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stressors, including physical illness. Children with DMDD have displayed elevated rates of social impair ments, school suspension, and service use. Irritability in adolescence has predicted the development of major depressive and dysthymic dis orders and generalized anxiety disorder (but not bipolar disorder) 20 years later, as well as lower educational attainment and income. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. 260 Part III u Behavioral and Psychiatric Disorders Table 39.6 DSM 5 Diagnostic Criteria for a Manic Episode A. A distinct period of abnormally and persistently elevated, expansive, or irritable mood and abnormally and persistently increased goal directed activity or energy, lasting at least 1 wk and present most of the day, nearly every day (or any duration if hospitalization is necessary). B. During the period of mood disturbance and increased energy or activity, three (or more) of the following symptoms (four if the mood is only irritable) are present to a significant degree and represent a noticeable change from usual behavior: 1. Inflated self esteem or grandiosity. 2. Decreased need for sleep (e.g., feels rested after only 3 hr of sleep). 3. More talkative than usual or pressure to keep talking. 4. Flight of ideas or subjective experience that thoughts are racing. 5. Distractibility (i.e., attention too easily drawn to unimportant or irrelevant external stimuli), as reported or observed. 6. Increase in goal directed activity (either socially, at work or school, or sexually) or psychomotor agitation (i.e., purposeless nongoal directed activity). 7. Excessive involvement in activities that have a high potential for painful consequences (e.g., engaging in unrestrained buying sprees, sexual indiscretions, or foolish business investments). C. The mood disturbance is sufficiently severe to cause marked impairment in social or occupational functioning or to necessitate hospitalization to prevent harm to self or others, or there are psychotic features. D. The episode is not attributable to the physiologic effects of a substance (e.g., a drug of abuse, a medication, other treatment) or to another medical condition. Note: A full manic episode that emerges during antidepressant treatment (e.g., medication, electroconvulsive therapy) but persists at a fully syndromal level beyond the physiologic effect of that treatment is sufficient evidence for a manic episode and, therefore, a bipolar I diagnosis. Note: Criteria A D constitute a manic episode. At least one lifetime manic episode is required for the diagnosis of bipolar I disorder. From the Diagnostic and Statistical Manual of Mental Disorders, 5th ed. p. 124. Copyright 2013. American Psychiatric Association. PREVENTION Experimental trials have sought to demonstrate the effectiveness of psychologic or educational strategies in preventing the onset of depres sive disorders in children and adolescents. These programs generally have provided information about the link between depressed mood, thoughts, and behaviors, as well as training in skills intended to modify these thoughts and behaviors. A Cochrane review found small effects of these programs on depression
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symptoms when implemented univer sally vs no intervention, with selective programs targeted at high risk groups performing better than universal programs; however, the effect of prevention programs was null compared with attention controls. Visit Elsevier eBooks at eBooks.Health.Elsevier.com for Bibliography. 39.2 Bipolar Disorders Colleen K. Manak and Rosa K. Kim The bipolar and related disorders include bipolar I, bipolar II, cyclo thymic, and other specifiedunspecified bipolar and related disorders, as well as bipolar and related disorder caused by another medical condition. A manic episode is characterized by a distinct period of at least 1 week in which there is an abnormally and persistently elevated, expan sive, or irritable mood and abnormally and persistently increased goal directed activity or energy that is present for most of the day, nearly every day (or any duration if hospitalization is necessary). The episode is associated with characteristic cognitive and behavioral symptoms, including disturbances in self regard, speech, attention, thought, activ ity, impulsivity, and sleep (Table 39.6). To diagnose bipolar I disorder, criteria must be met for at least one manic episode, and the episode must not be better explained by a psychotic disorder. The manic epi sode may be preceded and may be followed by hypomanic or major depressive episodes. Bipolar I disorder is rated as mild, moderate, or severe in the same way as the depressive disorders. To diagnose bipolar II disorder, criteria must be met for at least one hypomanic episode and at least one major depressive episode. A hypomanic episode is similar to a manic episode but is briefer (at least 4 days) and less severe (causes less impairment in functioning, is not associated with psychosis, and would not require hospitaliza tion) (Table 39.7). In bipolar II disorder, there must never have been a manic disorder, the episodes must not be better explained by a psy chotic disorder, and the symptoms of depression or the unpredict ability caused by frequent alternation between periods of depression and hypomania must cause clinically significant distress or functional impairment. Bipolar II disorder is also rated as mild, moderate, or severe. Cyclothymic disorder is characterized by a period of at least 1 year (in children and adolescents) in which there are numerous periods with hypomanic and depressive symptoms that do not meet criteria for a hypomanic episode or a major depressive episode, respectively (Table 39.8). EPIDEMIOLOGY The lifetime prevalence of bipolar disorder I among adults in the United States varies from 0.81.6, and bipolar II carries a lifetime prevalence of around 1.1. Bipolar I disorder affects males and females equally, whereas bipolar II disorder is more common in females. Life time rates of mania among youth have ranged from 0.11.7. The estimated annual number of U.S. office based visits of youth with a diagnosis of bipolar disorder increased from 25 per 100,000 population in 1994 1995 to 1,003100,000 in 2002 2003. U.S. hospital discharge diagnoses increased from 1.4 to 7.310,000 in 913 year old children and from 5.1 to 20.4 per 10,000 in 14 19 year
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olds. These increases were not found in U.K. diagnoses or hospital discharges, raising ques tions about whether bipolar disorder was being over diagnosed in the United States, with resultant increases in prescribing of antipsychotic and mood stabilizing medications. ETIOLOGY AND RISK FACTORS Twin studies suggest the heritability of bipolar disorder may be 6090; shared and unique environmental factors may account for 3040 and 1020, respectively. Offspring of parents with bipolar disorders are at high risk for early onset bipolar disorders as well as anxiety and behavioral disorders and mood dysregulation. There is an average 10 fold increased risk among adult relatives of individuals with bipolar disorder, with the magnitude of risk increasing with the degree of kinship. Bipolar disorder and schizophrenia likely share a common genetic origin, reflected in familial co aggregation of the two disorders. Studies to date suggest key roles for the amygdala, anterior paralim bic cortices, and their connections in the emotional dysregulation of bipolar disorder. Some of these abnormalities are apparent by adoles cence, whereas others appear to progress over adolescence into young adulthood. Dysthymic (sad), cyclothymic (labile), or hyperthymic (irritable) tem peraments may presage eventual bipolar disorder. Premorbid anxiety and dysphoria also are common. Environmental factors such as irri table and negative parenting styles, physical and sexual abuse, poor social support, and prenatal alcohol exposure may interact with genetic vulnerability to produce early onset of bipolar illness as well as negative prognostic indicators. Affective lability, in particular, has been associ ated with high levels of childhood trauma, and gradual sensitization to stressors has been linked to episode recurrence. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. Chapter 39 u Mood Disorders 261 SCREENING Cardinal manic symptoms of elation, increased energy, and grandiosity occurring in adolescents as a discrete episode representing an unequiv ocal and uncharacteristic change in functioning should alert pediat ric practitioners to the possibility of bipolar disorder. High scores on parent completed versions of mania specific rating scales (e.g., Gen eral Behavior Inventory, Child Mania Rating Scale, Young Mania Rating Scale) have been associated with increased likelihood of a bipolar diag nosis. However, screening tools for bipolar disorder have suboptimal psychometric properties when applied to young people. Because of the complexity of diagnosing and treating bipolar disorders, any suspected cases should be referred to the specialty mental health setting for com prehensive assessment and treatment. PRESENTATION In adolescents, the clinical manifestations of mania are similar to those in adults; psychosis (delusions, hallucinations) often is an associated symptom (see Chapter 47). Mood in a manic episode is often described as euphoric, excessively cheerful, high, or feeling on top of the world. During the episode, the adolescent may engage in multiple new proj ects that are initiated with little knowledge of the topic and often at unusual hours (middle of the night). Inflated self esteem is usually present, ranging
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from uncritical self confidence to marked grandiosity, and may reach delusional proportions. The adolescent may sleep little, if at all, for days and still feel rested and full of energy. Speech can be rapid, pressured, and loud and characterized by jokes, puns, amusing irrelevancies, and theatricality. Frequently there is a flight of ideas, evidenced by an almost continuous flow of accelerated speech, with abrupt shifts from one topic to another. Distractibility is evidenced by an inability to censor irrelevant extraneous stimuli, which often pre vents an individual with mania from engaging in a rational conversa tion. The expansive mood, grandiosity, and poor judgment often lead to reckless involvement in activities with high potential for personal harm. Controversy surrounds the applicability of the diagnostic criteria for mania to prepubertal children. It may be developmentally normal for children to be elated, expansive, grandiose, or talkative, reducing the specificity of these symptoms to this disorder. In addition, the distract ibility, overactivity, impulsivity, and irritability formerly ascribed to bipolar disorder by some investigators may be better explained by a diagnosis of ADHD, with or without comorbid ODD. The presentation of severe and pervasive irritability formerly diagnosed as bipolar dis order may be better captured by the diagnosis of DMDD. DIFFERENTIAL DIAGNOSIS Numerous psychiatric disorders, general medical conditions, and medications can generate manic like symptoms and must be distin guished from the bipolar and related disorders. The psychiatric disor ders include ADHD, ODD, and intermittent explosive, posttraumatic stress, depressive, anxiety, substance abuse, and borderline personality disorders. Medical conditions include neurologic disorders, endocrine disorders, infectious diseases, tumors, anemia, uremia, and vitamin deficiencies. Medications include androgens, bronchodilators, cardio vascular medications, corticosteroids, chemotherapy agents, thyroid preparations, and certain psychiatric medications (benzodiazepines, antidepressants, stimulants). The diagnosis of a bipolar disorder should be made after these other explanations for the observed symptoms have been ruled out. Substance induced mood disorder should also be considered and ruled out in patients presenting with mania. Table 39.7 DSM 5 Diagnostic Criteria for a Hypomanic Episode A. A distinct period of abnormally and persistently elevated, expansive, or irritable mood and abnormally and persistently increased goal directed activity or energy, lasting at least four consecutive days and present most of the day, nearly every day. B. During the period of mood disturbance and increased energy or activity, three (or more) of the following symptoms (four if the mood is only irritable) have persisted, represent a noticeable change from usual behavior, and have been present to a significant degree: 1. Inflated self esteem or grandiosity. 2. Decreased need for sleep (e.g., feels rested after only 3 hr of sleep). 3. More talkative than usual or pressure to keep talking. 4. Flight of ideas or subjective experience that thoughts are racing. 5. Distractibility (i.e., attention too easily drawn to unimportant or irrelevant external stimuli), as reported or observed. 6. Increase in goal directed activity (either socially, at work or school, or sexually) or psychomotor agitation (i.e., purposeless nongoal directed activity). 7. Excessive involvement in activities that have
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a high potential for painful consequences (e.g., engaging in unrestrained buying sprees, sexual indiscretions, or foolish business investments). C. The episode is associated with an unequivocal change in functioning that is uncharacteristic of the individual when not symptomatic. D. The disturbance in mood and the change in functioning are observable by others. E. The disturbance is not severe enough to cause marked impairment in social or occupational functioning or to necessitate hospitalization. If there are psychotic features, the episode is, by definition, manic. F. The episode is not attributable to the physiologic effects of a substance (e.g., a drug of abuse, a medication, other treatment) or to another medical condition. Note: A full hypomanic episode that emerges during antidepressant treatment (e.g., medication, electroconvulsive therapy) but persists at a fully syndromal level beyond the physiologic effect of that treatment is sufficient evidence for a hypomanic episode diagnosis. However, caution is indicated so that one or two symptoms (particularly increased irritability, edginess, or agitation following antidepressant use) are not taken as sufficient for diagnosis of a hypomanic episode, nor necessarily indicative of a bipolar diathesis. Note: Criteria A F constitute a hypomanic episode. Hypomanic episodes are common in bipolar I disorder but are not required for the diagnosis of bipolar I disorder. From the Diagnostic and Statistical Manual of Mental Disorders, 5th ed. p. 124. Copyright 2013. American Psychiatric Association. Table 39.8 A Comparison of Bipolar I and II and Cyclothymia in Children and Adolescents BIPOLAR I BIPOLAR II CYCLOTHYMIA Core feature(s) One manic episode One hypomanic episode AND one major depressive episode Symptoms of hypomania and depression, without meeting full criteria for a manic, hypomanic or depressive episode Duration Mania: 7 days Hypomania: 4 days Depressive episode: 14 days 1 year Associated symptoms Depressive episodes, hypomanic episodes, psychosis Chronic disruption in mood patterns Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. 262 Part III u Behavioral and Psychiatric Disorders For bipolar II disorder, the main differential is unipolar depression (MDD) or cyclothymic disorder, which are ruled out by the lack of a hypomanic episode and by not meeting full criteria for either a major depressive or hypomanic episode, respectively. COMORBIDITY The most common simultaneous comorbidities (ADHD, ODD, conduct disorder, anxiety) may be difficult to distinguish from mania because of considerable symptom overlap. Substance use also is a common comorbidity in adolescents, and presentations that appear to be manic may remit when the substances of abuse are discontinued. TREATMENT Pharmacologic Treatment Medication is the primary treatment for mania (Table 39.9). Studies have demonstrated the superiority of antipsychotics over mood stabi lizers in the treatment of mania. Risperidone and olanzapine are the most efficacious agents; quetiapine, risperidone, and olanzapine ranked as the most tolerable agents. The choice of antipsychotic medication is based on factors such as side effect profiles, comorbidities, adherence, and positive response of a family
