken 1-2 times daily has been shown to decrease overall depressive symptoms, emotional instability, insomnia, and somatization.102,103 Typically, dosages range from 200 to 600 mg daily, depending on the percentage of active constituents.104,105 Caution should be used in those with bipolar disorder, who are prone to manic episodes when given antidepressants or stimulants.104
Crocus sativus (saffron) is a well-known, brilliant, yellow-red, and precious spice that mostly grows in Greece, Iran, Morocco, and India; it is one of the most expensive botanicals in the world.106 It has a long history of traditional use, and is considered to be an antispasmodic, thymoleptic, carminative, cognition enhancer, aphrodisiac, and emmenagogue.107 This revered spice has also been shown clinically to benefit attention-deficit/hyperactivity disorder (ADHD),108 Alzheimer’s disease,109,110 anxiety,111 and depression.112 It is theorized that safranal (a carotenoid found in saffron) interacts with the GABAergic system,113 modulates levels of serotonin (possibly by inhibiting reuptake),111 and alters levels of dopamine and norepinephrine.114 Standardized extracts containing 2% safranal, 2% crocin, and small amounts of picrocrocin (percentage in studies unspecified), dosed at 15 mg twice daily, have been shown to significantly reduce numerous parameters of depression.115-117 Saffron is very safe and has no known drug-herb interactions.118
The use of pharmaceutical hormone replacement therapies (estrogen, progesterone, and testosterone) will not be discussed in this article; however, the prudent use of dehydroepiandrosterone (DHEA) and pregnenolone will be.
Pregnenolone is a ubiquitously produced endogenous neurosteroid, mostly made in the brain and adrenal glands from cholesterol. It is known as the master steroid hormone, since all steroid hormones, including cortisol, aldosterone, allopregnanolone, DHEA, progesterone, and testosterone, are made from it.119 Pregnenolone is thought to interact with the cannabinoid receptor-1 (CB1), one of the mechanisms for pregnenolone’s antidepressant effects.120 Pregnenolone and its metabolites have also been shown to modulate GABAA; N-methyl-D-aspartate (NMDA); and cholinergic, dopaminergic, and neurotrophic systems, thus affecting neuronal excitability.121,122
While some studies have used a dosage of around 500 mg daily for individuals with mood disorders,120 I have personally found a dose range of 50-100 mg per day to be effective. Monitoring serum pregnenolone levels every 3 to 6 months is advisable. Studies have revealed lower CSF pregnenolone levels in both patients with bipolar disorder and depression.123,124
DHEA is the most abundant neurosteroid hormone in the human body, secreted by the adrenal gland and produced in the brain.125 As a precursor to male and female sex hormones, DHEA has been shown to be effective in many health conditions; for depression and dysthymia, specifically, doses of 30-450 mg daily have been used in studies, with greater benefit observed at the lower-dose end.126,127 DHEA-S, the major circulating metabolite of DHEA, is not subject to DHEA’s day-to-day and diurnal changes.128,129 For this reason, DHEA-S should be tested prior to administering the hormone to ensure it may be of benefit, as well as ideally monitored every 3-6 months. Excessive administration of DHEA can cause acne and hirsutism,130 and as a precursor to estrogen and testosterone, there is a theoretical risk that long-term use could lead to hormone-sensitive cancers, especially if DHEA-S becomes elevated.
The aforementioned text is not an exhaustive list of safe and effective interventions for mood disorders, but rather a consolidation of what has better evidence clinically, both from published human studies and this author’s personal experience with patients. As with any health condition, individuals should not self-treat, but rather seek out a qualified healthcare professional to discuss their health concerns and options.
This is a slightly revised version of an article by Dr Born, published in the October 2019 issue (#435) of Townsend Letter.
- Cleveland Clinic. Mood Disorders. 2018. Available at: https://my.clevelandclinic.org/health/diseases/17843-mood-disorders. Accessed August 18, 2019.
- American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 5th Edition: DSM-5. Philadelphia, PA: American Psychiatric Publishing; 2013.
- National Institute of Mental Health. Any Mood Disorder. Last updated November 2017. Available at: https://www.nimh.nih.gov/health/statistics/any-mood-disorder.shtml. Accessed August 18, 2019.
- National Institute of Mental Health. Statistics. Last updated January 2018. Available at: https://www.nimh.nih.gov/health/statistics/index.shtml. Accessed August 18, 2019.
- World Health Organization. Mental Disorders. 2018. Available at: https://www.who.int/news-room/fact-sheets/detail/mental-disorders. Accessed August 18, 2019.
- Kurlansik SL, Ibay AD. Seasonal affective disorder. Am Fam Physician. 2012;86(11):1037-1041.
- World Health Organization. The Global Burden of Disease: 2004 Update. 2008. Available at: https://www.who.int/healthinfo/global_burden_disease/GBD_report_2004update_full.pdf?ua=1. Accessed August 18, 2019.
- Cloutier M, Greene M, Guerin A, et al. The economic burden of bipolar I disorder in the United States in 2015. J Affect Disord. 2018;226:45-51.
- Gregory C. Mood Disorders. Last updated October 21, 2019. Psycom. Available at: https://www.psycom.net/mood-disorders/. Accessed August 18, 2019.
- Malhi GS, Mann JJ. Depression. Lancet. 2018;392(10161):2299-2312.
- Pigott HE, Leventhal AM, Alter GS, Boren JJ. Efficacy and effectiveness of antidepressants: current status of research. Psychother Psychosom. 2010;79(5):267-279.
- Pompili M, Serafini G, Del Casale A, et al. Improving adherence in mood disorders: the struggle against relapse, recurrence and suicide risk. Expert Rev Neurother. 2009;9(7):985-1004.
- Mayo Clinic. Depression (major depressive disorder). February 3, 2018. Available at: https://www.mayoclinic.org/diseases-conditions/depression/symptoms-causes/syc-20356007. Accessed August 18, 2019.
- Lau JY, Eley TC. The genetics of mood disorders. Annu Rev Clin Psychol. 2010;6:313-337.
- Archer T, Oscar-Berman M, Blum K, Gold M. Epigenetic Modulation of Mood Disorders. J Genet Syndr Gene Ther. 2013;4(120). pii: 1000120.
- Detera-Wadleigh SD, McMahon FJ. Genetic association studies in mood disorders: issues and promise. Int Rev Psychiatry. 2004;16(4):301-310.
- Lynch B. Dirty Genes. New York, NY: Harper One; 2018.
- Amare AT, Schubert KO, Baune BT. Pharmacogenomics in the treatment of mood disorders: Strategies and Opportunities for personalized psychiatry. EPMA J. 2017;8(3):211-227.
- Brennan FX, Gardner KR, Lombard J, et al. A Naturalistic Study of the Effectiveness of Pharmacogenetic Testing to Guide Treatment in Psychiatric Patients With Mood and Anxiety Disorders. Prim Care Companion CNS Disord. 2015;17(2). doi: 10.4088/PCC.14m01717.
- Pickar D, Rubinow K. Pharmacogenomics of psychiatric disorders. Trends Pharmacol Sci. 2001;22(2):75-83.
- Qureshi NA, Al-Bedeh AM. Mood disorders and complementary and alternative medicine: a literature review. Neuropsychiatr Dis Treat. 2013;9:639-658.
- Elkins G, Rajab MH, Marcus J. Complementary and alternative medicine use by psychiatric inpatients. Psychol Rep. 2005;96:163-166.
- Simon GE, Cherkin DC, Sherman KJ, et al. Mental health visits to complementary and alternative medicine providers. Gen Hosp Psychiatry. 2004;26(3):171-177.
- Davison KM, Kaplan BJ. Nutrient intakes are correlated with overall psychiatric functioning in adults with mood disorders. Can J Psychiatry. 2012;57(2):85-92.
- Byrne A, Byrne DG. The effect of exercise on depression, anxiety and other mood states: a review. J Psychosom Res. 1993;37(6):565-574.
- Lakhan SE, Vieira KF. Nutritional therapies for mental disorders. Nutr J. 2008;7:2.
- Foster JA, McVey Neufeld KA. Gut-brain axis: how the microbiome influences anxiety and depression. Trends Neurosci. 2013;36(5):305-312.
- Sherwin E, Rea K, Dinan TG, Cryan JF. A gut (microbiome) feeling about the brain. Curr Opin Gastroenterol. 2016;32(2):96-102.
- Gaby A. Nutritional Medicine. 2nd ed. Concord, NH: Fritz Perlberg Publishing; 2017.
- Hutto BR. Folate and cobalamin in psychiatric illness. Compr Psychiatry. 1997;38(6):305-314.
- Hector M, Burton JR. What are the psychiatric manifestations of vitamin B12 deficiency? J Am Geriatr Soc. 1988;36(12):1105-1112.
- Coppen A, Bolander-Gouaille C. Treatment of depression: time to consider folic acid and vitamin B12. J Psychopharmacol. 2005;19(1):59-65.
- Higdon J. Folate. 2014. Linus Pauling Institute, Oregon State University. Available at: https://lpi.oregonstate.edu/mic/vitamins/folate. Accessed August 18, 2019.
- Alpert JE, Fava M. Nutrition and depression: the role of folate. Nutr Rev. 1997;55(5):145-149.
- Coppen AA, Bailey J. Enhancement of the antidepressant action of fluoxetine by folic acid: a randomised, placebo controlled trial. J Affect Dis. 2000;60(2):121-131.
- Behzadi AH, Omrani Z, Chalian M, et al. Folic acid efficacy as an alternative drug added to sodium valproate in the treatment of acute phase of mania in bipolar disorder: a double-blind randomized controlled trial. Acta Psychiatr Scand. 2009;120(6):441-445.
- Pietrzik K, Bailey L, Shane B. Folic acid and L-5-methyltetrahydrofolate: comparison of clinical pharmacokinetics and pharmacodynamics. Clin Pharmacokinet. 2010;49(8):535-548.
- Scaglione F, Panzavolta G. Folate, folic acid and 5-methyltetrahydrofolate are not the same thing. Xenobiotica. 2014;44(5):480-488.
- Clayton PT. B6-responsive disorders: a model of vitamin dependency. J Inherit Metab Dis. 2006;29(2-3):317-326.
- Krishnan AV, Feldman D. Mechanisms of the anti-cancer and anti-inflammatory actions of vitamin D. Annu Rev Pharmacol Toxicol. 2011;51:311-336.
- Autier P, Boniol M, Pizot C, Mullie P. Vitamin D status and ill health: a systematic review. Lancet Diabetes Endocrinol. 2014;2(1):76-89.
- Spedding S. Vitamin D and depression: a systematic review and meta-analysis comparing studies with and without biological flaws. Nutrients. 2014;6(4):1501-1518.
- Gloth FM 3rd, Alam W, Hollis B. Vitamin D vs broad spectrum phototherapy in the treatment of seasonal affective disorder. J Nutr Health Aging. 1999;3(1):5-7.
- Szabo L. The Man Who Sold America On Vitamin D – And Profited in the Process. August 24, 2018. Medscape. Available at: https://www.medscape.com/viewarticle/901146. Accessed August 18, 2019.
- Wallace TC, McBurney M, Fulgoni VL 3rd. Multivitamin/mineral supplement contribution to micronutrient intakes in the United States, 2007-2010. J Am Coll Nutr. 2014;33(2):94-102.
- DiNicolantonio JJ, O’Keefe JH, Wilson W. Subclinical magnesium deficiency: a principal driver of cardiovascular disease and a public health crisis. Open Heart. 2018;5(1):e000668.
- Wester PO. Magnesium. Am J Clin Nutr. 1987;45(5 Suppl):1305-1312.
- Altura BM. Basic biochemistry and physiology of magnesium: a brief review. Magnes Trace Elem. 1991-1992;10(2-4):167-171.
- Tarleton EK, Littenberg B, MacLean CD, et al. Role of magnesium supplementation in the treatment of depression: A randomized clinical trial. PLoS One. 2017;12(6):e0180067.
- Serefko A, Szopa A, Poleszak E. Magnesium and depression. Magnes Res. 2016;29(3):112-119.
- McCall KA, Huang C, Fierke CA. Function and mechanism of zinc metalloenzymes. J Nutr. 2000;130(5S Suppl):1437S-1446S.
- Li Z, Li B, Song X, Zhang D. Dietary zinc and iron intake and risk of depression: A meta-analysis. Psychiatry Res. 2017;251:41-47.
- Nowak G, Siwek M, Dudek D, et al. Effect of zinc supplementation on antidepressant therapy in unipolar depression: a preliminary placebo-controlled study. Pol J Pharmacol. 2003;55(6):1143-1147.
- Institute of Medicine (US) Panel on Micronutrients. Dietary reference intakes for vitamin A, vitamin K, arsenic, boron, chromium, copper, iodine, iron, manganese, molybdenum, nickel, silicon, vanadium, and zinc. Washington, DC: National Academies Press; 2001:442-501.
- Maroon JC, Bost JW. Omega-3 fatty acids (fish oil) as an anti-inflammatory: an alternative to nonsteroidal anti-inflammatory drugs for discogenic pain. Surg Neurol. 2006;65(4):326-331.
- Kang JX, Weylandt KH. Modulation of inflammatory cytokines by omega-3 fatty acids. Subcell Biochem. 2008;49:133-143.
- Su KP, Lai HC, Yang HT, et al. Omega-3 fatty acids in the prevention of interferon-alpha-induced depression: results from a randomized, controlled trial. Biol Psychiatry. 2014;76(7):559-566.
- Grosso G, Pajak A, Marventano S, et al. Role of omega-3 fatty acids in the treatment of depressive disorders: a comprehensive meta-analysis of randomized clinical trials. PLoS One. 2014;9(5):e96905.
- Lin PY, Su KP. A meta-analytic review of double-blind, placebo-controlled trials of antidepressant efficacy of omega-3 fatty acids. J Clin Psychiatry. 2007;68(7):1056-1061.
- Martins JG. EPA but not DHA appears to be responsible for the efficacy of omega-3 long chain polyunsaturated fatty acid supplementation in depression: evidence from a meta-analysis of randomized controlled trials. J Am Coll Nutr. 2009;28(5):525-542.
- Sarris J, Mischoulon D, Schweitzer I. Omega-3 for bipolar disorder: meta-analyses of use in mania and bipolar depression. J Clin Psychiatry. 2012;73(1):81-86.
- Carney MW, Toone BK, Reynolds EH. S-Adenosylmethionine and affective disorder. Am J Med. 1987;83(5A):104-106.
- Sharma A, Gerbarg P, Bottiglieri T, et al. S-Adenosylmethionine (SAMe) for Neuropsychiatric Disorders: A Clinician-Oriented Review of Research. J Clin Psychiatry. 2017;78(6):e656-e667.
- Papakostas GI, Mischoulon D, Shyu I, et al. S-adenosyl methionine (SAMe) augmentation of serotonin reuptake inhibitors for antidepressant nonresponders with major depressive disorder: a double-blind, randomized clinical trial. Am J Psychiatry. 2010;167(8):942-948.
- Carney MW, Chary TK, Bottiglieri T, Reynolds EH. The switch mechanism and the bipolar/unipolar dichotomy. Br J Psychiatry. 1989;154:48-51.
- Shaw K, Turner J, Del Mar C. Tryptophan and 5-hydroxytryptophan for depression. Cochrane Database Syst Rev. 2002;(1):CD003198.
- Kious BM, Sabic H, Sung YH, et al. An Open-Label Pilot Study of Combined Augmentation With Creatine Monohydrate and 5-Hydroxytryptophan for Selective Serotonin Reuptake Inhibitor- or Serotonin-Norepinephrine Reuptake Inhibitor-Resistant Depression in Adult Women. J Clin Psychopharmacol. 2017;37(5):578-583.
- Kahn RS, Westenberg HG. L-5-hydroxytryptophan in the treatment of anxiety disorders. J Affect Disord. 1985;8(2):197-200.
- van Praag HM, Korf J, Dols LC, Schut T. A pilot study of the predictive value of the probenecid test in application of 5-hydroxytryptophan as antidepressant. Psychopharmacologia. 1972;25(1):14-21.
- Kahn RS, Westenberg HG, Verhoeven WM, et al. Effect of a serotonin precursor and uptake inhibitor in anxiety disorders; a double-blind comparison of 5-hydroxytryptophan, clomipramine and placebo. Int Clin Psychopharmacol. 1987;2(1):33-45.
- Nakajima T, Kudo Y, Kaneko Z. Clinical evaluation of 5-hydroxy-L-tryptophan as an antidepressant drug. Folia Psychiatr Neurol Jpn. 1978;32(2):223-230.
- Jangid P, Malik P, Singh P, et al. Comparative study of efficacy of l-5-hydroxytryptophan and fluoxetine in patients presenting with first depressive episode. Asian J Psychiatr. 2013;6(1):29-34.
- James SJ, Slikker W 3rd, Melnyk S, et al. Thimerosal neurotoxicity is associated with glutathione depletion: protection with glutathione precursors. Neurotoxicology. 2005;26(1):1-8.
- Sadowska A, Verbraecken J, Darquennes K, De Backer WA. Role of N-acetylcysteine in the management of COPD. Int J Chron Obstruct Pulmon Dis. 2006;1(4):425-434.
- Palacio JR, Markert UR, Martínez P. Anti-inflammatory properties of N-acetylcysteine on lipopolysaccharide-activated macrophages. Inflamm Res. 2011;60(7):695-704.
- Harrison PM, Wendon JA, Gimson AE, et al. Improvement by acetylcysteine of hemodynamics and oxygen transport in fulminant hepatic failure. N Engl J Med. 1991;324(26):1852-1857.
- Ziment I. Acetylcysteine: a drug with an interesting past and a fascinating future. Respiration. 1986;50 Suppl 1:26-30.
- Ooi SL, Green R, Pak SC. N-Acetylcysteine for the Treatment of Psychiatric Disorders: A Review of Current Evidence. Biomed Res Int. 2018;2018:2469486.
- Dean O, Giorlando F, Berk M. N-acetylcysteine in psychiatry: current therapeutic evidence and potential mechanisms of action. J Psychiatry Neurosci. 2011;36(2):78-86.
- Minarini A, Ferrari S, Galletti M, et al. N-acetylcysteine in the treatment of psychiatric disorders: current status and future prospects. Expert Opin Drug Metab Toxicol. 2017;13(3):279-292.
- Grant JE, Odlaug BL, Kim SW. N-acetylcysteine, a glutamate modulator, in the treatment of trichotillomania: a double-blind, placebo-controlled study. Arch Gen Psychiatry. 2009;66(7):756-763.
- Hayces KC. A review on the biological function of taurine. Nutr Rev. 1976;34(6):161-165.
- Ripps H, Shen W. Review: taurine: a “very essential” amino acid. Mol Vis. 2012;18:2673-2686.
- Schaffer S, Kim HW. Effects and Mechanisms of Taurine as a Therapeutic Agent. Biomol Ther (Seoul). 2018;26(3):225-241.
- Benzie IFF, Wachtel-Galor S, eds. Chapter 11: Medical Attributes of St. John’s Wort (Hypericum perforatum). In: Herbal Medicine: Biomolecular and Clinical Aspects. 2nd edition. New York, NY: CRC Press/Taylor & Francis; 2011.
- Vorbach EU, Arnoldt KH, Hübner WD. Efficacy and tolerability of St. John’s wort extract LI 160 versus imipramine in patients with severe depressive episodes according to ICD-10. Pharmacopsychiatry. 1997;30 Suppl 2:81-85.
- van Gurp G, Meterissian GB, Haiek LN, et al. St John’s wort or sertraline? Randomized controlled trial in primary care. Can Fam Physician. 2002;48:905-912.
- Gastpar M, Singer A, Zeller K. Comparative efficacy and safety of a once-daily dosage of hypericum extract STW3-VI and citalopram in patients with moderate depression: a double-blind, randomised, multicentre, placebo-controlled study. Pharmacopsychiatry. 2006;39(2):66-75.
- Müller WE, Singer A, Wonnemann M, et al. Hyperforin represents the neurotransmitter reuptake inhibiting constituent of hypericum extract. Pharmacopsychiatry. 1998;31 Suppl 1:16-21.
- Calapai G, Crupi A, Firenzuoli F, et al. Serotonin, norepinephrine and dopamine involvement in the antidepressant action of hypericum perforatum. Pharmacopsychiatry. 2001;34(2):45-49.
- Linde K, Ramirez G, Mulrow CD, et al. St John’s wort for depression–an overview and meta-analysis of randomised clinical trials. BMJ. 1996;313(7052):253-258.
- Drugs.com. St. John’s Wort. 2000-2020. Available at: https://www.drugs.com/npp/st-john-s-wort.html. Accessed August 18, 2019.
- Wang Z, Gorski JC, Hamman MA, et al. The effects of St John’s wort (Hypericum perforatum) on human cytochrome P450 activity. Clin Pharmacol Ther. 2001;70(4):317-326.
- Sanmukhani J, Satodia V, Trivedi J, et al. Efficacy and safety of curcumin in major depressive disorder: a randomized controlled trial. Phytother Res. 2014;28(4):579-585.
- Nq QX, Koh SSH, Chan HW, Ho CYX. Clinical Use of Curcumin in Depression: A Meta-Analysis. J Am Med Dir Assoc. 2017;18(6):503-508.
- Esmaily H, Sahebkar A, Iranshahi M, et al. An investigation of the effects of curcumin on anxiety and depression in obese individuals: A randomized controlled trial. Chin J Integr Med. 2015;21(5):332-338.
- Kulkarni SK, Dhir A. An Overview of Curcumin in Neurological Disorders. Indian J Pharm Sci. 2010;72(2):149-154.
- Kelly GS. Rhodiola rosea: a possible plant adaptogen. Altern Med Rev. 2001;6(3):293-302.
- Chen Q, Zeng YS, Qu ZQ, et al. The effects of Rhodiola rosea extract on 5-HT level, cell proliferation and quantity of neurons at cerebral hippocampus of depressive rats. Phytomedicine. 2009;16(9):830-838.
- Panossian A, Nikoyan N, Ohanyan N, et al. Comparative study of Rhodiola preparations on behavioral despair of rats. Phytomedicine. 2008;15(1-2):84-91.
- van Diermen D, Marston A, Bravo J, et al. Monoamine oxidase inhibition by Rhodiola rosea L. roots. J Ethnopharmacol. 2009;122(2):397-401.
- Darbinyan G, Aslanyan G, Amroyan E, et al. Clinical trial of Rhodiola rosea L. extract SHR-5 in the treatment of mild to moderate depression. Nord J Psychiatry. 2007;61(5):343-348.
- Ross M. Rhodiola rosea (SHR-5), Part 2: A standardized extract of Rhodiola rosea is shown to be effective in the treatment of mild to moderate depression. Holist Nurs Pract. 2014;28(3):217-221.
- Brown RP, Gerbarg PL, Ramazanov Z. Rhodiola rosea: A Phytomedicinal Overview. HerbalGram. 2002;56:40-52. Available at: http://cms.herbalgram.org/herbalgram/issue56/article2333.html?ts=1578841493&signature=cc4d6dbf7169d10853eea0a63508a12f. Accessed August 18, 2019.
- Hudson H. Rhodiola rosea: An overview of its versatility, effectiveness and indications. Sponsored by Gaia Herbs.
- Baraghani A. What Is Saffron, the World’s Most Legendary Spice? February 5, 2018. Available at: https://www.bonappetit.com/story/what-is-saffron. Accessed August 18, 2019.
- Rios JL, Recio MC, Giner RM, Máñez S. An update review of saffron and its active constituents. Phytother Res. 1996;10(3):189-193.
- Baziar S, Aqamolaei A, Khadem E, et al. Crocus sativus L. Versus Methylphenidate in Treatment of Children with Attention-Deficit/Hyperactivity Disorder: A Randomized, Double-Blind Pilot Study. J Child Adolesc Psychopharmacol. 2019;29(3):205-212.
- Akhondzadeh S, Sabet MS, Harirchian MH, et al. Saffron in the treatment of patients with mild to moderate Alzheimer’s disease: a 16-week, randomized and placebo-controlled trial. J Clin Pharm Ther. 2010;35(5):581-588.
- Akhondzadeh S, Shafiee Sabet M, Harirchian MH, et al. A 22-week, multicenter, randomized, double-blind controlled trial of Crocus sativus in the treatment of mild-to-moderate Alzheimer’s disease. Psychopharmacology. 2010;207(4):637-643.
- Mazidi M, Shemshian M, Mousavi SH, et al. A double-blind, randomized and placebo-controlled trial of Saffron (Crocus sativus L.) in the treatment of anxiety and depression. J Complement Integr Med. 2016;13(2):195-199.
- Dwyer AV, Whitten DL, Hawrelak JA. Herbal Medicines, other than St. John’s Wort, in the Treatment of Depression: A Systematic Review. Altern Med Rev. 2011;16(1):40-49.
- Marañón JA, et al. GABA receptors mediates the activity of safranal from IRIDAFRAN saffron extract. Int Soc Nutraceutical Func Foods. 2012. [Poster presentation]
- Talaei A, Hassanpour Moghadam M, Sajadi Tabassi SA, Mohajeri SA. Crocin, the main active saffron constituent, as an adjunctive treatment in major depressive disorder: a randomized, double-blind, placebo-controlled, pilot clinical trial. J Affect Disord. 2015;174:515-516.
- Akhondzadeh S, Tahmacebi-Pour N, Noorbala AA, et al. Crocus sativus L. in the Treatment of Mild to Moderate Depression: A Double-blind, Randomized and Placebo-controlled Trial. Phytother Res. 2005;19(2):148-151.
- Noorbala AA, Akhondzadeh S, Tahmacebi-Pour N, Jamshidi AH. Hydro-alcoholic extract of Crocus sativus L. versus fluoxetine in the treatment of mild to moderate depression: a double-blind, randomized pilot trial. J Ethnopharmacol. 2005;97(2):281-284.
- Akhondzadeh S, Fallah-Pour H, Afkham K, et al. Comparison of Crocus sativus L. and imipramine in the treatment of mild to moderate depression: A pilot double-blind randomized trial. BMC Complement Altern Med. 2004;4:12.
- Stargrove MB, Treasure J, McKee DL. Herb, Nutrient and Drug Interactions. Maryland Heights, MO: Mosby; 2008.
- Devlin TM, ed. Textbook of Biochemistry with Clinical Correlations. 3rd edition. New York, NY: Wiley-Liss Inc; 1992.
- Brown ES, Park J, Marx CE, et al. A randomized, double-blind, placebo-controlled trial of pregnenolone for bipolar depression. Neuropsychopharmacology. 2014;39(12):2867-2873.
- Ritsner MS, Gibel A, Shleifer T, et al. Pregnenolone and dehydroepiandrosterone as an adjunctive treatment in schizophrenia and schizoaffective disorder: an 8-week, double-blind, randomized, controlled, 2-center, parallel-group trial. J Clin Psychiatry. 2010;71(10):1351-1362.
- Marx CE, Keefe RS, Buchanan RW, et al. Proof-of-concept trial with the neurosteroid pregnenolone targeting cognitive and negative symptoms in schizophrenia. Neuropsychopharmacology. 2009;34(8):1885-1903.
- Osuji IJ, Vera-Bolaños E, Carmody TJ, Brown ES. Pregnenolone for cognition and mood in dual diagnosis patients. Psychiatry Res. 2010;178(2):309-312.
- George MS, Guidotti A, Rubinow D, et al. CSF neuroactive steroids in affective disorders: pregnenolone, progesterone, and DBI. Biol Psych. 1994;35(10):775-780.
- Kroboth PD, Salek FS, Pittenger AL, et al. DHEA and DHEA-S: A review. J Clin Pharmacol. 1999;39(4):327-348.