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member. Among traditional mood stabilizers, only lithium is FDA approved for the treatment of bipolar disorder from age 12 years; its efficacy and tolerability compared to placebo has been demonstrated in ran domized controlled trials (RCTs). There also is evidence that lithium reduces the risk of suicide and total deaths in patients with both unipo lar and bipolar depressive disorder. Given the co occurrence of sleep disturbance with bipolar disorders, the use of medications to help regulate sleep can have a significant ben efit on mood and functioning. Medications to promote sleep, includ ing benzodiazepines, benzodiazepine receptor agonists, and melatonin receptor agonists have some evidence for the treatment of sleep in bipolar disorder in adults. When treating children and adolescents, it is important to monitor for paradoxical activationdisinhibition when using benzodiazepines. Medication trials should be systematic and their duration sufficient (generally 6 8 weeks) to determine effectiveness. Care should be taken to avoid unnecessary polypharmacy, in part by discontinuing agents that have not demonstrated significant benefit. Because these medica tions are associated with significant side effects, careful monitoring of baseline and follow up indices is imperative (see Chapter 33). The regimen needed to stabilize acute mania should be maintained for 12 24 months. Maintenance therapy is often needed for adolescents with bipolar I disorder, and some patients need lifelong medication. Any attempts to discontinue prophylactic medication should be done gradually while closely monitoring the patient for relapse. Antidepressants alone should not be prescribed for depressive symp toms in confirmed cases of bipolar I disorder because of the risk of manic switch. For treatment of depression in bipolar II, antidepressant medication may be used cautiously. Comorbid ADHD can be treated with a stimulant once a mood stabilizer has been initiated. Psychotherapies Psychotherapy is a potentially important adjunctive treatment for bipolar disorders. Therapies with some evidence of efficacy, primarily as adjunctive to pharmacotherapy, include multifamily psychoeduca tional psychotherapy and family focused treatment, child and family focused CBT, dialectical behavioral therapy, and interpersonal and social rhythm therapy. Active components of these therapies include family involvement and psychoeducation, along with self regulation, cognitive restructuring, communication, problem solving, and emo tion regulation skills. Factors that adversely influence response to ther apy include high conflict families and sleep impairment, suggesting the importance of targeting these factors in treatment. Sleep hygiene is an important factor in the treatment of mania, and there is support for the use of CBT in treating insomnia related to bipolar disorder. Ensur ing patients get adequate rest will help with recovery and the preven tion of future episodes of mania. LEVEL OF CARE Most youths with bipolar disorders can be safely and effectively treated as outpatients, provided that an appropriate schedule of visits and labo ratory monitoring can be maintained through the course of treatment. Youths who are suicidal, homicidal, psychotic, or present an inten tional danger to themselves or others typically require inpatient care. Clinical Course and Prognosis The mean age of onset of the first manic episode is approximately 18
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years old for bipolar I disorder. Premorbid problems are common in bipolar disorder, especially temperamental difficulties with mood and behavioral regulation. Premorbid anxiety also is common. The early course of adolescent onset bipolar I disorder appears to be more chronic and refractory to treatment than adult onset bipolar disorder. Comorbidity predicts functional impairment, and age at onset pre dicts duration of episodes. Sleep impairment and family conflict are inversely related to favorable treatment response, suggesting impor tant targets for treatment. The bipolar disorders are highly recurrent, and 7080 of bipolar I patients will have additional mood episodes. Recurrent episodes can approximate 4 in 10 years, with the inter episode interval shortening as the patient ages. Although the majority of patients with bipolar I return to a fully functional level between epi sodes, approximately 30 continue to be symptomatic and function ally impaired between episodes. The initial presentation of bipolar I disorder is often a major depres sive episode. Switching from a depressive episode to a manic episode by adulthood may occur in 1020 of youth, both spontaneously and during depression treatment. Factors that predict the eventual devel opment of mania in depressed youth include a depressive episode characterized by rapid onset, psychomotor retardation, and psychotic features; a family history of affective disorders, especially bipolar disor der; and a history of mania or hypomania after antidepressant therapy. The mean age of onset of bipolar II disorder is 20 years old. The ill ness most often begins with a depressive episode and is not recognized as bipolar II disorder until a hypomanic episode occurs, in about 12 of individuals with the initial diagnosis of major depression. Many individuals experience several episodes of major depression before experiencing the first recognized hypomanic episode. Anxiety, sub stance misuse, or eating disorders may also precede the onset of bipolar II, complicating its detection. About 515 of individuals with bipolar II disorder will ultimately develop a manic episode, which changes the diagnosis to bipolar I disorder. Depression in bipolar I or II usually has an earlier age of onset, more frequent episodes of shorter duration, an abrupt onset and offset, is linked to comorbid substance misuse, and is triggered by stressors. Atypical symptoms such as hypersomnia, lability, and weight instabil ity are also common in bipolar depression, reported in up to 90 of cases vs 50 in unipolar depression. Psychosis, psychomotor retarda tion, and catatonia are also more characteristic of bipolar depression, Table 39.9 U.S. Food and Drug AdministrationApproved Treatments for Bipolar Disorder in Youth MEDICATION INDICATION (APPROVED AGES) Aripiprazole Mania (10 17 yr) Asenapine Maniamixed episode (10 17 yr) Lithium Acute maniabipolar maintenance (717 yr) Lurasidone Bipolar depression (10 17 yr) Olanzapine Maniamixed episode (13 17 yr) Quetiapine Mania (10 17 yr) Risperidone Maniamixed episode (10 17 yr) Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. Chapter 40 u Suicide
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and Attempted Suicide 263 whereas somatic complaints are more frequent in unipolar depression. A family history of mania is also a relevant discriminating factor. Provision of clinical services is poor for youth with bipolar disor der. In one healthcare system study spanning 2 year follow up after diagnosis, despite complex drug regimens, medication appointments were infrequent, averaging one visit every 2 months. More than 50 of patients needed one or more hospitalizations, and almost half had psychiatric emergency department visits. In a national study, 38 of youths diagnosed with bipolar disorder had received no treatment at all. SEQUELAE Bipolar disorder has one of the higher rates of suicide among men tal health diagnoses, with a lifetime risk of suicide in individuals with bipolar disorder estimated to be at least 15 times that of the general population. Factors associated with suicide attempts include female gender, young age at illness onset, depressive polarity of first illness episode or current or most recent episode, comorbid anxiety disorder, any comorbid substance use disorder, borderline personality disorder, and first degree family history of suicide. In contrast, completed sui cides are associated with male sex and a first degree family history of suicide. Despite patients with bipolar disorder having normal or even superior cognition before diagnosis, bipolar disorder has been associ ated with decrements in executive function and verbal memory. Youths with bipolar disorder are also at high risk for substance abuse, anti social behavior, impaired academic performance, impaired family and peer relationships, and poor adjustment to life stressors. PREVENTION Although empirical support is sparse, one study demonstrated the effectiveness of family focused treatment vs an educational control in hastening and sustaining recovery from mood symptoms in a high familial risk cohort of youths with subsyndromal symptoms of mania. Family focused treatment is a manualized psychoeducational inter vention designed to reduce family stress, conflict, and affective arousal by enhancing communication and problem solving between youths and their caregivers. Pharmacologic interventions for subsyndromal mania have produced equivocal results. Visit Elsevier eBooks at eBooks.Health.Elsevier.com for Bibliography. Youth suicide is a major public health concern. In 2021, suicide was the second leading cause of death in adolescents and young adults (aged 10 24 years) and the tenth leading cause of death for all ages. The rates of emergency department (ED) visits for psychiatric chief complaints have also increased over time, with a 2.5 fold increase in suicide related visits in adolescents. There are numerous genetic, psychiatric, social, cultural, and environmental risk factors for suicidal behavior (Fig. 40.1). There are also many protective factors and interventions that can reduce rates of self injury and suicide. Knowledge of these risk factors and protective factors may facilitate identification and treat ment in youths at highest risk for intentional harm to themselves. Chapter 40 Suicide and Attempted Suicide Jennifer A. Zaspel and Rosa K. Kim EPIDEMIOLOGY Suicide rates for children and adolescents have been increasing over time, with the overall suicide rates increasing by 35 since 1999. It is estimated that 46 of
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people who die by suicide were diagnosed with a psychiatric condition at the time of their death. Linear trends in suicide attempts from 20092019 have also increased and specifically among certain demographic groups. A better understanding of which groups are at risk for suicide and parasuicidal behavior can help pediatricians identify and support those who are at risk (Table 40.1). Suicidal Ideation and Attempts More than 30 of 9th 12th grade students in the United States felt so sad or hopeless almost every day for 2 or more weeks in a row dur ing the previous year that they stopped doing usual activities. During that same period, 18.8 of the students reported that they had seri ously considered attempting suicide, and 8.9 reported that they had attempted suicide one or more times. A suicide attempt in the previ ous year that resulted in an injury, poisoning, or overdose that had to be treated by a physician or nurse was reported by 2.5 of students. Ingestion is the most common method of attempted suicide. The 1519 year old age group is the most likely to intentionally harm them selves by ingestion, receive treatment in the ED, and survive. Attempts are more common in adolescent females than males and in Hispanic females than their non Hispanic counterparts. LGBTQ and bullied youths also have disproportionately high rates of suicidal ideation and suicide attempts (see Chapter 154). Prior self harm (self injury) from poisoning, drowning, firearms, fires, asphyxiation (hanging), and traffic injury are risk factors for suicide. Repeated episodes of self harm are a higher risk factor than a single episode (see Chapter 46). Attempters who have made prior suicide attempts, who used a method other than ingestion, who have a plan, who have no regret, and who still want to die are at increased risk for completed suicide. Nonetheless, a significant number of children and adolescents who have completed suicide had no previous attempts. Suicide Completions In the United States, completed suicide is very rare before age 10. Rates of completed suicide increase steadily across adolescence into young adulthood, peaking in the early 20s. The male to female ratio for completed suicide rises with age from 3:1 in children to approxi mately 4:1 in those aged 15 24 and greater than 6:1 among those ages 20 24. Although exact rates have changed over time, firearms, suffo cation, and poisoning remain the most common methods of suicide (Fig. 40.2). For both male and female youth ages 15 24, suicide rates remain highest among Indigenous American and Indigenous Alaskan youth and White youth relative to Black, Asian or Pacific Islander, and His panic youth. However, rates have been rising for both Black and Asian or Pacific Islander youth, with the rates in Black males increasing 47 between 2013 and 2019 (12.2100,000 to 17.9100,000 individu als) and Asian or Pacific Islander males increasing 40 between 2013 and 2019 (12.0100,000 to 16.8100,000 individuals). Similar increases have also been seen in female youth in these groups in this
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time, with a rate increase of 59 among Black female youth (2.7 to 4.3100,000) and 42 among Asian or Pacific Islander (3.6 to 5.1100,000). In 2021, the combined (male and female, age 1024) suicide rates among Indig enous youths increased 16 (over 2018 rates); Increases were also noted among Black youths (36) and Hispanic youths (8). RISK FACTORS Multiple risk factors predispose youth to suicide (see Fig. 40.1, Table 40.1). Dynamic risk factors are those that change over time and are most amenable to risk mitigation through treatment, resources, and support. Static risk factors are those that increase an individuals risk of suicide attempt and completion but are not amenable to direct inter vention. They include genetic factors, demographic information, an individuals past psychiatric history, family psychiatric history, and history of suicidal and parasuicidal behavior. The risk associated with each factor varies, with the highest risk associated with a personal Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. 264 Part III u Behavioral and Psychiatric Disorders Fig. 40.1 Risk factors for suicide and the strength of the associa tion throughout life. The strength of the association between each risk factor and suicide is indicat ed by the shading (darker shad ing indicates a stronger associa tion). (From Fazel S, Runeson B. Suicide published correction appears in. N Engl J Med. 2020 Mar 12;382:1078; N Engl J Med. 2020;382:266274:Fig. 1, p 267.) Predisposition Childhood Adolescence Adulthood Older Adults Genetic and epigenetic factors Family history Earlylife adversity Psychiatric disorders Severe mental illness Depression Personality disorders Substance misuse Physical health problems Lack of social support Economic factors Life events Effects of the media Access to lethal means Individual risk factors Environmental risk factors history of a suicide attempt. Risk is also cumulative, with childhood adversity leading to an increased lifetime risk of suicide. Access to Firearms Firearms are the most lethal method of suicide completion; the death rate with respect to firearms is approximately 8090, whereas the death rate is only 1.54 for drug overdoses. Firearms have long been the most common method of completed suicide across all ages and genders and have become the most common method of suicide com pletion for adolescent males (see Fig. 40.2). Limiting access to lethal means, in particular firearms, reduces rates of completed suicide. Suicide Contagion Suicide attempts may also be precipitated by exposure to news of another persons suicide or by reading about or viewing a suicide por trayed in a romantic light in the media. Media coverage of suicide is linked to fluctuating incidence rates of suicides, particularly among adolescents. Glorification of suicide whether in news or in fictional media has been associated with an increase in suicides. When media coverage includes a detailed description of specific means used, the use of that particular method may increase in the overall population. Preexisting Psychiatric Illness Approximately 90 of youths
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who complete suicide have a preexist ing psychiatric illness, most often major depression. Among females, chronic anxiety, especially panic disorder, also is associated with sui cide attempts and completion. Among males, conduct disorder and substance use confer increased risk. Comorbidity of a substance use disorder, a depressive disorder, andor conduct disorder are linked to suicide by firearm. Schizophrenia spectrum disorders are linked to sui cide attempts and completions (see Chapter 47.1). Suicidal and Parasuicidal Behavior History of a previous suicide attempt is recognized as the strongest pre dictive risk factor for future suicidal behavior. Individual definitions of suicide attempts can vary; therefore parasuicidal behavior should be explored when considering past attempts. Some patients may not consider an aborted attempt or interrupted attempt an actual suicide attempt, but these behaviors carry considerable risk, as do researching suicide methods, preparatory acts, rehearsals, giving away possessions, and making arrangements for responsibilities (e.g., finding someone else to care for a pet or family member in their planned absence). Nonsuicidal self injury (NSSI) is the direct and deliberate destruc tion of ones own body tissue with the absence of intent to die (see Chap ter 46). The most common self harm behavior is cutting or carving, but other behaviors include scratching, burning, punching or hitting one self, biting, and others. NSSI is common among adolescents, especially females. Up to 47.4 of youth with a diagnosis of depression engage in NSSI, and lifetime prevalence rates of NSSI are between 17 and 60. Although the intent of these behaviors may not be to cause death, they are important to note, as they are strong predictors of future suicidality if left untreated. Seventy percent of adolescents who engaged in NSSI report a lifetime suicide attempt, and 55 reported multiple attempts. Individuals who are most likely to engage in NSSI are those who have a family member or close friend who have engaged in self harm and those who believe that peers engage in self harm. Protective Factors Protective factors (Table 40.2) can provide a counterbalance for those contemplating suicide. Internal protective factors are those that are inherent to the individual. External protective factors are typically dependent on relationships and interactions with others. Protective factors, even if present, may not counteract significant acute risk. ASSESSMENT AND INTERVENTION All suicidal ideation (including planning) and suicide attempts should be taken seriously and require a thorough assessment by a child trained mental health clinician to evaluate the youths current state of mind, ongoing risk of harm, and next best steps in treatment. Emergency mental health assessment is needed for immediate threat to self (i.e., active suicidal ideation with plan and intent); urgent mental health assessment (48 72 hours) is needed for severe psychiatric symptoms, significant change in overall functioning, and suicidal ideation with out intent or plan. Routine mental health assessment is appropriate for mild to moderate psychiatric symptoms without suicidal ideation. Pediatric practitioners should expect the mental health clinician to evaluate the presence and degree of suicidality and underlying risk fac
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tors. The reliability and validity of child interviewing are affected by Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. Chapter 40 u Suicide and Attempted Suicide 265 childrens level of cognitive development as well as their understanding of the relationship between their emotions and behavior. Confirma tion of the youths suicidal behavior can be obtained from information gathered by interviewing others who know the child or adolescent. A discrepancy between patient and parent reports is not unusual, with both children and adolescents more likely to disclose suicidal ideation and suicidal actions than their parents. Suicide Inquiry In the mental health assessment, suicidal ideation is assessed by explicit questions posed in a nonjudgmental, noncondescending, matter of fact approach. The clinician should explore all aspects of suicidal ideation (i.e., frequency, intensity), suicide plan, parasuicidal behaviors like preparatory acts or writing notes, and intent associated with their thoughts. The assessment of a suicide attempt should also include a detailed exploration of the hours immediately preceding an attempt to identify precipitants as well as the circumstances of the attempt itself to better understand the patients intent and potential lethality. It is important to recognize that suicidal ideation is dynamic in nature and should be considered on an individual basis; a patient should be compared to their own baseline when assessing for risk of harm to self. Children Under 12 Years Although suicidal ideation and attempts are less frequent in children under 12 than older teens and adults, they do occur. A developmen tal approach must be taken, as children vary in their understanding of death, moral reasoning, and cognitive reasoning based on age and whether they are following a typical developmental trajectory. A young child may not recognize that their means are not lethal, but that fact should not discount their intent. Unlike adolescents, Black male children are most likely to complete suicide, most often by hanging or strangulation. Children who are at risk of suicide may be less likely to demonstrate classical symp toms of depression than teens and are more likely to attempt at home. Children who die by suicide have higher rates of attention deficit hyperactivity disorder (ADHD), emphasizing the importance of impulsivity in suicide attempts. Relationship problems are the most common precipitating circumstance, but the specific relationship dif fers along developmental lines. Younger adolescents are more likely to have had relationship problems with peers or a significant other, whereas children are more likely to have had relationship problems with family. Determining Risk The calculation of the level of risk of harm to self is complex, requiring a determination across a spectrum of risk. At the low end of the risk spectrum are youth with thoughts of death or wanting to die but with out suicidal thoughts, intent, or plan. Those with specific suicide plans, preparatory acts or suicide rehearsals, low probability of being found
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during an attempt, and clearly articulated intent are at the high end. A history of suicide attempts, presently impaired judgment, and poor social support further exacerbates the heightened risk. Among adoles cents who consider self harm, those who carry out self injury are more likely to have family or friends who have engaged in self harm. When considering all aspects of a suicide risk assessment, positive responses to a suicide inquiry carry more weight and concern than risk factors alone. Levels of Psychiatric Care For youth who are an imminent danger to themselves (i.e., have active thoughts of killing themselves with plan and intent), inpatient level of psychiatric care is necessary to ensure safety, clarify diagnoses, and plan comprehensive treatment. These patients can be hospitalized voluntarily or involuntarily. It is helpful for the pediatric practitioner to have an office protocol to follow in these situations. This protocol should take into consideration state laws regarding involuntary hospi talization, transportation options, nearest emergency assessment site, necessary forms for hospitalization, and available emergency mental health consultants. For those youth suitable for treatment in the outpatient setting (e.g., suicidal ideation without plan or intent, intact mental sta tus, few or no other risk factors for suicidality, willing and able to participate in outpatient treatment; has caregivers able to provide emotional support, supervision, safeguarding, and adherence to follow up), an appointment should be scheduled within a few days with a mental health clinician. Ideally, this appointment should be scheduled before leaving the assessment venue. A procedure should be in place to contact the family to encourage mental health follow up and provide additional support or resources, if needed. Some Table 40.1 Dynamic and Static Risk Factors for Suicide in Children and Adolescents DYNAMIC RISK FACTORS Psychiatric symptoms Anhedonia Feelings of hopelessness, helplessness, or worthlessness Impulsivity Insomnia Command hallucinations Agitation Anxiety or panic Poor coping Changes in psychiatric treatment Recent discharge from a psychiatric hospital Change in treatment plan Change in treatment team Psychosocial stressors or precipitants Events that can cause humiliation, shame, or despair (e.g., loss of a relationship, death of a loved one, housing insecurity, academic problems, newly diagnosed medical condition) Ongoing medical illness Substance intoxication Family turmoilchaosconflict Social isolation Bullying or being bullied Pending legal situation Suicide in the community (contagion) STATIC RISK FACTORS Demographics Age: 14 25 Sex: male Race: White, Indigenous American, and Native Alaskan LGBTQ identification Preexisting andor current psychiatric illness Mood disorder Psychotic disorder Substance abuse disorder ADHD Eating disorder Posttraumatic stress disorder Cluster B personality traitsdisorders Conduct disorder or behaviors (antisocial behavior, aggression) History of trauma, abuse, or neglect Past suicidal and parasuicidal behavior Previous suicide attempts Aborted or interrupted suicide attempts Nonsuicidal self injury (self harm) thoughts andor action Family history Psychiatric illness Psychiatric hospitalization Suicide attempts and completions ADHD, Attention deficithyperactivity disorder. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved.
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266 Part III u Behavioral and Psychiatric Disorders evidence suggests that quick and consistent follow up with a team approach, including both primary care and mental health, can be helpful in enhancing treatment plan engagement among patients who are suicidal. Safety Planning Safety planning is a brief psychosocial intervention that has been shown to reduce suicidal behavior and increase engagement in treat ment. Safety plan development consists of working ideally with both the patient and their caregivers to identify individual warning signs and symptoms related to self harm and suicidal behavior, outlining healthy coping skills and people or places that can provide distraction, identifying loved ones and professionals who can be contacted dur ing a crisis, and agreeing on ways to make the home environment safe (e.g., removing firearms, locking up medications). Studies have repeat edly refuted the efficacy of safety or suicide contracts in mitigating risk of completing suicide, and some have shown them to be harmful to the therapeutic relationship. PREVENTION The previously mentioned risk factors associated with suicide are relatively common and individually not strong predictors of sui cide. The assessment is complicated by patients who may attempt to conceal their suicide thoughts and by those who express sui cidal thoughts without serious intent. Suicide screening has been challenging because most screening instruments have variable sensitivity and specificity. In addition, the follow up mental health evaluations for those who screen positive has been poor. Prevention strategies in the pediatric medical home include training staff to recognize and respond to the warning signs of sui cide (Table 40.3), screening for and treating depression, educating Percentage of Suicide Deaths by Method Among Male and Female Adolescents Age 10 to 19 Years, 19992020 100 80 60 20 40 0 S ui ci de d ea th s, S ui ci de d ea th s, Male adolescents 2000 2005 2010 2015 2020 Year 100 80 60 20 40 0 Female adolescents 2000 2005 2010 2015 2020 Year Asphyxiation Method of suicide death Firearm Other Fig. 40.2 Percentage of suicide deaths by method among male and female adolescents, age 10 to 19 years, 19992020. Locally estimated scat terplot smoothing regression estimated percentages of suicide deaths by method with 95 CIs. Asphyxiation includes suicide deaths involving hanging, strangulation, and suffocation; Firearm includes suicide deaths involving firearm use; and Other includes suicide deaths involving poison ing, drowning, fall, fire, and cuts. (Data from Centers for Disease Control and Prevention. Multiple cause of death: 19992020 request form. Updated July 27, 2022. Accessed July 11, 2022. https:wonder.cdc.govwonderhelpmcd.html.) Table 40.2 Protective Factors Against Suicide in Children and Adolescents PROTECTIVE FACTORS Internal protective factors Positive coping skills Frustration tolerance Religious faith Fear of consequences of an attempt (e.g., disfigurement, hospitalization, effects on familyfriends) Future oriented thinking Fear of lost opportunities External protective factors Responsibilities for others (e.g., other children in the home, pets) Positive therapeutic or mentoring relationships (e.g., physician, therapist, teacher, coach) Social supports Living with others Table 40.3 Warning Signs of Suicide Seek help as
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soon as possible by contacting a mental health professional or by calling the National Suicide Prevention Lifeline at 1 800 273 TALK if you or someone you know exhibits any of the following signs: Threatening to hurt or kill oneself or talking about wanting to hurt or kill oneself. Looking for ways to kill oneself by seeking access to firearms, available pills, or other means. Talking or writing about death, dying, or suicide when these actions are out of the ordinary for the person. Feeling hopeless. Feeling rage or uncontrolled anger or seeking revenge. Acting reckless or engaging in risky activities, seemingly without thinking. Feeling trapped, like theres no way out. Increasing alcohol or drug use. Withdrawing from friends, family, and society. Feeling anxious, agitated, or unable to sleep, or sleeping all the time. Experiencing dramatic mood changes. Seeing no reason for living, or having no sense of purpose in life. Developed by the U.S. Department of Health and Human Services, Substance Abuse and Mental Health Services Administration (SAMHSA). https:www.nimh.nih.gov healthpublicationswarningsignsofsuicide Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. Chapter 40 u Suicide and Attempted Suicide 267 patientsparents about warning signs for suicide, and restricting access to lethal means. Pediatric practitioners should consider counseling parents to remove firearms from the home entirely or securely lock guns and ammunition in separate locations. Anec dotal evidence suggests youths frequently know where guns and keys to gun cabinets are kept, even though parents may think they do not. The same recommendation applies to restricting access to potentially lethal prescription and nonprescription medications (e.g., containers of 25 acetaminophen tablets) and alcohol. These approaches emphasize the importance of restriction of access to means of suicide to prevent self harm. SCREENING AND EARLY TREATMENT In 2022, the U.S. Preventive Services Task Force (USPSTF) con cluded that there is insufficient evidence to recommend universal suicide screening in the primary care setting for children and ado lescents. The American Academy of Pediatrics does recommend universal suicide screening for all children 12 years old. In addi tion, in 2018 the American Academy of Pediatrics and the USPFTS (2022) recommended annual universal depression screening for youths 12 and older, which often includes suicide screening as part of validated tools. Pediatric practitioners should also consider sui cide potential and the need for mental health assessment in the Fig. 40.3 Ask Suicide Screening Ques tionsSuicide Risk Screening Tool. (ASQ Tool courtesy National Institute of Men tal Health. National Institutes of Health, Bethesda, Maryland. Accessed at https: www.nimh.nih.govresearchresearch conducted at nimhasq toolkit materials, May 9, 2022.) Provide resources to all patients 247 National Suicide Prevention Lifeline 1800273TALK (8255) En Espaol: 18886289454 247 Crisis Text Line: Text HOME to 741741 1. In the past few weeks, have you wished you were dead? ?Yes ?No 2. In the past few weeks, have you felt that you or your family
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?Yes ?No 3. In the past week, have you been having thoughts about killing yourself? would be better off if you were dead? ?Yes ?No 4. Have you ever tried to kill yourself? ?Yes ?No If yes, how? When? If the patient answers Yes to any of the above, ask the following acuity question: 5. Are you having thoughts of killing yourself right now? ?Yes ?No If yes, please describe: Next steps: If patient answers No to all questions 1 through 4, screening is complete (not necessary to ask question 5). No intervention is necessary (Note: Clinical judgment can always override a negative screen). If patient answers Yes to any of questions 1 through 4, or refuses to answer, they are considered a positive screen. Ask question 5 to assess acuity: ? Yes to question 5 acute positive screen Patient requires a STAT safetyfull mental health evaluation. Patient cannot leave until evaluated for safety. Keep patient in sight. Remove all dangerous objects from room. Alert physician or clinician responsible for patients care. ? No to question 5 nonacute positive screen Patient requires a brief suicide safety assessment to determine if a full mental health evaluation is needed. Patient cannot leave until evaluated for safety. Alert physician or clinician responsible for patients care. as l .Ask SuicideScreening uestions NIMH TOOLKIT Suicide Risk Screening Tool Ask the patient: asQ Suicide Risk Screening Toolkit NATIONAL INSTITUTE OF MENTAL HEALTH (NIMH) (imminent risk identified) (potential risk identified) Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. 268 Part III u Behavioral and Psychiatric Disorders context of concerning information elicited in childparent psy chosocial histories (e.g., HEADSS Psychosocial Risk Assessment; see Chapter 32, Table 32.2), general screening measure scores out of the normal range (e.g., Pediatric Symptom Checklist Internal izing Sub Scale; see Table 28.5), or self reported statements or behaviors from patients and parents. The Ask Suicide Screening Questionnaire (ASQ) is a validated four item measure shown in the ED setting to have high sensitivity and negative predictive value in identifying youth at risk for suicide ideation and behavior (Fig. 40.3). Other common screening tools are the Columbia Sui cide Severity Rating Scale (C SSRS) Screener (Table 40.4) and the Patient Health Questionnaire (PHQ 2PHQ 9). These scales have also been used in the emergency room setting. Through follow up office visits, pediatric practitioners can help support and facilitate the implementation of psychotherapies that target the specific psychiatric disorders and the emotional dyspho ria or behavioral dysregulation that accompany suicidal ideation or behavior. In conjunction with a child and adolescent psychiatrist, psychotropic medications may be used as indicated to treat under lying psychiatric disorders. Both dialectical behavioral therapy and cognitive behavioral therapy are effective in reducing harm but must be combined with appropriate psychopharmacology of an underlying disorder. Pediatric practitioners also can encourage social connectedness to peers and to