- Wolkowitz OM, Reus VI, Keebler A, et al. Double-blind treatment of major depression with dehydroepiandrosterone. Am J Psychiatry. 1999;156(4):646-649.
- Bloch M, Schmidt PJ, Danaceau MA, et al. Dehydroepiandrosterone treatment of midlife dysthymia. Biol Psychiatry. 1999;45(12):1533-1541.
- Kamin HS, Kertes DA. Cortisol and DHEA in Development and Psychopathology. Horm Behav. 2017;89:69-85.
- Starka L, Dušková M, Hill M. Dehydroepiandrosterone: a neuroactive steroid. J Steroid Biochem Mol Biol. 2015;145:254-260.
- Drugs.com. Dehydroepiandrosterone. Last updated November 1, 2019. Available at: https://www.drugs.com/npp/dehydroepiandrosterone.html. Accessed January 13, 2020.
Todd A. Born, ND, CNS, is a naturopathic doctor, certified nutrition specialist, co-owner, and medical director of Born Integrative Medicine Specialists, PLLC. He is also Allergy Research Group’s Head of New Product Development, Product Manager, Scientific Advisor, and Editor-in-Chief of their science-based Focus Newsletter. Dr Born graduated from Bastyr University and completed his residency at the Bastyr Center for Natural Health, its 13 teaching clinics, with rotations at Seattle-area hospitals. He uses a wide range of therapeutic modalities. Strong interests include difficult and refractory cases, GI issues, neurological disorders, endocrinology, CVD, diabetes, autoimmune disease, developmental and behavioral issues, HIV/AIDS, and geriatrics. | <urn:uuid:928c7526-2f11-45b8-856b-66f1ace97aa6> | {
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Are you wondering why your child struggles with numbers and finds it difficult to solve the seemingly simple tasks?
Dyscalculia is usually perceived as a specific learning difficulty for mathematics, or, more appropriately, arithmetic. In isolated dyscalculia, there are no deficits in reading or writing. Dyscalculia is classified under WHO ICD-10, a classification system for diseases and mental disorders, as:
“The deficit concerns mastery of basic computational skills of
addition, subtraction, multiplication, and division rather than of the more
abstract mathematical skills involved in algebra, trigonometry,
geometry, or calculus.”
Signs and Symptoms
With Dyscalculia the computational difficulties can appear from the very beginning of learning numbers at school. However, if the child has a generally high level of learning and achievement, deficiencies in arithmetic can only be noticed at a later stage, namely when school demands increase. The first signs of dyscalculia can already be seen in preschool age. The understanding of numbers and quantities, counting skills as well as simple addition and subtraction tasks are difficult. However, since
Children affected by dyscalculia are more prone to mental health problems such as depressive or psychosomatic symptoms. Some children are becoming more and more withdrawn because of school difficulties, others are more prone to aggressive behaviour. In addition to dyscalculia, your child may also experience dyslexia or an attention deficit disorder (ADD) with or without additional hyperactivity disorder (ADHD).
Frequency and Causes
According to international studies, about 3 to 8% of all children and adolescents suffer from dyscalculia. It has not yet been clarified whether girls or boys are affected more frequently. Some studies have found no difference in this regard, while others show that girls are more likely to suffer from dyscalculia. The causes of dyscalculia are still not known today. However, it is believed that there are several factors that influence computational skills, such as genetic, neuroscience, and cognitive factors.
In addition, the child’s relationship with parents, peers, teachers, financial security and way of parenting can compound existing computational issues. It also matters whether the child has deficits in other areas, such as ADHD or mental health problems.
Activities in the Brain
What happens inside a brain with dyscalculia? Using fMRI and EEG studies, scientists have found that we have a kind of innate number sense in the parietal lobe of our brain. This serves the quantity comprehension and thus the development of the later calculation abilities. Dyscalculics show significantly less activation in this region. This is related to the fact that children with dyscalculia, even with increasing age, still mainly work with the frontal lobe, which is responsible for learning new content.
Effects of Dyscalculia
Contrary to widespread opinion you do not grow out of dyscalculia. Studies have shown that dyscalculics leave school early and are less likely to acquire a vocational qualification than peers without dyscalculia. Furthermore, their everyday life is heavily affected, as they can for example have difficulties when using money or reading clocks.
However, if dyscalculia is diagnosed early and the therapy is appropriate, the prognosis is good that arithmetic can still be learned later.
Assessment and Diagnosis
A diagnosis should be made as early as possible and by experienced specialists. The Dyslexia Centre in London or the British Dyslexia Association, for example, recommend professional Educational Psychologists for assessments and diagnosis.
Treatment after Diagnosis
The earlier therapy is started, the better the chances of development. Highly recommended are individualised therapies by trained specialists, because then not only the dyscalculia is in focus, but the entire situation such as depression or psychosomatic symptoms. This is the best way to control the difficulties of computation and mental health difficulties in the long term. The first attempt is to give children access to understanding numbers and quantities.
Only in a second step, simple arithmetic operations are then discussed. Funding programs must be long-term, as dyscalculia can not be treated in a few weeks. In addition, one to one therapy is more effective than group therapy or in class. Instead of abruptly stopping therapy, it is advisable to increase the duration between sessions to gradually stop it.
However far down the path of dyscalculia whether it be at the beginning of identifying or you are already challenging your difficulties with numbers, always remember that there are others on the same journey as you and they can help you. One place you can find these people is in our Dyscalculia Support Group on Facebook – Join here. | <urn:uuid:0edf8062-6521-4f5a-b73c-84b4970f43f7> | {
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Remember Measles? It's Back!
Measles is making a comeback. The Centers for Disease Control and Prevention (CDC) recently reported 477 confirmed cases of the measles (rubeola) in the first six months of 2014. A graph created by the CDC shows the rapid increase in cases and outbreaks this year compared to past years.
Measles was deemed “eliminated” in the United States in 2000, but remains vulnerable because the disease is still prevalent in many parts of the world, and travelers continue to bring it into the country. The Philippines, for example, is experiencing a large, ongoing measles outbreak, which has led the CDC to issue a Travelers’ Health Notice.
Look for the Signs
Providers should be on the lookout for measles, the CDC advises. Measles is an acute viral respiratory illness. Indications include:
- Coryza (rhinitis)
- Conjunctivitis (pink eye)
- Pathognomonic enanthema (Koplick’s spots) – Little spots inside the mouth that are surrounded by a red ring.
- Maculopapular rash – A combination of both macules (flat, discolored areas) and papules (small, raised bumps).
Complications of measles may include:
- Otitis media (middle ear infection)
- Laryngotracheobronchitis (croup)
There is no treatment for measles, but the provider may treat the symptoms, for which an appropriate evaluation and management code can be reported.
The majority of reported cases occurred in unvaccinated people. The CDC recommends the Measles-Mumps-Rubella (MMR) and Varicella (VAR) vaccines, or the combination Measles-Mumps-Rubella-Varicella (MMRV) vaccine, for children 1-12 years of age, given in two separate doses: the first dose at 12-15 months of age and the second dose at 4-6 years of age.
For this service, you would report the appropriate CPT® vaccine product code:
- 90705 Measles virus vaccine, live, for subcutaneous use
- 90707 Measles, mumps and rubella virus vaccine (MMR), live, for subcutaneous use
- 90708 Measles and rubella virus vaccine, live, for subcutaneous use
- 90710 Measles, mumps, rubella, and varicella vaccine (MMRV), live, for subcutaneous use
Remember to also code the administration of the vaccine (90460-90474).
Measles is classified to ICD-9-CM category 055. The fourth digit depends on whether the patient experienced a complication, such as:
- 055.0 Postmeasles encephalitis
- 055.1 Postmeasles pneumonia
- 055.2 Postmeasles otitis media
- 055.71 Measles keratoconjunctivitis
- 055.79 Measles with other specified complications
- 055.8 Measles with unspecified complication
Assign 055.9 for measles without mention of complication.
ICD-10-CM coding is similar, but with a few more options:
- B05.0 Measles complicated by encephalitis
- B05.1 Measles complicated by meningitis
- B05.2 Measles complicated by pneumonia
- B05.3 Measles complicated by otitis media
- B05.4 Measles with intestinal complications
- B05.81 Measles keratitis and keratoconjunctivitis
- B05.89 Other measles complications
Assign B05.9 for measles without mention of complication. | <urn:uuid:b5de55a7-ac52-4053-a15a-637b6193326c> | {
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|Other names||Septicemia, blood poisoning|
|Blood culture bottles: orange cap for anaerobes, green cap for aerobes, and yellow cap for blood samples from children|
|Symptoms||Fever, increased heart rate, low blood pressure, increased breathing rate, confusion|
|Causes||Immune response triggered by an infection|
|Risk factors||Young or old age, cancer, diabetes, major trauma, burns|
|Diagnostic method||Systemic inflammatory response syndrome (SIRS), qSOFA|
|Treatment||Intravenous fluids, antimicrobials|
|Prognosis||10 to 80% risk of death|
|Frequency||0.2–3 per 1000 a year (developed world)|
Sepsis is a life-threatening condition that arises when the body's response to infection causes injury to its tissues and organs. Common signs and symptoms include fever, increased heart rate, increased breathing rate, and confusion. There may also be symptoms related to a specific infection, such as a cough with pneumonia, or painful urination with a kidney infection. The very young, old, and people with a weakened immune system may have no symptoms of a specific infection, and the body temperature may be low or normal instead of having a fever. Severe sepsis is sepsis causing poor organ function or blood flow. The presence of low blood pressure, high blood lactate, or low urine output may suggest poor blood flow. Septic shock is low blood pressure due to sepsis that does not improve after fluid replacement.
Sepsis is an inflammatory immune response triggered by an infection. Bacterial infections are the most common cause, but fungal, viral, and protozoan infections can also lead to sepsis. Common locations for the primary infection include the lungs, brain, urinary tract, skin, and abdominal organs. Risk factors include being very young, older age, a weakened immune system from conditions such as cancer or diabetes, major trauma, or burns. Previously, a sepsis diagnosis required the presence of at least two systemic inflammatory response syndrome (SIRS) criteria in the setting of presumed infection. In 2016, a shortened sequential organ failure assessment score (SOFA score), known as the quick SOFA score (qSOFA), replaced the SIRS system of diagnosis. qSOFA criteria for sepsis include at least two of the following three: increased breathing rate, change in the level of consciousness, and low blood pressure. Sepsis guidelines recommend obtaining blood cultures before starting antibiotics; however, the diagnosis does not require the blood to be infected. Medical imaging is helpful when looking for the possible location of the infection. Other potential causes of similar signs and symptoms include anaphylaxis, adrenal insufficiency, low blood volume, heart failure, and pulmonary embolism.
Sepsis requires immediate treatment with intravenous fluids and antimicrobials. Ongoing care often continues in an intensive care unit. If an adequate trial of fluid replacement is not enough to maintain blood pressure, then the use of medications that raise blood pressure becomes necessary. Mechanical ventilation and dialysis may be needed to support the function of the lungs and kidneys, respectively. A central venous catheter and an arterial catheter may be placed for access to the bloodstream and to guide treatment. Other helpful measurements include cardiac output and superior vena cava oxygen saturation. People with sepsis need preventive measures for deep vein thrombosis, stress ulcers, and pressure ulcers unless other conditions prevent such interventions. Some might benefit from tight control of blood sugar levels with insulin. The use of corticosteroids is controversial, with some reviews finding benefit, and others not.
Disease severity partly determines the outcome. The risk of death from sepsis is as high as 30%, as high as 50% from severe sepsis, and up to 80% from septic shock. Sepsis affected about 49 million people in 2017, with 11 million deaths (1 in 5 deaths worldwide). In the developed world, approximately 0.2 to 3 people per 1000 are affected by sepsis yearly, resulting in about a million cases per year in the United States. Rates of disease have been increasing. Sepsis is more common among males than females. Descriptions of sepsis date back to the time of Hippocrates. The terms "septicemia" and "blood poisoning" have been used in various ways and are no longer recommended.
In addition to symptoms related to the actual cause, people with sepsis may have a fever, low body temperature, rapid breathing, a fast heart rate, confusion, and edema. Early signs include a rapid heart rate, decreased urination, and high blood sugar. Signs of established sepsis include confusion, metabolic acidosis (which may be accompanied by a faster breathing rate that leads to respiratory alkalosis), low blood pressure due to decreased systemic vascular resistance, higher cardiac output, and disorders in blood-clotting that may lead to organ failure.
Infections leading to sepsis are usually bacterial but may be fungal or viral. Gram-positive bacteria were the primary cause of sepsis before the introduction of antibiotics in the 1950s. After the introduction of antibiotics, gram-negative bacteria became the predominant cause of sepsis from the 1960s to the 1980s. After the 1980s, gram-positive bacteria, most commonly staphylococci, are thought to cause more than 50% of cases of sepsis. Other commonly implicated bacteria include Streptococcus pyogenes, Escherichia coli, Pseudomonas aeruginosa, and Klebsiella species. Fungal sepsis accounts for approximately 5% of severe sepsis and septic shock cases; the most common cause of fungal sepsis is an infection by Candida species of yeast, a frequent hospital-acquired infection.
The most common sites of infection resulting in severe sepsis are the lungs, the abdomen, and the urinary tract. Typically, 50% of all sepsis cases start as an infection in the lungs. In one third to one-half of cases, the source of infection is unclear.
Early diagnosis is necessary to properly manage sepsis, as the initiation of rapid therapy is key to reducing deaths from severe sepsis. Some hospitals use alerts generated from electronic health records to bring attention to potential cases as early as possible.
Within the first three hours of suspected sepsis, diagnostic studies should include white blood cell counts, measuring serum lactate, and obtaining appropriate cultures before starting antibiotics, so long as this does not delay their use by more than 45 minutes. To identify the causative organism(s), at least two sets of blood cultures using bottles with media for aerobic and anaerobic organisms are necessary. At least one should be drawn through the skin and one through each vascular access device (such as an IV catheter) that has been in place more than 48 hours. Bacteria are present in the blood in only about 30% of cases. Another possible method of detection is by polymerase chain reaction. If other sources of infection are suspected, cultures of these sources, such as urine, cerebrospinal fluid, wounds, or respiratory secretions, also should be obtained, as long as this does not delay the use of antibiotics.
Within six hours, if blood pressure remains low despite initial fluid resuscitation of 30 ml/kg, or if initial lactate is ≥ four mmol/l (36 mg/dl), central venous pressure and central venous oxygen saturation should be measured. Lactate should be re-measured if the initial lactate was elevated. Evidence for point of care lactate measurement over usual methods of measurement, however, is poor.
Within twelve hours, it is essential to diagnose or exclude any source of infection that would require emergent source control, such as a necrotizing soft tissue infection, an infection causing inflammation of the abdominal cavity lining, an infection of the bile duct, or an intestinal infarction. A pierced internal organ (free air on an abdominal x-ray or CT scan), an abnormal chest x-ray consistent with pneumonia (with focal opacification), or petechiae, purpura, or purpura fulminans may indicate the presence of an infection.
|Temperature||<36 °C (96.8 °F) or >38 °C (100.4 °F)|
|Respiratory rate||>20/min or PaCO2<32 mmHg (4.3 kPa)|
|WBC||<4x109/L (<4000/mm³), >12x109/L (>12,000/mm³), or 10% bands|
Previously, SIRS criteria had been used to define sepsis. If the SIRS criteria are negative, it is very unlikely the person has sepsis; if it is positive, there is just a moderate probability that the person has sepsis. According to SIRS, there were different levels of sepsis: sepsis, severe sepsis, and septic shock. The definition of SIRS is shown below:
In 2016 a new consensus was reached to replace screening by systemic inflammatory response syndrome (SIRS) with qSOFA. However, the American College of Chest Physicians (CHEST) raised concerns that qSOFA and SOFA criteria may lead to delayed diagnosis of serious infection, leading to delayed treatment. Although SIRS criteria can be too sensitive and not specific enough in identifying sepsis, SOFA also has its limitations and is not intended to replace the SIRS definition. qSOFA has also been found to be poorly sensitive though decently specific for the risk of death with SIRS possibly better for screening.
More specific definitions of end-organ dysfunction exist for SIRS in pediatrics.
Consensus definitions, however, continue to evolve, with the latest expanding the list of signs and symptoms of sepsis to reflect clinical bedside experience.
A 2013 review concluded moderate-quality evidence exists to support the use of the procalcitonin level as a method to distinguish sepsis from non-infectious causes of SIRS. The same review found the sensitivity of the test to be 77% and the specificity to be 79%. The authors suggested that procalcitonin may serve as a helpful diagnostic marker for sepsis, but cautioned that its level alone does not definitively make the diagnosis. A 2012 systematic review found that soluble urokinase-type plasminogen activator receptor (SuPAR) is a nonspecific marker of inflammation and does not accurately diagnose sepsis. This same review concluded, however, that SuPAR has prognostic value, as higher SuPAR levels are associated with an increased rate of death in those with sepsis.
The differential diagnosis for sepsis is broad and has to examine (to exclude) the non-infectious conditions that may cause the systemic signs of SIRS: alcohol withdrawal, acute pancreatitis, burns, pulmonary embolism, thyrotoxicosis, anaphylaxis, adrenal insufficiency, and neurogenic shock. Hyperinflammatory syndromes such as hemophagocytic lymphohistiocytosis (HLH) may have similar symptoms and are on the differential diagnosis..
In common clinical usage, neonatal sepsis refers to a bacterial blood stream infection in the first month of life, such as meningitis, pneumonia, pyelonephritis, or gastroenteritis, but neonatal sepsis also may be due to infection with fungi, viruses, or parasites. Criteria with regard to hemodynamic compromise or respiratory failure are not useful because they present too late for intervention.
This section needs expansion with: Viral sepsis. You can help by adding to it. (March 2020)
Sepsis is caused by a combination of factors related to the particular invading pathogen(s) and to the status of the immune system of the host. The early phase of sepsis characterized by excessive inflammation (sometimes resulting in a cytokine storm) may be followed by a prolonged period of decreased functioning of the immune system. Either of these phases may prove fatal. On the other hand, systemic inflammatory response syndrome (SIRS) occurs in people without the presence of infection, for example, in those with burns, polytrauma, or the initial state in pancreatitis and chemical pneumonitis. However, sepsis also causes similar response to SIRS.
Bacterial virulence factors, such as glycocalyx and various adhesins, allow colonization, immune evasion, and establishment of disease in the host. Sepsis caused by gram-negative bacteria is thought to be largely due to a response by the host to the lipid A component of lipopolysaccharide, also called endotoxin. Sepsis caused by gram-positive bacteria may result from an immunological response to cell wall lipoteichoic acid. Bacterial exotoxins that act as superantigens also may cause sepsis. Superantigens simultaneously bind major histocompatibility complex and T-cell receptors in the absence of antigen presentation. This forced receptor interaction induces the production of pro-inflammatory chemical signals (cytokines) by T-cells.
There are a number of microbial factors that may cause the typical septic inflammatory cascade. An invading pathogen is recognized by its pathogen-associated molecular patterns (PAMPs). Examples of PAMPs include lipopolysaccharides and flagellin in gram-negative bacteria, muramyl dipeptide in the peptidoglycan of the gram-positive bacterial cell wall, and CpG bacterial DNA. These PAMPs are recognized by the pattern recognition receptors (PRRs) of the innate immune system, which may be membrane-bound or cytosolic. There are four families of PRRs: the toll-like receptors, the C-type lectin receptors, the NOD-like receptors, and the RIG-I-like receptors. Invariably, the association of a PAMP and a PRR will cause a series of intracellular signalling cascades. Consequentially, transcription factors such as nuclear factor-kappa B and activator protein-1, will up-regulate the expression of pro-inflammatory and anti-inflammatory cytokines.
Upon detection of microbial antigens, the host systemic immune system is activated. Immune cells not only recognise pathogen-associated molecular patterns, but also damage-associated molecular patterns from damaged tissues. An uncontrolled immune response is then activated because leukocytes are not recruited to the specific site of infection, but instead they are recruited all over the body. Then, an immunosuppression state ensues when the proinflammatory T helper cell 1 (TH1) is shifted to TH2, mediated by interleukin 10, which is known as "compensatory anti-inflammatory response syndrome". The apoptosis (cell death) of lymphocytes further worsens the immunosuppression. Subsequently, multiple organ failure ensues because tissues are unable to use oxygen efficiently due to inhibition of cytochrome c oxidase.
Inflammatory responses cause multiple organ dysfunction syndrome through various mechanisms as described below. Increased permeability of the lung vessels causes leaking of fluids into alveoli, which results in pulmonary edema and acute respiratory distress syndrome (ARDS). Impaired utilization of oxygen in the liver impairs bile salt transport, causing jaundice (yellowish discoloration of skin). In kidneys, inadequate oxygenation results in tubular epithelial cell injury (of the cells lining the kidney tubules), and thus causes acute kidney injury (AKI). Meanwhile, in the heart, impaired calcium transport, and low production of adenosine triphosphate (ATP), can cause myocardial depression, reducing cardiac contractility and causing heart failure. In the gastrointestinal tract, increased permeability of the mucosa alters the microflora, causing mucosal bleeding and paralytic ileus. In the central nervous system, direct damage of the brain cells and disturbances of neurotransmissions causes altered mental status. Cytokines such as tumor necrosis factor, interleukin 1, and interleukin 6 may activate procoagulation factors in the cells lining blood vessels, leading to endothelial damage. The damaged endothelial surface inhibits anticoagulant properties as well as increases antifibrinolysis, which may lead to intravascular clotting, the formation of blood clots in small blood vessels, and multiple organ failure.
The low blood pressure seen in those with sepsis is the result of various processes, including excessive production of chemicals that dilate blood vessels such as nitric oxide, a deficiency of chemicals that constrict blood vessels such as vasopressin, and activation of ATP-sensitive potassium channels. In those with severe sepsis and septic shock, this sequence of events leads to a type of circulatory shock known as distributive shock.
Early recognition and focused management may improve the outcomes in sepsis. Current professional recommendations include a number of actions ("bundles") to be followed as soon as possible after diagnosis. Within the first three hours someone with sepsis should have received antibiotics and, intravenous fluids if there is evidence of either low blood pressure or other evidence for inadequate blood supply to organs (as evidenced by a raised level of lactate); blood cultures also should be obtained within this time period. After six hours the blood pressure should be adequate, close monitoring of blood pressure and blood supply to organs should be in place, and the lactate should be measured again if initially it was raised. A related bundle, the "Sepsis Six", is in widespread use in the United Kingdom; this requires the administration of antibiotics within an hour of recognition, blood cultures, lactate and hemoglobin determination, urine output monitoring, high-flow oxygen, and intravenous fluids.
Apart from the timely administration of fluids and antibiotics, the management of sepsis also involves surgical drainage of infected fluid collections and appropriate support for organ dysfunction. This may include hemodialysis in kidney failure, mechanical ventilation in lung dysfunction, transfusion of blood products, and drug and fluid therapy for circulatory failure. Ensuring adequate nutrition—preferably by enteral feeding, but if necessary, by parenteral nutrition—is important during prolonged illness. Medication to prevent deep vein thrombosis and gastric ulcers also may be used.
Two sets of blood cultures (aerobic and anaerobic) are recommended without delaying the initiation of antibiotics. Cultures from other sites such as respiratory secretions, urine, wounds, cerebrospinal fluid, and catheter insertion sites (in-situ more than 48 hours) are recommended if infections from these sites are suspected. In severe sepsis and septic shock, broad-spectrum antibiotics (usually two, a β-lactam antibiotic with broad coverage, or broad-spectrum carbapenem combined with fluoroquinolones, macrolides, or aminoglycosides) are recommended. However, combination of antibiotics is not recommended for the treatment of sepsis but without shock and immunocompromised persons unless the combination is used to broaden the anti-bacterial activity. The choice of antibiotics is important in determining the survival of the person. Some recommend they be given within one hour of making the diagnosis, stating that for every hour of delay in the administration of antibiotics, there is an associated 6% rise in mortality. Others did not find a benefit with early administration.
Several factors determine the most appropriate choice for the initial antibiotic regimen. These factors include local patterns of bacterial sensitivity to antibiotics, whether the infection is thought to be a hospital or community-acquired infection, and which organ systems are thought to be infected. Antibiotic regimens should be reassessed daily and narrowed if appropriate. Treatment duration is typically 7–10 days with the type of antibiotic used directed by the results of cultures. If the culture result is negative, antibiotics should be de-escalated according to person's clinical response or stopped altogether if infection is not present to decrease the chances that the person is infected with multiple drug resistance organisms. In case of people having high risk of being infected with multiple drug resistance organisms such as Pseudomonas aeruginosa, Acinetobacter baumannii, addition of antibiotic specific to gram-negative organism is recommended. For Methicillin-resistant Staphylococcus aureus (MRSA), vancomycin or teicoplanin is recommended. For Legionella infection, addition of macrolide or fluoroquinolone is chosen. If fungal infection is suspected, an echinocandin, such as caspofungin or micafungin, is chosen for people with severe sepsis, followed by triazole (fluconazole and itraconazole) for less ill people. Prolonged antibiotic prophylaxis is not recommended in people who has SIRS without any infectious origin such as acute pancreatitis and burns unless sepsis is suspected.
Once daily dosing of aminoglycoside is sufficient to achieve peak plasma concentration for clinical response without kidney toxicity. Meanwhile, for antibiotics with low volume distribution (vancomycin, teicoplanin, colistin), loading dose is required to achieve adequate therapeutic level to fight infections. Frequent infusions of beta-lactam antibiotics without exceeding total daily dose would help to keep the antibiotics level above minimum inhibitory concentration (MIC), thus providing better clinical response. Giving beta-lactam antibiotics continuously may be better than giving them intermittently. Access to therapeutic drug monitoring is important to ensure adequate drug therapeutic level while at the same time preventing the drug from reaching toxic level.
The Surviving Sepsis Campaign has recommended 30 ml/kg of fluid to be given in adults in the first three hours followed by fluid titration according to blood pressure, urine output, respiratory rate, and oxygen saturation with a target mean arterial pressure (MAP) of 65 mmHg. In children an initial amount of 20ml/kg is reasonable in shock. In cases of severe sepsis and septic shock where a central venous catheter is used to measure blood pressures dynamically, fluids should be administered until the central venous pressure (CVP) reaches 8–12 mmHg. Once these goals are met, the central venous oxygen saturation (ScvO2), i.e., the oxygen saturation of venous blood as it returns to the heart as measured at the vena cava, is optimized. If the ScvO2 is less than 70%, blood may be given to reach a hemoglobin of 10 g/dL and then inotropes are added until the ScvO2 is optimized. In those with acute respiratory distress syndrome (ARDS) and sufficient tissue blood fluid, more fluids should be given carefully.
Crystalloid is recommended as the fluid of choice for resuscitation. Albumin can be used if large amount of crystalloid is required for resuscitaition. Crystalloid solutions shows little difference with hydroxyethyl starch in terms of risk of death. Starches also carry an increased risk of acute kidney injury, and need for blood transfusion. Various colloid solutions (such as modified gelatin) carry no advantage over crystalloid. Albumin also appears to be of no benefit over crystalloids.
The Surviving Sepsis Campaign recommended packed red blood cells transfusion for hemoglobin levels below 70 g/L if there is no myocardial ischemia, hypoxemia, or acute bleeding. In a 2014 trial, blood transfusions to keep target hemoglobin above 70 or 90 g/L did not make any difference to survival rates; meanwhile, those with a lower threshold of transfusion received fewer transfusions in total. Erythropoietin is not recommended in the treatment of anemia with septic shock because it may precipitate blood clotting events. Fresh frozen plasma transfusion usually does not correct the underlying clotting abnormalities before a planned surgical procedure. However, platelet transfusion is suggested for platelet counts below (10 × 109/L) without any risk of bleeding, or (20 × 109/L) with high risk of bleeding, or (50 × 109/L) with active bleeding, before a planned surgery or an invasive procedure. IV immunoglobulin is not recommended because its beneficial effects are uncertain. Monoclonal and polyclonal preparations of intravenous immunoglobulin (IVIG) do not lower the rate of death in newborns and adults with sepsis. Evidence for the use of IgM-enriched polyclonal preparations of IVIG is inconsistent. On the other hand, the use of antithrombin to treat disseminated intravascular coagulation is also not useful. Meanwhile, the blood purification technique (such as hemoperfusion, plasma filtration, and coupled plasma filtration adsorption) to remove inflammatory mediators and bacterial toxins from the blood also does not demonstrate any survival benefit for septic shock.
If the person has been sufficiently fluid resuscitated but the mean arterial pressure is not greater than 65 mmHg, vasopressors are recommended. Norepinephrine (noradrenaline) is recommended as the initial choice.
Norepinephrine is often used as a first-line treatment for hypotensive septic shock because evidence shows that there is a relative deficiency of vasopressin, when shock continues for 24 to 48 hours. Norepinephrine raises blood pressure through a vasoconstriction effect, with little effect on stroke volume and heart rate. In some people, the required dose of vasopressor needed to increase the mean arterial pressure can become exceedingly high that it becomes toxic. In order to reduce the required dose of vasopressor, epinephrine may be added. Epinephrine is not often used as a first-line treatment for hypotensive shock because it reduces blood flow to the abdominal organs and increases lactate levels. However, one of the adrenaline side effects is that it reduces blood flow to abdominal organs and may cause increased lactate levels. Vasopressin can be used in septic shock because studies have shown that there is a relative deficiency of vasopressin when shock continues for 24 to 48 hours. However, vasopressin reduces blood flow to the heart, finger/toes, and abdominal organs, resulting in a lack of oxygen supply to these tissues. Dopamine is typically not recommended. Although dopamine is useful to increase the stroke volume of the heart, it causes more abnormal heart rhythms than norepinephrine and also has an immunosuppressive effect. Dopamine is not proven to have protective properties on the kidneys. Dobutamine can also be used in hypotensive septic shock to increase cardiac output and correct blood flow to the tissues. Dobutamine is not used as often as epinephrine due to its associate side effects, which include reducing blood flow to the gut. Additionally, dobutamine increases the cardiac output by abnormally increasing the heart rate.
The use of steroids in sepsis is controversial. Studies do not give a clear picture as to whether and when glucocorticoids should be used. The 2016 Surviving Sepsis Campaign recommends low dose hydrocortisone only if both intravenous fluids and vasopressors are not able to adequately treat septic shock. A 2015 Cochrane review found low-quality evidence of benefit, as did two 2019 reviews.
During critical illness, a state of adrenal insufficiency and tissue resistance to corticosteroids may occur. This has been termed critical illness–related corticosteroid insufficiency. Treatment with corticosteroids might be most beneficial in those with septic shock and early severe ARDS, whereas its role in others such as those with pancreatitis or severe pneumonia is unclear. However, the exact way of determining corticosteroid insufficiency remains problematic. It should be suspected in those poorly responding to resuscitation with fluids and vasopressors. Neither ACTH stimulation testing nor random cortisol levels are recommended to confirm the diagnosis. The method of stopping glucocorticoid drugs is variable, and it is unclear whether they should be slowly decreased or simply abruptly stopped. However, the 2016 Surviving Sepsis Campaign recommended to taper steroids when vasopressors are no longer needed.
A target tidal volume of 6 mL/kg of predicted body weight (PBW) and a plateau pressure less than 30 cm H2O is recommended for those who require ventilation due to sepsis-induced severe ARDS. High positive end expiratory pressure (PEEP) is recommended for moderate to severe ARDS in sepsis as it opens more lung units for oxygen exchange. Predicted body weight is calculated based on sex and height, and tools for this are available. Recruitment maneuvers may be necessary for severe ARDS by briefly raising the transpulmonary pressure. It is recommended that the head of the bed be raised if possible to improve ventilation. However, β2 adrenergic receptor agonists are not recommended to treat ARDS because it may reduce survival rates and precipitate abnormal heart rhythms. A spontaneous breathing trial using continuous positive airway pressure (CPAP), T piece, or inspiratory pressure augmentation can be helpful in reducing the duration of ventilation. Minimizing intermittent or continuous sedation is helpful in reducing the duration of mechanical ventilation.
General anesthesia is recommended for people with sepsis who require surgical procedures to remove the infective source. Usually inhalational and intravenous anesthetics are used. Requirements for anesthetics may be reduced in sepsis. Inhalational anesthetics can reduce the level of proinflammatory cytokines, altering leukocyte adhesion and proliferation, inducing apoptosis (cell death) of the lymphocytes, possibly with a toxic effect on mitochondrial function. Although etomidate has a minimal effect on the cardiovascular system, it is often not recommended as a medication to help with intubation in this situation due to concerns it may lead to poor adrenal function and an increased risk of death. The small amount of evidence there is, however, has not found a change in the risk of death with etomidate.
Paralytic agents are not suggested for use in sepsis cases in the absence of ARDS, as a growing body of evidence points to reduced durations of mechanical ventilation, ICU and hospital stays. However, paralytic use in ARDS cases remains controversial. When appropriately used, paralytics may aid successful mechanical ventilation, however evidence has also suggested that mechanical ventilation in severe sepsis does not improve oxygen consumption and delivery.
Early goal directed therapy (EGDT) is an approach to the management of severe sepsis during the initial 6 hours after diagnosis. It is a step-wise approach, with the physiologic goal of optimizing cardiac preload, afterload, and contractility. It includes giving early antibiotics. EGDT also involves monitoring of hemodynamic parameters and specific interventions to achieve key resuscitation targets which include maintaining a central venous pressure between 8–12 mmHg, a mean arterial pressure of between 65–90 mmHg, a central venous oxygen saturation (ScvO2) greater than 70% and a urine output of greater than 0.5 ml/kg/hour. The goal is to optimize oxygen delivery to tissues and achieve a balance between systemic oxygen delivery and demand. An appropriate decrease in serum lactate may be equivalent to ScvO2 and easier to obtain.
In the original trial, early goal directed therapy was found to reduce mortality from 46.5% to 30.5% in those with sepsis, and the Surviving Sepsis Campaign has been recommending its use. However, three more recent large randomized control trials (ProCESS, ARISE, and ProMISe), did not demonstrate a 90-day mortality benefit of early goal directed therapy when compared to standard therapy in severe sepsis. It is likely that some parts of EGDT are more important than others. Following these trials the use of EGDT is still considered reasonable.
Neonatal sepsis can be difficult to diagnose as newborns may be asymptomatic. If a newborn shows signs and symptoms suggestive of sepsis, antibiotics are immediately started and are either changed to target a specific organism identified by diagnostic testing or discontinued after an infectious cause for the symptoms has been ruled out. Despite early intervention, death occurs in 13% of children who develop septic shock, with the risk partly based on other health problems. Those without multiple organ system failure or who require only one inotropic agent mortality is low.
Treating fever in sepsis, including people in septic shock, has not been associated with any improvement in mortality over a period of 28 days. Treatment of fever still occurs for other reasons.
Recombinant activated protein C (drotrecogin alpha) was originally introduced for severe sepsis (as identified by a high APACHE II score), where it was thought to confer a survival benefit. However, subsequent studies showed that it increased adverse events—bleeding risk in particular—and did not decrease mortality. It was removed from sale in 2011. Another medication known as eritoran also has not shown benefit.
In those with high blood sugar levels, insulin to bring it down to 7.8–10 mmol/L (140–180 mg/dL) is recommended with lower levels potentially worsening outcomes. Glucose levels taken from capillary blood should be interpreted with care because such measurements may not be accurate. If a person has an arterial catheter, arterial blood is recommended for blood glucose testing.
Intermittent or continuous renal replacement therapy may be used if indicated. However, sodium bicarbonate is not recommended for a person with lactic acidosis secondary to hypoperfusion. Low molecular weight heparin (LMWH), unfractionated heparin (UFH), and mechanical prophylaxis with intermittent pneumatic compression devices are recommended for any person with sepsis at moderate to high risk of venous thromboembolism. Stress ulcer prevention with proton-pump inhibitor (PPI) and H2 antagonist are useful in a person with risk factors of developing upper gastrointestinal bleeding (UGIB) such as on mechanical ventilation for more than 48 hours, coagulation disorders, liver disease, and renal replacement therapy. Achieving partial or full enteral feeding (delivery of nutrients through a feeding tube) is chosen as the best approach to provide nutrition for a person who is contraindicated for oral intake or unable to tolerate orally in the first seven days of sepsis when compared to intravenous nutrition. However, omega-3 fatty acids are not recommended as immune supplements for a person with sepsis or septic shock. The usage of prokinetic agents such as metoclopramide, domperidone, and erythromycin are recommended for those who are septic and unable to tolerate enteral feeding. However, these agents may precipitate prolongation of the QT interval and consequently provoke a ventricular arrhythmia such as torsades de pointes. The usage of prokinetic agents should be reassessed daily and stopped if no longer indicated.
Severe sepsis will prove fatal in approximately 20–35% of people, and septic shock will prove fatal in 30–70% of people. Lactate is a useful method of determining prognosis, with those who have a level greater than 4 mmol/L having a mortality of 40% and those with a level of less than 2 mmol/L having a mortality of less than 15%.
There are a number of prognostic stratification systems, such as APACHE II and Mortality in Emergency Department Sepsis. APACHE II factors in the person's age, underlying condition, and various physiologic variables to yield estimates of the risk of dying of severe sepsis. Of the individual covariates, the severity of underlying disease most strongly influences the risk of death. Septic shock is also a strong predictor of short- and long-term mortality. Case-fatality rates are similar for culture-positive and culture-negative severe sepsis. The Mortality in Emergency Department Sepsis (MEDS) score is simpler, and useful in the emergency department environment.
Some people may experience severe long-term cognitive decline following an episode of severe sepsis, but the absence of baseline neuropsychological data in most people with sepsis makes the incidence of this difficult to quantify or to study.
Sepsis causes millions of deaths globally each year and is the most common cause of death in people who have been hospitalized. The number of new cases worldwide of sepsis is estimated to be 18 million cases per year. In the United States sepsis affects approximately 3 in 1,000 people, and severe sepsis contributes to more than 200,000 deaths per year.
Sepsis occurs in 1–2% of all hospitalizations and accounts for as much as 25% of ICU bed utilization. Due to it rarely being reported as a primary diagnosis (often being a complication of cancer or other illness), the incidence, mortality, and morbidity rates of sepsis are likely underestimated. A study of U.S. states found approximately 651 hospital stays per 100,000 population with a sepsis diagnosis in 2010. It is the second-leading cause of death in non-coronary intensive care unit (ICU) and the tenth-most-common cause of death overall (the first being heart disease). Children under 12 months of age and elderly people have the highest incidence of severe sepsis. Among people from the U.S. who had multiple sepsis hospital admissions in 2010, those who were discharged to a skilled nursing facility or long-term care following the initial hospitalization were more likely to be readmitted than those discharged to another form of care. A study of 18 U.S. states found that, amongst people with Medicare in 2011, sepsis was the second most common principal reason for readmission within 30 days.
Several medical conditions increase a person's susceptibility to infection and developing sepsis. Common sepsis risk factors include age (especially the very young and old); conditions that weaken the immune system such as cancer, diabetes, or the absence of a spleen; and major trauma and burns.
From 1979 to 2000, data from the United States National Hospital Discharge Survey showed that the incidence of sepsis increased fourfold, to 240 cases per 100,000 population, with higher incidence in men when compared to women. During the same time frame, the in-hospital case fatality rate was reduced from 28% to 18%. However, according to the nationwide inpatient sample from the United States, the incidence of severe sepsis increased from 200 per 10,000 population in 2003 to 300 cases in 2007 for population aged more than 18 years. The incidence rate is particularly high among infants, with the incidence of 500 cases per 100,000 population. Mortality related to sepsis increases with age, from less than 10% in the age group of 3 to 5 years to 60% by sixth decade of life. The increase in average age of the population, alongside the presence of more people with chronic diseases or on immunosuppressive medications, and also the increase in the number of invasive procedures being performed, has led to an increased rate of sepsis.
The term "σήψις" (sepsis) was introduced by Hippocrates in the fourth century BC, and it meant the process of decay or decomposition of organic matter. In the eleventh century, Avicenna used the term "blood rot" for diseases linked to severe purulent process. Though severe systemic toxicity had already been observed, it was only in the 19th century that the specific term – sepsis – was used for this condition.
The terms "septicemia", also spelled "septicaemia", and "blood poisoning" referred to the microorganisms or their toxins in the blood. The International Statistical Classification of Diseases and Related Health Problems (ICD) version 9, which was in use in the US until 2013, used the term septicemia with numerous modifiers for different diagnoses, such as "Streptococcal septicemia"., All those diagnoses have been converted to sepsis, again with modifiers, in ICD-10, such as "Sepsis due to streptococcus".
The current terms are dependent on the microorganism that is present: bacteremia if bacteria are present in the blood at abnormal levels and are the causative issue, viremia for viruses, and fungemia for a fungus.
By the end of the 19th century, it was widely believed that microbes produced substances that could injure the mammalian host and that soluble toxins released during infection caused the fever and shock that were commonplace during severe infections. Pfeiffer coined the term endotoxin at the beginning of the 20th century to denote the pyrogenic principle associated with Vibrio cholerae. It was soon realised that endotoxins were expressed by most and perhaps all gram-negative bacteria. The lipopolysaccharide character of enteric endotoxins was elucidated in 1944 by Shear. The molecular character of this material was determined by Luderitz et al. in 1973.
It was discovered in 1965 that a strain of C3H/HeJ mice were immune to the endotoxin-induced shock. The genetic locus for this effect was dubbed Lps. These mice were also found to be hypersusceptible to infection by gram-negative bacteria. These observations were finally linked in 1998 by the discovery of the toll-like receptor gene 4 (TLR 4). Genetic mapping work, performed over a period of five years, showed that TLR4 was the sole candidate locus within the Lps critical region; this strongly implied that a mutation within TLR4 must account for the lipopolysaccharide resistance phenotype. The defect in the TLR4 gene that led to the endotoxin resistant phenotype was discovered to be due to a mutation in the cytoplasm.
Controversy occurred in the scientific community over the use of mouse models in research into sepsis in 2013, when scientists published a review of the mouse immune system compared to the human immune system, and showed that on a systems level, the two worked very differently; the authors noted that as of the date of their article over 150 clinical trials of sepsis had been conducted in humans, almost all of them supported by promising data in mice, and that all of them had failed. The authors called for abandoning the use of mouse models in sepsis research; others rejected that but called for more caution in interpreting the results of mouse studies, and more careful design of preclinical studies. One approach is to rely more on studying biopsies and clinical data from people who have had sepsis, to try to identify biomarkers and drug targets for intervention.
Sepsis was the most expensive condition treated in United States' hospital stays in 2013, at an aggregate cost of $23.6 billion for nearly 1.3 million hospitalizations. Costs for sepsis hospital stays more than quadrupled since 1997 with an 11.5 percent annual increase. By payer, it was the most costly condition billed to Medicare and the uninsured, the second-most costly billed to Medicaid, and the fourth-most costly billed to private insurance.
A large international collaboration entitled the "Surviving Sepsis Campaign" was established in 2002 to educate people about sepsis and to improve outcomes with sepsis. The Campaign has published an evidence-based review of management strategies for severe sepsis, with the aim to publish a complete set of guidelines in subsequent years.
Some authors suggest that initiating sepsis by the normally mutualistic (or neutral) members of the microbiome may not always be an accidental side effect of the deteriorating host immune system. Rather it is often an adaptive microbial response to a sudden decline of host survival chances. Under this scenario, the microbe species provoking sepsis benefit from monopolizing the future cadaver, utilizing its biomass as decomposers, and then transmitting through soil or water to establish mutualistic relations with new individuals. The bacteria Streptococcus pneumoniae, Escherichia coli, Proteus spp., Pseudomonas aeruginosa, Staphylococcus aureus, Klebsiella spp., Clostridium spp., Lactobacillus spp., Bacteroides spp. and the fungi Candida spp. are all capable of such a high level of phenotypic plasticity. Evidently, not all cases of sepsis arise through such adaptive microbial strategy switches.
Septicemia... has been used... in a variety of ways... We therefore suggest that this term be eliminated from current usage.
We believe that adopting a more restrictive definition that requires further progression along the sepsis pathway may delay intervention in this highly time-dependent condition, with additional risk to patients.
We hope this editorial will clarify that the qSOFA is meant to be used to raise suspicion of sepsis and prompt further action—it is not a replacement for SIRS and is not part of the definition of sepsis.
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Schizophrenia is a severe mental sickness in which people depict reality abnormally. It may result in a consolidation of hallucinations, delusions, and intense disordered thinking and attitude that damage daily working, and can be wrecking. The accurate cause of schizophrenia is still unknown, but factors like genetics, environment, brain chemistry, and structure might play a crucial role. There are various types of schizophrenia, each of which is distinguished from the rest due to its unique characteristics.
Paranoid Schizophrenia is characterized by hallucinations and delusions, the person finds it difficult to differentiate between what’s real and what’s not. They face problems in leading a normal life. It is the most commonly diagnosed subtype of this chronic illness. Disorganized speech and disorganized behavior are some of the symptoms that develop during Paranoid Schizophrenia. This subtype can be controlled with medications and therapy, medications termed as the antipsychotics help to alleviate some of the major symptoms like delusions and hallucinations. If detected at an early stage, it can be controlled well, but if the person has reached the later stage, then hospitalization is essential.
Hebephrenic Schizophrenia also termed as the disorganized subtype of Schizophrenia. The inappropriate emotional response, false beliefs, false perceptions, inappropriate laughter, incoherent speech, and thought, etc. are its characteristics. It used to be considered as a subtype, but since 2013, it is no longer included under the heading Schizophrenia. A person suffering through this specific type finds it difficult to carry out daily activities like eating, showering, etc.
Catatonic Schizophrenia affects the way we move, i.e the patient will be mute and still or they might become hyperactive for no reason. A major sign that you are suffering from it is that you will not carry out motor activities normally even though you are physically capable of doing so. Other symptoms might include parroting other person’s behavior, sluggish response, staring, repeated movements, etc. It usually appears during the late teens or young adulthood. This disorder stays lifelong but through treatment, you can ease out its symptoms. We are yet to discover what exactly triggers this disorder but factors like a family history of schizophrenia, drugs, and alcohol addiction can play an important role.
The term Undifferentiated Schizophrenia is used when the patient demonstrates symptoms that fit into two or more subtypes of schizophrenia. Eg: The person suffering from this might display the symptoms of paranoid schizophrenia-like hallucinations and delusions. At the same time also demonstrate the symptoms of catatonic schizophrenia-like repeated movements, standing mute and still. The treatment includes medications, therapies, and support groups.
Simple Schizophrenia demonstrates symptoms such as lack of motivation, lack of initiative, apathy, avolition, low activity, etc. Use of the antipsychotic medications is usually the first line of treatment used. Delusions and hallucinations are not noticeable, and this disorder is less psychotic compared to the hebephrenic, paranoid, and catatonic subtypes.
Residual schizophrenia is a subtype of schizophrenia in which the person displays only negative symptoms of schizophrenia. To better understand this type, it is essential to know the difference between positive and negative symptoms of schizophrenia. Positive symptoms include hallucination, talking in a made-up language, delusions, inappropriate behavior, etc., whereas negative symptoms include lack of interest, flat or blunt emotions, lack of normal range of thoughts, etc. To be diagnosed with this disorder, people must display positive symptoms for at least six months. Once the positive symptoms disappear, negative symptoms will continue for some time. During this phase where only negative symptoms are displayed, a person is categorized as a residual schizophrenic.
People suffering from cenesthopathic schizophrenia encounter unusual bodily sensations. This subtype is majorly characterized by abnormal and strange body sensations, eg: the patient might feel as if he is coiled in wire, his body parts are burning, etc. 18% of the schizophrenic patients suffer from this particular subtype. This type is included in the category of ‘other schizophrenia’ according to ICD-10 but isn’t specifically defined. The word cenesthopathy is derived from the Greek word ‘koinos’ meaning feeling and ‘pathos’ meaning suffering.
Unspecified psychotic spectrum is diagnosis assigned to persons who are displaying symptoms of schizophrenia or any other psychotic symptoms but they fail to meet the entire diagnostic criteria or any other psychotic disorder. The symptoms generate stress and damage functioning in social, occupational, or other areas of functioning. In simple words, symptoms match the general conditions for a diagnosis but fail to fit into any of the categories. The treatment is conducted after a detailed analysis of the symptoms, the treatment includes therapy, counseling, and medications. This type is different from undifferentiated schizophrenia. In it, there is a combination of symptoms from two or more types. Whereas, unspecified subtype the symptom does not entirely meet any category.
Read Also: Different Types Of Insomnia. | <urn:uuid:4304113c-420c-4782-abfc-61e2a730d899> | {
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Hemophilia – the hemophilia
This leads to serious complications if those injured. Overall, the disease is divided into two major types, hemophilia A and B, and several subtypes of missing coagulation factor, of which human possesses several. However, the mechanisms of the different types are comparatively similar.
Name (s):Hemophilia; Hemophilia; royal diseaseType of disease: hereditary disease Distribution: Worldwide First mention of the disease: Circa 5th century in the Talmud treatable: treatable; but not curable Type of trigger: gene mutation How many sufferers: About 0; 01% of the world population Which specialist should you visit:GP; Pediatrician; orthopedist; Hämostaseologe; Specialist in human genetics ICD-10 code (s): D66; D67; D68
Hemophilia is a rare hereditary disease. The sex-linked X chromosome disorder manifests almost exclusively in males, although the genetic mutation causing the disorder is localized on the X chromosome and can be inherited from the mother of male children or the mother or father of female children.
This is because the trait is recessive, which means that only a properly functioning copy of the clotting factor gene is necessary for normal coagulation. Females have two X chromosomes and thus redundant copies of the blood coagulation factor gene.
A woman who inherits a mutated copy on an X chromosome has also inherited a second X chromosome from the other parent who probably carries an unmutated copy of the gene capable of directing a suitable coagulation.
Such a normal coagulation female, but possessing a single mutated copy of the gene, is called a carrier. Men have only one X chromosome inherited from their mother and have also received a Y chromosome from their father instead of a second X. If your only X chromosome contains the hemophilia mutation, unlike women, you will not have a second copy to ensure normal function.
Each child of a carrier has a 50% chance to inherit the mutation of his mother and afterwards to be a hemophile (son) or carrier (daughter). The daughter of a male hemophile will always inherit his mutation, while a son can never inherit it, as he receives the father’s Y chromosome, but not his X chromosome.
A woman is rarely affected by hemophilia when she inherits mutant X chromosomes from both a hemophiliac father and a host mother.
Haemophilia is transmitted through a defective X chromosome, although it does not necessarily occur recessively in every generation. In the following, carriers also pass on their genetic make-up to their own offspring, without being registered as a blood-man himself.
For this reason, the first signs are absolutely necessary to tell a doctor, so that the appropriate prophylactic steps can be initiated and the person concerned can be protected.
If the subject injures a blood vessel, he will notice the very slow or sometimes seemingly non-existent bleeding in the damaged body area. In addition, ad hoc bleeding occurs in many cases – usually without an obvious wound being perceived.
In this regard, those affected are colloquially referred to as hemophiliacs, which is to be found to a considerable extent in men. In the three stages of mild, moderate and severe, the patient denies his possible injuries due to the recessive inherited disease to varying degrees of stress.
Patients are always dependent on the use of coagulants in the case of major injuries, as otherwise, in the worst case, death can result from bleeding.
If a person suffers from hemophilia, then he can not be cured by this. Reversing a gene mutation is still not possible. Only a few alternative therapies that add blood clotting factors to the blood are possible. However, current research is working intensively on using genetic engineering to develop a remedy for hemophilia.
A hereditary disease
Haemophilia is one of the so-called hereditary diseases. This means that the problem that causes the disease is in the genes of the parents, which are then transferred to an embryo at fertilization. In hemophilia this affects the so-called X chromosome.
Female animals have two X chromosomes, whereas males have one X and one Y chromosome. Thus, when a female embryo arises, each of them gets a chromosome of mother and father. A male embryo in turn receives the Y- from the father and an X-chromosome from the mother.
Since the mutations that cause the disease hemophilia are X-linked recessive, a woman bearing the defect on one of her X chromosomes may not be affected because the equivalent allele on her other chromosome compensates for the mutation to generate necessary coagulation factors.
The affected mutation gene remains inactive in this sense. However, the Y chromosome in the male does not have a gene factor VIII or IX factor which is responsible for the two major types of hemophilia. If the genes responsible for the production of Factor VIII or Factor IX on a male X chromosome are absent, there is no equivalent on the Y chromosome to compensate for the mutation so that the deficient gene is not masked and the Disorder develops.
Since a man, as already mentioned, receives his single X chromosome from his mother, the male offspring of a healthy woman carrying the deficient gene in inactive form has a 50% chance of getting the gene from her and thus inheriting the disease. If, on the other hand, the intact and active X chromosome is passed on, the disease does not arise.
It is also possible, however, that the mother herself suffers from hemophilia, as both chromosomes are affected. Under these circumstances, the likelihood is 100% that the offspring will also contract hemophilia.
Therefore, hemophilia is much more common in men than in women. However, it may be possible for female carriers to become mild hemophiliacs by improper inactivation of the X chromosomes.
Hemophiliac daughters are currently more prevalent than previously, as improved treatments for the disease have enabled more hemophilic men to survive adulthood and become parents. Adult women may experience menorrhagia (severe periods) due to the tendency to bleed.
The pattern of heredity found in hemophilia is called cross-inheritance. This type of pattern is also found, for example, in color blindness, which also occurs much more frequently in men than in women.
A mother who is a carrier has a 50% chance of passing the defective X chromosome to her daughter, while a concerned father always passes the affected gene to his daughters. Since the mutation is recessive and non-dominant, the healthy gene will subsequently correct the mutation.
A son can not inherit the defective gene from his father because he receives a Y chromosome from him. Genetic testing and genetic counseling is recommended for families with hemophilia. Prenatal tests, such as amniocentesis, are available to pregnant women who may be carriers of the disease.
Spontaneous or inherited
Of course, as with all genetic disorders, it is also possible for a human to acquire them spontaneously through mutation, rather than receive them from the parents when they are raised by heredity.
Spontaneous mutations account for about one third of all hemophilia A cases. About 30% of cases of hemophilia B are also the result of a spontaneous gene mutation. When a woman gives birth to a hemophilic son, either the woman is the carrier of the blood disease or hemophilia is the result of a spontaneous mutation.
Until modern direct DNA testing, however, it was impossible to determine if a woman with only healthy children was a carrier or not. In general, the healthier she was, the higher the likelihood that she was not a wearer.
If a man has been infected with the disease and has children with a woman who is not the mother of the mutation, his daughters will be carriers of haemophilia. His sons, however, will not be affected by the disease. The disease is X-linked and the father can not pass hemophilia through the Y chromosome.
Persons with less than one percent active factor are classified as severe hemophilia sufferers, those with one to five percent active factor have moderate hemophilia and those with mild hemophilia even up to 40% of the normal level of active coagulation factors.
In the following hereditary disease, the patient suffers from a reduced coagulation function of his own blood.
What is hemophilia??
Hemophilia, also commonly referred to as hemophilia, is a mostly inherited genetic disorder that interferes with the body’s ability to produce blood clots. Consequently, these people are not given a process that causes bleeding to be stopped.