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community organizations, as well as promote help seeking (e.g., talking to a trusted adult when distressed) and wellness behaviors. In the event of a completed sui cide, pediatricians can offer support to the family, particularly by monitoring for pathologic bereavement responses in siblings and parents. SCHOOL RESOURCES Screening for suicide in schools is also fraught with problems related to low specificity of screening instruments, paucity of referral sites, and variable acceptability among school administrators. Gatekeeper (e.g., student support personnel) training appears effective in improving skills among school personnel and is highly acceptable to administra tors but has not been shown to prevent suicide. School curricula (e.g., Signs of Suicide) have shown some preventive potential by teaching students to recognize the signs of depression and suicide in themselves and others and providing them with specific action steps necessary for responding to these signs. Peer helpers have not generally been shown to be efficacious. Visit Elsevier eBooks at eBooks.Health.Elsevier.com for Bibliography. Table 40.4 Columbia Suicide Severity Rating Scale Screener 1. Have you wished you were dead or wished you could go to sleep and not wake up? 2. Have you actually had any thoughts about killing yourself? If Yes to 2, answer questions 3, 4, 5, and 6. If No to 2, go directly to question 6. 3. Have you thought about how you might do this? 4. Have you had any intention of acting on these thoughts of killing yourself, as opposed to you having the thoughts but you definitely would not act on them? 5. Have you started to work out or worked out the details of how to kill yourself? Do you intend to carry out this plan? 6. Have you done anything, started to do anything, or prepared to do anything to end your life? RESPONSE PROTOCOL TO SCREENING (BASED ON LAST ITEM ANSWERED YES) Item 1Mental Health Referral at discharge Item 2Mental Health Referral at discharge Item 3Care Team Consultation (Psychiatric Nurse) and Patient Safety MonitorProcedures Item 4Psychiatric Consultation and Patient Safety MonitorProcedures Item 5Psychiatric Consultation and Patient Safety MonitorProcedures Item 6If over 3 months ago, Mental Health Referral at discharge If 3 months ago or less, Psychiatric Consultation and Patient Safety Monitor From Posner K. Columbia Lighthouse Project. The Columbia Suicide Severity Rating Scale (C SSRS) ScreenerRecent. https:cssrs.columbia.eduthecolumbiascalecssrsrisk identification Eating disorders (EDs) are characterized by body dissatisfaction related to overvaluation of a thin body ideal, associated with dysfunc tional patterns of cognition and weight control behaviors that result in significant biologic, psychologic, and social complications. EDs can develop in individuals of any age, gender, sexual orientation, ethnicity, or cultural background. Early intervention in EDs improves outcome. DEFINITIONS Anorexia nervosa (AN) involves significant overestimation of body size and shape, with a relentless pursuit of thinness that, in the restric tive subtype, typically combines excessive dieting and compulsive exercising. In the binge purge subtype, patients might intermittently overeat and then attempt to rid themselves of calories by vomiting or taking laxatives, still with a strong drive for thinness
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(Table 41.1). Bulimia nervosa (BN) is characterized by episodes of eating large amounts of food in a brief period, followed by compensatory vomiting, laxative use, exercise, or fasting to rid the body of the effects of overeat ing in an effort to avoid obesity (Table 41.2). Children and adolescents with EDs may not fulfill criteria for AN or BN in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM 5) and may fall into a subcategory of Other Specified Feeding and Eating Disorders (OSFED). Youth with these subthresh old conditions merit close monitoring over time because they may be early in the course of an illness. Avoidantrestrictive food intake disorder (ARFID) involves limiting food intake based on the subjective qualities of food (e.g., appearance, color, smell, taste, texture or consistency), fear of adverse consequences of eating (e.g., choking, gagging or vomiting), or lack of interest in eat ing, but without concern about body image, weight, shape, or size. However, significant unintended weight loss or nutritional deficiencies and problems with social interactions can occur as a result (Table 41.3). Binge eating disorder (BED), in which binge eating is not followed regularly by any compensatory behaviors (vomiting, laxatives), is a stand alone category in DSM 5 but shares many features with obesity (see Chapter 65). Chapter 41 Eating Disorders Taylor B. Starr and Richard E. Kreipe Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. Chapter 41 u Eating Disorders 269 EPIDEMIOLOGY The classic presentation of AN is an early to middle adolescent female of above average intelligence and socioeconomic status who is a conflict avoidant, risk aversive perfectionist and is struggling with dis turbances of anxiety andor mood. BN tends to emerge in later adoles cence, sometimes evolving from AN, and is typified by impulsivity and features of borderline personality disorder associated with depression and mood swings. ARFID typically presents in late childhood, is more common in males, and more often co occurs with anxiety disorders and autism spectrum disorder. The 0.51 and 35 incidence rates among younger and older adolescent females for AN and BN, respec tively, probably reflect ascertainment bias in sampling and underdiag nosis in cases not fitting the common profile. The same may be true of the significant gender disparity, in which female patients account for approximately 85 of patients with diagnosed EDs. No single factor causes the development of an ED; sociocultural studies indicate a complex interplay of culture, ethnicity, gender, peers, and family. The gender dimorphism is presumably related to females having a stronger relationship between body image and self evaluation, as well as the influence of the Western cultures thin body ideal. Eth nicity appears to moderate the association between risk factors and disordered eating, with African American and Caribbean females reporting lower body dissatisfaction and less dieting than Hispanic and non Hispanic White females. Because peer
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acceptance is central to healthy adolescent growth and development, especially in early adoles cence, when AN tends to have its initial prevalence peak, the potential influence of peers on EDs is significant, as are the relationships among peers, body image, and eating. Teasing by peers or by family members (especially males) may be a contributing factor for overweight females. Table 41.1 DSM 5 Diagnostic Criteria for Anorexia Nervosa A. Restriction of energy intake relative to requirements, leading to a significantly low body weight in the context of age, sex, developmental trajectory, and physical health. Significantly low weight is defined as a weight that is less than minimally normal or, for children and adolescents, less than that minimally expected. B. Intense fear of gaining weight or of becoming fat, or persistent behavior that interferes with weight gain, even though at a significantly low weight. C. Disturbance in the way in which ones body weight or shape is experienced, undue influence of body weight or shape on self evaluation, or persistent lack of recognition of the seriousness of the current low body weight. Specify whether: Restricting type (ICD 10 CM code F50.01): During the last 3 mo, the individual has not engaged in recurrent episodes of binge eating or purging behavior (i.e., self induced vomiting or the misuse of laxatives, diuretics, or enemas). This subtype describes presentations in which weight loss is accomplished primarily through dieting, fasting, andor excessive exercise. Binge eatingpurging type (ICD 10 CM code F50.02): During the last 3 mo, the individual has engaged in recurrent episodes of binge eating or purging behavior (i.e., self induced vomiting or the misuse of laxatives, diuretics, or enemas). Specify if: In partial remission: After full criteria for anorexia nervosa were previously met, Criterion A (low body weight) has not been met for a sustained period, but either Criterion B (intense fear of gaining weight or becoming fat or behavior that interferes with weight gain) or Criterion C (disturbances in self perception of weight and shape) is still met. In full remission: After full criteria for anorexia nervosa were previously met, none of the criteria has been met for a sustained period of time. Specify current severity: The minimum level of severity is based, for adults, on current BMI (see the following) or, for children and adolescents, on BMI percentile. The ranges below are derived from World Health Organization categories for thinness in adults; for children and adolescents, corresponding BMI percentiles should be used. The level of severity may be increased to reflect clinical symptoms, the degree of functional disability, and the need for supervision. Mild: BMI 17 kgm2 Moderate: BMI 16 16.99 kgm2 Severe: BMI 15 15.99 kgm2 Extreme: BMI 15 kgm2 From the Diagnostic and Statistical Manual of Mental Disorders, 5th ed. pp. 338339. Copyright 2013. American Psychiatric Association. Table 41.2 DSM 5 Diagnostic Criteria for Bulimia Nervosa A. Recurrent episodes of binge eating. An episode of binge eating is characterized by both of the following: 1. Eating, in a discrete
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period of time (e.g., within any 2 hr period), an amount of food that is definitely larger than what most individuals would eat in a similar period of time under similar circumstances. 2. A sense of lack of control over eating during the episode (e.g., a feeling that one cannot stop eating or control what or how much one is eating). B. Recurrent inappropriate compensatory behaviors to prevent weight gain, such as self induced vomiting; misuse of laxatives, diuretics, or other medications; fasting; or excessive exercise. C. The binge eating and inappropriate compensatory behaviors both occur, on average, at least once a week for 3 mo. D. Self evaluation is unduly influenced by body shape and weight. E. The disturbance does not occur exclusively during episodes of anorexia nervosa. Specify if: In partial remission: After full criteria for bulimia nervosa were previously met, some, but not all, of the criteria have been met for a sustained period of time. In full remission: After full criteria for bulimia nervosa were previously met, none of the criteria has been met for a sustained period of time. Specify current severity: The minimum level of severity is based on the frequency of inappropriate compensatory behaviors (see the following). The level of severity may be increased to reflect other symptoms and the degree of functional disability. Mild: An average of 1 3 episodes of inappropriate compensatory behaviors per week. Moderate: An average of 4 7 episodes of inappropriate compensatory behaviors per week. Severe: An average of 8 13 episodes of inappropriate compensatory behaviors per week. Extreme: An average of 14 or more episodes of inappropriate compensatory behaviors per week. From the Diagnostic and Statistical Manual of Mental Disorders, 5th ed. p. 345. Copyright 2013. American Psychiatric Association. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. 270 Part III u Behavioral and Psychiatric Disorders Family influence in the development of EDs is even more complex because of the interplay of environmental and genetic factors; shared elements of the family environment and immutable genetic factors account for approximately equal amounts of the variance in disordered eating. There are associations between parents and childrens eating behaviors; dieting and physical activity levels suggest parental rein forcement of body related societal messages. The influence of inherited genetic factors on the emergence of EDs during adolescence is also sig nificant, but not directly. Rather, the risk for developing an ED appears to be mediated through a genetic predisposition to anxiety (see Chap ter 38), depression (see Chapter 39), or obsessive compulsive traits that may be modulated through the internal milieu of puberty. There is no evidence to support the outdated notion that parents or family dynam ics cause an ED; rather, the family dynamics may represent responses to having a family member with a potentially life threatening condi tion. The supportive influence on recovery of
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parents as nurturing caregivers cannot be overestimated. PATHOLOGY AND PATHOGENESIS The emergence of EDs coinciding with the processes of adolescence (e.g., puberty, identity, autonomy, cognition) indicates the central role of development. EDs may be viewed as a final common path way, with a number of predisposing factors that increase the risk of developing an ED, precipitating factors often related to develop mental processes of adolescence triggering the emergence of the ED, and perpetuating factors that cause an ED to persist. A history of sexual trauma is more common in children with BN, and when present with any ED makes recovery more difficult. EDs often begin with dieting but gradually progress to unhealthy habits that lessen the negative impact of associated psychosocial problems to which the affected person is vulnerable because of premorbid biologic and psychologic characteristics, family interactions, and social climate. When persistent, the biologic effects of starvation and malnutrition (e.g., true loss of appetite, hypothermia, gastric atony, amenorrhea, sleep disturbance, fatigue, weakness, depression), combined with the psychologic rewards of increased sense of mastery and reduced emotional reactivity, actually maintain and reward pathologic ED behaviors. This positive reinforcement of behaviors and consequences, gen erally viewed by parents and others as negative, helps to explain why persons with an ED characteristically deny that a problem exists and resist treatment. With significantly low caloric intake, patients ini tially exhibit extreme irritability, but over time experience emotional numbness, which reinforces continued caloric restriction. Although noxious, purging can be reinforcing because of a reduction in anxi ety triggered by overeating; purging also can result in short term, but reinforcing, improvement in mood related to changes in neurotrans mitters. In addition to an imbalance in neurotransmitters, most nota bly serotonin and dopamine, alterations in functional anatomy also support the concept of EDs as brain disorders. The cause and effect relationship in central nervous system (CNS) alterations in EDs is not clear, nor is their reversibility. CLINICAL MANIFESTATIONS Except for ARFID, in which weight loss is unintentional, a central fea ture of EDs is the overestimation of body size, shape, or parts (e.g., abdomen, thighs) leading to intentional weight control practices to reduce weight (AN) or prevent weight gain (BN). Associated practices include severe restriction of caloric intake and behaviors intended to reduce the effect of calories ingested, such as compulsive exercising or purging by inducing vomiting or taking laxatives. Eating and weight loss habits commonly found in EDs can result in a wide range of energy intake and output, the balance of which leads to a wide range in weight, from extreme loss of weight in AN to fluctuation around a normal to moderately high weight in BN. Reported eating and weight control habits thus inform the initial primary care approach (Table 41.4). Although weight control patterns guide the initial pediatric approach, an assessment of common symptoms and findings on physi cal examination is essential to identify targets for intervention. When reported symptoms of excessive weight loss (feeling tired and cold; lacking energy; orthostasis; difficulty
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concentrating) are explicitly linked by the clinician to their associated physical signs (hypothermia with acrocyanosis and slow capillary refill; loss of muscle mass; bra dycardia with orthostasis), it becomes more difficult for the patient to deny that a problem exists. Furthermore, awareness that bothersome symptoms can be eliminated by healthier eating and activity patterns can increase a patients motivation to engage in treatment. Tables 41.5 and 41.6 detail common symptoms and signs that should be addressed in a pediatric assessment of a suspected ED. DIFFERENTIAL DIAGNOSIS In addition to identifying symptoms and signs that deserve targeted intervention for patients who have an ED, a comprehensive history and physical examination are required to rule out other conditions in the differential diagnosis. Weight loss can occur in any condition with increased catabolism (e.g., hyperthyroidism, malignancy, occult chronic infection) or malabsorption (e.g., celiac disease) or in other disorders (Addison disease, type 1 diabetes mellitus, stimulant abuse), but these illnesses are generally associated with other findings and are not usually associated with decreased caloric intake. Patients with inflammatory bowel disease can reduce intake to minimize abdomi nal cramping; eating can cause abdominal discomfort and early satiety in AN because of gastric atony associated with significant weight loss, not malabsorption. Likewise, signs of weight loss in AN might include hypothermia, acrocyanosis with slow capillary refill, and neutropenia similar to some features of sepsis, but the overall picture in EDs is one of relative cardiovascular stability compared with sepsis. Endocrinop athies are also in the differential of EDs. With BN, voracious appetite in the face of weight loss might suggest diabetes mellitus, but blood glucose levels are normal or low in EDs. Adrenal insufficiency mim ics many physical symptoms and signs found in restrictive AN but is associated with elevated potassium levels and hyperpigmentation. Thy roid disorders may be considered, because of changes in weight, but the overall presentation of AN includes symptoms of both underactive and Table 41.3 DSM 5 Diagnostic Criteria for Avoidant Restrictive Food Intake Disorder A. An eating or feeding disturbance (e.g., apparent lack of interest in eating or food; avoidance based on the sensory characteristics of food; concern about aversive consequences of eating) as manifested by persistent failure to meet appropriate nutritional andor energy needs associated with one (or more) of the following: 1. Significant weight loss (or failure to achieve expected weight gain or faltering growth in children). 2. Significant nutritional deficiency. 3. Dependence on enteral feeding or oral nutritional supplements. 4. Marked interference with psychosocial functioning. B. The disturbance is not better explained by lack of available food or by an associated culturally sanctioned practice. C. The eating disturbance does not occur exclusively during the course of anorexia nervosa or bulimia nervosa, and there is no evidence of a disturbance in the way in which ones body weight or shape is experienced. D. The eating disturbance is not attributable to a concurrent medical condition or not better explained by another mental disorder. When the eating disturbance occurs in the