As a result, people will bleed longer after an injury, have more bruising, and be at increased risk for bleeding in the joints or brain. Those who suffer from a mild variant of the disease may have symptoms only after an accident or during surgery.
The strong course leads to more serious restrictions in everyday life. Hemorrhaging into a joint can cause permanent damage, while bleeding in the brain can lead to long-term headaches, seizures, or a decreased state of consciousness.
There are two main types of hemophilia, referred to as hemophilia A and B, which were determined in 1952: The Hemophilia A, which occurs due to the low coagulation factor VIII, and the Hemophilia B, which arises due to the low coagulation factor IX.
Both species are typically inherited from parents via an X chromosome with a non-functional gene. Rarely, a new mutation can occur during early development.
Still more rarely does hemophilia occur later in life due to antibodies that form against a coagulation factor. Other types of this disorder include hemophilia C, which develops due to insufficient factor XI, and parahemophilia, which occurs due to insufficient factor V..
Acquired hemophilia is associated with cancer and various autoimmune diseases. The diagnosis is that the blood is tested for coagulability and coagulation factors.
prevention & cure
An actual prevention In terms of hemophilia, there is no, because it is an inherited gene mutation that can not be corrected in retrospect. It is only possible during pregnancy to have the embryo tested for coagulation factors.
If the results point to this disease, then an abortion is possible. However, many doctors do not recommend this because the progress of medicine can enable a partially normal everyday life even with this disease.
The cure hemophilia is not yet possible. But there are different therapeutic approaches. As a rule, the treatment by replacing the missing blood coagulation factors. This can happen regularly or during bleeding episodes.
The replacement can take place at home or in the hospital. The coagulation factors are produced in this method either from human blood or from recombinant proteins (factors produced by genetic engineering). However, up to 20% of people develop antibodies to coagulation factors, which makes the treatment extremely difficult.
In addition, that can drug Desmopressin can be used in patients with mild hemophilia A. There are also a number of studies in the field of genetic engineering that deal with haemophilia. The first experiments with humans were already carried out here and were quite successful.
Overall, hemophilia is one of the comparatively rare hereditary diseases. For one thing, in the majority of cases it occurs only in men. On the other hand, the gene mutation per se is rather rare.
Since hemophilia A and B are both X-linked recessive disorders, women are rarely severely affected, as previously noted. However, some women with a non-functional gene on one of the X chromosomes may be mildly symptomatic.
An exception forms Hemophilia C. It occurs equally in both sexes. Studies have found that this disease is predominantly found in people who are descendants of Ashkenazi Jews.
In the 19th century, this disease was particularly well known. This was based on the fact that haemophilia was common within the royal families of Europe. This is the basis for the common name of hemophilia as a royal disease.
causes & formation
The hemophilia causes vary depending on which type it is. Therefore, a distinction is made in the causes and the origin between hemophilia A and B as well as the subtypes (eg hemophilia C).
Haemophilia A is inherited as an X-linked recessive trait. It occurs in men and in homozygous women. This means that the disease only occurs in females if the father is hemophilic, ie has a damaged X chromosome, and the mother is also the carrier of the disease and has also passed on a mutated gene to the daughter.
However, it is known that mild hemophilia A can also occur in heterozygous women in whom the mutant gene does not become completely inactive. Therefore, it is recommended that levels of Factor VIII and IX be measured prior to surgery and for clinically significant bleeding in all known or potential carriers.
About 5-10% of people with hemophilia A are affected because they produce a dysfunctional version of the factor VIII protein. The remainder of the disease is affected by this disease because factor VIII is produced in insufficient quantities. Consequently, there is no qualitative but quantitative shortage here.
Of those patients who have a severe form of hemophilia A that has less than one percent of active Factor VIII, about half have the same mutation. It is an inversion within the factor VIII gene that leads to complete elimination of protein production.
In contrast to hemophilia A, the concerns Hemophilia B Factor IX of blood clotting. The Facto IX gene is also located on the X chromosome. Its mutation also corresponds to an X-linked recessive trait, which explains why almost only men are affected.
In 1990, some physicians showed that two genetic mutations prevent two key proteins from clinging to the DNA of people with a rare and unusual form of hemophilia B. These people have excessive bleeding during childhood.
However, these bleeding problems decrease after puberty. This lack of protein attachment to the DNA knocked out the gene that produces coagulation factor IX, which prevents excessive bleeding.
Factor IX deficiency leads to an increased tendency to bleeding, either spontaneously or in response to mild trauma. Factor IX deficiency can lead to disruption of the coagulation cascade and trauma to spontaneous bleeding.
Factor IX becomes active during coagulation by cofactor factor VIII. Platelets provide a binding site for both cofactors. Finally, Factor IX, when activated, activates factor X, which promotes the conversion of fibrinogen into fibrin, which are essential elements of wound closure and are often referred to as the coagulation substrate.
In addition to haemophilia A and B, there are some more subtypes, which can influence the specific genes in different ways and thus inhibit the coagulation factors. This includes, for example, the Hemophilia C, also known as plasma thromboplastin antecedent deficiency or Rosenthal syndrome.
It is a mild form of hemophilia affecting both sexes due to a factor XI deficiency. This form concerns a specific gene mutation that predominantly occurs in Jewish people of Ashkenazi descent.
Hemophilia C is caused by a lack of coagulation factor XI and differs from hemophilia A and B in that it does not lead to bleeding into the joints.
In addition, it has an autosomal recessive inheritance, since the gene for factor XI is located on chromosome 4 (near the prekallikrein gene, and thus it is not completely recessive.) In contrast to other hemophilia, individuals can also be found are heterozygous, show an increased bleeding tendency.
An exact cause of hemophilia C does not exist. Here are various mutations in question, which can be acquired in the course of life. Comparatively many mutations exist and the risk of bleeding is not always affected by the severity of the deficiency. Hemophilia C is occasionally developed in patients with systemic lupus erythematosus due to inhibitors of the FXI protein.
However, a single mutation is not responsible here. Rather, the various forms of hemophilia can be caused by a variety of different mutations. The result is always a lack of a certain factor, which is decisive for the blood clotting.
For this reason, initial diagnosis is usually done by measuring protein activity rather than genetic testing, although genetic testing is recommended for family members as soon as a known case of hemophilia has been identified.
About one third of patients have no family history. Therefore, the disease does not arise as a hereditary disease, but it is suspected that subsequent or spontaneous mutations are responsible for the disease.
symptoms & sign
Characteristic symptoms of hemophilia usually vary with the severity. In general, the symptoms are internal or external bleeding episodes that are simply called bleeding.
People with severe hemophilia experience significantly heavier and more frequent bleeding, while people with mild hemophilia usually have minor symptoms, such as after surgery or severe trauma. In moderate hemophilia symptoms vary and may manifest in a spectrum between severe and mild forms.
By both Hemophilia A and B there is spontaneous bleeding, but a normal bleeding time, an average prothrombin time, a normal thrombin time, but prolonged partial thromboplastin time. Internal bleeding is common in people with severe hemophilia and in some people with moderate hemophilia.
The most characteristic Type of internal bleeding is a joint bleeding in which blood enters the joint space. This is most common in severe hemophiliacs and can occur spontaneously without obvious trauma. If these patients are not treated promptly, joint bleeding can result in permanent joint damage and disfigurement.
Bleeding in the soft tissues such as muscles and subcutaneous tissue are less severe, but can cause damage and must also be treated.
children & baby
children with mild to moderate haemophilia may have no signs or symptoms at birth, especially if they are not pruned. Their first symptoms are often frequent and large bruises and hematomas, which arise as a result of falls when learning to walk. It also causes swelling and bruising due to bleeding in the joints, soft tissues and muscles.
Children with mild hemophilia may not have any noticeable symptoms for years. Often the first sign of very mild hemophilia is heavy bleeding during a dental procedure, accident or surgery.
women, The carriers are usually have enough coagulation factors from their normal gene to prevent serious bleeding problems, though some may appear as mild bleeding. Here only symptoms appear, if surgical interventions are made or serious injuries exist.
Depending on severity
It can be seen later that haemophilia, regardless of type, can lead to internal and external bleeding episodes. Depending on the severity of the disease and the number of functional coagulation factors, these only occur as a result of injury or entirely spontaneously.
In people who have one mild form of hemophilia and have about 40% active coagulation factors, shows only after major surgery and injuries increased bleeding tendency.
Patients who have a sdifficult course form can suffer from sudden bleeding. This also means that there is no way to prevent them or, if necessary, to prepare for a bleeding episode. If a person has moderate hemophilia, a combination of the common symptoms may occur. Here, for example, show faster hematomas and it comes simultaneously to bleeding in the joints. But a complication-free life is possible and bleeding episodes occur spontaneously in mild trauma.
The specific symptoms of hemophilia are therefore a significantly longer bleeding and at the same time a bad wound healing. As an early indication is for example a longer bleeding by venipuncture or heel bruise.
inwardly & externally
Bleeding can theoretically occur anywhere in the body, superficial bleeding, such as those caused by abrasions or shallow cuts, can persist longer in terms of healing time, and the scab can be easily broken due to the lack of fibrin, which in turn can lead to re-bleeding.
Superficial bleeding can be annoying. However, they do not represent an actual danger to the patient. Only in the case of a large number of cuts or bruises can relatively much blood be lost.
Then the patient may show symptoms of anemia or iron deficiency. Tiredness, pain in the muscles and joints as well as breathing problems and indigestion are the result.
at internal bleeding Of course, the situation is completely different. Here, bleeding episodes, especially if they occur spontaneously, can be dangerous and life-threatening. As a rule, the joints, muscles, digestive tract and brain are affected.
Muscle and joint bleeding, which as hemarthroses are always indicative of hemophilia, while gastrointestinal bleeding and cerebral hemorrhage are also relevant to other coagulation disorders.
Repeated bleeding into an articular capsule can cause permanent joint damage and disfigurement, leading to chronic arthritis and disability. Joint damage is not caused by blood in the capsule but by the healing process.
When the blood in the joint is broken down by enzymes in the body, the bone in that area is also broken down, causing a lot of pain to the person affected by the disease. Depending on which parts of the body are still affected by bleeding, it can also lead to many other possible symptoms that result from the functional impairment of the organs.
diagnosis & examination
Until a few years ago, a person could only be screened for symptoms of hemophilia if they had already occurred. Today it is possible thanks to genetic testing, the disease probability to determine before a pregnancy. However, there are other diagnostic procedures. These depend primarily on whether a history exists and when the first symptoms begin.
So hemophilia can be in front, while or after birth be diagnosed. If a family history exists, parents have several options to choose from. For example, it is possible to find out about the hemophilia and the likelihood of its occurrence in the offspring before pregnancy.
Genetic tests and a consultation through a Specialist in human genetics are available to determine the risk of transmitting the disease to a child. As a rule, an examination of both parents is carried out here, on the one hand checking the coagulation factors in the blood and, on the other hand, detecting gene defects by means of a tissue sample.
Shows up at the mother a carrier gene, there is a 50% chance that either a hemophiliac carrier or a hemophile will be born. Own one man a mutated X chromosome, he is hemophilic himself. Then a possible daughter 100% even the mutated gene received. On son however, the Y chromosome inherits and is not affected by the disease afterwards.
To have both parents a mutated X chromosome, which is comparatively rare, there is still a 50% chance that the son Hemophilia will suffer. A daughter would be 100% self-carrier of the mutation, but can also suffer 50% of the disease, as it inherits a mutated gene from the mother.
A human geneticist will always educate about these possibilities. Afterwards, parents learn before they can conceive to what extent the future child could be hemophilic.
But even during pregnancy, a woman in whose family haemophilia is common, can be tested on these. One of the common tests is, for example, the chorionic villus sampling. A small sample of the placenta is removed from the uterus and usually tested for hemophilia during weeks 11 to 14 of pregnancy.
But it is also one amniocentesis possible. Amniocentesis, also known as amniocentesis, is usually performed during weeks 15 through 20 weeks of gestation. In this case, liquid is taken with a cannula directly from the amniotic sac, in which cells of the embryo are located.
An amniocentesis is now a relatively frequent procedure. Nevertheless, there is a risk of miscarriage or premature labor, as a result of premature birth.
Whether afterwards Amniocentesis makes sense, should be discussed with the treating gynecologist. In those cases where it has been shown during pregnancy that the fetus will suffer from a severe form of hemophilia, a woman may have over one abortion think. However, most doctors advise against this, because thanks to modern medicine for hemophilia patients a relatively normal life is possible.
A hemophilia test is also possible after birth. Here can blood directly from the umbilical cord can be tested, which can be tested directly after birth, if hemophilia is present. This procedure is usually appropriate if there is a family history and no pregnancy test was performed during pregnancy for safety reasons.
The decisive factor is whether the coagulation factor IX (B), XI (C), V (paraphilia) or VIII (A) is affected. Finally, the number of coagulation factors present can also be recognized. In this way it can be determined how severe the hemophilia will be afterwards.
Severe haemophilia is present when there is less than one percent coagulation factors, moderate hemophilia results from approximately five percent active factors, and mild disease consists of five to forty percent of functional coagulation factors.
In addition to the hereditary variant sometimes acquired hemophilia also occurs. Decisive here can be an autoimmune disease, a cancer but also a birth.
Then of course one Genetic test provide hardly meaningful results. Here also a blood test is carried out. As a rule, a reduction in the active factor V or VIII is shown. In addition, there is sometimes evidence of antibodies advisable against these factors in the blood.
If hemophilia is mild, it may not be diagnosed until surgery or injury bleeding occur.
Obviously the sufferer suffers from haemophilia if he is too many and too long bleeding symptoms inclines. With only a small wound, the blood seems to exit the wound without stopping, which can turn out to be a major problem for large or deep injuries.
If the care or the medical care is not given immediately, the body can lose so much blood in such a short time that on the one hand the consciousness of the affected person is disturbed and on the other hand important body and circulatory functions can not be maintained to the extent it the normal case estimated.
Less problematic in the shallow stages, but nevertheless become omnipresent to those suffering from hemophilia spontaneous bleeding which, however, heal quickly and sometimes even almost unnoticed. Despite the occurrence of symptoms of possible hemorrhages on the whole body, the joints in those affected show as the primary indicator of such genetic disease.
After an accident or trauma, there is often an initial bleeding in the areas of the large joints. To stabilize this body region, the body compresses that site with more vascular systems. Actually counterproductive for the future, this measure proves to be a strong potential for further joint bleeding.
wounds & hematomas
at lacerations, but also at Scraping and cutting wounds, is to register a cover by the platelets in the first moments. In the course of apparent healing, however, blood breaks through the crust again and again and thus maintains the flow of effusion and prevents the healing – the pressure in the blood vessels pulsates the blood repeatedly through the newly formed protective layer and is noted as striking permanent tearing.
Close-up of a hematoma
Shutterstock / Stephane Bidouze
This process is also followed by another feature of the disease – the hematoma. Even without external action, this pressure on the wound or in the case of non-open injuries of the small capillaries can cause subcutaneous or intramuscular bruising. These are now increased in the body of those affected and often seen.
In addition, as a result of this dysfunction there is a risk of internal bleeding, so that obstruction of the urinary tract due to thrombi or renal bleeding can be diagnosed with concomitant colic.
According to the stages It can lead to simple hemorrhages, hematomas with concomitant pain or even above-average nosebleeds. In particular, female patients could also complain of greater menstrual bleeding or the increased formation of bruises – especially in so-called medical trivial and especially in childbirth these signs are correct to interpret.
at children the carry-over of the coagulation cascade can be noticed, especially in developing age, by joint bleeding or apparently suddenly broken wounds.
Furthermore, the symptoms also leave on the Von Willebrand disease or that Owren syndrome conclude – a test for hypoproacelioma should also be considered.
Due to regular bleeding – and in addition usually accompanying inflammation – it can lead to significant joint stiffness. Because this form of osteoarthritis – one speaks of hemarthrosis – may be related to surgery on the elbow, knee, shoulder or ankle.
In addition, it can be more dangerous if the areas of the skull are integrated into the bleeding character – here urgent medical advice must be sought.
frequency & statistics
Although haemophilia, often called hemophilia, is known to most people, it is still a very rare hereditary disease. It is assumed that worldwide only 0.01% the population of Hemophilia A and 0.04% of hemophilia B are affected.
In most cases, these are males, because the disease is inherited via the X chromosome. women can compensate for such mutations by another X chromosome and develop thereafter no disease. Of course, this is not possible for men.
How much women currently suffering from hemophilia is not known. This also applies to the possible presence of a mutated gene in women. Since the disease does not break out here, women may not know that they carry the blood, and thus can pass it on.
For this reason, annually about 1000 people born with hemophilia. The numbers, however, may well deviate from reality. This is mainly due to the fact that in other countries there is no adequate documentation of hemophilia and especially mild forms are not always diagnosed.
ancestry & countries
However, in contrast to other countries, in Germany predominantly the so-called Hemophilia A which leads to a greater tendency to hemorrhage than haemophilia B. Therefore, only one third of those affected worldwide are affected by severe haemophilia.
It has been assumed for some time that certain ethnicities be predisposed to the occurrence of hemophilia. For example, Ashkenazi Jews, mainly from Northern or Eastern Europe, as well as some tribes of Finland are much more affected by haemophilia than other people.
However, this can not be attributed to specific gene variants in these people, but rather to coincidences as well as a specific partner choice within closed communities, which have subsequently favored a transfer.
Therefore, two categorical hemophilia are to be distinguished, whereby variant A can only occur in male subjects due to an X chromosome defect as hereditary coagulation defect. Women have a balance due to their second X chromosome.
The lack of antihemophilic globulin now causes the partially grueling phenomena. The second form of hemophilia, meanwhile, will cause only very slow blood clotting due to the deficit of the Christmas factor.
Furthermore, a very rare autosomal coagulation defect – depending on the autosomes and therefore not gender specific – can occur, which also causes an enlargement of the coagulation cascades.
With the existence of potential intermediate forms such as parahemophilia due to a lack of coagulation factor or Angiohämophilie together with reduced carrier protein for the coagulation factor, it is necessary to force the individual diagnosis.
Even the simplest forms of tripping or kinking may mean a new hemorrhage for the hemophiliac patient, which, depending on its extent, may possibly be treated again by a doctor.
Likewise, stretching the neck while sleeping at night is a cause of bleeding. Serious accidents and inflammations of the body cause a corresponding sensitivity through increased vascularization – paradoxically, that these lay the foundation for frequently occurring, more or less extensive, bleeding.
In addition, an experienced trauma can cause a muscle bleeding, this form is less common, but also more devastating. Should it come to a muscle bleeding, the patient is confronted with a very high probability of crippling the tissue.
It becomes dangerous for the subject when forearm or calf muscle should be affected. For this reason, hemophiliacs should receive all vaccinations strictly subcutaneously and not intramuscularly.
complications & consequences
Hemophilia, of course, causes discomfort when bleeding occurs. Overall, however, serious complications are only to be expected, even if there is severe or moderate hemophilia. After this, complications may arise from the disease itself or the appropriate treatment.
As an essential and relatively common complication occur deep internal bleeding on. These include, for example, deep muscle bleeding. These usually lead to severe swelling, numbness or body aches. But also bleeding in organs are possible.
A particular problem arises especially if this is the case brain is affected. A intracranial hemorrhage is a serious medical emergency caused by the build-up of pressure in the skull, which forms when blood accumulates under the skull. This can cause disorientation, nausea, loss of consciousness, brain damage and even the death of the person affected.
Frequently in terms of hemophilia is also the so-called hemarthrosis, So a haemophilic arthropathy. Here, blood enters the joints and gradually destroys the cartilage. If the hemorrhage does not drain early, ie is drained off, the joint capsules become inflamed and synovitis develops. Iron can also accumulate in the joints as a result of the influence of blood, which in turn leads to signs of inflammation.
The immune response to the inflammatory processes and the permanent iron deposition also stimulates angiogenesis (cleavage of blood vessels), which can ultimately destroy cartilage and bone completely. This manifests itself not only in severe pain, but also in disfigurements of the affected joint regions, curvatures and progressive paralysis.
In addition to the complications that arise from the disease itself, but also show serious side effects of various treatment methods. For example, it is common practice for affected individuals to receive clotting factors via human blood during the periods of bleeding.
In such transfusions it has come several times to various infections. These result from the frequency of transfusions themselves, but also from impurities in the blood.
Although rigorous testing is testing the donor blood for various infectious agents, it has come to devastating disease transmission throughout history. For example, in the 1980s, donor blood transmitted HIV. But also infections with herpes are possible.
Research is currently underway on whether cancer cells, which can be found in the blood, especially in metastatic cancer, after a transfusion in the body of the recipient spread and there can also lead to metastases. Clear results are not yet available.
Most physicians also rate the likelihood of such cancer cell transmission as relatively low. Absolute security, however, does not exist in transfusions of foreign blood.
Other side effects also arise when the body has a coagulation factor immune response There are antibodies against coagulation factors are formed. This makes the factors significantly less effective.
In addition, the frequent Immune reaction contribute to a weakening of the patient’s health. This is especially unfavorable when there is an acute bleeding episode.
Overall, the complications of hemophilia are known and are well considered by the treating physicians during a therapy. However, it is imperative that one regular examination of hemophilia patients takes place and first symptoms of hemorrhage are immediately examined and treated. In addition, a therapy should always be accompanied by a doctor.
When to the doctor?
When should you go to the doctor?
Here you can seek advice from a human geneticist or haemostaseologist to have specific tests done and then determine the risk of a child developing hemophilia. This can certainly play a role in the decision for a child.
In addition, it is also advisable for a woman expecting a child to consult a gynecologist with questions about hemophilia insofar as the child’s producer is hemophilic or has a family history of hemophilia. Here it is also possible to perform tests before birth that provide certainty about the health status of the child. Such tests are also possible after birth.
A doctor should also be consulted if a child shows an increased tendency to bleed. This means that, especially at the stage of life in which the child is learning to walk, hematomas are much faster and the bruises are unusually large.
In some cases, acquired hemophilia is also possible. The symptoms are initially less pronounced. However, it is worthwhile to contact a doctor if it is noticed that bruises are significantly larger and heal cuts and scrapes very badly.
In addition, it is of course advisable to seek medical help immediately if complications with the disease occur. These include, for example, joint pain, severe fatigue, muscle aches, headache, drowsiness and diminished consciousness. Doctors, such as dentists, should also contact a specialist if a patient has an increased tendency to bleed.
treatment & therapy
There is no long-term cure for hemophilia. Thereafter, the treatment is for the symptoms of gene mutation and is essentially done by replacing the missing blood coagulation factors.
Coagulation factors can be supplied by transfusion of foreign blood or by chemically prepared combination preparations. Factor replacement can thus be isolated from either human blood serum, recombinant or a combination of the two.
Commercially produced factor concentrates, such as a recombinant factor VIII, come in powder form into an ampule which must be mixed with sterile water prior to intravenous injection. Finally, this mixture is passed via a transfusion into the bloodstream of the patient.
Such coagulation factors are usually not needed in mild hemophilia. In moderate hemophilia, coagulation factors are typically used only when bleeding or bleeding is to be prevented in certain events, such as surgery.
For severe hemophilia, preventive use is often recommended two or three times a week and can be continued for life. The rapid treatment of bleeding episodes reduces the overall damage to the body.
Of course, the factors that are administered via blood or combination will depend on the underlying condition. Factor VIII is in the presence of hemophilia A and Factor IX used in hemophilia B.
Some people develop during a therapy antibody against the surrogate factors that are given to them so that the amount of the factor must be increased or nonhuman substitutes must be administered.
If a person reacts refractory to the replacement coagulation factor due to circulating antibodies, this can be partially overcome with recombinant human factor VII.
However, coagulation factors of other organisms are also suitable. Is often used as well as the Factor VIII from the pig. At the beginning of 2008, a haemophilic factor was also approved in America, consisting of the genes of Chinese ovary cells Hamsterart was extracted.
This sounds unusual at first. However, research into hematopoietic blood formation has been going on since the 1980s. This is intended, inter alia, to prevent anemia in dialysis patients.
countries & risks
In most countries, factor products are comparatively easy to obtain and are now a relatively safe treatment method. While products with a recombinant coagulation factor provide greater purity and safety, as a concentrate they are extremely expensive and not generally available in developing countries.
In many cases, factor products are of any kind in developing countries difficult to obtain.
In addition, regardless of the fact that regular screening of the samples and transfusions are performed under sterile conditions, transfusions do indeed result risks.
In addition to rare bacterial transmissions, allergic reactions and the transmission of harmful lymphocytes, for example, an iron storage in long-term transfusions is not uncommon.
This can be followed by a hemochromatosis form. For this reason, it is advised to start regular treatment only when symptoms of haemophilia appear.
drugs & medicines
In addition to the transmission of coagulation factors, there are a number of drugs, which can be used to treat mild hemophilia. Among other things, desmopressin, a synthetically produced protein, can be used in patients with mild hemophilia A. Tranexamic acid or epsilonaminocaproic acid may be co-administered with coagulation factors to prevent the breakdown of clots.
Essential elements of a hemophilia treatment also provide Painkiller, steroids and physical therapies They are mainly used to treat pain and swelling after joint bleeding.
In addition, it is mostly tried by means of drains remove the excess blood from the joints to prevent damage to the cartilage and joint capsule.
However, there are also some medications that can be quite dangerous when taken by hemophilia: Anticoagulants such as heparin and warfarin are for people with hemophilia contraindicated, as these can increase the coagulation difficulties.
Also contraindicated are those drugs that blood thinning side effects to have. For example, medicines containing aspirin, ibuprofen, or naproxen sodium should not be taken, as they are known to have a prolonged bleeding time as a common side effect.
With the administration of the missing Coagulation factor Hemophilia can be counteracted extremely efficiently and with little stress for the patient. Without major restrictions on everyday life, the therapy is thus primarily prophylactic. Required proteins are embedded here from the purified blood of various canned foods and blood stores to the individual physical needs of the subject.
Despite advanced medicine, it is recommended that body-weighted and distressing sports how to avoid athletics or martial arts.
The hemophilia certainly attracts some anatomical consequences with himself. In favorable cases, orthopedic devices such as special shoes or walking aids are enough for coping with everyday life. Nevertheless, there are some cases where one surgery and thus a joint replacement remained essential.
Due to potentially possible abnormalities In terms of bone structure or muscle, hemophilia can also result in lengthy physiotherapy for the patient. According to recent findings, a cure of hemophilia is not possible.
However, the medical options allow those affected almost uninfluenced life with the disease. On-demand treatment after the onset of a symptom or continuous treatment with intravenously injected factor concentrate is determined by the attending physician according to personal needs.
Overall, the treatment methods has been increasingly improved over the past decades. For this reason, sufferers can often lead a relatively normal life.
In addition, there are several research projects, who deal with new forms of therapy or a simplification of current therapies.
The most promising tests are shown here Genetic Engineering. Here, for example, mutated genes are to be repaired, so that afterwards a normal coagulation factor production should be possible.
However, most approaches to gene therapy are currently still in the pipeline phase of development. In the coming years, however, this could bring about new treatments or even a cure.
Hemophilia Prevention – Possible prevention measures
An actual prevention of hemophilia is of course not possible. After all, it is a hereditary disease that occurs independently of one’s own behavior insofar as the responsible mutation gene was inherited.
However, there are ways that Prevent spread of the disease. If a person has noticed that in the family history several persons were born with haemophilia or they themselves suffer from this disease, then a human geneticist can be visited. Together with the partner, he uses genetic tests to calculate the likelihood that offspring will develop hemophilia.