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context of another condition or disorder, the severity of the eating disturbance exceeds that routinely associated with the condition or disorder and warrants additional clinical attention. Specify if: In remission: After full criteria for avoidantrestrictive food intake disorder were previously met, the criteria have not been met for a sustained period of time. From the Diagnostic and Statistical Manual of Mental Disorders, 5th ed. p. 334. Copyright 2013. American Psychiatric Association. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. Chapter 41 u Eating Disorders 271 Table 41.4 Eating and Weight Control Habits Commonly Found in Children and Adolescents with an Eating Disorder (ED) HABIT PROMINENT FEATURE CLINICAL COMMENTS REGARDING ED HABITS ANOREXIA NERVOSA BULIMIA NERVOSA ANOREXIA NERVOSA BULIMIA NERVOSA Overall intake Inadequate energy (calories), although volume of food and beverages may be high because of very low caloric density of intake as a result of diet and nonfat choices Variable, but calories normal to high; intake in binges is often forbidden food or drink that differs from intake at meals Consistent inadequate caloric intake leading to wasting of the body is an essential feature of diagnosis Inconsistent balance of intake, exercise, and vomiting, but severe caloric restriction is short lived Food Counts and limits calories, especially from fat; emphasis on healthy food choices with reduced caloric density Monotonous, limited good food choices, often leading to vegetarian or vegan diet Strong feelings of guilt after eating more than planned leads to exercise and renewed dieting Aware of calories and fat, but less regimented in avoidance than AN Frequent dieting interspersed with overeating, often triggered by depression, isolation, or anger Obsessive compulsive attention to nutritional data on food labels and may have logical reasons for food choices in highly regimented pattern, such as sports participation or family history of lipid disorder Choices less structured, with more frequent diets Beverages Water or other low or no calorie drinks; nonfat milk Variable, diet soda common; may drink alcohol to excess Fluids often restricted to avoid weight gain Fluids ingested to aid vomiting or replace losses Meals Consistent schedule and structure to meal plan Reduced or eliminated caloric content, often starting with breakfast, then lunch, then dinner Volume can increase with fresh fruits, vegetables, and salads as primary food sources Meals less regimented and planned than in AN; more likely impulsive and unregulated, often eliminated following a binge purge episode Rigid adherence to rules governing eating leads to sense of control, confidence, and mastery Elimination of a meal following a binge purge only reinforces the drive for binge later in the day Snacks Reduced or eliminated from meal plan Often avoided in meal plans, but then impulsively eaten Snack foods removed early because unhealthy Snack comfort foods can trigger a binge Dieting Initial habit that becomes progressively restrictive, although often appearing superficially healthy Beliefs and rules about the patients
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idiosyncratic nutritional requirements and response to foods are strongly held Initial dieting gives way to chaotic eating, often interpreted by the patient as evidence of being weak or lazy Distinguishing between healthy meal planning with reduced calories and dieting in ED may be difficult Dieting tends to be impulsive and short lived, with diets often resulting in unintended weight gain Binge eating None in restrictive subtype, but an essential feature in binge purge subtype Essential feature, often secretive Shame and guilt prominent afterward Often subjective (more than planned but not large) Relieves emotional distress, may be planned Exercise Characteristically obsessive compulsive, ritualistic, and progressive May excel in dance, long distance running Less predictable May be athletic, or may avoid exercise entirely May be difficult to distinguish active thin vs ED Males often use exercise as means of purging Vomiting Characteristic of binge purge subtype May chew, then spit out, rather than swallow, food as a variant Most common habit intended to reduce effects of overeating Can occur after meal as well as a binge Physiologic and emotional instability prominent Strongly addictive and self punishing, but does not eliminate calories ingestedmany still absorbed Laxatives If used, generally to relieve constipation in restrictive subtype, but as a cathartic in binge purge subtype Second most common habit used to reduce or avoid weight gain, often used in increasing doses for cathartic effect Physiologic and emotional instability prominent Strongly addictive, self punishing, but ineffective means to reduce weight (calories are absorbed in small intestine, but laxatives work in colon) Diet pills Very rare, if used; more common in binge purge subtype Used to either reduce appetite or increase metabolism Use of diet pills implies inability to control eating Control over eating may be sought by any means AN, Anorexia nervosa; BN, bulimia nervosa. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. 272 Part III u Behavioral and Psychiatric Disorders Table 41.5 Symptoms Commonly Reported by Patients with an Eating Disorder (ED) SYMPTOMS DIAGNOSIS CLINICAL COMMENTS REGARDING ED SYMPTOMSANOREXIA NERVOSA BULIMIA NERVOSA Body image Feels fat, even with extreme emaciation, often with specific body distortions (e.g., stomach, thighs); strong drive for thinness, with self efficacy closely tied to appraisal of body shape, size, andor weight Variable body image distortion and dissatisfaction, but drive for thinness is less than desire to avoid gaining weight Challenging patients body image is both ineffective and countertherapeutic clinically Accepting patients expressed body image but noting its discrepancy with symptoms and signs reinforces concept that patient can feel fat but also be too thin and unhealthy Metabolism Hypometabolic symptoms include feeling cold, tired, and weak and lacking energy May be both bothersome and reinforcing Variable, depending on balance of intake and output and hydration Symptoms are evidence of bodys shutting down in an attempt to conserve calories with an inadequate diet Emphasizing reversibility of symptoms
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with healthy eating and weight gain can motivate patients to cooperate with treatment Skin Dry skin, delayed healing, easy bruising, gooseflesh Orange yellow skin on hands No characteristic symptom; self injurious behavior may be seen Skin lacks good blood flow and ability to heal in low weight Carotenemia with large intake of carotene foods; reversible Hair Lanugo type hair growth on face and upper body Slow growth and increased loss of scalp hair No characteristic symptom Body hair growth conserves energy Scalp hair loss can worsen during refeeding telogen effluvium (resting hair is replaced by growing hair) Reversible with continued healthy eating Eyes No characteristic symptom Subconjunctival hemorrhage Caused by increased intrathoracic pressure during vomiting Teeth No characteristic symptom Erosion of dental enamel Decay, fracture, and loss of teeth Intraoral stomach acid resulting from vomiting etches dental enamel, exposing softer dental elements Salivary glands No characteristic symptom Enlargement (no to mild tenderness) Caused by chronic binge eating and induced vomiting, with parotid enlargement more prominent than submandibular; reversible Heart Dizziness, fainting in restrictive subtype Palpitations more common in binge purge subtype Dizziness, fainting, palpitations Dizziness and fainting due to postural ortho static tachycardia and dysregulation at hypothalamic and cardiac level with weight loss, as a result of hypovolemia with binge purge Palpitations and arrhythmias often caused by electrolyte disturbance Symptoms reverse with weight gain andor cessation of binge purge Abdomen Early fullness and discomfort with eating Constipation Perceives contour as fat, often preferring well defined abdominal musculature Discomfort after a binge Cramps and diarrhea with laxative abuse Weight loss is associated with reduced volume and tone of GI tract musculature, especially the stomach Laxatives may be used to relieve constipation or as a cathartic Symptom reduction with healthy eating can take weeks to occur Extremities and musculoskeletal Cold, blue hands and feet No characteristic symptoms Self cutting or burning on wrists or arms Energy conserving low body temperature with slow blood flow most notable peripherally Quickly reversed with healthy eating Nervous system No characteristic symptom No characteristic symptom Neurologic symptoms suggest diagnosis other than ED Mental status Depression, anxiety, obsessive compulsive symptoms, alone or in combination Depression; PTSD; borderline personality disorder traits Underlying mood disturbances can worsen with dysfunctional weight control practices and can improve with healthy eating AN patients might report emotional numbness with starvation preferable to emotionality associated with healthy eating AN, Anorexia nervosa; ED, eating disorder; GI, gastrointestinal; PTSD, posttraumatic stress disorder. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. Chapter 41 u Eating Disorders 273 Table 41.6 Signs Commonly Found in Patients with Eating Disorder Relative to Prominent Feature of Weight Control PHYSICAL SIGN PROMINENT FEATURE CLINICAL COMMENTS RELATED TO ED SIGNSRESTRICTIVE INTAKE BINGE EATINGPURGING General appearance Thin to cachectic, depending on balance of intake and output Might wear bulky clothing to hide thinness and might resist being examined Thin
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to overweight, depending on the balance of intake and output through various means Examine in hospital gown Weight loss more rapid with reduced intake and excessive exercise Binge eating can result in large weight gain, regardless of purging behavior Appearance depends on balance of intake and output and overall weight control habits Weight Low and falling (if previously overweight, may be normal or high); may be falsely elevated if patient drinks fluids or adds weights to body before being weighed Highly variable, depending on balance of intake and output and state of hydration Falsification of weight is unusual Weigh in hospital gown with no underwear, after voiding (measure urine SG) Remain in gown until physical exam completed to identify possible fluid loading (low urine SG, palpable bladder) or adding weights to body Metabolism Hypothermia: temp 35.5C (95.9F), pulse 60 beatsmin Slowed psychomotor response with very low core temperature Hypoglycemia Hypokalemia Amenorrhea Delayed puberty Variable, but hypometabolic state is less common than in AN Hypometabolism related to disruption of hypothalamic control mechanisms as a result of weight loss Signs of hypometabolism (cold skin, slow capillary refill, acrocyanosis) most evident in hands and feet, where energy conservation is most active Metabolic acidosis or alkalosis Skin Dry, scaly Increased prominence of hair follicles Orange or yellow hands Hair loss Calluses over proximal knuckle joints of hand (Russell sign) Carotenemia with large intake of carotene foods Russell sign: maxillary incisors abrasion develops into callus with chronic digital pharyngeal stimulation, usually on dominant hand Hair Lanugo type hair growth on face and upper body Scalp hair loss, especially prominent in parietal region No characteristic sign Body hair growth conserves energy Scalp hair loss telogen effluvium can worsen weeks after refeeding begins, as hair in resting phase is replaced by growing hair Eyes No characteristic sign Subconjunctival hemorrhage Increased intrathoracic pressure during vomiting Teeth Caries Eroded dental enamel and decayed, fractured, missing teeth Perimolysis (dental erosions) worse on lingual surfaces of maxillary teeth, is intensified by brushing teeth without preceding water rinse Salivary glands No characteristic sign Enlargement, relatively nontender Parotid submandibular involvement with frequent and chronic binge eating and induced vomiting Throat No characteristic sign Absent gag reflex Extinction of gag response with repeated pharyngeal stimulation Heart Bradycardia, hypotension, and orthostatic pulse differential 25 beatsmin Hypovolemia if dehydrated Changes in AN resulting from central hypo thalamic and intrinsic cardiac function Orthostatic changes less prominent if athletic, more prominent if associated with purging Abdomen Scaphoid, organs may be palpable but not enlarged, stool filled left lower quadrant Constipation Transaminitis Increased bowel sounds if recent laxative use Presence of organomegaly requires investigation to determine cause Constipation prominent with weight loss Pancreatitis Esophageal or gastric ulceration or perforation Extremities and musculoskeletal system Cold, acrocyanosis, slow capillary refill Edema of feet Loss of muscle, subcutaneous, and fat tissue Osteopenia No characteristic sign, but may have rebound edema after stopping chronic laxative use Signs of hypometabolism (cold) and cardiovascular dysfunction (slow capillary refill and acrocyanosis) in hands and feet Edema,
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caused by capillary fragility more than hypoproteinemia in AN, can worsen in early phase of refeeding Nervous system No characteristic sign Peripheral neuropathy No characteristic sign Water loading before weigh ins can cause acute hyponatremia Mental status Anxiety about body image, irritability, depressed mood, oppositional to change Depression, evidence of PTSD, more likely suicidal than AN Mental status often improves with healthier eating and weight; SSRIs only shown to be effective for BN AN, Anorexia nervosa; BN, bulimia nervosa; ED, eating disorder; PTSD, posttraumatic stress disorder; SG, specific gravity; SSRIs, selective serotonin reuptake inhibitors. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. 274 Part III u Behavioral and Psychiatric Disorders overactive thyroid, such as hypothermia, bradycardia, and constipa tion, as well as weight loss and excessive physical activity, respectively. In the CNS, craniopharyngiomas and Rathke pouch tumors can mimic some of the findings of AN, such as weight loss and growth failure, and even some body image disturbances, but the latter are less fixed than in typical EDs and are associated with other findings, including evidence of increased intracranial pressure. Mitochondrial neurogastrointestinal encephalomyopathy, caused by a mutation in the TYMP gene, presents with gastrointestinal dysmotility, cachexia, ptosis, peripheral neuropathy, ophthalmoplegia, and leukoencepha lopathy. Symptoms begin during the second decade of life and are often initially diagnosed as AN. Early satiety, vomiting, cramps, con stipation, and pseudoobstruction result in weight loss often before the neurologic features are noticed (see Chapter 638.2). Acute or chronic oromotor dysfunction and obsessive compulsive disorder may mimic an ED. Fear of choking may lead to avoidance restrictive food intake disorder. Any patient with an atypical presentation of an ED, based on age, sex, or other factors not typical for AN or BN, deserves a scrupulous search for an alternative explanation. In ARFID, disturbance in the neurosen sory processes associated with eating, not weight loss, is the central concern and must be recognized for appropriate treatment. Patients can have both an underlying illness and an ED. The core features of dysfunctional eating habits (body image disturbance and change in weight) can co occur with conditions such as diabetes mellitus, where patients might manipulate their insulin dosing to lose weight. LABORATORY FINDINGS Because the diagnosis of an ED is made clinically, there is no confir matory laboratory test. Laboratory abnormalities, when found, are the result of malnutrition secondary to weight control behaviors or medical complications; studies should be chosen based on history and physical examination. A routine screening battery typically includes complete blood count, erythrocyte sedimentation rate (should be normal), and biochemical profile. Common abnormalities in ED include low white blood cell count with normal hemoglobin and differential; hypokale mic, hypochloremic metabolic alkalosis from severe vomiting; mildly elevated liver enzymes, cholesterol, and cortisol levels; low gonado tropins and blood glucose with marked weight loss; and generally normal total protein, albumin, and renal
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function. An electrocardio gram (ECG) may be useful when profound bradycardia or arrhythmia is detected; the ECG usually has low voltage, with nonspecific ST or T wave changes. Although prolonged QTc has been reported, prospec tive studies have not found an increased risk for this. Nonetheless, when a prolonged QTc is present in a patient with ED, it may increase the risk for ventricular dysrhythmias. COMPLICATIONS No organ is spared the harmful effects of dysfunctional weight con trol behaviors, but the most concerning targets of medical complica tions are the heart, brain, gonads, and bones. Some cardiac findings in EDs (e.g., sinus bradycardia, hypotension) are physiologic adap tations to starvation that conserve calories and reduce afterload. Cold, blue hands and feet with slow capillary refill that can result in tissue perfusion insufficient to meet demands also represent energy conserving responses associated with inadequate intake. All these acute changes are reversible with restoration of nutri tion and weight. Significant orthostatic pulse changes, ventricular dysrhythmias, or reduced myocardial contractility reflect myocar dial impairment that can be lethal. In addition, with extremely low weight, refeeding syndrome (a result of the rapid drop in serum phosphorus, magnesium, and potassium with excessive reintro duction of calories, specifically carbohydrates), is associated with acute tachycardia and heart failure and neurologic symptoms (see Chapter 63). With long term malnutrition, the myocardium appears to be more prone to tachyarrhythmias, the second most common cause of death in these patients after suicide. In BN, dysrhythmias can also be related to electrolyte imbalance. Clinically, the primary CNS area affected acutely in EDs, especially with weight loss, is the hypothalamus. Hypothalamic dysfunction is reflected in problems with thermoregulation (warming and cooling), satiety, sleep, autonomic cardioregulatory imbalance (orthostasis), and endocrine function (reduced gonadal and excessive adrenal cor tex stimulation), all of which are reversible. Anatomic studies of the brain in ED have focused on AN, with the most common finding being increased ventricular and sulcal volumes that normalize with weight restoration. Persistent gray matter deficits following recovery, related to the degree of weight loss, have been reported. Elevated medial tempo ral lobe cerebral blood flow on positron emission tomography, similar to that found in psychotic patients, suggests that these changes may be related to body image distortion. Also, visualizing high calorie foods is associated with exaggerated responses in the visual association cortex that are similar to those seen in patients with specific phobias. Patients with AN might have an imbalance between serotonin and dopamine pathways related to neurocircuits in which dietary restraint reduces anxiety. Reduced gonadal function occurs in male and female patients; it is clinically manifested in AN as amenorrhea in female patients and erectile dysfunction in males. It is related to understimulation from the hypothalamus as well as cortical suppression related to physical and emotional stress. Amenorrhea precedes significant dieting and weight loss in up to 30 of females with AN, and most adolescents with EDs perceive the absence of menses positively. The primary health concern is the negative effect of
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decreased ovarian function and estrogen on bones. Decreased bone mineral density (BMD) with osteopenia or the more severe osteoporosis is a significant complication of EDs (more pronounced in AN than BN). Data do not support the use of sex hor mone replacement therapy because this alone does not improve other causes of low BMD (low body weight, lean body mass, low insulin like growth factor 1, high cortisol). TREATMENT Principles Guiding Primary Care Treatment The approach in primary care should facilitate the acceptance by the ED patient (and parents) of the diagnosis and initial treatment recom mendations. A nurturant authoritative approach using the biopsy chosocial model is useful. A pediatrician who explicitly acknowledges that the patient may disagree with the diagnosis and treatment rec ommendations and may be ambivalent about changing eating habits, while also acknowledging that recovery requires strength, courage, willpower, and determination, demonstrates nurturance. Parents also find it easier to be nurturing once they learn that the development of an ED is neither a willful decision by the patient nor a reflection of poor parenting. Framing the ED as a maladaptive coping mechanism for a complex variety of issues with both positive and negative aspects avoids blame or guilt and can prepare the family for professional help that will focus on strengths and restoring health, rather than on the deficits in the adolescent or the family. The authoritative aspect of a physicians role comes from expertise in health, growth, and physical development. A goal of primary care treat ment should be attaining and maintaining health, not merely weight gain, although weight gain is a means to the goal of wellness. Providers who frame themselves as consultants to the patient with authoritative knowledge about health can avoid a countertherapeutic authoritarian stance. Primary care health focused activities include monitoring the patients physical status, setting limits on behaviors that threaten the patients health, involving specialists with expertise in EDs on the treat ment team, and continuing to provide primary care for health mainte nance, acute illness, or injury. The biopsychosocial model uses a broad ecologic framework, starting with the biologic impairments of physical health related to dysfunctional weight control practices, evidenced by symptoms and signs. Explicitly linking ED behaviors to symptoms and signs can increase motivation to change. In addition, there are usually unresolved psychosocial conflicts in both the intrapersonal (self esteem, self efficacy) and the interpersonal (family, peers, school) Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. Chapter 41 u Eating Disorders 275 domains. Weight control practices initiated as coping mechanisms become reinforced because of positive feedback. That is, external rewards (e.g., compliments about improved physical appearance) and internal rewards (e.g., perceived mastery over what is eaten or what is done to minimize the effects of overeating through exercise or purging) are more powerful to maintain behavior than negative feedback (e.g., conflict with parents,
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peers, and others about eating) is to change it. Thus, when definitive treatment is initiated, more productive alternative means of coping must be developed. Nutrition and Physical Activity The primary care provider generally begins the process of prescrib ing nutrition, although a dietitian should be involved eventually in the meal planning and nutritional education of patients with AN or BN. Framing food as fuel for the body and the source of energy for daily activities emphasizes the health goal of increasing the patients energy level, endurance, and strength. For patients with AN and low weight, the nutrition prescription should work toward gradually increasing weight at the rate of about 0.5 1 lbweek, by increasing energy intake by 100 200 kcal increments every few days, toward a target of approximately 90 of average body weight for sex, height, and age. Weight gain will not occur until intake exceeds output, and eventual intake for continued weight gain can exceed 4,000 kcal day, especially for patients who are anxious and have high levels of thermogenesis from nonexercise activity. Stabilizing intake is the goal for patients with BN, with a gradual introduction of forbid den foods while also limiting foods that might trigger a binge. When initiating treatment of an ED in a primary care setting, the clinician should be aware of common cognitive patterns. Patients with AN typically have all or none thinking (related to perfection ism) with a tendency to overgeneralize and jump to catastrophic conclusions, while assuming that their body is governed by rules that do not apply to others. These tendencies lead to the dichoto mization of foods into good or bad categories, having a day ruined because of one unexpected event, or choosing foods based on rigid self imposed restrictions. These thoughts may be related to neu rocircuitry and neurotransmitter abnormalities associated with executive function and rewards. Weight loss in the absence of body shape, size, or weight concerns should raise suspicion about ARFID, because the emotional distress associated with forced eating is not associated with gaining weight, but with the neurosensory experi ence of eating. A standard nutritional balance of 1520 calories from protein, 5055 from carbohydrate, and 2530 from fat is appropriate. The fat content may need to be lowered to 1520 early in the treatment of AN because of continued fat phobia. With the risk of low BMD in patients with AN, calcium and vitamin D supplements are often needed to attain the recommended 1,300 mgday intake of calcium. Refeeding can be accomplished with frequent small meals and snacks consisting of a variety of foods and beverages (with minimal diet or fat free products), rather than fewer high volume high calorie meals. Some patients find it easier to take in part of the additional nutrition as canned supplements (medicine) rather than food. Regardless of the source of energy intake, the risk for refeeding syndrome (e.g., see the previous section on Complica tions) increases with the degree of weight loss and the rapidity of caloric increases (see
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Chapter 63). Therefore, if the weight has fallen below 80 of expected weight for height, refeeding should proceed carefully (not necessarily slowly) and possibly in the hos pital (Table 41.7). Patients with AN tend to have a highly structured day with restrictive intake, in contrast to BN, which is characterized by a lack of structure, resulting in chaotic eating patterns and binge purge episodes. All patients with AN, BN, or ED NOS benefit from a daily structure for healthy eating that includes three meals and at least one snack a day, distributed evenly over the day, based on balanced meal planning. Breakfast deserves special emphasis because it is often the first meal eliminated in AN and is often avoided the morning after a binge purge episode in BN. In addition to structuring meals and snacks, patients should plan structure in their activities. Although overexercising is common in AN, completely prohibiting exercise can lead to further restriction of intake or to surreptitious exercise; inactivity should be limited to situations in which weight loss is dra matic or there is physiologic instability. Also, healthy exercise (once a day, for no more than 30 min, at no more than moderate intensity) can improve mood and make increasing calories more acceptable. Because patients with AN often are unaware of their level of activity and tend toward progressively increasing their output, exercising without either a partner or supervision is not recommended. Primary Care Treatment Follow up primary care visits are essential in the management of EDs. Close monitoring of the response of the patient and the family to suggested interventions is required to determine which patients can remain in primary care treatment (patients with early, mildly disordered eating), which patients need to be referred to individ ual specialists for co management (mildly progressive disordered eating), and which patients need to be referred for interdisciplin ary team management (EDs). Between the initial and subsequent visits, the patient can record daily caloric intake (food, drink, amount, time, location), physical activity (type, duration, inten sity), and emotional state (e.g., angry, sad, worried) in a journal that is reviewed jointly with the patient in follow up. Focusing on the recorded data helps the clinician to identify dietary and activity deficiencies and excesses, as well as behavioral and mental health patterns, and helps the patient to become objectively aware of the relevant issues to address in recovery. Given the tendency of patients with AN to overestimate their caloric intake and underestimate their activity level, before reviewing the journal record it is important at each visit to measure weight, with out underwear, in a hospital gown after voiding; urine specific grav ity; temperature; and blood pressure and pulse in supine, sitting, and standing positions as objective data. In addition, a targeted physical examination focused on hypometabolism, cardiovascular stability, and mental status, as well as any related symptoms, should occur at each visit to monitor progress (or regression). Table 41.7 Potential Indications for Inpatient Medical Hospitalization of Patients with Anorexia Nervosa PHYSICAL
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AND LABORATORY Heart rate 50 beatsmin Other cardiac rhythm disturbances Blood pressure 8050 mm Hg Postural hypotension resulting in 10 mm Hg decrease or 25 beats min increase Hypokalemia Hypophosphatemia Hypoglycemia Dehydration Body temperature 36.1C (97F) 80 healthy body weight Hepatic, cardiac, or renal compromise PSYCHIATRIC Suicidal intent and plan Very poor motivation to recover (in family and patient) Preoccupation with ego syntonic thoughts Coexisting psychiatric disorders MISCELLANEOUS Requires supervision after meals and while using the restroom Failed day treatment Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. 276 Part III u Behavioral and Psychiatric Disorders Referral to Mental Health Services In addition to referral to a registered dietitian, mental health and other services are important elements of treatment of ED patients. Depend ing on availability and experience, these services can be provided by a psychiatric social worker, psychologist, or psychiatrist, who should team with the primary care provider. ARFID presents the challenge of working with patients negative experiences of eating, or fear of trauma such as vomiting or choking, while also addressing inadequate nutritional needs. Although patients with AN often are prescribed a selective serotonin reuptake inhibitor (SSRI) because of depressive symptoms, there is no evidence of efficacy for patients at low weight; food remains the initial treatment of choice to treat depression in AN. SSRIs, very effective in reducing binge purge behaviors regardless of depression, are considered a standard element of therapy in BN. SSRI dosage in BN, however, may need to increase to an equivalent of 60 mg of fluoxetine to maintain effectiveness. Cognitive behavioral therapy, which focuses on restructuring thinking errors and establishing adaptive patterns of behavior, is more effective than interpersonal or psychoanalytic approaches in ED patients. Dialectical behavioral therapy, in which distorted thoughts and emotional responses are challenged, analyzed, and replaced with healthier ones, with an emphasis on mindfulness, requires adult thinking skills and is useful for older patients with BN. Group ther apy can provide much needed support, but it requires a skilled clini cian. Combining patients at various levels of recovery who experience variable reinforcement from dysfunctional coping behaviors can be challenging if group therapy patients compete with each other to be thinner or take up new behaviors such as vomiting. The younger the patient, the more intimately the parents need to be involved in therapy. The only treatment approach with evidence based effectiveness in the treatment of AN in children and adolescents is family based treatment, exemplified by the Maudsley approach. This three phase intensive outpatient model helps parents play a posi tive role in restoring their childs eating and weight to normal, then returns control of eating to the child, who has demonstrated the ability to maintain healthy weight, and then encourages healthy progression in the other domains of adolescent development. Features of effective family treatment include (1) an agnostic approach in which the
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cause of the disease is unknown and irrelevant to weight gain, emphasizing that parents are not to blame for EDs; (2) parents being actively nurtur ing and supportive of their childs healthy eating while reinforcing lim its on dysfunctional habits, rather than an authoritarian food police or complete hands off approach; and (3) reinforcement of parents as the best resource for recovery for almost all patients, with professionals serving as consultants and advisors to help parents address challenges. Referral to an Interdisciplinary Eating Disorder Team The treatment of a child or adolescent diagnosed with an ED is ideally provided by an interdisciplinary team (physician, nurse, dietitian, men tal health provider) with expertise treating pediatric patients. Because such teams, often led by specialists in adolescent medicine at medical centers, are not widely available, the primary care provider might need to convene such a team. Adolescent medicinebased programs report encouraging treatment outcomes, possibly related to patients entering earlier into care and the stigma that some patients and parents may associate with psychiatry based programs. Specialty centers focused on treating EDs are generally based in psychiatry and often have separate tracks for younger and adult patients. The elements of treatment noted earlier (cognitive behavioral, dialectical behavioral, family based), as well as individual and group treatment, should all be available as part of interdisciplinary team treatment. Comprehensive services ide ally include intensive outpatient and partial hospitalization as well as inpatient treatment. Regardless of the intensity, type, or location of the treatment services, the patient, parents, and primary care provider are essential members of the treatment team. A recurring theme in effec tive treatment is helping patients and families reestablish connections that are disrupted by the ED. Inpatient medical treatment of EDs is generally limited to patients with AN to stabilize and treat life threatening starvation and to pro vide supportive mental health services. Inpatient medical care may be required to avoid refeeding syndrome in severely malnourished patients, provide nasogastric tube feeding for patients unable or unwilling to eat, or initiate mental health services, especially family based treatment, if this has not occurred on an outpatient basis (see Table 41.7). Admission to a general pediatric unit is advised only for short term stabilization in preparation for transfer to a medical unit with expertise in treating pediatric EDs. Inpatient psychiatric care of EDs should be provided on a unit with expertise in managing often challenging behaviors (e.g., hiding or discarding food, vomiting, sur reptitious exercise) and emotional problems (e.g., depression, anxiety). Suicidal risk is small, but patients with AN might threaten suicide if made to eat or gain weight in an effort to get their parents to back off. An ED partial hospital program offers outpatient services that are less intensive than round the clock inpatient care. Generally held 4 5 daysweek for 6 to 9 hours each session, partial hospital program ser vices typically are group based and include eating at least two meals as well as opportunities to address issues in a setting that