Subsequently, it is up to the parents to decide whether to give up their own children or risk their child’s illness. However, with hemophilia quality of life, as well as their average life expectancy, is minimized thanks to modern treatments, avoidance of pregnancy in the case of hemophilia risk is not mandatory.
Other preventive measures concern the stability of the health of those affected. This includes, for example, that none Painkiller be taken. Especially aspirin and ibuprofen, which are available without a prescription and are often consumed by many people, are considered dangerous for people with hemophilia.
In addition, in hemophilia are also contraindicated activities with a high probability for diverse trauma and injury, like motorcycling and skateboarding.
Popular sports with a lot of physical contact with others and an increased risk of injury such as American football, hockey, boxing, wrestling and rugby or certain martial arts should rather not be operated by people with hemophilia.
Other active sports such as football, baseball and basketball also have one high injury rate, However, all in all, they have less contact with players who may end up traumatized and may be treated with caution and only in consultation with a doctor.
suitable However, for people with hemophilia, sports activities that spare the body and prevent serious injury are unlikely. For this example, swimming is suitable. This sport is also considered gentle on the joints, which can be beneficial for hemophilia patients who have already bleeding into the joints and are therefore physically limited.
Prognosis for healing
At this point, it should first be noted that hemophilia is still not curable and only the symptoms can be treated. As with most aspects of the disease, life expectancy varies according to severity and adequate treatment.
People with severe hemophilia who do not receive adequate, modern treatment have a much shorter lifespan and often do not reach sexual maturity. Before the 1960s, when effective treatment was not yet available, the average life expectancy was only 11 years.
In the 1980s, the life expectancy of the average hemophiliacs who received appropriate treatment was already 50 to even 60 years. Today, haemophiliacs with appropriate treatment typically have a near-normal quality of life with an average lifespan that is only about 10 years shorter than that of an unaffected man.
However, people who have only a mild form of hemophilia are not limited in terms of their quality of life and life expectancy. Often no preventive therapy is necessary here.
Replacement factors intended to cause coagulation are given to such patients on their own prior to surgery or acute injury. As a result, these people are not confronted with the side effects of frequent blood transfusions.
causes of death
Since the 1980s, the primary cause of death of people with severe hemophilia has become bleeding contagions with HIV or AIDS or others infectious diseases postponed. These are caused by a treatment with contaminated blood products.
Even today, despite the screening and testing of blood samples, particularly in countries with low safety standards, contaminated samples can be administered. In Germany this is comparatively unlikely. However, it is always possible that still unknown pathogens are passed on by means of transfusion.
Healthy liver and liver with cirrhosis
The second most frequent cause of death in severe hemophilia complications is the intracranial hemorrhage, which today accounts for one-third of all deaths in people with hemophilia.
Two other major causes of death Blocking are airways for internal bleeding as well as hepatitis infections that lead to cirrhosis of the liver.
Two studies conducted in the Netherlands have investigated hemophilia patients over a period of several years. Both studies found that viral infections were common in hemophiliacs due to frequent blood transfusions. The life expectancy of men was about 59 years.
On the other hand, if no viral infection was transmitted, patients could become around 75 years old. However, these statistics for the prognosis are unreliable as a significant improvement in the control of infection and the efficacy of antiretroviral drugs has been reported since these studies were conducted. Overall, the prognosis for hemophilia is therefore good in western countries.
History of hemophilia
Although haemophilia is a very rare hereditary disease, it is still known to most people, at least as hemophilia. It is also quite common in the media and is featured in medical series or historical films.
This is probably due to the relatively interesting history of this disease. The first mentions of hemophilia are already evident in the fifth century in the Talmud.
10 – 18 century.
Specifically, the suffering is described later by the Andalusian doctor Abulcasis, who has become known mainly for his invention of surgical instruments for Kautarisation (tissue removal and stopping bleeding by burning). In the tenth century he described families whose men died of bleeding after only minor trauma.
While many other such descriptive and practical references to the disease appear in later historical writings, scientific analysis began only at the beginning of the nineteenth century.
In 1803, John Conrad Otto, a Philadelphia doctor, wrote a report on a family whose members are suffering from profuse bleeding, which can be breastfed worse than usual and also occur spontaneously.
The affected men referred to Otto as a hemophiliac. He realized that the disorder was hereditary, affecting mainly men, but passed down by healthy women. His work was the second paper describing important features of an X-linked genetic disorder.
The first paper is a description of the color blindness of John Dalton, who studied his own family. Since the mechanisms of inheritance in color blindness and hemophilia are the same, Otto Dalton’s study could certainly be used as a template.
Otto traced the disease back to a woman who settled in 1720 near Plymouth in the United States. However, the idea that affected men could pass on the property to their unaffected daughters did not come to him.
This was not described until 1813, when John F. Hay published a report on this in an English medical journal. This eventually led other doctors to deal with the issue of hemophilia, which led to the discovery of other bleeding disorders.
For example, a Finnish physician discovered a similar hereditary bleeding disorder in the 1820s, more commonly found in southwestern Finland. This was the so-called von Willebrand disease (also Willebrand-Jürgens syndrome), which is also due to a functional impairment of the coagulation factors.
Up to Beginning of the 19th century Haemophilia was predominantly referred to as hemophilia. It was not until 1828 that the term hemophilia, which is still used today, became established. This is derived from the term hemorrhage, and was first used by the Swiss physician Friedrich Hopff.
Although the physicians of the time were able to deduce the exact mechanism of action, they remained undetected until the 20th century. Only in the 1930s, the two American doctors Patek and Taylor discovered the antihemophilic globulin.
This test consisted of transferring hemophiliac blood to another hemophiliac. The fact that this corrected the coagulation problem showed that there was more than one form of hemophilia. This finally allowed more specific therapies to be developed. The delivery of donor blood containing coagulation factors has become the standard treatment for hemophilia.
Transfusion therapy has long been considered a very safe treatment. In the 1980s, however, the case of boy Ryan White caused a scandal that led to innovations in therapy. Ryan White was an American hemophile who became infected with HIV at the age of 13 through contaminated blood products.
By the end of 1985, many people with hemophilia were given coagulation factor products that posed a risk for HIV and hepatitis C infection. The plasma used to make the preserved blood was neither screened nor tested, nor were most products virally inactivated.
By the time this was recognized, tens of thousands worldwide were already infected as a result of contaminated factor products. After that, scientists persistently worked on various methods of examining blood samples and killing possible pathogens. Nevertheless, blood preserves remained dangerous until the end of the 80s. Today, infection as a result of blood transfusion represents a relatively low risk.
Hemophilia – the royal disease
For most people, hemophilia is not only known for the blood transfusion scandal in the late 1980s, but because of many haemophilia cases in aristocratic homes. This prejudice is actually based on historical facts. Haemophilia actually played an important role in the European royal family and is therefore sometimes referred to as a royal disease.
Carrier of the gene mutation of the X chromosome was demonstrable Victoria the Queen of England. She passed on the mutation for hemophilia B to her son Leopold and, through two of her daughters, Alice and Beatrice, to various royals throughout the European continent. This included the King Family from Spain, Germany and Russia.
In Russia Alexey Nikolaevich Romanov, the son and heir of Tsar Nicholas II, was known to suffer from hemophilia, which he had received from his mother, Empress Alexandra, one of Queen Victoria’s granddaughters.
The hemophilia of Alexei was used to form the Russian mystic Grigori Rasputin at the imperial court. It has been claimed that Rasputin has successfully treated the hemophilia of Alexei.
At that time, the usual treatment of aspirin was done by professional doctors, which aggravated rather than worsened the problem. It is believed that by working simply against medical treatment, Rasputin has made a visible and significant improvement in the condition of Alexei Nikolaevich. In retrospect, the son of the last Tsar was considered very lively.
For this reason, it is believed that he suffered only from moderate hemophilia. This was nevertheless guarded as a state secret. However, when the German Kaiser Wilhelm II visited Russia, the disease could no longer be hidden from him, as he himself had hemophiliacs in his family and immediately recognized the corresponding signs.
In Spain had Queen Victoria’s youngest daughter, Princess Beatrice, a daughter Victoria Eugenie von Battenberg, who later became Queen of Spain. Two of her sons were hemophiles and both died from minor car accidents:
Her eldest son, Prince Alfonso of Spain, died at the age of 31 of internal bleeding after his car hit a telephone booth. Her youngest son, Don Gonzalo, died of stomach ache at the age of 19, after a minor car accident in which he and his sister collided against a wall.
No one seemed injured or sought immediate medical attention. Gonzalo died of internal bleeding two days later. Again, historians suspect that there was a mild form of hemophilia.
No living member of the current or former ruling dynasties Europe It is known to have symptoms of hemophilia, or it is believed that it carries the gene in it.
The last descendant of Victoria, who is known to be suffering from the disease, is Don Gonzalo, although since his birth in 1914, dozens of descendants of Queen Victoria were born. This also applies to male descendants of potential wearers.
However, hemophilia is usually hidden in women who only inherit the gene from a parent. Consequently, there is still a chance that hemophilia will continue to exist in the aristocratic circles and the disease will once again erupt.
This is particularly likely in offspring of Princess Beatrice, the youngest daughter of Queen Victoria. It is considered a proven carrier of the mutation gene. Marriage within noble circles can easily lead to hereditary diseases.
After all, incest is likely here in the broadest sense, which is derived from the fact that was married within noble families over the centuries, with each other. This could now also favor the occurrence of hemophilia.
Are there alternative treatments for hemophilia?
This is mainly because the therapy in this disease is not directed against the actual cause, but against specific symptoms. A replacement of the missing blood coagulation factors is afterwards unavoidable, but can hardly be given with home remedies or alternative therapies. However, some methods of attendant treatment are suitable.
This concerns primarily the replacement of analgesics. The common drugs that are approved for the treatment of pain in Germany, can cause serious complications in hemophilia patients.
Among other things, aspirin and ibuprofen have a blood-thinning effect and lead to an increased probability of hemophilia bleeding. The light pain treatment can be carried out afterwards with herbs or essential oils.
But also heat treatments are possible. However, other pain therapies, such as acupuncture, are foreseeable. Here it comes to small injuries of the skin, which in turn can cause strong bleeding.
If a haemophilia suffer from bleeding into the joints, this often leads to the destruction of the cartilage tissue. For this reason, exercise therapies in this disease are an optimal adjunct to normal treatment.
Hemophilia home remedies
Helpful home remedies for hemophilia
Home remedies are basically not intended in the treatment of hemophilia. Here are usually only a few measures that serve to provide relief in pain, as common painkillers may not be taken.
In addition, it is recommended that health be kept as stable as possible. Again, there are preventive measures that can be easily adhered to.
- Heat treatment with hot water bottle or warm coils
- enough sleep
- Waiver of alcohol and cigarettes
- a healthy and balanced diet
- physical activity, such as swimming the walks (but no sport with high risk of injury)
The exact data on the dosage and the type of application can be found in the package leaflet or clarified with the responsible health practitioner.
medicinal herbs & medicinal plants
Medicinal herbs can take on different functions in hemophilia. On the one hand, various teas and tinctures can be used to relieve pain caused by bleeding or illnesses.
However, care should be taken that the plants used do not dilute the blood, as this increases the risk of bleeding and spontaneous bleeding episodes.
In addition to the treatment of pain, balancing the iron balance is also possible with medicinal herbs. Due to heavy bleeding this can be significantly lowered, which can lead to tiredness and difficulty concentrating. However, some plants can counteract this.
Medicinal plants recommended for the concomitant treatment of hemophilia include the following:
The exact data on the dosage and the type of application can be found in the package leaflet or clarified with the responsible health practitioner.
Just like medicinal herbs and medicinal plants, essential oils can also be used to combat pain. As a result, however, only limited success can be achieved. In addition, special care should always be taken when using such oils.
Many people, for example, can not tolerate the resulting vapors and react to oils with irritation of the mucous membranes, allergic reactions, dry eyes or breathing difficulties.
However, for those who tolerate oils, they can apply them to the skin in the form of tinctures or create a relaxing indoor climate by means of a fragrance lamp, which can reduce stress and thereby relieve pain.
The oils that may be used to treat hemophilia include the following:
The exact data on the dosage and the type of application can be found in the package leaflet or clarified with the responsible health practitioner.
homeopathy & globules
Homeopathic remedies have been on the rise for several years. Many people trust in globules rather than conventional medicine. In hemophilia, however, such is not replaceable. An accompanying therapy with homeopathic remedies can hardly be successful.
This is mainly due to the fact that active ingredients present in globules are present in a very low dose and are often so diluted that they can not have any measurable influence on the human body. For this reason, homeopathy can not be recommended at this point.
It is possible to take globules especially if pain relief is to be achieved and the patient believes in the successes of homeopathy. Under certain circumstances, the so-called placebo effect arises here. Means di eligible for this are, for example, the following:
Schüssler salts were developed at a time when modern medicine was still in its infancy and the body’s mechanisms of action were comparatively undetected.
For this reason, the basic assumption on which the development of the salts is based is fundamentally wrong: the physician Schuessler, who developed this method, believed that every disease was based on a deficiency of a particular mineral. After the supply of the missing substance, the illness should afterwards be considered cured.
Today, of course, it is known that this theory is baseless. Nevertheless, some people firmly believe in achieving health benefits with Schüssler salts.
Here, the placebo effect may provide real relief of pain or even symptom relief. With regard to hemophilia, however, Schüssler salts should only be taken concomitantly and after consultation with the attending physician.
Salts – List
- No. 2Calcium phosphoricum: Classically, this remedy is used more against toothache, nevertheless, it can also help with hemophilia remedy. Because it provides the body with important elements that it needs to restore or completely rebuild solid tissue. These include, among other things, overused lutic vessels.
- No. 13Kalium arsenicumAll in all, this remedy has a very stabilizing effect on the human organism and helps it recover better through rest. Not least because of this, it can be very helpful to give this medicine a chance, even though it does not directly correlate with the health of the blood.
- No. 17 Manganum sulfuricum: This is a means of strengthening the nerves. Since these are often very much overused in the case of diseases, it can not hurt to use the help of this Schüssler salt to promote the healing and accelerate in any case.
- No. 8 Sodium chloratum: This is a remedy that is very often used against common colds, but also against the loss of fluids in general. Not least because of this, it can be very important to give this drug a chance.
- No. 21 Zincum chloratum: This ingredient strengthens the immune system and promotes the healing of wounds and open areas. This can be very helpful especially for diseases with the blood. Treatment with this remedy is therefore highly recommended in the present disease and should be considered in any case.
diet & nutrition
Diet plays no essential role in terms of hemophilia. Although the human genetic apparatus is certainly influenced by food and can even be caused by contaminated food gene mutations, severe hemophilia is usually possible only through heredity.
Mild forms can also be caused by autoimmune diseases or cancer. In principle, no cases are known in which food intake has triggered haemophilia.
If a person already suffers from hemophilia, no cure or blatant symptom relief can be achieved with food. However, it is possible to keep your health stable through a balanced diet. Of course this also favors a treatment afterwards.
In addition, there are a few factors that can be quite interesting for hemophiles when eating. This includes, for example, that a normal weight is held. Many patients with severe hemophilia tend to bleed into the joints. These are heavily used in the episode.
overweight could affect this even further negatively. For this reason, doctors and nutritionists advise that a food diary be kept and portions always checked for the amount and calories contained.
iron & folic acid
Another problem can be with hemophiliacs iron deficiency represent. Especially if after a surgical procedure, the blood loss was correspondingly large, the iron balance can be compensated by appropriate food again. Among the cheap foods here include spinach, broccoli, fennel or beans.
Fiber-containing whole grains are also among the main suppliers of iron. Millet, lentils or oatmeal should therefore be on the menu. Animal foods are best consumed by the body in terms of iron content.
However, the fats contained in these products are also characterized by an increase in cholesterol levels. For this reason, try to consume meat only in moderation.
Small bleeding that occurs with regularity usually also leads to a decrease in folic acid levels. This usually worsens the well-being of those affected. Nutritionists advise for this reason to keep the folic acid level high enough fresh fruit and vegetables.
FAQ – questions & reply
Here are answers to frequently asked questions about hemophilia.
Incest – transmission?
If hemophilia is transmitted by incest?
The haemophilia is mainly known that it is widely used in European aristocratic homes. These are often associated with incestuous marriages. For this reason, it is suspected that hemophilia is a result of incest.
This assumption is not true. Hemophilia can also be inherited if only one parent carries the mutant X chromosome. For example, if the mother is a carrier, there is a 50% chance that her son will become a hemophiliac and an equally high risk that a daughter herself becomes the carrier of the mutated gene.
If the father is hemophilic, the son can not be, since he inherits from his father not the X but the Y chromosome. The daughter of a hemophile, however, will certainly become a carrier. If both parents have corresponding gene mutations, which may be the case irrespective of mutual relatives, the risk also increases for girls to develop hemophilia.
Consequently, it can be seen that haemophilia, like any other hereditary disease, may be favored in incest. However, an incestuous relationship is not mandatory for the development of this disease.
In addition, such a compound does not always have to develop a hereditary disease in the offspring. In this case also healthy children can be begotten. Only the probability of the occurrence of hereditary diseases, which are already common in the family, increases.
Are there gene therapies for the treatment of hemophilia?
Gene therapy is extensively researched and sometimes even used in many diseases that are based on mutations in the genetic material. This is also the case with regard to hemophilia.
In patients with severe hemophilia, gene therapy may reduce the symptoms to those that a mild or moderate person with hemophilia may have. The best results were achieved in hemophilia B..
Currently, various studies on the comprehensive use of gene therapies in humans are being researched. The first attempts are already completed and were able to achieve above-average results.
However, the technology has not yet matured and therefore can not yet be applied nationwide. However, physicians believe it is very likely that gene therapies will be established in the next few years and will certainly supplant or replace conventional medical approaches.
Hemophilia – Deadly?
Haemophilia is deadly?
Only a century ago, there was no adequate therapy to treat haemophilia and its symptoms accordingly. On the contrary, penicillin and aspirin were often used for therapy, which even negatively affected the disease.
Patients suffering from a severe form of hemophilia only managed to reach the age of 11 on average. Today, the situation is different. Thanks to the transfusion of blood coagulation factors that can compensate for the lack of it, most people can live a relatively normal life regardless of the disease.
Only with serious complications that are left untreated, a life threat is possible. However, most patients reach an almost average age. Hemophilia can not be classified as lethal for this reason.
Blood type crucial?
Does hemophilia depend on the particular blood group??
Human blood is made up of different elements. These include the red blood cells whose specific surface causes the classification in a blood group. The hemophilia is not bound to the red blood cells, but to the so-called coagulation factors, which are also part of the blood mixture.
These coagulation factors are always the same in healthy people. In hemophilia, however, a gene mutation results in either a specific coagulation factor not being formed or not being sufficiently produced. Consequently, a dependency on the blood group is involved, which means that every person who has an appropriately mutated gene can be affected by this disease.
Women also suffer from haemophilia?
As the coagulation factor is recessively inherited on the X chromosome, only males are affected by hemophilia. They have only one X chromosome, which is in any case active afterwards. On the other hand, girls and women have two X chromosomes.
The recessive gene variant, which is transmitted in hemophilia, is finally not used. Coagulation factors are thus formed by the healthy gene. This means that hemophilia in women occurs only when both chromosomes are damaged.
However, this presupposes that both father and mother are gene carriers. However, this combination is rarely found in practice, as hemophilia is a very rare hereditary disease altogether. Theoretically, there is the possibility that women also develop hemophilia.
Another possibility arises when, despite the recessive inheritance in carriers of the mutated gene, this is active. Here it comes to very mild forms of the disease, which usually only affect the person affected, if surgical procedures are performed or a serious injury exists. However, this variant is also rare to find.
Infection with AIDS?
Do you get AIDS from hemophilia treatment??
Hemophilia has also become known in the past because AIDS or HIV has been transmitted in the treatment of this disease. The reason for this is that HIV remained unexplored for a long time because this disease was discovered very late. In addition, a lot of myths about HIV. This included, for example, that it is a disease that occurs only among homosexual people.
Among other things, blood transfusions, which are routinely administered to heavy blood, have not been studied for the presence of HI viruses. For this reason, tens of thousands of hemophilia patients worldwide have been infected with the dangerous virus.
This triggered a scandal, but led to more intensive research into the preservation of blood. Since the 90s, a blood transfusion is therefore considered relatively safe. However, there is no 100% certainty that foreign blood does not contain any infectious agents. For this reason, artificial coagulation factors are used in the treatment of hemophiliacs.
Overall, therefore, that the hemophilia treatment does not lead to AIDS. Only in rare cases do contaminated canned foods cause infection with the HI virus or other diseases such as hepatitis.
Video on hemophilia
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MindTap Chapter 13 Final Test
Terms in this set (25)
The autonomic nervous system can be described as being self-governing, automatic, or ___________________
The words that BEST illustrate the action of the sympathetic nervous system are fright, fight, and _________ .
Drugs that mimic the action of the sympathetic nervous system are called sympathomimetic or _______________ .
Adrenergics can be administered intravenously, subcutaneously, or _____________________ .
The MOST commonly used adrenergic blockers are known as alpha- and _______________ -blockers.
Drugs that mimic the action of the parasympathetic nervous system are commonly known as __________________ .
Drugs that block the action of the parasympathetic nervous system are known as ________________________ .
The parasympathetic nerve fibers synthesize and liberate ____________________________ as a mediator.
Only ____________________ , a cholinergic blocker, acts as a bronchodilator and reduces the incidence of laryngospasm that can occur during general anesthesia.
Chemical substances called ___________________ are released at nerve endings to transmit nerve impulses.
A health care practitioner is administering adrenergic blockers. She knows that this will block what type of response?
a. Sympathetic response
b. Autonomic response
c. Parasympatholytic response
d. Cholinergic response
At a health fair, a nurse explains to students the difference between the sympathetic and parasympathetic nervous system. What could the nurse say about the sympathetic nervous system response?
a. It speeds up the responses in the body.
b. It dilates the peripheral blood vessels.
c. It slows responses in the body.
d. It prevents a cholinergic response
An adrenergic medication is ordered for a client. The provider has ordered epinephrine subcutaneously. What can the health care provider tell the client to expect after taking this?
a. Low blood pressure
b. Racing of heart
d. Low blood sugar and hunger
A client is using a sympathomimetic. The health care provider knows that this medication should be used with caution when the client has which of the following?
b. Sulfa allergy
c. Open angle glaucoma
A client has been prescribed a cholinergic drug. How can the health care provider describe the action of a cholinergic drug such as bethanechol?
a. Slows the heart rate
b. Lowers GI peristalsis
c. Decreases contraction of the urinary bladder
d. Increases intraocular pressure
An older adult client is being treated for benign prostatic hypertrophy and is prescribed the cholinergic doxazosin. The health care practitioner knows this medication has what effect?
a. It stimulates the bladder neck.
b. It acts as an alpha blocker.
c. It acts as an adrenergic receptor agonist.
d. It stimulates the binding of the neurotransmitter norepinephrine.
The term parasympathetic is synonymous with which of the following?
d. Cholinergic blocker
What BEST describes the action of propranolol (Inderal)?
a. Blocks the beta receptors
b. Works on the central nervous system
c. Stimulates the alpha receptors
d. Stimulates the beta receptors
A client is being treated in the emergency department for bradycardia secondary to a Lyme disease infection. The client has a sudden decrease in his heart rate and requires medication to speed it up. What medication will have this action?
b. Atropine sulfate
The student is reviewing her anatomy and physiology materials on the autonomic nervous system. She knows that the sympathetic and the parasympathetic nervous systems act on the same organs but produce opposite effects. What is the parasympathetic response to the gastrointestinal tract?
a. Decreases gastric contractions
b. Decreases salivation
c. Slows down peristalsis
d. Speeds up peristalsis
The body has specific receptors that respond to stimulation of chemicals called neurotransmitters. What are these receptors called?
a. Alpha- and gamma-receptors
b. Alpha- and beta-receptors
c. Beta- and gamma-receptors
d. Alpha- and omega-receptors
In reviewing a medication that has an adrenergic beta-2 response, the health care practitioner knows it will have which effect on the bronchioles?
a. Has no effect on the respiratory system
b. Increases respiratory secretions
c. Dilates the bronchioles
d. Constricts the bronchioles
In providing discharge instructions to a client with hypertension, the health care practitioner instructs him not to use over-the-counter cold medicines and diet pills, because they may have adrenergic properties. What is one of these properties?
a. Low blood sugar
b. Decreased blood pressure
c. Decreased heart rate
d. Increased blood pressure
A client is given Urecholine for postoperative urinary retention. The client has also been taking pilocarpine ophthalmic for glaucoma. What does the health care practitioner instruct the client to report?
a. Elevated blood pressure or decreased blood sugar
b. Increased respiratory rate, hypertension, or diarrhea
c. Gastric pain, cramping, diarrhea, increased salivation, bradycardia, or orthostatic hypotension
d. Dry mouth, constipation, or bowel obstruction
A client is taking an over-the-counter nasal decongestant. The nurse tells the client that an overdose might lead to which of the following?
a. Increased salivation
b. Rebound congestion
c. A runny nose
d. All of these
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Cognitive symptoms refer to the difficulties with concentration and memory. These can include:
1. Disorganized thinking
2. Slow thinking
3. Difficulty understanding
4. Poor concentration
5. Poor memory
6. Difficulty expressing thoughts
7. Difficulty integrating thoughts, feelings and behavior.
Each schizophrenic falls under a subtype of schizophrenia defined by a unique indicator. This indicator may be one dominant symptom only or a combination of positive and negative symptoms. People with schizophrenia are classified into 5 sub-types, namely “Paranoid Type”, “Disorganized Type”, “Catatonic Type”, “Undifferentiated Type” and “Residual Type”.
For example, schizoaffective disorder exhibits schizophrenia alongside another mental disorder. Undifferentiated schizophrenia can be thought of as “general” schizophrenia, as it doesn’t display any one dominant symptom. Below are the different types of schizophrenia and their characteristics.
There are different kinds of schizophrenia. The International Classification of
Diseases (ICD-10) manual describes them as below:
1.Paranoid schizophrenia: These persons are very suspicious of others and often have grand schemes of persecution at the root of their behavior. Halluciations, and more frequently delusions, are a prominent and common part of the illness.
-Common form of schizophrenia.
-Prominent hallucinations and/or delusions.
-May develop at a later age than other types of schizophrenia.
-Speech and emotions may be unaffected.
2. Hebephrenic schizophrenia (Disorganized schizophrenia): In this case the person is verbally incoherent and may have moods and emotions that are not appropriate to the situation. Hallucinations are not usually present.
– Disorganized behavior (e.g., difficulty starting or finishing a task, difficulty acting appropriately in social situations)
-Disorganised thoughts: other people may find it difficult to understand others.
-Pranks, giggling, health complaints and grimacing.
-Short-lasting delusions and hallucinations.
-Usually develops between 15 and 25 years old.
-Disorganized speech (e.g., word salad, incoherence, perseverance)
-Flat or inappropriate affect (e.g., poor eye contact, lack of facial expressions)
3. Catatonic schizophrenia: In this case, the person is extremely withdrawn, negative and isolated, and has marked psychomotor disturbances.
-Rarer than other types.
-Unusual movements, often switching between being very active and very still.
-You may not talk at all.
.Undifferentiated schizophrenia: Conditions meeting the general diagnostic criteria for schizophrenia but not conforming to any of the above subtypes, or exhibiting the features of more than one of them without a clear predominance of a particular set of diagnostic characteristics.
One’s diagnosis may have some signs of paranoid, hebephrenic or catatonic schizophrenia, but doesn’t obviously fit into one of these types alone.
5. Residual schizophrenia: In this case the person is not currently suffering from delusions, hallucinations, or disorganized speech and behavior, but lacks motivation and interest in day-to-day living. One may be diagnosed with this if he/she has a history of psychosis but only have negative symptoms.
6. Simple schizophrenia:
-Rarely diagnosed in the UK.
-Negative symptoms are prominent early and get worse quickly.
-Positive symptoms are rare.
7. Cenesthopathic schizophrenia:
People with cenesthopathic schizophrenia experience unusual bodily sensations.
8. Unspecified schizophrenia:
Symptoms meet the general conditions for a diagnosis, but do not fit in to any of the above categories.
9. Schizoaffective Disorder: These people have symptoms of schizophrenia as well as mood disorder such as major depression, bipolar mania, or mixed mania.
Schizoaffective disorder is a mixture of schizophrenia and either depression or bipolar disorder. This type of schizophrenia is typically hard to diagnose because of the myriad of symptoms that depression or bipolar disorder may bring.
Depression is marked by prolonged feelings of sadness and worthlessness, as well as cognitive problems like problems with concentrating and remembering details. On the other hand, bipolar disorder causes shifts in mood — one moment you may feel elated, and then you suddenly feel low, often to the point of sadness.
The cycle between high and low emotions may become so intense and frequent that they begin to interfere with your daily life and affect your relationships and work or academic performance. The two tables below indicate the symptoms for the mental disorders that may coexist with schizophrenia.
-Weight gain or loss
-Changes in sleeping patterns
-Lack of energy
-Loss of interest in hobbies or favorite activities
-Feelings of worthlessness or hopelessness
-Guilt or self-blame
-Troubles with thinking or concentration
-Thoughts of death or suicide
Bipolar Disorder Symptoms:
Bipolar Mania (High):
• Euphoria or irritability
• Increased energy and activity
• Excessive talk or racing thoughts
• Inflated self-esteem
• Unusual energy, plus a lowered need for sleep
• Reckless pursuit of gratification
Bipolar Depression (Low):
• Depressed mood and low-self esteem
• Low energy levels and apathy
• Sadness, loneliness, helplessness, guilt
• Slow speech, fatigue and poor coordination
• Insomnia or oversleeping
• Suicidal thoughts and feelings
• Poor concentration
10. Disorders Related to (or sometimes with similar symptoms to) Schizophrenia/ Schizophrenia Spectrum Disorders:
Knowing the symptoms of these disorders, and how they can be similar and different from schizophrenia, can help prevent a possible misdiagnosis. The concentration on predominant symptoms at presentation has helped mental health professionals distinguish and better treat other mental disorders that resemble schizophrenia, creating the schizophrenia spectrum of disorders.
-Schizoid Personality: Schizoid personality disorder (SPD) is a chronic and pervasive condition characterized by social isolation and feelings of indifference toward other people. Those who suffer from this disorder are often described as distant or withdrawn.
-Schizophreniform Disorder: Schizophreniform disorder has identical features to schizophrenia but the duration of symptoms is less. The patient has experienced symptoms for longer than one week but less than six months. This diagnosis is often considered the first step towards an eventual schizophrenia diagnosis, which requires continuous signs of disturbance for at least six months.
-Schizotypal Personality: develops by early adulthood and is characterized by pervasive deficits in social and interpersonal skills, eccentric behavior, discomfort forming close personal relationships, as well as cognitive and perceptual distortions. Someone with schizotypal personality disorder may have ideas of reference. These are unlike delusions of reference, in which a person’s behavior is altered by their belief that something is referential to them personally.
-Bipolar Disorder (Manic Depression) – frequently misdiagnosed as schizophrenia (and vice versa).
-Asperger’s Syndrome – a type of Autism that may be misdiagnosed
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From Wikipedia, the free encyclopedia
- For the Hebrew Bible term and its varied meanings, see Tzaraath. For other uses, see Leprosy (disambiguation).
|Leprosy (Hansen's disease)|
|Classification and external resources|
A 24-year-old man infected with leprosy.
|eMedicine||med/1281 derm/223 neuro/187|
Leprosy or Hansen's disease (HD), named after physician Gerhard Armauer Hansen, is a chronic disease caused by the bacteria Mycobacterium leprae and Mycobacterium lepromatosis. Leprosy is primarily a granulomatous disease of the peripheral nerves and mucosa of the upper respiratory tract; skin lesions are the primary external sign. Left untreated, leprosy can be progressive, causing permanent damage to the skin, nerves, limbs and eyes. Contrary to myth, leprosy does not cause body parts to fall off, although they can become numb and/or diseased as a result of the disease.
Historically, leprosy has affected humanity for at least 4,000 years, and was well-recognized in the civilizations of ancient China, Egypt, and India. DNA taken from the shrouded remains of a man discovered in a tomb next to the Old City of Jerusalem shows him to be the first human proven to have suffered from leprosy. In 1995, the World Health Organization (WHO) estimated that between 2 and 3 million people were permanently disabled because of leprosy. In the past 20 years, 15 million people worldwide have been cured of leprosy. Although the forced quarantine or segregation of patients is unnecessary in places where adequate treatments are available, many leper colonies still remain around the world in countries such as India (where there are still more than 1,000 leper colonies), China, Romania, Egypt, Nepal, Somalia, Liberia, Vietnam, and Japan. Leprosy was once believed to be highly contagious and sexually transmitted, and was treated with mercury—all of which applied to syphilis which was first described in 1530. It is now thought that many early cases of leprosy could have been syphilis. Leprosy is in fact neither sexually transmitted nor is it highly infectious after treatment, as approximately 95% of people are naturally immune and sufferers are no longer infectious after as little as 2 weeks of treatment. However, before treatment was developed, leprosy was certainly contagious.
The age-old social stigma, in other words, leprosy stigma associated with the advanced form of leprosy lingers in many areas, and remains a major obstacle to self-reporting and early treatment. Effective treatment for leprosy appeared in the late 1930s with the introduction of dapsone and its derivatives. However, leprosy bacilli resistant to dapsone soon evolved and, due to overuse of dapsone, became widespread. It was not until the introduction of multidrug therapy (MDT) in the early 1980s that the disease could be diagnosed and treated successfully within the community.
MDT for multibacillary leprosy consists of rifampicin, dapsone, and clofazimine taken over 12 months. Dosages adjusted appropriately for children and adults are available in all Primary Health Centres in the form of blister packages. Single dose MDT for single lesion leprosy consists of rifampicin, ofloxacin, and minocycline. The move towards single dose treatment strategies has reduced the prevalence of disease in some regions since prevalence is dependent on duration of treatment.
World Leprosy Day was created to draw awareness to leprosy and its sufferers.
There are several different approaches for classifying leprosy, but parallels exist.
- The World Health Organization system distinguishes "paucibacillary" and "multibacillary" based upon the proliferation of bacteria ("pauci-" refers to a low quantity.)
- The SHAY scale provides five gradations.
- The ICD-10, though developed by the WHO, uses Ridley-Jopling and not the WHO system. It also adds an indeterminate ("I") entry.
- In MeSH, three groupings are used.
|WHO||Ridley-Jopling||ICD-10||MeSH||Description||Lepromin test||Immune target|
|Paucibacillary||tuberculoid ("TT"), borderline tuberculoid ("BT")||A30.1, A30.2||Tuberculoid||It is characterized by one or more hypopigmented skin macules and anaesthetic patches, where skin sensations are lost because of damaged peripheral nerves that have been attacked by the human host's immune cells.||Positive||bacillus (Th1)|
|Multibacillary||midborderline or borderline ("BB")||A30.3||Borderline||Borderline leprosy is of intermediate severity and is the most common form. Skin lesions resemble tuberculoid leprosy but are more numerous and irregular; large patches may affect a whole limb, and peripheral nerve involvement with weakness and loss of sensation is common. This type is unstable and may become more like lepromatous leprosy or may undergo a reversal reaction, becoming more like the tuberculoid form.|
|Multibacillary||borderline lepromatous ("BL"), and lepromatous ("LL")||A30.4, A30.5||Lepromatous||It is associated with symmetric skin lesions, nodules, plaques, thickened dermis, and frequent involvement of the nasal mucosa resulting in nasal congestion and epistaxis (nose bleeds) but typically detectable nerve damage is late.||Negative||plasmid inside bacillus (Th2)|
There is a difference in immune response to the tuberculoid and lepromatous forms.
Hansen's disease may also be divided into the following types::344-346
Mycobacterium leprae and Mycobacterium lepromatosis are the causative agents of leprosy.
Due to extensive loss of genes necessary for independent growth, M. leprae and M. lepromatosis are unculturable in the laboratory, a factor which leads to difficulty in definitively identifying the organism under a strict interpretation of Koch's postulates. The use of non-culture-based techniques such as molecular genetics has allowed for alternative establishment of causation.
Several genes have been associated with a susceptibility to leprosy:
The mechanism of transmission of leprosy is prolonged close contact and transmission by nasal droplet. The only animal other than humans that is known to contract leprosy is the nine-banded armadillo. The bacterium can also be grown in the laboratory by injection into the footpads of mice. There is evidence that not all people who are infected with M. leprae develop leprosy, and genetic factors have long been thought to play a role, due to the observation of clustering of leprosy around certain families, and the failure to understand why certain individuals develop lepromatous leprosy while others develop other types of leprosy. It is estimated that due to genetic factors, only 5% of the population is susceptible to leprosy. This is mostly because the body is naturally immune to the bacteria, and those persons who do become infected are experiencing a severe allergic reaction to the disease. However, the role of genetic factors is not entirely clear in determining this clinical expression. In addition, malnutrition and prolonged exposure to infected persons may play a role in development of the overt disease.
The incubation period for the bacteria can last anywhere from two to ten years.
The most widely held belief is that the disease is transmitted by contact between infected persons and healthy persons. In general, closeness of contact is related to the dose of infection, which in turn is related to the occurrence of disease. Of the various situations that promote close contact, contact within the household is the only one that is easily identified, although the actual incidence among contacts and the relative risk for them appear to vary considerably in different studies. In incidence studies, infection rates for contacts of lepromatous leprosy have varied from 6.2 per 1000 per year in Cebu, Philippines to 55.8 per 1000 per year in a part of Southern India.
Two exit routes of M. leprae from the human body often described are the skin and the nasal mucosa, although their relative importance is not clear. It is true that lepromatous cases show large numbers of organisms deep down in the dermis. However, whether they reach the skin surface in sufficient numbers is doubtful. Although there are reports of acid-fast bacilli being found in the desquamating epithelium (sloughing of superficial layer of skin) of the skin, Weddell et al. had reported in 1963 that they could not find any acid-fast bacilli in the epidermis, even after examining a very large number of specimens from patients and contacts. In a recent study, Job et al. found fairly large numbers of M. leprae in the superficial keratin layer of the skin of lepromatous leprosy patients, suggesting that the organism could exit along with the sebaceous secretions.
The importance of the nasal mucosa was recognized as early as 1898 by Schäffer, particularly that of the ulcerated mucosa. The quantity of bacilli from nasal mucosal lesions in lepromatous leprosy was demonstrated by Shepard as large, with counts ranging from 10,000 to 10,000,000. Pedley reported that the majority of lepromatous patients showed leprosy bacilli in their nasal secretions as collected through blowing the nose. Davey and Rees indicated that nasal secretions from lepromatous patients could yield as much as 10 million viable organisms per day.
The entry route of M. leprae into the human body is also not definitively known: the skin and the upper respiratory tract are most likely. While older research dealt with the skin route, recent research has increasingly favored the respiratory route. Rees and McDougall succeeded in the experimental transmission of leprosy through aerosols containing M. leprae in immune-suppressed mice, suggesting a similar possibility in humans. Successful results have also been reported on experiments with nude mice when M. leprae were introduced into the nasal cavity by topical application. In summary, entry through the respiratory route appears the most probable route, although other routes, particularly broken skin, cannot be ruled out. The CDC notes the following assertion about the transmission of the disease: "Although the mode of transmission of Hansen's disease remains uncertain, most investigators think that M. leprae is usually spread from person to person in respiratory droplets."
In leprosy both the reference points for measuring the incubation period and the times of infection and onset of disease are difficult to define; the former because of the lack of adequate immunological tools and the latter because of the disease's slow onset. Even so, several investigators have attempted to measure the incubation period for leprosy. The minimum incubation period reported is as short as a few weeks and this is based on the very occasional occurrence of leprosy among young infants. The maximum incubation period reported is as long as 30 years, or over, as observed among war veterans known to have been exposed for short periods in endemic areas but otherwise living in non-endemic areas. It is generally agreed that the average incubation period is between three and five years.
In a recent trial, a single dose of rifampicin reduced the rate at which contacts acquired leprosy in the two years after contact by 57%; 265 treatments with rifampicin prevented one case of leprosy in this period. A non-randomized study found that rifampicin reduced the number of new cases of leprosy by 75% after three years.
Until the development of promin in the 1940s, there was no effective treatment for leprosy. The efficacy of promin was first discovered by Guy Henry Faget and his co-workers in 1943. Later dapsone was developed. However, it is only weakly bactericidal against M. leprae and it was considered necessary for patients to take the drug indefinitely. Moreover, when dapsone was used alone, the M. leprae population quickly evolved antibiotic resistance; by the 1960s, the world's only known anti-leprosy drug became virtually useless.
The search for more effective anti-leprosy drugs than dapsone led to the use of clofazimine and rifampicin in the 1960s and 1970s. Later, Indian scientist Shantaram Yawalkar and his colleagues formulated a combined therapy using rifampicin and dapsone, intended to mitigate bacterial resistance. Multidrug therapy (MDT) and combining all three drugs was first recommended by a WHO Expert Committee in 1981. These three anti-leprosy drugs are still used in the standard MDT regimens. None of them are used alone because of the risk of developing resistance.
Because this treatment was quite expensive, it was not quickly adopted in most endemic countries. In 1985 leprosy was still considered a public-health problem in 122 countries. The 44th World Health Assembly (WHA), held in Geneva in 1991, passed a resolution to eliminate leprosy as a public-health problem by the year 2000—defined as reducing the global prevalence of the disease to less than 1 case per 100,000. At the Assembly, the World Health Organization (WHO) was given the mandate to develop an elimination strategy by its member states, based on increasing the geographical coverage of MDT and patients’ accessibility to the treatment.
The WHO Study Group's report on the Chemotherapy of Leprosy in 1993 recommended two types of standard MDT regimen be adopted. The first was a 24-month treatment for multibacillary (MB or lepromatous) cases using rifampicin, clofazimine, and dapsone. The second was a six-month treatment for paucibacillary (PB or tuberculoid) cases, using rifampicin and dapsone. At the First International Conference on the Elimination of Leprosy as a Public Health Problem, held in Hanoi the next year, the global strategy was endorsed and funds provided to WHO for the procurement and supply of MDT to all endemic countries.
Between 1995 and 1999, WHO, with the aid of the Nippon Foundation (Chairman Yōhei Sasakawa, World Health Organization Goodwill Ambassador for Leprosy Elimination), supplied all endemic countries with free MDT in blister packs, channelled through Ministries of Health. This free provision was extended in 2000 with a donation by the MDT manufacturer Novartis, which will run until at least the end of 2010. At the national level, non-government organizations (NGOs) affiliated to the national programme will continue to be provided with an appropriate free supply of this WHO supplied MDT by the government.
MDT remains highly effective, and patients are no longer infectious after the first monthly dose. It is safe and easy to use under field conditions due to its presentation in calendar blister packs. Relapse rates remain low, and there is no known resistance to the combined drugs. The Seventh WHO Expert Committee on Leprosy, reporting in 1997, concluded that the MB duration of treatment—then standing at 24 months—could safely be shortened to 12 months "without significantly compromising its efficacy."
Persistent obstacles to the elimination of the disease include improving detection, educating patients and the population about its cause, and fighting social taboos about a disease whose patients have historically been considered "unclean" or "cursed by God" as outcasts. Where taboos are strong, patients may be forced to hide their condition (and avoid seeking treatment) to avoid discrimination. The lack of awareness about Hansen's disease can lead people to falsely believe that the disease is highly contagious and incurable.
The ALERT hospital and research facility in Ethiopia provides training to medical personnel from around the world in the treatment of leprosy, as well as treating many local patients. Surgical techniques, such as for the restoration of control of movement of thumbs, have been developed.
In 1999, the world incidence of Hansen's disease was estimated to be 640,000. In 2000, 738,284 cases were identified. In 1999, 108 cases occurred in the United States. In 2000, the World Health Organization (WHO) listed 91 countries in which Hansen's disease is endemic. India, Myanmar and Nepal contained 70% of cases. India reports over 50% of the world's leprosy cases. In 2002, 763,917 new cases were detected worldwide, and in that year the WHO listed Brazil, Madagascar, Mozambique, Tanzania and Nepal as having 90% of Hansen's disease cases.
According to recent figures from the WHO, new cases detected worldwide have decreased by approximately 107,000 cases (or 21%) from 2003 to 2004. This decreasing trend has been consistent for the past three years. In addition, the global registered prevalence of HD was 286,063 cases; 407,791 new cases were detected during 2004.
In the United States, Hansen's disease is tracked by the Centers for Disease Control and Prevention (CDC), with a total of 92 cases being reported in 2002. Although the number of cases worldwide continues to fall, pockets of high prevalence continue in certain areas such as Brazil, South Asia (India, Nepal), some parts of Africa (Tanzania, Madagascar, Mozambique) and the western Pacific.
At highest risk are those living in endemic areas with poor conditions such as inadequate bedding, contaminated water and insufficient diet, or other diseases (such as HIV) that compromise immune function. Recent research suggests that there is a defect in cell-mediated immunity that causes susceptibility to the disease. Less than ten percent of the world's population is actually capable of acquiring the disease. The region of DNA responsible for this variability is also involved in Parkinson disease, giving rise to current speculation that the two disorders may be linked in some way at the biochemical level. In addition, men are twice as likely to contract leprosy as women. According to The Leprosy Mission Canada, most people-–about 95 % of the population-–are naturally immune.
Although annual incidence—the number of new leprosy cases occurring each year—is important as a measure of transmission, it is difficult to measure in leprosy due to its long incubation period, delays in diagnosis after onset of the disease and the lack of laboratory tools to detect leprosy in its very early stages. Instead, the registered prevalence is used. Registered prevalence is a useful proxy indicator of the disease burden as it reflects the number of active leprosy cases diagnosed with the disease and receiving treatment with MDT at a given point in time. The prevalence rate is defined as the number of cases registered for MDT treatment among the population in which the cases have occurred, again at a given point in time.
New case detection is another indicator of the disease that is usually reported by countries on an annual basis. It includes cases diagnosed with onset of disease in the year in question (true incidence) and a large proportion of cases with onset in previous years (termed a backlog prevalence of undetected cases). The new case detection rate (NCDR) is defined by the number of newly detected cases, previously untreated, during a year divided by the population in which the cases have occurred.
Endemic countries also report the number of new cases with established disabilities at the time of detection, as an indicator of the backlog prevalence. However, determination of the time of onset of the disease is generally unreliable, is very labor-intensive and is seldom done in recording these statistics.
|New case detection during the year|
|Start of 2006||2001||2002||2003||2004||2005|
|South-East Asia||133,422 (0.81)||668,658||520,632||405,147||298,603||201,635|
|Eastern Mediterranean||4,024 (0.09)||4,758||4,665||3,940||3,392||3,133|
|Western Pacific||8,646 (0.05)||7,404||7,154||6,190||6,216||7,137|
|New case detection|
|Start of 2004||Start of 2005||Start of 2006||During 2003||During 2004||During 2005|
|Brazil||79,908 (4.6)||30,693 (1.7)||27,313 (1.5)||49,206 (28.6)||49,384 (26.9)||38,410 (20.6)|
|Mozambique||6,810 (3.4)||4,692 (2.4)||4,889 (2.5)||5,907 (29.4)||4,266 (22.0)||5,371 (27.1)|
|Nepal||7,549 (3.1)||4,699 (1.8)||4,921 (1.8)||8,046 (32.9)||6,958 (26.2)||6,150 (22.7)|
|Tanzania||5,420 (1.6)||4,777 (1.3)||4,190 (1.1)||5,279 (15.4)||5,190 (13.8)||4,237 (11.1)|
As reported to WHO by 115 countries and territories in 2006, and published in the Weekly Epidemiological Record the global registered prevalence of leprosy at the beginning of the year was 219,826 cases. New case detection during the previous year (2005 - the last year for which full country information is available) was 296,499. The reason for the annual detection being higher than the prevalence at the end of the year can be explained by the fact that a proportion of new cases complete their treatment within the year and therefore no longer remain on the registers. The global detection of new cases continues to show a sharp decline, falling by 110,000 cases (27%) during 2005 compared with the previous year.
Table 1 shows that global annual detection has been declining since 2001. The African region reported an 8.7% decline in the number of new cases compared with 2004. The comparable figure for the Americas was 20.1%, for South-East Asia 32% and for the Eastern Mediterranean it was 7.6%. The Western Pacific area, however, showed a 14.8% increase during the same period.
Table 2 shows the leprosy situation in the four major countries which have yet to achieve the goal of elimination at the national level. It should be noted that: a) Elimination is defined as a prevalence of less than 1 case per 10,000 population; b) Madagascar reached elimination at the national level in September 2006; c) Nepal detection reported from mid-November 2004 to mid-November 2005; and d) D.R. Congo officially reported to WHO in 2008 that it had reached elimination by the end of 2007, at the national level.
Current situation in China
As is the case with much of the rest of the world, China also has many leprosy recovered patients who have been isolated from the rest of society. In the '50s the Chinese government created "Recovered Villages" in rural remote mountaintops for the recovered patients. Although leprosy is now curable with the advent of the multi-drug treatment, the villagers remain because they have been stigmatized by the outside world. Health NGOs such as Joy in Action have arisen in China to especially focus on improving the conditions of "Recovered Villages".
The word leprosy comes from ancient Greek λέπρα [léprā], "a disease which makes the skin scaly", in turn a nominal derivation of the verb λέπω [lépō], "to peel, scale off". The word came into the English language via Latin and Old French. The first attested English use is in the Ancrene Wisse, a 13th-century manual for nuns ("Moyseses hond..bisemde o þe spitel uuel & þuhte lepruse." The Middle English Dictionary, s.v., "leprous"). A roughly contemporaneous use is attested in the Anglo-Norman Dialogues of Saint Gregory, "Esmondez i sont li lieprous" (Anglo-Norman Dictionary, s.v., "leprus").
Historically, individuals with Hansen's disease have been known as lepers; however, this term is falling into disuse as a result of the diminishing number of leprosy patients and the pejorative connotations of the term. Because of the stigma to patients, some prefer not to use the word "leprosy," though the term is used by the U.S. Centers for Disease Control and Prevention and the World Health Organization.
Historically, the term Tzaraath from the Hebrew Bible was, erroneously, commonly translated as leprosy, although the symptoms of Tzaraath were not entirely consistent with leprosy and rather referred to a variety of disorders other than Hansen's disease.
In particular, tinea capitis (fungal scalp infection) and related infections on other body parts caused by the dermatophyte fungus Trichophyton violaceum are abundant throughout the Middle East and North Africa today and might also have been common in biblical times. Similarly, the related agent of the disfiguring skin disease favus, Trichophyton schoenleinii, appears to have been common throughout Eurasia and Africa before the advent of modern medicine. Persons with severe favus and similar fungal diseases (and potentially also with severe psoriasis and other diseases not caused by microorganisms) tended to be classed as having leprosy as late as the 17th century in Europe. This is clearly shown in the painting The Regents of the Leper Hospital in Haarlem 1667 by Jan de Bray (Frans Hals Museum, Haarlem, the Netherlands), where a young Dutchman with a vivid scalp infection, almost certainly caused by a fungus, is shown being cared for by three officials of a charitable home intended for leprosy sufferers. The use of the word "leprosy" before the mid-19th century, when microscopic examination of skin for medical diagnosis was first developed, can seldom be correlated reliably with Hansen's disease as we understand it today.
The Oxford Illustrated Companion to Medicine holds that the mention of leprosy, as well as cures for it, were already described in the Hindu religious book Atharva-veda. Writing in the Encyclopedia Britannica 2008, Kearns & Nash state that the first mention of leprosy is in the Indian medical treatise Sushruta Samhita (6th century BC). The Cambridge Encyclopedia of Human Paleopathology (1998) holds that: "The Sushruta Samhita from India describes the condition quite well and even offers therapeutic suggestions as early as about 600 BC" The surgeon Sushruta lived in the Indian city of Kashi by the 6th century BC, and the medical treatise Sushruta Samhita-—attributed to him—-made its appearance during the 1st millennium BC. The earliest surviving excavated written material which contains the works of Sushruta is the Bower Manuscript—-dated to the 4th century AD, almost a millennium after the original work. In 1881, around 120,000 leprosy patients existed in India. The central government passed the Lepers Act of 1898, which provided legal provision for forcible confinement of leprosy sufferers in India. In 2009, a 4,000-year-old skeleton was uncovered in India that was shown to contain traces of leprosy. The discovery was made at a site called Balathal, which is today part of Rajasthan, and is believed[by whom?] to be the oldest case of the disease ever found. This pre-dated the previous earliest recognised case, dating back to 6th-century Egypt, by 1,500 years. It is believed that the excavated skeleton belonged to a male, who was in his late 30s and belonged to the Ahar Chalcolithic culture. Archaeologists have stated that not only does the skeleton represent the oldest case of leprosy ever found, but is also the first such example that dates back to prehistoric India. This finding supports one of the theories regarding the origin of the disease, which is believed to have originated in either India or Africa, before being subsequently spread to Europe by the armies of Alexander the Great.
Japan has had a unique history of segregation of patients into sanatoriums based on leprosy prevention laws of 1907, 1931 and 1953, and hence, it intensified leprosy stigma. The 1953 law was abrogated in 1996. There are still 2717 ex-patients in 13 national sanatoriums and 2 private hospitals as of 2008. In a document written in 833, leprosy was described as " is caused by a parasite which eats five organs of the body. The eyebrows and eyelashes come off, and the nose is deformed. The disease brings hoarseness, and necessitates amputations of the fingers and toes. Do not sleep with the patients, as the disease is transmittable to those nearby.", the first document concerning infectivity.
In the West, the earliest known description of leprosy there was made by the Roman encyclopedist Aulus Cornelius Celsus (25 BC – 37 AD) in his De Medicina; he called leprosy "elephantiasis". The Roman author Pliny the Elder (23–79 AD) mentioned the same disease. Although "sara't" of Leviticus (Old Testament) is translated as "lepra" in the 5th century AD Vulgate, the original term sara't found in Leviticus was not the elephantiasis described by Celsus and Pliny; in fact, sara't was used to describe a disease which could affect houses and clothing. Katrina C. D. McLeod and Robin D. S. Yates state that sara't "denotes a condition of ritual impurity or a temporary form of skin disease."
Numerous leprosaria, or leper hospitals, sprang up in the Middle Ages; Matthew Paris, a Benedictine Monk, estimated that in the early thirteenth century there were 19,000 across Europe. The first recorded Leper colony was in Harbledown. These institutions were run along monastic lines and, while lepers were encouraged to live in these monastic-type establishments, this was for their own health as well as quarantine. Indeed, some medieval sources indicate belief that those suffering from leprosy were considered to be going through Purgatory on Earth, and for this reason their suffering was considered holier than the ordinary person's. More frequently, lepers were seen to exist in a place between life and death: they were still alive, yet many chose or were forced to ritually separate themselves from mundane existence. The Order of Saint Lazarus was a hospitaller and military order of monks that began as a leper hospital outside Jerusalem in the twelfth century and remained associated with leprosy throughout its history. The first monks in this order were leper knights and they originally had leper grand masters, although these aspects of the order changed over the centuries.