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more closely approximates real life than inpatient treatment. That is, patients sleep at home and are free living on weekends, exposing them to challenges that can be processed during the 25 40 hours each week in program, as well as sharing group and family experiences. Supportive Care In relation to pediatric EDs, support groups are primarily designed for parents. Because their daughter or son with an ED often resists the diagnosis and treatment, parents often feel helpless and hopeless. Because of the historical precedent of blaming parents for causing EDs, parents often express feelings of shame and isolation (www.maudsley parents.org). Support groups and multifamily therapy sessions bring parents together with other parents whose families are at various stages of recovery from an ED in ways that are educational and encouraging. Patients often benefit from support groups after intensive treatment or at the end of treatment because of residual body image or other issues after eating and weight have normalized. PROGNOSIS With early diagnosis and effective treatment, 80 of youth with AN recover: They develop normal eating and weight control habits, resume menses, maintain average weight for height, and function in school, work, and relationships, although some still have poor body image. With weight restoration, fertility returns as well, although the weight for resumption of menses (approximately 92 of average body weight for height) may be lower than the weight for ovulation. The prognosis for BN is less well established, but outcome improves with multidimensional treatment that includes SSRIs and attention to mood, past trauma, impulsivity, and any existing psychopathol ogy. Since the diagnosis of ARFID was only established in 2013, little is known about its long term prognosis, although anecdotal evidence suggests that weight restoration is not actively resisted as it is in AN. PREVENTION Given the complexity of the pathogenesis of EDs, prevention is diffi cult. Targeted preventive interventions can reduce risk factors in older adolescents and college age women. Universal prevention efforts to promote healthy weight regulation and discourage unhealthy dieting have not shown effectiveness in middle school students. Programs that include recovered patients or focus on the problems associated with EDs can inadvertently normalize or even glamorize EDs and should be discouraged. Visit Elsevier eBooks at eBooks.Health.Elsevier.com for Bibliography. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. Chapter 42 u Disruptive, Impulse Control, and Conduct Disorders 277 The disruptive, impulse control, and conduct disorders (CDs) are interrelated sets of psychiatric symptoms characterized by a core deficit in self regulation of anger, aggression, defiance, and antisocial behav iors that typically begin in childhood or adolescence. These disorders include oppositional defiant, intermittent explosive, conduct, and other specifiedunspecified disruptiveimpulse controlCDs, as well as pyro mania, kleptomania, and antisocial personality disorder. Although all involve difficulty with both emotional and behavioral self regulation, the disorders vary by the relative intensity of problems with emotional regulation (e.g.,
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anger outbursts) vs behavioral regulation (e.g., defi ance, aggression, violating the rights of others or societal norms). DESCRIPTION Oppositional defiant disorder (ODD) is characterized by a persistent pattern lasting at least 6 months of angryirritable mood, argumenta tivedefiant behavior, andor vindictiveness exhibited during interac tion with at least one individual who is not a sibling (Table 42.1). For preschool children, the behavior must occur on most days, whereas in school age children, the behavior must occur at least once a week. The severity of the disorder is considered mild if symptoms are confined to only one setting (e.g., at home, at school, at work, with peers), moderate if symptoms are present in at least two settings, and severe if symptoms are present in three or more settings. Intermittent explosive disorder (IED) is characterized by recur rent verbal or physical aggression that is grossly disproportionate to the provocation or to any precipitating psychosocial stressors (Table 42.2). The outbursts, which are impulsive andor anger based rather than premeditated andor instrumental, typically onset rap idly, last 30 minutes, and frequently occur in response to a minor provocation by a close intimate. CD is characterized by a repetitive and persistent pattern over at least 12 months of serious aggressive, destructive, andor rule violating behavior in which the basic rights of others or major age appropriate societal norms or rules are violated (Table 42.3). The symptoms of CD are divided into four major categories: aggression to people and animals, destruction of property, deceitfulness or theft, and serious rule violations (e.g., truancy, running away). Three sub types of CD (which have different prognostic significance) are based on the age of onset: childhood onset type, adolescent onset type, and unspecified. A small proportion of individuals with CD exhibit char acteristics (lack of remorseguilt, callouslack of empathy, uncon cerned about performance, shallowdeficient affect) that qualify for the with limited prosocial emotions specifier. CD is classified as mild when few if any symptoms over those required for the diagnosis are present, and the symptoms cause relatively minor harm to oth ers. CD is classified as severe if many symptoms over those required for the diagnosis are present, and the symptoms cause considerable harm to others. Moderate severity is intermediate between mild and severe. Other specifiedunspecified disruptiveimpulse controlCD (subsyndromal disorder) applies to presentations in which symptoms characteristic of the disorders in this class are present and cause clini cally significant distress or functional impairment, but do not meet full diagnostic criteria for any of the disorders in this class. EPIDEMIOLOGY The prevalence of ODD is approximately 3, and in preadolescents is more common in males than females (1.4:1). One year prevalence rates for IED and CD approximate 3 and 4, respectively. For CD, prevalence rates rise from childhood to adolescence and are higher among males than females. CLINICAL COURSE Oppositional behavior can occur in all children and adolescents at times, particularly during the toddler and early teenage periods when autonomy and independence are normative developmental tasks. Oppositional behavior becomes a
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concern when it is frequent, intense, persistent, and pervasive and when it affects the childs social, family, andor academic life. Some of the earliest manifestations of opposition ality are stubbornness (3 years), defiance and temper tantrums (4 5 years), and argumentativeness (6 years). Approximately 65 of chil dren with ODD exit from the diagnosis after a 3 year follow up; ear lier age at onset of oppositional symptoms conveys a poorer prognosis. ODD often precedes the development of CD and there is an approxi mately 30 higher likelihood of CD when ODD is comorbid with attention deficithyperactivity disorder (ADHD). ODD also increases the risk for the development of depressive and anxiety disorders. The defiant, argumentative, and vindictive symptoms carry most of the risk for CD, whereas the angry, irritable mood symptoms carry most of the risk for depression and anxiety. IED usually begins in late childhood or adolescence and appears to follow a persistent course over many years, with recurrent periods of impulsive and aggressive outbursts. The onset of CD may occur as early as the preschool years, but the first significant symptoms usually emerge during the period from middle childhood through middle adolescence; onset is rare after age 16 years. Symptoms of CD vary with age as the individual develops increased physical strength, cognitive abilities, and sexual maturity. Symptoms that emerge first tend to be less serious (e.g., lying), while those emerging later tend to be more severe (e.g., sexual or physical assault). Severe behaviors emerging at an early age convey a poor prog nosis. In the majority of individuals, the disorder remits by adulthood; in a substantial fraction, antisocial personality disorder develops. Indi viduals with CD also are at risk for the later development of mood, anxiety, posttraumatic stress, impulse control, psychotic, somatic symptom, and substance related disorders. DIFFERENTIAL DIAGNOSIS The disorders in this diagnostic class share a number of characteristics with each other as well as with disorders from other classes, and as such must be carefully differentiated. ODD can be distinguished from CD by the absence of physical aggression and destructiveness and by the presence of angry, irritable mood. ODD can be distinguished from IED by the lack of serious aggression toward others (e.g., physical assault). IED can be distinguished from CD by the lack of predatory aggression and other, nonaggressive symptoms of CD. The oppositionality seen in ODD, the explosivity seen in IED, and the aggressiondestructiveness seen in CD must be distinguished from those symptoms occurring in the context of other psychiatric disor ders, particularly ADHD, depression, and bipolar, substance related, autism spectrum, or psychotic disorders. COMORBIDITY Rates of ODD are much higher in children with ADHD, which suggests shared temperamental risk factors. Depressive, anxiety, and substance related disorders are most often comorbid with IED. ADHD and ODD are both common in individuals with CD, and this comorbid presenta tion predicts worse outcomes. CD may also occur with anxiety, depres sive, bipolar, learning, language, and substance related disorders. SEQUELAE The disruptive, impulse control, and CDs
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are associated with a wide range of psychiatric disorders in adulthood and with many other adverse outcomes, such as suicidal behavior, physical injury, Chapter 42 Disruptive, Impulse Control, and Conduct Disorders Erica H. Lee, Keneisha R. Sinclair McBride, David R. DeMaso, and Heather J. Walter Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. 278 Part III u Behavioral and Psychiatric Disorders delinquency and criminality, legal problems, substance use, unplanned pregnancy, social instability, marital failure, and academic and occupa tional underachievement. ETIOLOGY AND RISK FACTORS At the individual level, a number of neurobiologic markers (lower heart rate and skin conductance reactivity, reduced basal cortisol reactivity, abnormalities in the prefrontal cortex and amygdala, serotonergic abnor malities) have been variously associated with aggressive behavior disor ders. Other biologic risk factors include pre , peri , and postnatal insults; cognitive and linguistic impairment, particularly language based learning deficits; difficult temperamental characteristics, particularly negative affec tivity, emotional reactivity, poor frustration tolerance, and impulsivity; cer tain personality characteristics (novelty seeking, reduced harm avoidance, and reward dependence); and certain cognitive characteristics (cognitive rigidity, hostile attributions for ambiguous social cues). At the family level, a consistently demonstrated risk factor is ineffective parenting. Parents of behaviorally disordered children are more inconsis tent in their use of rules, issue more and unclear commands, are more likely to respond to their child based on their own mood rather than the childs behavior, are more likely to utilize a harsh or neglectful parenting style, are less likely to monitor their childrens whereabouts, and are relatively unre sponsive to their childrens prosocial behavior. Complicating this asso ciation is the consistent finding that temperamentally difficult children are more likely to elicit negative parenting responses, including physical punishment, which can exacerbate anger and oppositionality in the child. Other important family level influences include impaired parentchild attachment, child maltreatment (physical and sexual abuse, neglect), expo sure to marital conflict and domestic violence, family poverty and crime, frequent changes in caregivers, and family genetic liability (family history of the disorders in this class along with substance use, depressive, bipolar, schizophrenic, somatization, and personality disorders, as well as ADHD, have all been shown to be associated with the development of behavior disorders). Peer level influence on the development of behavior problems includes peer rejection in childhood and antisocial peer groups. Neighborhood influences include social processes such as collective efficacy, social con trol, and exposure to violence. Culturally, it is helpful to consider the context in which undesirable behaviors occur to better understand their function. PREVENTION An effective conduct problem prevention program was Fast Track, a multicomponent school based intervention comprising a classroom curriculum targeted at conflict resolution and interpersonal skills, parent training, and interventions targeted at the school environment. Imple mented in grades 1 through 10, former program participants at age 25 had a lower prevalence of any externalizing, internalizing, or substance
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Table 42.1 DSM 5 Diagnostic Criteria for Oppositional Defiant Disorder A. A pattern of angryirritable mood, argumentativedefiant behavior, or vindictiveness lasting at least 6 mo as evidenced by at least four symptoms from any of the following categories, and exhibited during interaction with at least one individual who is not a sibling: ANGRYIRRITABLE MOOD 1. Often loses temper. 2. Is often touchy or easily annoyed. 3. Is often angry and resentful. ARGUMENTATIVEDEFIANT BEHAVIOR 4. Often argues with authority figures or, for children and adolescents, with adults. 5. Often actively defies or refuses to comply with requests from authority figures or with rules. 6. Often deliberately annoys others. 7. Often blames others for his or her mistakes or misbehavior. VINDICTIVENESS 8. Has been spiteful or vindictive at least twice within the past 6 mo. Note: The persistence and frequency of these behaviors should be used to distinguish a behavior that is within normal limits from a behavior that is symptomatic. For children younger than 5 yr, the behavior should occur on most days for a period of at least 6 mo unless otherwise noted (Criterion A8). For individuals 5 yr or older, the behavior should occur at least once per week for at least 6 mo, unless otherwise noted (Criterion A8). Although these frequency criteria provide guidance on a minimal level of frequency to define symptoms, other factors should be considered, such as whether the frequency and intensity of the behaviors are outside a range that is normative for the individuals developmental level, gender, and culture. B. The disturbance in behavior is associated with distress in the individual or others in his or her immediate social context (e.g., family, peer group, work colleagues), or it impacts negatively on social, educational, occupational, or other important areas of functioning. C. The behaviors do not occur exclusively during the course of a psychotic, substance use, depressive, or bipolar disorder. Also, the criteria are not met for disruptive mood dysregulation disorder. From the Diagnostic and Statistical Manual of Mental Disorders, 5th ed. pp. 462463. Copyright 2013. American Psychiatric Association. Table 42.2 DSM 5 Diagnostic Criteria for Intermittent Explosive Disorder A. Recurrent behavioral outbursts representing a failure to control aggressive impulses as manifested by either of the following: 1. Verbal aggression (e.g., temper tantrums, tirades, verbal arguments or fights) or physical aggression toward property, animals, or other individuals, occurring twice weekly, on average, for a period of 3 mo. The physical aggression does not result in damage or destruction of property and does not result in physical injury to animals or other individuals. 2. Three behavioral outbursts involving damage or destruction of property andor physical assault involving physical injury against animals or other individuals occurring with a 12 mo period. B. The magnitude of aggressiveness expressed during the recurrent outbursts is grossly out of proportion to the provocation or to any precipitating psychosocial stressors. C. The recurrent aggressive outbursts are not premeditated (i.e., they are impulsive andor anger based) and are not committed to achieve some