Radegund was noted for washing the feet of lepers. Orderic Vitalis writes of a monk, Ralf, who was so overcome by the plight of lepers that he prayed to catch leprosy himself (which he eventually did). The leper would carry a clapper and bell to warn of his approach, and this was as much to attract attention for charity as to warn people that a diseased person was near.
After the end of the 17th century, Norway and Iceland were the only countries in Western Europe where leprosy was a significant problem. During the 1830s, the number of lepers in Norway rose rapidly, causing an increase in medical research into the condition, and the disease became a political issue. Norway appointed a medical superintendent for leprosy in 1854 and established a national register for lepers in 1856, the first national patient register in the world.
Mycobacterium leprae, the causative agent of leprosy, was discovered by G. H. Armauer Hansen in Norway in 1873, making it the first bacterium to be identified as causing disease in humans. He worked at St. Jørgens Hospital in Bergen, founded early in the fifteenth century. St. Jørgens is today a museum, Lepramuseet, probably the best preserved leprosy hospital in Northern Europe.
There were cases of leprosy in Atlantic Canada at the end of the 19th century. The patients were first housed on Sheldrake Island in the Miramichi river and later transferred to Tracadie [disambiguation needed]. Catholic nuns (the religieuses hospitalières de Saint-Joseph, RHSJ) came to take care of the sick. They opened the first French-language hospital in New-Brunswick and many more followed. Many hospitals opened by the RHSJ nuns are still in use today. The last hospital to house lepers in Tracadie was demolished in 1991. Its lazaretto section had been closed since 1965. In a century of existence, it had housed not only acadian victims of the disease, but people from all over Canada as well as sick immigrants from Iceland, Russia and China, among other nations.
Society and culture
|Lists of miscellaneous information should be avoided. Please relocate any relevant information into appropriate sections or articles. (December 2009)|
Lepers in the Bible
- The Bible has a number of references such as Moses's sister (), Moses (), commander of the army of Syria Naaman the Syrian and later the prophet Elisha's servant Gehazi (), and several people Jesus healed (, ), though the afflictions mentioned and symptoms described are now thought not to be, or not exclusively to be, the result of Hansen's Disease (see discussion at 'Tzaraath').
Famous persons with leprosy
- King Baldwin IV of Jerusalem, who was portrayed as a character in the film Kingdom of Heaven
- Saint Damien of Molokaʻi was a Roman Catholic missionary-priest who contracted leprosy while serving the leper colony at Molokaʻi and continued to serve the lepers until he died from the effects of the disease himself. He was canonized on October 11, 2009 at a Vatican ceremony presided over by Pope Benedict XVI
- Robert Vincent Giglio III
- Vietnamese poet Han Mac Tu
- King Louis I of France, known as the Leper King
- Possibly Robert the Bruce, King of Scots
- Otani Yoshitsugu, a Japanese daimyo
- The protagonist of The Chronicles of Thomas Covenant, the Unbeliever contracts leprosy, the central point of the entire series.
- In Hamlet, a Shakespearean play, the ghost of old king Hamlet, prince Hamlet's father, claimed to have been poisoned by a 'leprous distillment', as he contracted several symptoms similar to those of leprosy such as pustulating boils.
- In the original book (and movies based on the book) Ben Hur, the mother and sister of Judah Ben-Hur, the protagonist, contract leprosy while in prison.
- Rachel Kalama in the novel Molokai is sent away from Honolulu to live on the leper colony in Molokai.
- In the novel Healing Water by Joyce Moyer Hostetter, a Hawaiian teenager struggles to survive the leper colony of Molokai in the 1860s.
- The Island is a historical novel written by Victoria Hislop, much of which is set in a leper colony on the Mediterranean island of Spinalonga
- Caius Merlyn Brittanicus from The Camulod Chronicles contracts leprosy while trying to save a bleeding leper from freezing to death.
- The protagonist of the book The Leper by Steve Thayer is an American soldier who is infected during World War I and contracts the disease
- In the 1973 film Papillon, Steve McQueen portrays a prisoner of Devil's Island who during an attempted escape encounters a leper colony.
- In Tess Gerritsen's 2003 novel The Sinner, Maura's post-mortem tests on an unidentified body found in an abandoned Boston warehouse show this victim to be Indian leprosy victim born perhaps 40 or 50 years before the date of the corpse being studied
- In the TV-series Monk, S05-E10, Derek Bronson, of Bronson Technologies suffers from leprosy.
- In The Simpsons episode "Little Big Mom", Lisa fools Bart and Homer into thinking they have leprosy. Ned Flanders sends them to the island of Molokai for treatment.
- The Sherlock Holmes short-story "The Adventure of the Blanched Soldier" concerns a soldier who is thought to have contracted leprosy, but turns out that the real problem is ichthyosis.
- Dante from The Last Vampire series by Christopher Pike appeared to Sita to suffer from leprosy.
- ^ Sasaki S, Takeshita F, Okuda K, Ishii N (2001). "Mycobacterium leprae and leprosy: a compendium". Microbiol Immunol 45 (11): 729–36. PMID 11791665. http://www.jstage.jst.go.jp/article/mandi/45/11/729/_pdf.
- ^ a b c "New Leprosy Bacterium: Scientists Use Genetic Fingerprint To Nail 'Killing Organism'". ScienceDaily. 2008-11-28. http://www.sciencedaily.com/releases/2008/11/081124141047.htm. Retrieved 2010-01-31.
- ^ a b Kenneth J. Ryan, C. George Ray, editors. (2004). Ryan KJ, Ray CG. ed. Sherris Medical Microbiology (4th ed.). McGraw Hill. pp. 451–3. ISBN 0838585299. OCLC 52358530 61405904.
- ^ "Lifting the stigma of leprosy: a new vaccine offers hope against an ancient disease". Time 119 (19): 87. May 1982. PMID 10255067. http://www.time.com/time/magazine/article/0,9171,925377,00.html.
- ^ Kulkarni GS (2008). Textbook of Orthopedics and Trauma (2 ed.). Jaypee Brothers Publishers. p. 779. ISBN 8184482426, 9788184482423.
- ^ Holden (2009). "Skeleton Pushes Back Leprosy's Origins". ScienceNOW. http://sciencenow.sciencemag.org/cgi/content/full/2009/527/1. Retrieved 2010-01-31.
- ^ a b c d e f "Leprosy". WHO. 2009-08-01. http://www.who.int/mediacentre/factsheets/fs101/en/. Retrieved 2010-01-31.
- ^ "DNA of Jesus-Era Shrouded Man in Jerusalem Reveals Earliest Case of Leprosy". ScienceDaily. 2009-12-16. http://www.sciencedaily.com/releases/2009/12/091216103558.htm. Retrieved 2010-01-31.
- ^ a b WHO (1995). [Expression error: Missing operand for > "Leprosy disabilities: magnitude of the problem"]. Weekly Epidemiological Record 70 (38): 269–75. PMID 7577430.
- ^ a b Walsh F (2007-03-31). "The hidden suffering of India's lepers". BBC News. http://news.bbc.co.uk/2/hi/programmes/from_our_own_correspondent/6510503.stm.
- ^ Lyn TE (2006-09-13). "Ignorance breeds leper colonies in China". Independat News & Media. http://www.iol.co.za/index.php?set_id=1&click_id=117&art_id=qw1158139440409B243. Retrieved 2010-01-31.
- ^ Radan S, Hutt A (2001-11-06). "Europe's last leper colony lives on". BBC News. http://news.bbc.co.uk/2/hi/europe/1639335.stm. Retrieved 2010-01-31.
- ^ "“Making Peace With Vietnam” to be screened at Beijing film festival". Radio the Voice of Vietnam. 2009-02-08. http://english.vovnews.vn/Home/Making-Peace-With-Vietnam-to-be-screened-at-Beijing-film-festival/20092/101642.vov. Retrieved 2010-01-31.
- ^ Japan repealed its "Leprosy Prevention Laws" in 1996 but former patients still reside in sanatoriums. See Koizumi apologises for leper colonies. BBC News. May 25, 2001 and Ex-Hansen's disease patients still struggling with prejudice Japan Times June 7, 2007.
- ^ Syphilis through history Encyclopædia Britannica
- ^ "about leprosy: frequently asked questions". American Leprosy Missions, Inc. http://www.leprosy.org/getinformed/aboutleprosy/leprosyfaq.php. Retrieved September 19, 2009.
- ^ "about leprosy: statistics". American Leprosy Missions, Inc. http://www.leprosy.org/getinformed/aboutleprosy/statistics.php. Retrieved September 19, 2009.
- ^ "about leprosy: the basics". American Leprosy Missions, Inc. http://www.leprosy.org/getinformed/aboutleprosy/basics.php. Retrieved September 19, 2009.
- ^ Jopling WH (March 1991). [Expression error: Missing operand for > "Leprosy stigma"]. Lepr Rev 62 (1): 1–12. PMID 2034017.
- ^ a b "Communicable Diseases Department, Leprosy FAQ". World Health Organization. 2006-05-25. http://www.searo.who.int/en/section10/section373_11716.htm. Retrieved 2010-01-31.
- ^ Smith DS (2008-08-19). "Leprosy: Overview". eMedicine Infectious Diseases. http://emedicine.medscape.com/article/220455-overview. Retrieved 2010-02-01.
- ^ Singh N, Manucha V, Bhattacharya SN, Arora VK, Bhatia A (June 2004). [Expression error: Missing operand for > "Pitfalls in the cytological classification of borderline leprosy in the Ridley-Jopling scale"]. Diagn. Cytopathol. 30 (6): 386–8. doi:10.1002/dc.20012. PMID 15176024.
- ^ Ridley DS, Jopling WH (1966). [Expression error: Missing operand for > "Classification of leprosy according to immunity. A five-group system"]. Int. J. Lepr. Other Mycobact. Dis. 34 (3): 255-73. PMID 5950347.
- ^ Modlin RL (June 1994). [Expression error: Missing operand for > "Th1-Th2 paradigm: insights from leprosy"]. J. Invest. Dermatol. 102 (6): 828–32. doi:10.1111/1523-1747.ep12381958. PMID 8006444.
- ^ James, William D.; Berger, Timothy G.; et al. (2006). Andrews' Diseases of the Skin: clinical Dermatology. Saunders Elsevier. ISBN 0-7216-2921-0.
- ^ Jardim MR, Antunes SL, Santos AR, et al. (July 2003). [Expression error: Missing operand for > "Criteria for diagnosis of pure neural leprosy"]. J. Neurol. 250 (7): 806–9. doi:10.1007/s00415-003-1081-5. PMID 12883921.
- ^ Mendiratta V, Khan A, Jain A (2006). [Expression error: Missing operand for > "Primary neuritic leprosy: a reappraisal at a tertiary care hospital"]. Indian J Lepr 78 (3): 261–7. PMID 17120509.
- ^ Ishida Y, Pecorini L, Guglielmelli E (July 2000). [Expression error: Missing operand for > "Three cases of pure neuritic (PN) leprosy at detection in which skin lesions became visible during their course"]. Nihon Hansenbyo Gakkai Zasshi 69 (2): 101–6. PMID 10979277.
- ^ Mishra B, Mukherjee A, Girdhar A, Husain S, Malaviya GN, Girdhar BK (1995). [Expression error: Missing operand for > "Neuritic leprosy: further progression and significance"]. Acta Leprol 9 (4): 187–94. PMID 8711979.
- ^ Talwar S, Jha PK, Tiwari VD (September 1992). [Expression error: Missing operand for > "Neuritic leprosy: epidemiology and therapeutic responsiveness"]. Lepr Rev 63 (3): 263–8. PMID 1406021.
- ^ McMurray DN (1996). Mycobacteria and Nocardia. in: Baron's Medical Microbiology (Baron S et al., eds.) (4th ed.). Univ of Texas Medical Branch. ISBN 0-9631172-1-1. OCLC 33838234. http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=mmed.section.1833.
- ^ Bhattacharya S, Vijayalakshmi N, Parija SC (1 October 2002). "Uncultivable bacteria: Implications and recent trends towards identification". Indian journal of medical microbiology 20 (4): 174–7. PMID 17657065. http://www.ijmm.org/article.asp?issn=0255-0857;year=2002;volume=20;issue=4;spage=174;epage=177;aulast=Bhattacharya.
- ^ Rojas-Espinosa O, Løvik M (2001). [Expression error: Missing operand for > "Mycobacterium leprae and Mycobacterium lepraemurium infections in domestic and wild animals"]. Rev. - Off. Int. Epizoot. 20 (1): 219–51. PMID 11288514.
- ^ Hastings RC, Gillis TP, Krahenbuhl JL, Franzblau SG (1988-07-01). "Leprosy". Clin. Microbiol. Rev. 1 (3): 330–48. PMID 3058299. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=3058299.
- ^ Alcaïs A, Mira M, Casanova JL, Schurr E, Abel L (2005). [Expression error: Missing operand for > "Genetic dissection of immunity in leprosy"]. Curr. Opin. Immunol. 17 (1): 44–8. doi:10.1016/j.coi.2004.11.006. PMID 15653309.
- ^ "AR Dept of Health debunks leprosy fears". 2008-02-08. http://www.kfsm.com/Global/story.asp?S=7845322. Retrieved 2008-04-08.
- ^ Kaur H, Van Brakel W (2002). [Expression error: Missing operand for > "Dehabilitation of leprosy-affected people—a study on leprosy-affected beggars"]. Leprosy review 73 (4): 346–55. PMID 12549842.
- ^ Doull JA, Guinto RA, Rodriguez RS, et al. (1942). [Expression error: Missing operand for > "The incidence of leprosy in Cordova and Talisay, Cebu, Philippines"]. International Journal of Leprosy 10: 107–131.
- ^ Noordeen S, Neelan P (1978). [Expression error: Missing operand for > "Extended studies on chemoprophylaxis against leprosy"]. Indian J Med Res 67: 515–27. PMID 355134.
- ^ Weddell G, Palmer E (1963). [Expression error: Missing operand for > "The pathogenesis of leprosy. An experimental approach"]. Leprosy Review 34: 57–61. PMID 13999438.
- ^ Job C, Jayakumar J, Aschhoff M (1999). [Expression error: Missing operand for > ""Large numbers" of Mycobacterium leprae are discharged from the intact skin of lepromatous patients; a preliminary report"]. Int J Lepr Other Mycobact Dis 67 (2): 164–7. PMID 10472371.
- ^ Arch Dermato Syphilis 1898; 44:159–174
- ^ Shepard C (1960). [Expression error: Missing operand for > "Acid-fast bacilli in nasal excretions in leprosy, and results of inoculation of mice"]. Am J Hyg 71: 147–57. PMID 14445823.
- ^ Pedley J (1973). [Expression error: Missing operand for > "The nasal mucus in leprosy"]. Lepr Rev 44 (1): 33–5. PMID 4584261.
- ^ Davey T, Rees R (1974). [Expression error: Missing operand for > "The nasal dicharge in leprosy: clinical and bacteriological aspects"]. Lepr Rev 45 (2): 121–34. PMID 4608620.
- ^ Rees R, McDougall A (1977). [Expression error: Missing operand for > "Airborne infection with Mycobacterium leprae in mice"]. J Med Microbiol 10 (1): 63–8. doi:10.1099/00222615-10-1-63. PMID 320339.
- ^ Chehl S, Job C, Hastings R (1985). [Expression error: Missing operand for > "Transmission of leprosy in nude mice"]. Am J Trop Med Hyg 34 (6): 1161–6. PMID 3914846.
- ^ CDC Disease Info hansens_t Hansen's Disease (Leprosy)
- ^ Montestruc E, Berdonneau R (1954). [Expression error: Missing operand for > "2 New cases of leprosy in infants in Martinique"] (in French). Bull Soc Pathol Exot Filiales 47 (6): 781–3. PMID 14378912.
- ^ Moet FJ, Pahan D, Oskam L, Richardus JH (2008). [Expression error: Missing operand for > "Effectiveness of single dose rifampicin in preventing leprosy in close contacts of patients with newly diagnosed leprosy: cluster randomised controlled trial"]. BMJ 336: 761. doi:10.1136/bmj.39500.885752.BE. PMID 18332051.
- ^ Bakker MI, Hatta M, Kwenang A, et al. (1 April 2005). "Prevention of leprosy using rifampicin as chemoprophylaxis". Am J Trop Med Hyg 72 (4): 443–8. PMID 15827283. http://www.ajtmh.org/cgi/content/abstract/72/4/443?ijkey=4b15a78b876fd990dfd877ee89b22399c026501c&keytype2=tf_ipsecsha.
- ^ Fine PE, Smith PG (1996). [Expression error: Missing operand for > "Vaccination against leprosy—the view from 1996"]. Lepr Rev 67 (4): 249–52. PMID 9033195.
- ^ Karonga prevention trial group (1996). [Expression error: Missing operand for > "Randomized controlled trial of single BCG, repeated BCG, or combined BCG and killed Mycobacterium leprae vaccine for prevention of leprosy and tuberculosis in Malawi"]. Lancet 348: 17–24. doi:10.1016/S0140-6736(96)02166-6. PMID 8691924.
- ^ Rees RJ, Pearson JM, Waters MF (1970). [Expression error: Missing operand for > "Experimental and clinical studies on rifampicin in treatment of leprosy"]. Br Med J 688 (1): 89–92. doi:10.1136/bmj.1.5688.89. PMID 4903972.
- ^ Yawalkar SJ, McDougall AC, Languillon J, Ghosh S, Hajra SK, Opromolla DV, Tonello CJ (1982). [Expression error: Missing operand for > "Once-monthly rifampicin plus daily dapsone in initial treatment of lepromatous leprosy"]. Lancet 8283 (1): 1199–1202. doi:10.1016/S0140-6736(82)92334-0. PMID 6122970.
- ^ "Chemotherapy of Leprosy". WHO Technical Report Series 847. WHO. 1994. http://www.who.int/lep/mdt/chemotherapy/en/index.html. Retrieved 2007-03-24.
- ^ "Seventh WHO Expert Committee on Leprosy". WHO Technical Report Series 874. WHO. 1998. http://www.who.int/lep/resources/expert/en/index.html. Retrieved 2007-03-24.
- ^ "Mortality and Burden of Disease Estimates for WHO Member States in 2002" (xls). World Health Organization. 2002. http://www.who.int/entity/healthinfo/statistics/bodgbddeathdalyestimates.xls.
- ^ Last Days Of A Leper Colony. CBC News. March 22, 2003.
- ^ Surgery grants for leprosy sufferers in India. Times of India. February 2, 2009.
- ^ CDC Leprosy Fact Sheet.
- ^ a b What is Leprosy?, The Leprosy Mission Canada
- ^ World Health Organization. (1985). [Expression error: Missing operand for > "Epidemiology of leprosy in relation to control. Report of a WHO Study Group"]. World Health Organ Tech Rep Ser (Geneva: World Health Organization) 716: 1–60. ISBN 9241207167. OCLC 12095109. PMID 3925646.
- ^ "Global leprosy situation, 2006" (PDF). Weekly Epidemiological Record 81 (32): 309–16. August 2006. PMID 16903018. http://www.who.int/lep/resources/wer8132.pdf.
- ^ Artscroll Tanakh, 6
- ^ Kane J, Summerbell RC, Sigler L, Krajden S, Land G (1997). Laboratory Handbook of Dermatophytes: A clinical guide and laboratory manual of dermatophytes and other filamentous fungi from skin, hair and nails. Star Publishers (Belmont, CA). ISBN 0898631572. OCLC 37116438.
- ^ Lock et al; p. 420
- ^ a b Kearns & Nash (2008)
- ^ Aufderheide, A. C.; Rodriguez-Martin, C. & Langsjoen, O. (1998) The Cambridge Encyclopedia of Human Paleopathology. Cambridge University Press ISBN 0521552036; p. 148.
- ^ Dwivedi & Dwivedi (2007)
- ^ Kutumbian, P. (2005) Ancient Indian Medicine. Orient Longman ISBN 8125015213; pp. XXXII-XXXIII
- ^ Leprosy - Medical History of British India, National Library of Scotland
- ^ Robbins G, Tripathy VM, Misra VN, Mohanty RK, Shinde VS, et al. (2009). Ancient Skeletal Evidence for Leprosy in India (2000 B.C.) PLoS ONE 4(5): e5669. doi:10.1371/journal.pone.0005669
- ^ a b "Skeleton shows earliest evidence of leprosy". Associated Press. 2009-05-27. http://www.google.com/hostednews/ap/article/ALeqM5idNIe5ytThacobusirf-k5Bfwl_gD98E87F80. Retrieved 2009-05-29.
- ^ a b "Skeleton Pushes Back Leprosy's Origins". Science Now. 2009-05-27. http://sciencenow.sciencemag.org/cgi/content/full/2009/527/1?rss=1. Retrieved 2009-05-29.
- ^ "Leprosy belonged to Ahar Chalcolithic era: Expert". The Times of India. 2009-05-29. http://timesofindia.indiatimes.com/Pune/Leprosy-belonged-to-Ahar-Chalcolithic-era-Expert/articleshow/4590778.cms. Retrieved 2009-05-29.
- ^ "‘Oldest evidence of leprosy found in India’". The Times of India. 2009-05-27. http://timesofindia.indiatimes.com/Health--Science/Oldest-proof-of-leprosy-found-in-India/articleshow/4585654.cms. Retrieved 2009-05-29.
- ^ Hansen's disease in Japan: a brief history Kikuchi I Int J Dermatol 1997:36:629-633.
- ^ Cite error: Invalid
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mcleod_yates_152_153; see Help:Cite error.
- ^ "Leprosy". Catholic Encyclopedia. New York: Robert Appleton Company. 1913. http://sources.wikipedia.org/wiki/Catholic_Encyclopedia_(1913)/Leprosy.
- ^ Brody, Saul Nathaniel (1974). The Disease of the Soul: Leprosy in Medieval Literature. Ithaca: Cornell Press.
- ^ "The Leprosy Archives in Bergen, Norway". http://digitalarkivet.uib.no/lepra-eng/intro.htm. Retrieved 2009-05-30.
- ^ Hansen GHA (1874). [Expression error: Missing operand for > "Undersøgelser Angående Spedalskhedens Årsager (Investigations concerning the etiology of leprosy)"] (in Norwegian). Norsk Mag. Laegervidenskaben 4: 1–88.
- ^ Irgens L (2002). [Expression error: Missing operand for > "The discovery of the leprosy bacillus"]. Tidsskr nor Laegeforen 122 (7): 708–9. PMID 11998735.
- ^ Bymuseet i Bergen
- ^ http://personal.nbnet.nb.ca/rhsjnda/Page20.html
- 1877: Lewis, T. R.; D. D. Cunningham (1877). Leprosy In India. Calcutta: Office Of The Superintendent Of Government Printing. http://books.google.com/books?id=wHMIAAAAQAAJ. Retrieved 2009-08-07.
- 1895: Ashmead, Albert S. (1895). Pre-Columbian Leprosy. Chicago: American Medical Association Press. http://books.google.com/books?id=imSHLN5DvgYC. Retrieved 2009-08-07.
- 1895: Prize Essays On Leprosy. London: The New Sydenham Society. 1895. http://books.google.com/books?id=qUEJAAAAIAAJ. Retrieved 2009-08-07.
- 1896: Impey, S. P. (1896). A Handbook On Leprosy. Philadelphia: P. Blakiston, Son & Co.. http://books.google.com/books?id=wHMIAAAAQAAJ. Retrieved 2009-08-07.
- 1916: "Fighting Leprosy In The Philippines". The World's Work: A History of Our Time XXXI: 310–320. January 1916. http://books.google.com/books?id=09_Sr9emceQC&pg=PA310. Retrieved 2009-08-04.
- 1991:William Jopling. Leprosy stigma. Lepr Rev 1991, 62, 1-12.
- Documentary film about leprosy
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Adolescence is a period of development of the individual that extends from 10 to 19 years and has particular biological and psychological characteristics. This definition, which varies according to the source, is not consensual as regards the psychological, physical and social development of each one.
Adolescence begins with pubertal phenomena that will result in many changes in the body, and totally alter the relationship to the body at different ages. The start of puberty can take place between 9 and 15 years in the boy whereas in the girl it can take place between 8 and 13 years.
The majority of individuals begin and model their drinking in adolescence. Alcohol, as well as tobacco, is one of the first products encountered by the adolescent, one of the most accessible and therefore logically the one most often consumed. The annual epidemiological work of the French Observatory on Drugs and Drug Addiction (OFDT) clearly underlines this.
Unlike their elders, adolescents consume alcohol preferentially outside meals. This consumption is initially occasional, discontinuous, often at the family home during festive events, authorized by the parents themselves. In fact, 70-80% of teenagers before the age of 11 have already tasted beer, wine or champagne and more than 20% have already been drunk.
The risks associated with alcohol use vary according to the pubertal stage of the adolescent: a 14 year old adolescent reacts very differently to alcohol exposure depending on the pubertal period in which he is. The risks associated with the use of alcohol also vary according to the stage of psychological development of the consumer.
The psychotropic effect of alcohol is generally more harmful in developing subjects, as it affects a brain in full pubertal maturation and can interrupt natural neurobiological programs.
Clinically, this may lead to cognitive impairment, altering interactions with others and / or the environment.
Studies in functional magnetic resonance imaging (MRI) have revealed some abnormalities in adolescents with pathological alcohol consumption.
The search for sensations and the search for novelties are factors that must be taken into account both in the understanding of consumer behavior at the level of society and when it comes to addressing, on an individual level, a given teenager. Finally, the peer group occupies a central place in the adolescent’s life and there is a profound desire to experiment with new behaviors to shape one’s own identity.
Different epidemiological studies such as the Survey of Representations, Opinions and Perceptions on Psychotropic Drugs (EROPP), Health and Consumer Surveys in the Defense Preparation Appeal (ESCAPAD), the French Observatory of Drugs (OFDT), the Health Barometer, the European School Survey Project on Alcohol and Other Drugs (ESPAD) and INSERM, are used to assess levels of alcohol use among adolescents and recent developments in the different forms of consumption at the end of adolescence.
Over the past thirty years, regular consumption of wine has gradually been replaced, especially for the new generations, by occasional consumption of beer – the drink most frequently consumed by adolescents with little variation depending on the socio-economic level -, d the main characteristics of which are detailed below.
Compared to other countries such as Denmark, Greece, Belgium and the United Kingdom, where the figures are high, the percentage of 15-year-olds drinking beer at least once a week is relatively low (20 % for boys and 8% for girls).Moreover, the proportion of young people who consume beer regularly decreased in France in 16 years, unlike some countries like Russia. The daily consumption of young people decreases significantly in favor of consumption over the weekend.
The analysis of the ESCAPAD survey shows that 76% of girls and 84% of boys have ever used alcohol in the last 30 days. An important point to note is the difference in regular use of alcohol, defined by 10 drinks during the last month, according to sex. Indeed, 21% of boys have a regular use of alcohol whereas this figure is 8% for girls.
Regular drunkenness, defined by at least 10 drunkenness during the year, is rare before the age of 16, as opposed to 17-18 years when most boys and girls consume alcohol.
In Europe, 7% of French teenagers aged 16 declare a regular use, placing France in 21st place among the European countries, Holland being the country with the highest regular consumption (25%) and Finland the one where it is the lowest (3%). Differences in alcohol consumption between countries can be explained.
These include the national contexts of alcohol consumption, the social status of alcohol, the influence of advertising campaigns, the role of the family environment, relationships between young people and the weight of initiation and regular consumption.
Risk factors for installing an addictive driving:
In order to assess the risks of alcohol consumption, it is imperative to investigate the existence of unsafe drinking patterns and individual and environmental risk factors during the first interviews with the adolescent.
Modalities of consumption at risk:
These forms of risky use correspond to the age at which the drug is consumed, the self-therapeutic nature of the consumption, the solitary or massive use of alcohol, the repetition of consumption, the cumulative consumption of psychoactive substances and at risk under the influence of alcohol. We detail them in the following.
Age of early onset:
It is a risk factor for the further development of harmful use for health (or abuse) and / or dependence, especially if the consumption repeats. Particular care must be taken when the use is very early due to the possible long-term medical, psychological, psychiatric and social consequences.
Cumulative consumption of psychoactive substances:
Autotherapeutic use – anxiolytic, antidepressant or hypnotic – may be indicative of underlying psychopathological disorders in a number of adolescents.
Alcohol solitary use:
Apart from the usual situations of consumption, it is often synonymous with an increase in consumption.
Repetition of consumption:
It is a mode of consumption to be taken into consideration: the greater the number of drinking, the longer the time of exposure to the effects of alcohol over life, the greater the risk of complications.
The effect sought by frequent consumption and / or in high quantities, by consumption outside socially regulated conditions, is that of a search for “stoning”, anesthesia, escape and forgetting of reality.
Alone or coupled with the consumption of other products (cannabis, cocaine, psychotropic drugs, ecstasy …) they can be massive and frequent. In general, frequent use of cannabis is associated and was preceded by the consumption of tobacco and alcohol. The increase in alcohol intoxication and tobacco use was shown to be correlated with cannabis use.
Some situations at risk:
For example, driving vehicles (scooters, motorcycles, cars) under the influence of alcohol must attract the attention of the practitioner. A blood alcohol concentration of 0.5 g / l multiplies the risk of an accident by a factor of 2. Beyond 0.8 g / l, this risk is multiplied by 10. Young drivers are particularly affected by the problem of drinking and driving. As cannabis use is frequently associated, the accidental road hazard is potentiated (multiplied by a factor of 15). Recent prevention campaigns have insisted on this important risk. Other situations such as unprotected intercourse, behavioral problems and pregnancy under the influence of alcohol should also be sought.
Individual and environmental risk factors:
Individual risk factors include genetic, psychological and psychiatric factors.
Individual psychological factors:
Among the individual psychological factors, it is important to specify the personality traits of the subject; the existence of personality traits such as low self-esteem, shyness, self-depreciation, excessive emotional reactions, difficulties in dealing with certain events, difficulties in having stable relationships and resolving interpersonal problems must be account.
Individual psychiatric factors:
Different pathologies can exist and must be the subject of a precise analysis during the various interviews. This may include conduct disorder, attention deficit hyperactivity, depression, repeated suicide attempts, bipolar disorder, anxiety disorders (obsessive-compulsive disorder, phobic disorder , panic disorder, generalized anxiety disorder, post-traumatic stress disorder), eating disorder, borderline or other personality disorder such as antisocial personality.
A statistically significant correlation between family history of alcohol dependence and early age of consumption was found. Intra-family functioning, education, parental tolerance for alcohol use and for breaking rules, life events are risk factors for the installation of addictive behavior. As we have seen above, the role of friends is indisputable in the initiation of alcohol, tobacco or other drugs, but does not explain the pathological behavior of drinking alone. Finally, the loss of social benchmarks such as poverty, precariousness, unemployment, lack of schooling, marginality is also an important risk factor.
Any adolescent, during a consultation in general medicine, school or a specialist should benefit from a tracking on his use of psychoactive substances.
After researching risk factors for the installation of an addictive alcoholic behavior, the clinician will define the type of consumption of the patient, be able to use locating questionnaires and evaluate the overall impact of consumption.
Different types of consumption:
It is socially accepted consumption without any physical, psychological or social complications.
Harmful Health Use (ICD-10) or Alcohol Abuse (DSM IV TR):
The harmful use for health or alcohol abuse can be a modality of consumption quite common in adolescents.
According to the Tenth International Classification of Diseases (WHO), the diagnostic criteria for harmful use of alcohol for health are as follows.
It is a mode of alcohol consumption that is detrimental to health.
Complications can be physical (hepatitis, polyneuropathy, pancreatitis …) or psychic (major depressive episode secondary to high alcohol consumption, attempted suicide …).
The diagnosis is based on clear evidence that the use of alcohol alone or in combination with other substances has led to psychological or physical problems.
This mode of consumption often gives rise to criticism and often has negative social consequences. Disapproval by others or by the cultural environment, and negative social consequences (police arrest, temporary detention, separation, etc.) are not enough to make the diagnosis.
This diagnosis is not made when the subject has a syndrome of addiction, a psychotic disorder or other specific disorder related to the use of alcohol or other psychoactive substances.
According to DSM IV revised version (DSM IV-TR), the diagnostic criteria for alcohol abuse are as follows.
Inadequate use of alcohol leading to functional impairment or clinically significant suffering characterized by the presence of at least one of the following events over a 12-month period:
• repeated use of alcohol leading to inability to fulfill major obligations at work, at school, or at home (repeated absences or poor performance at work due to alcohol use, absences , temporary or permanent school disqualifications, neglect of children or household chores);
• repeated use of alcohol in situations where it can be physically dangerous (eg, when driving a moped, scooter, car or operating a machine while is under the influence of alcohol);
• relationship to the use of alcohol;
• alcohol use in spite of persistent or recurring interpersonal or social problems caused or exacerbated by the effects of alcohol (eg, disputes with the spouse about the consequences of intoxication, fights).
The symptoms have never met the criteria for substance dependence for this class of substance.
Addiction is a rare phenomenon in adolescence.
We will use the diagnostic criteria of DSM IV to define it.
This is an inadequate use of a clinically significant substance that leads to a functional impairment or suffering, characterized by the presence of three (or more) of the following symptoms at any one time continuous period of 12 months:
• tolerance, defined by any of the following symptoms: C require significantly higher amounts of the substance to achieve intoxication or the desired effect; C significantly decreased in the case of continuous use of the same quantity of the substance;
• weaning characterized by one or the other of the following manifestations:
C weaning syndrome characteristic of the substance; C the same substance (or a very close substance) is taken to relieve or avoid withdrawal symptoms;
• the substance is often taken in greater quantities or for a longer period than expected;
• there is a persistent desire, or unsuccessful effort, to decrease or control the use of the substance;
• a significant amount of time has gone into activities necessary to obtain the substance (eg, to smoke continuously), or to recover from its effects;
• significant social, occupational or recreational activities are abandoned or reduced because of the use of the substance;
• the use of the substance is continued although the person is aware of a persistent or recurring psychological or physical problem that may have been caused or exacerbated by the substance (eg continued cocaine use although the person admitted cocaine-related depression, or continued alcoholic beverages, although the subject acknowledged an aggravation of an ulcer as a result of alcohol consumption).
• with physical dependence: presence of tolerance or withdrawal;
• no physical dependence: no tolerance or withdrawal.
Clinical features of the adolescent:
Various elements concerning the pathological consumption of alcohol in adolescents have been raised in the literature.
Consumption behaviors during adolescence are much less fixed than in adults. As we have seen, these behaviors are different according to sex and variable according to individuals.
Dependence is a very rare phenomenon, but harmful use of alcohol for health (or abuse) is possible in adolescents.
In the adolescent, we speak of alcohol misuse because the adolescent does not completely answer the various diagnostic criteria of abuse or dependency defined in the adult.
Alcohol misuse in adolescents does not meet the WHO criteria (21 drinks per week in men and 14 drinks per week in women) and manifests itself in weekend drinks in large quantities between buddies, with the search for sensations and drunkenness.
Unlike adults, there are no biologic markers (CDT [desulphurised transferrin] …) to detect and affirm a disorder related to the use of alcohol in adolescents.
Consequences of pathological alcohol consumption :
The somatic complications of alcohol consumption usually found in adults such as alcoholic hepatitis, cirrhosis, peripheral neuropathies, and pancreatitis are very rare in adolescence.
The main consequences of an alcohol misuse in the adolescent are on the one hand social and on the other hand psychological.
Socially, school absenteeism, school failure, behavioral problems with fighting, delinquency, risk-taking in the sphere of sexual life (absence of contraception and protection in the event of sexual intercourse, sexual violence) and road accidents. In the latter case, the risk of accidents is magnified by the relative inexperience of many young people, by a denial of the danger and by the fact that their bodies are not yet accustomed to the consumption of large quantities of alcohol.
Psychologically, it is essentially hyperactivity with attention deficit, anxiety, depression and attempted suicide.
No longitudinal studies have been performed in France to assess the evolution of adolescent misuse in adults.However, prospective studies have provided some answers: a relative stability of pathological consumption behaviors has been shown over time (over a 2-year period, 50% of problematic consumers remained in this category); in a prospective follow-up of six years, compared to a control population, there was a 3.7-fold increase in alcohol abuse or dependence on previous pathological drinking.
Several French and English-language instruments are used to identify and evaluate the pathological consumption of alcohol and other psychoactive substances, particularly illicit substances, in adolescents. Alcohol misuse is commonly associated with cannabis in adolescents.
We will not make an exhaustive list of the existing tools, we will take as examples some of them that have been the subject of work in France.
The CRAFFT questionnaire was constructed and validated in the United States for the early detection of harmful uses of various addictive substances (cannabis, alcohol, other products) in adolescents. CRAFFT is the acronym for Car, Relax, Alone, Forget, Family / Friends, Trouble.
ADOSPA, French version of CRAFFT, is the acronym for the following items: Auto / motorcycle (Driving under influence or someone under the influence of alcohol or other drugs), Relaxation (self-treatment) (Problems, Friends / family (reproaches made by friends or family).
This tool was subjected to a general population validation study which showed that this tool was performing well in the early identification of regular uses, the daily use of cannabis and mixed drunkenness. At the score of 2, CRAFFTADOSPA showed qualities of widespread identification of the harmful use and at the score of 3, it detected the gravity of the consumptions. The recommendations recommended by the authors were that a score greater than or equal to 2 at CRAFFT-ADOSPA indicated a moderate risk and a score of 3 or more a high risk of harmful use in the adolescent or the young adult.
The POSIT, an acronym for the Problem Oriented Screening Instrument for Teenagers, is a locator instrument for adolescents aged 12 to 19 years that was developed by the National Institute on Drug Abuse (NIDA) in the United States and validated in schools. It identifies psychological and social health issues that may warrant further evaluation and require treatment. It is a questionnaire that evaluates 10 areas (or factors) classified from A to J: psychoactive substance use, physical health, mental health, intrafamilial relationships, relationships with family, academic situation, vocational guidance, social skills, recreation and aggressive behavior / delinquency. It contains 139 simple closed questions (yes / no).
Other questionnaires, such as the RISQ (Research and Intervention on Psychoactive Substances – Quebec), DEPADO (ADOlescents Screening), ADI (Adolescent Drinking Index), ADIS (Adolescent Drug Involvement Scale), ADAD Drug Abuse Diagnosis), the DAP (Drug and Alcohol Problem) can be cited.
Before a teen consumes, talk with him about the harms and risks of alcohol, tobacco, cannabis and / or other illicit psychoactive products is a first approach.
It is essential to prevent this by informing the population known to be the most vulnerable to alcohol and its close circle, especially to adults in contact with adolescents (educators, teachers, teachers, school doctors, school nurses).
Identify the various signs of appeal of the adolescent in difficulty and the factors of vulnerability and risk favoring early use, work on the fact that the adolescent is sometimes out of step with his / her own beliefs of a risky behavior, inform on the apparent and damaging consequences of alcohol (more than the inventory of somatic consequences) are important elements to be taken into account.
First, a therapeutic alliance should be established with the adolescent and his / her parents in order to establish a dialogue that is often broken and to recognize the difficulties and sufferings of the patient. It should be borne in mind that the adolescent builds his / her own identity and remains very sensitive to the role of peers who influence their relationships and consumption.
An overall assessment of the situation highlights individual risk factors, environmental factors, type of consumption (whether it is festive or occasional use, abuse or harmful use, dependence), possible consumptions (cannabis, other drugs …) and the importance of the risks incurred in order to adapt therapeutic management. Different therapeutic objectives will be proposed depending on the severity of the situation (binge drinking, associated psychopathology, harmful use for health or poly-consumptions).
In the adolescent, we must neither trivialize nor dramatize the consumption of alcohol and avoid confrontation.Depending on the clinical history, it is necessary to involve the family more or less in the care because its role is essential and to strengthen their skills is useful.
The different types of intervention used are most often based on validated techniques in adults, which adapt to the specific characteristics of adolescent development and its problems at this time of life. An orientation in the event of real problems with alcohol towards places of listening can facilitate a start of care.
Different therapeutic techniques:
In a patient in difficulty with alcohol and in request of assistance, the practitioner puts in place strategies to reduce or stop drinking.
It is necessary to inform the teenager about the product and its short-term damage more than long-term. Educational work plays a benchmark and information role in dealing with the risks the young person may face in order to respond to or oppose it.
Awareness of the risk involved often involves the use of self-evaluation scales associated with clinical interviewing to provide an informative exchange.
It may be useful to propose, as in adults, a therapeutic withdrawal time, and to emphasize that abstinence may have positive consequences on the overall functioning of the adolescent.
Different therapeutic techniques can be used.
Short intervention strategies have demonstrated their effectiveness in alcohol misuse. These are interventions of short duration and limited duration (12 sessions over a semester, for example), which are often inspired by motivational techniques.
They can be used on an outpatient basis or during hospitalization. They include a short evaluation with feedback, different objectives to be achieved, references to self-help techniques, and an assessment of changes in consumption patterns.
Motivational interviews, a patient-centered approach, invited to talk about the positive and negative aspects of its use, showed a statistically significant reduction in alcohol behaviors in adolescents with alcohol problems.
Cognitive and behavioral therapies with work on beliefs and expectations, developing coping skills, assertiveness.
Systemic family therapies: many studies have shown their efficacy.
Family speaking groups, telephone support.
The combination of these different therapeutic techniques with pharmacotherapy may be necessary in some cases.
Finally, work involving social actors coupled with these different techniques is a must.
How to deal with harmful use of alcohol for adolescent health:
We should not just inform the patient at this stage. Most often, there are risk factors that cause difficulties that need to be identified. Having established a relationship of trust, the search for psychological suffering, relational or educational difficulties is an essential step in the care of the patient.
The management of the psychopathological disorders found is done by a psychotherapeutic approach and if necessary pharmacological associated with a regular and attentive medical follow-up.
Family support can be offered in case of conflict.
The minor must be protected by identifying and eliminating risky situations and harmful relationships with a young person who is ready to modify them.
In the absence of severity criteria, it is preferable not to stigmatize the adolescent by directing him at this stage towards a specialized structure.
How to deal with alcohol dependence in adolescents:
Adolescent dependence remains a rare phenomenon.
This type of addictive behavior is characterized by daily and repeated use, excesses, poly-consumptions, family and social problems that are often serious. Specific therapeutic measures will be implemented within the framework of an institutional network with a coherent and reassuring management.
The initiation to alcohol, easy to access as tobacco and to the particular social status in France, is a significant phenomenon of adolescence. Dependence is a rare phenomenon at this time of life, it is more frequently found a harmful use of alcohol for health or even the notion of misuse, the peculiarities of adolescence making that these subjects do not fully fill the first two diagnostic categories mentioned above. Nevertheless, the pathological consumption of alcohol has harmful effects, in itself disrupting the psychic and social functioning of individuals, and at the root of an increased risk of certain psychiatric pathologies suicide) and road accidents. These pathological drinks are influenced by individual, familial and environmental risk factors that the practitioner should seek.
The training in addictology, the prevention and the use of different therapeutic techniques in case of a known disorder are essential to take charge of this type of patient.
Finally, it is necessary to develop longitudinal prospective studies in France on cohorts of statistically satisfactory size in order to evaluate the cognitive, psychological and somatic repercussions of the pathological consumptions begun in adolescence in adults. | <urn:uuid:3b35e60b-1c55-4635-ab21-b29cb80026c0> | {
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Dehydration Classification and external resources
Nurses encourage a patient to drink an oral rehydration solution to reduce dehydration he acquired from cholera.
ICD-10 E86 ICD-9 276.5
In physiology and medicine, dehydration (hypohydration) is defined as the excessive loss of body fluid. It is literally the removal of water (Ancient Greek: ὕδωρ hýdōr) from an object; however, in physiological terms, it entails a deficiency of fluid within an organism. Dehydration of skin and mucous membranes can be called medical dryness.
There are three types of dehydration: hypotonic or hyponatremic (primarily a loss of electrolytes, sodium in particular), hypertonic or hypernatremic (primarily a loss of water), and isotonic or isonatremic (equal loss of water and electrolytes). In humans, the most commonly seen type of dehydration by far is isotonic (isonatraemic) dehydration which effectively equates with hypovolemia, but the distinction of isotonic from hypotonic or hypertonic dehydration may be important when treating people who become dehydrated. Physiologically, dehydration, despite the name, does not simply mean loss of water, as water and solutes (mainly sodium) are usually lost in roughly equal quantities to how they exist in blood plasma. In hypotonic dehydration, intravascular water shifts to the extravascular space, exaggerating intravascular volume depletion for a given amount of total body water loss. Neurological complications can occur in hypotonic and hypertonic states. The former can lead to seizures, while the latter can lead to osmotic cerebral edema upon rapid rehydration.
Signs and symptoms
Symptoms may include headaches similar to what is experienced during a hangover, a sudden episode of visual snow, decreased blood pressure (hypotension), and dizziness or fainting when standing up due to orthostatic hypotension. Untreated dehydration generally results in delirium, unconsciousness, swelling of the tongue and, in extreme cases, death.
Dehydration symptoms generally become noticeable after 2% of one's normal water volume has been lost. Initially, one experiences thirst and discomfort, possibly along with loss of appetite and dry skin. This can be followed by constipation. Athletes may suffer a loss of performance of up to 30% and experience flushing, low endurance, rapid heart rates, elevated body temperatures, and rapid onset of fatigue.
Symptoms of mild dehydration include thirst, decreased urine volume, abnormally dark urine, unexplained tiredness, irritability, lack of tears when crying, headache, dry mouth, dizziness when standing due to orthostatic hypotension, and in some cases insomnia. Other possible symptoms include cloudy urine and stinging during urination. Blood tests may show hyperalbuminemia. Mild dehydration also has been shown to negatively impact people’s moods. Experiments by the USDA's Agricultural Research Service has shown that dehydration is associated with confusion, fatigue, and negative moods. Mild dehydration, which includes water losses between 1% and 2%, observed in the experiment are comparable to mild dehydration experienced by people in their everyday lives.
In moderate to severe dehydration, there may be no urine output at all. Other symptoms in these states include lethargy or extreme sleepiness, seizures, sunken fontanel (soft spot) in infants, fainting, and sunken eyes.
The symptoms become increasingly severe with greater water loss. One's heart and respiration rates begin to increase to compensate for decreased plasma volume and blood pressure, while body temperature may rise because of decreased sweating. At around 5% to 6% water loss, one may become groggy or sleepy, experience headaches or nausea, and may feel tingling in one's limbs (paresthesia). With 10% to 15% fluid loss, muscles may become spastic, skin may shrivel and wrinkle (decreased skin turgor), vision may dim, urination will be greatly reduced and may become painful, and delirium may begin. Losses greater than 15% are usually fatal.
In people over age 50, the body’s thirst sensation diminishes and continues diminishing with age. Many senior citizens suffer symptoms of dehydration. Dehydration along with hyperthermia results in the elderly dying suddenly during extreme hot weather.
Diseases of the gastrointestinal tract can lead to dehydration in various ways. Often, dehydration becomes the major problem in an otherwise self-limited illness. Fluid loss may even be severe enough to become life-threatening.
In numerous studies of terminally ill patients who have chosen to die, it has been shown that deaths by terminal dehydration are generally peaceful, and are not associated with suffering when supplemented with adequate pain medication.
In humans, dehydration can be caused by a wide range of diseases and states that impair water homeostasis in the body. These include:
- External or stress-related causes
- Prolonged physical activity with sweating without consuming adequate water, especially in a hot and/or dry environment
- Prolonged exposure to dry air, e.g., in high-flying airplanes (5%–12% relative humidity)
- Blood loss or hypotension due to physical trauma
- Shock (hypovolemic)
- Use of methamphetamine, amphetamine, caffeine and other stimulants
- Excessive consumption of alcoholic beverages
- Electrolyte disturbance
- Recent rapid weight loss may reflect progressive depletion of fluid volume (the loss of 1 L of fluid results in a weight loss of 1 kg (2.2 lb)).
- Patient refusal of nutrition and hydration
- Inability to swallow (obstruction of the oesophagus)
Other causes of obligate water loss
- Severe hyperglycemia, especially in diabetes mellitus
- Diabetes insipidus
- Acute emergency dehydration event
- Foodborne illness
Dehydration is best avoided by drinking sufficient water. The greater the amount of water lost through perspiration, the more water must be consumed to replace it and avoid dehydration. Since the body cannot tolerate large deficits or excesses in total body water, consumption of water must be roughly concurrent with the loss (in other words, if one is perspiring, one should also be drinking some water frequently).
For routine activities in which a person is not perspiring to any large degree, drinking when one is thirsty is sufficient to maintain hydration. However, during exercise, relying on thirst alone may be insufficient to prevent dehydration from occurring. This is particularly true in hot environments or for those older than 65. For an exercise session, an accurate determination of how much fluid is necessary to consume during the workout can be made by performing appropriate weight measurements before and after a typical exercise session, to determine how much fluid is lost during the workout.
Drinking water beyond the needs of the body entails little risk when done in moderation, since the kidneys will efficiently remove any excess water through the urine with a large margin of safety.
A person's body, during an average day in a temperate climate such as the United Kingdom, loses approximately 2.5 litres of water. This can be through the lungs as water vapor (about 350ml), through the skin by perspiration (100ml) and by diffusion through the skin (350ml), or through the kidneys as urine (1000-2000ml, about 900ml of which is obligatory water excretion that gets rid of solutes). Some water (about 150-200ml, in the absence of diarrhea) is also lost through the bowels. In warm or humid weather or during heavy exertion, however, the water loss can increase by an order of magnitude or more through perspiration; all of which must be promptly replaced. In extreme cases, the losses may be great enough to exceed the body's ability to absorb water from the gastrointestinal tract; in these cases, it is not possible to drink enough water to stay hydrated, and the only way to avoid dehydration is to either pre-hydrate or find ways to reduce perspiration (through rest, a move to a cooler environment, etc.)
A useful rule of thumb for avoiding dehydration in hot or humid environments or during strenuous activity involves monitoring the frequency and character of urination. If one develops a full bladder at least every 3–5 hours and the urine is only lightly colored or colorless, chances are that dehydration is not occurring; if urine is deeply colored or urination occurs only after many hours or not at all, water intake may not be adequate to maintain proper hydration.
When large amounts of water are being lost through perspiration and concurrently replaced by drinking, maintaining proper electrolyte balance becomes an issue. Drinking fluids that are hypertonic or hypotonic with respect to perspiration may have grave consequences (hyponatremia or hypernatremia, principally) as the total volume of water turnover increases.
The treatment for minor dehydration often considered the most effective, is drinking water and stopping fluid loss. Plain water restores only the volume of the blood plasma, inhibiting the thirst mechanism before solute levels can be replenished. Solid foods can contribute to fluid loss from vomiting and diarrhea.
In more severe cases, correction of a dehydrated state is accomplished by the replenishment of necessary water and electrolytes (through oral rehydration therapy or fluid replacement by intravenous therapy). As oral rehydration is less painful, less invasive, less expensive, and easier to provide, it is the treatment of choice for mild dehydration. Solutions used for intravenous rehydration must be isotonic or hypotonic. Pure water injected into the veins will cause the breakdown (lysis) of red blood cells (erythrocytes).
For severe cases of dehydration where fainting, unconsciousness, or other severely inhibiting symptom is present (the patient is incapable of standing or thinking clearly), emergency attention is required. Fluids containing a proper balance of replacement electrolytes are given orally or intravenously with continuing assessment of electrolyte status; complete resolution is the norm in all but the most extreme cases.
Some research indicates that artificial hydration to alleviate symptoms of dry mouth and thirst in the dying patient may be futile.
- Ira R. Byock, M.D., "Patient Refusal of Nutrition and Hydration: Walking the Ever-Finer Line." American Journal Hospice & Palliative Care, pp. 8–13. (March/April 1995)
- ^ thefreedictionary.com > dehydration citing:
- Dorland's Medical Dictionary for Health Consumers. © 2007
- The American Heritage® Medical Dictionary Copyright © 2007
- Mosby's Medical Dictionary, 8th edition. © 2009
- Mosby's Dental Dictionary, 2nd edition. © 2008
- ^ TheFreeDictionary.com --> dehydration Citing The American Heritage Science Dictionary 2005. Retrieved on July 2, 2009
- ^ Lennox H Huang (Nov 3, 2009). Dehydration. eMedicine. http://emedicine.medscape.com/article/906999-overview
- ^ MedicineNet > Definition of Hypovolemia Retrieved on July 2, 2009
- ^ TheFreeDictionary.com --> hypovolemia Citing Saunders Comprehensive Veterinary Dictionary, 3 ed. Retrieved on July 2, 2009
- ^ Bean, Anita (2006). The Complete Guide to Sports Nutrition. A & C Black Publishers Ltd.. pp. 81–83. ISBN 0713675586.
- ^ http://www.ars.usda.gov/is/pr/2009/091123.htm#_top
- ^ Printz LA (April 1992). "Terminal dehydration, a compassionate treatment". Archives of Internal Medicine 152 (4): 697–700. doi:10.1001/archinte.152.4.697. PMID 1373053. http://archinte.ama-assn.org/cgi/pmidlookup?view=long&pmid=1373053.
- ^ Sullivan RJ (April 1993). "Accepting death without artificial nutrition or hydration". Journal of General Internal Medicine 8 (4): 220–224. doi:10.1007/BF02599271. PMID 8515334.
- ^ Dehydration Symptoms - Benefits of Drinking Water - Signs of Fluid Imbalance
- ^ "Water, Water, Everywhere". WebMD. http://www.webmd.com/balance/features/water-water-everywhere.
- ^ Dr. Mark Dedomenico. "Metabolism Myth #5". MSN Health. http://health.msn.com/blogs/healthy-diet-fit-body-post.aspx?post=1188190. [dead link]
- ^ a b "Exercise and Fluid Replacement". American College of Sports Medicine. http://journals.lww.com/acsm-msse/Fulltext/2007/02000/Exercise_and_Fluid_Replacement.22.aspx.
- ^ Nancy Cordes (April 2, 2008). "Busting The 8-Glasses-A-Day Myth". CBS. http://www.cbsnews.com/stories/2008/04/02/eveningnews/main3991145.shtml.
- ^ ""Drink at Least 8 Glasses of Water a Day" - Really?". Dartmouth Medical School. http://dms.dartmouth.edu/news/2002_h2/08aug2002_water.shtml.
- ^ Major Minerals. SparkNotes. http://www.sparknotes.com/health/minerals/major/section1.html
- ^ "Formulating carbohydrate-electrolyte drinks for optimal efficacy." Murray, R. & Stofan, J. (2001).
- ^ "Healthwise Handbook," Healthwise, Inc. 1999
- ^ JE Ellershaw, JM Sutcliffe, CM Saunders (1995). Dehydration and the dying patient. Journal of pain and symptom. http://linkinghub.elsevier.com/retrieve/pii/0885392494001233
- Dehydration Causes and Symptoms
- Water requirements in adults
- Definition of dehydration by the U.S. National Institutes of Health's MedlinePlus medical encyclopedia
- Rehydration Project at rehydrate.org
- About dehydration
- Are you drinking enough?
Water-electrolyte imbalance and acid-base imbalance (E86–E87, 276) Volume status Electrolyte Acid-baseBoth
- External or stress-related causes
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