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tangible objective (e.g., money, power, intimidation). D. The recurrent aggressive outbursts cause either marked distress in the individual or impairment in occupational or interpersonal functioning, or as associated with financial or legal consequences. E. Chronologic age is at least 6 yr (or equivalent developmental level). F. The recurrent aggressive outbursts are not better explained by another mental disorder (e.g., major depressive disorder, bipolar disorder, disruptive mood dysregulation disorder, a psychotic disorder, antisocial personality disorder, borderline personality disorder) and are not attributable to another medical condition (e.g., head trauma, Alzheimer disease) or to the physiologic effects of a substance (e.g., a drug of abuse, a medication). For children ages 6 18 yr, aggressive behavior that occurs as part of an adjustment disorder should not be considered for this diagnosis. Note: This diagnosis can be made in addition to the diagnosis of attention deficithyperactivity disorder, conduct disorder, oppositional defiant disorder, or autism spectrum disorder when recurrent impulsive aggressive outbursts are in excess of those usually seen in these disorders and warrant clinical attention. From the Diagnostic and Statistical Manual of Mental Disorders, 5th ed. p. 466. Copyright 2013. American Psychiatric Association. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. Chapter 42 u Disruptive, Impulse Control, and Conduct Disorders 279 abuse problem than program nonparticipants. Program participants also had lower violent and drug crime conviction scores, lower risky sexual behavior scores, and higher well being scores. Another useful prevention program, the Seattle Social Development Project, was also a multicompo nent school based intervention with teacher, parent, and student compo nents targeting classroom management, interpersonal problem solving, child behavior management, and academic support skills. Implemented in grades 1 through 6, outcomes at age 19 years demonstrated that the intervention decreased lifetime drug use and delinquency for participant males compared with males in comparator communities but had no sig nificant effects on females. SCREENINGCASE FINDING The parents of children presenting in the primary care setting should be queried about angry mood or aggressive, defiant, or antisocial behavior as part of the routine clinical interview. A typical screen ing question would be, Does name have a lot of trouble controlling hisher anger or behavior? A number of standardized broad band screening instruments widely used in the primary care setting (e.g., Pediatric Symptom Checklist, Strengths and Difficulties Questionnaire) have items specific to angry mood and aggressive behavior, and as such can also be used to identify problems in this domain. EARLY INTERVENTION Youth (andor their parents) presenting in the primary care setting who self report or respond affirmatively to queries about difficulties manag ing angry mood or aggressive or antisocial behavior should be afforded the opportunity to talk about the situation with the pediatric practitio ner (separately with older youth as indicated). By engaging in active listening (e.g., I hear how you have been feeling. Tell me more about what happened
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to make you feel that way), the pediatric practitioner can establish therapeutic rapport and begin to assess the onset, duration, context, severity, and complexity of the symptoms, and associated dan gerousness, distress, and functional impairment. In the absence of acute dangerousness (e.g., homicidality, assaultiveness, psychosis, substance abuse) and significant distress or functional impairment, the pediatric practitioner can schedule a follow up appointment within a few weeks to conduct a behavior assessment. At this follow up visit, to assist with decision making about appropriate level of care, a focused symptom rating scale can be administered (Table 42.4) and additional risk factors explored (e.g., see the previous section on Etiology and Risk Factors). For mild symptoms (manageable by the parent and not function ally impairing) and in the absence of major risk factors, guided self help (anticipatory guidance) and monitoring with a scheduled follow up may suffice. Guided self help can include provision of educational materials (pamphlets, books, videos, workbooks, internet sites) that provide infor mation to the youth about dealing with anger provoking situations, and advice to parents about strengthening the parentchild relationship, effec tive parenting strategies, and the effects of adverse environmental expo sures on the development of behavior problems. In a Cochrane review, media based parenting interventions had a moderate positive effect on child behavior problems, either alone or as an adjunct to medication. An example of a self help program for parents is the Positive Parenting Pro gram (Triple P; http:www.triplep parenting.com), online version, in which parents can purchase 6 8 modules of instruction addressing tech niques for positive parenting and strategies for encouraging good behavior, teaching new emotional and behavioral skills, and managing misbehavior with youth from toddlers to teens (see Chapter 20). If a mental health clinician has been co located or integrated into the primary care setting, all parents of young children (universal prevention), as well as the parents of youth with mild behavior problems (indicated prevention), could be provided with a brief version of behavioral parent training. For example, Incredible Years (http:www.incredibleyears.com) has a 4 8 session universal prevention version to help parents promote their 26 year old childrens emotional regulation, social competence, problem solving, and reading readiness. A randomized trial in pediatric practices found that Incredible Years significantly improved parenting practices and 24 year olds disruptive behaviors compared to a wait list control. Incredible Years positive effects on parenting and child behavior have been found for populations diverse in race, cultural background, and socioeconomic status. Similarly, the Triple P program has seminar (three, 90 minute sessions), brief (15 30 min consultations), and primary care (four, 20 30 minute consultations) versions for the parents of youth from birth to the teenage years, specifically designed for implementation in the primary care setting. The Triple P interventions, supported by an extensive evidence base, focus on strengthening the parentchild relation ship, identifying and monitoring the frequency of a problem behavior, and implementing and reviewing the effects of a targeted behavior plan. Meta analyses have found that gains
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from Triple P are maintained over time. TREATMENT For youth who continue to have mild to moderate behavior problems after several weeks of guided self help or a brief course of behavioral parent training, or who from the outset exhibit moderate to severe symptoms, or who have a history of maltreatment or severe family dysfunction or psy chopathology, assessment and treatment in the specialty mental health set ting by a child trained mental health clinician should be provided. The youths problem behavior may predominantly occur at home, at school, with peers, or in the community, or it may be pervasive. If possible, interventions need to address each context specifically, rather than assum ing generalizability of treatment. Thus, for behaviors mostly manifested in the home setting, behavioral parent training would be the treatment of Table 42.3 DSM 5 Diagnostic Criteria for Conduct Disorder A. A repetitive and persistent pattern of behavior in which the basic rights of others or major age appropriate societal norms or rules are violated, as manifested by the presence of at least 3 of the following 15 criteria in the past 12 mo from any of the following categories, with at least one criterion present in the past 6 mo: AGGRESSION TO PEOPLE AND ANIMALS 1. Often bullies, threatens, or intimidates others. 2. Often initiates physical fights. 3. Has used a weapon that can cause serious physical harm to others (e.g., a bat, brick, broken bottle, knife, gun). 4. Has been physically cruel to people. 5. Has been physically cruel to animals. 6. Has stolen while confronting a victim (e.g., mugging, purse snatching, extortion, armed robbery). 7. Has forced someone into sexual activity. DESTRUCTION OF PROPERTY 8. Has deliberately engaged in fire setting with the intention of causing serious damage. 9. Has deliberately destroyed others property (other than by fire setting). DECEITFULNESS OR THEFT 10. Has broken into someone elses house, building, or car. 11. Often lies to obtain good or favors or to avoid obligations (i.e., cons others). 12. Has stolen items of nontrivial value without confronting a victim (e.g., shoplifting, but without breaking and entering; forgery). SERIOUS VIOLATIONS OF RULES 13. Often stays out at night despite parental prohibitions, beginning before age 13 yr. 14. Has run away from home overnight at least twice while living in the parental or parental surrogate home, or once without returning for a lengthy period. 15. Is often truant from school, beginning before age 13 yr. B. The disturbance in behavior causes clinically significant impairment in social, academic, or occupational functioning. C. If the individual is age 18 yr or older, criteria are not met for antisocial personality disorder. From the Diagnostic and Statistical Manual of Mental Disorders, 5th ed. pp. 469471. Copyright 2013. American Psychiatric Association. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. 280 Part III u Behavioral and Psychiatric Disorders
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choice, whereas for behaviors manifested mostly at school, consultation with the teacher regarding an assessment for a 504 plan or individualized education plan (IEP) can be useful. School based services can include a functional behavioral analysis to determine the function of the problematic behavior for the child, and development of a behavioral intervention plan to direct the child toward alternative positive behaviors that can achieve the same goal. School based services should be considered whenever a child is subjected to repeated disciplinary action in school or suspensions for misbehavior. When there are pervasive problems, including aggression toward peers, cognitive behavioral therapy (CBT) with the childteen can be employed in addition to the other interventions. Behavioral parent training has been extensively studied for the treat ment of youth problem behavior. These programs work by reshaping nega tive family patterns that may trigger or reinforce problem behaviors. They are typically 10 15 weeks in duration and focus on some combination of the following components: understanding social learning principles, developing a warm supportive relationship with the child, encouraging child directed interaction and play, providing a predictable structured household environment, setting clear and simple household rules, con sistently praising and materially or socially rewarding positive behavior, consistently ignoring annoying behavior (followed by praise when the annoying behavior ceases), giving effective commands, and consistently giving consequences (e.g., time out, loss of privileges) for dangerous or destructive behavior. Other important targets for parenting training include understanding developmentally appropriate moods and behav ior, managing difficult temperamental characteristics, fostering the childs social and emotional development, and protecting the child from trau matic exposures. Parent training can be implemented with families in individual or group formats. Specific parent training programs include Incredible Years and Triple P, described earlier, and ParentChild Interac tion Therapy, Helping the Noncompliant Child, and Parent Management Training Oregon. Predictors of nonresponse to these interventions have included greater initial symptom severity as well as involvement of the parent with child protection services. Difficulty with adherence to the complete treatment regimen has lim ited the effectiveness of parent training programs. Estimates of premature termination are as high as 5060, and termination within five treatment sessions is not uncommon. Predictors of premature termination have included single parent status, low family income, low parental education levels, young maternal age, minority group status, and life stresses. CBT for youth with disruptive behavior also has been extensively stud ied. Common CBT techniques for disruptive behavior include identifying the antecedents and consequences of disruptive or aggressive behavior, learning strategies for recognizing and regulating anger expression, problem solving and cognitive restructuring (perspective taking) tech niques, and modeling and rehearsing socially appropriate behaviors that could replace angry or aggressive reactions. Programs typically are deliv ered in 16 20 weekly sessions. Multicomponent treatments for serious behavior disorders such as CD target the broader social context. Multidimensional Treatment Foster Care, delivered in a foster care setting for 6 9 months, typically includes foster parent training and support; family therapy for biologic parents; youth anger management, social
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skills, and problem solving train ing; school based behavioral interventions and academic support; and psychiatric consultation and medication management, when needed. Multisystemic Therapy, typically lasting 3 5 months, generally includes social competence training, parent and family skills training, medica tions, academic engagement and skills building, school interventions and peer mediation, mentoring and after school programs, and involve ment of child serving agencies. Due to the strength of the supporting evidence, these multicomponent programs have been designated well established treatments for adolescents involved in the juvenile justice system. Predictors of nonresponse to multicomponent treatments have included higher frequency of rule breaking behavior and predatory aggression, higher psychopathy scores, and comorbid mood disorders. Psychosocial interventions should be considered the first line inter vention; pharmacotherapy may provide benefit, particularly if psycho social treatment has not led to adequate improvement. Three classes of medication, stimulants, 2 adrenergic agonists, and atypical antipsy chotics, have evidence for the management of impulsive, anger driven aggressive behavior, although none is approved by the U.S. Food and Drug Administration (FDA) for this indication, except irritability aggression in autism. Resource limitations may necessitate provision of pharmacotherapy in the primary care setting; the safety and efficacy of this practice can be enhanced by regular consultation with a child and adolescent psychiatrist or developmental behavioral pediatrician. There are favorable effects of stimulants on oppositional behavior, anger outbursts, and aggression in youths, with or without comorbid ADHD. The doses of stimulants used for aggression are similar to those used for ADHD. An extended release 2 adrenergic agonist (guanfacine) is effica cious for oppositionality comorbid with ADHD, with a dose of 1 4 mg day, dosed according to weight. There is evidence for efficacy of risperi done in reducing aggression and conduct problems in children age 5 18 years. The suggested usual daily dose of risperidone for severe aggression is 1.5 2 mg for children and 2 4 mg for adolescents, titrating up as needed and tolerated from starting doses of 0.25 mg (children) or 0.5 mg (adoles cents). The use of this class of medication should be reserved for severe presentations in which the safety of self andor others is compromised. Medication trials should be systematic, and the duration of trials should be sufficient (generally 6 8 weeks for atypical antipsychotics; shorter for stimulants and agonists) to determine the agents effectiveness. The short term goal of medication treatment is to achieve at least a 50 reduc tion in aggressive symptoms, as assessed by a focused symptom rating scale (see Table 42.4); the ultimate goal is to achieve symptom remission (below clinical cutpoint on the rating scale). A second medication of the same class can be considered if there is insufficient evidence of response to the maximal tolerated dose. Care should be taken to avoid unnecessary polypharmacy, in part by discontinuing agents that have not demonstrated significant benefit. Discontinuation of the medication should be consid ered after a symptom free interval. LEVEL OF CARE Most children and adolescents with a behavior disorder can be
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safely and effectively treated in the outpatient setting. Youths with intractable CD may benefit from residential or specialized foster care treatment, where more intensive treatments can be provided. Visit Elsevier eBooks at eBooks.Health.Elsevier.com for Bibliography. Table 42.4 Selected AngerAggression Rating Scales NAME OF INSTRUMENT INFORMANT(S) AGE RANGE (YR) NO. OF ITEMS Childrens Aggression Scale Parent, Teacher 5 18 33 (P), 23 (T) Eyberg Child Behavior Inventory Parent 2 16 36 Outburst Monitoring Scale Parent 12 17 20 Sutter Eyberg Student Behavior InventoryRevised Teacher 2 16 38 Vanderbilt ADHD Diagnostic Rating Scales Parent, Teacher 6 12 55 (P), 43 (T) Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. Chapter 43 u Tantrums and Breath Holding Spells 281 Temper tantrums are common during early childhood. They are typically developmentally normative expressions of childrens frus tration with their own limitations or anger about not being able to get their way. It is important for parents to recognize the different trig gers for tantrums to determine the best course of action to prevent or manage this behavior as it arises. Dealing with tantrum behavior can become very frustrating for parents and these feelings should be validated, while also helping make sure parents are aware that many tantrums can be averted by awareness or attunement to certain cues given by their child. In particular, parents should be aware that when a child is tired, hungry, or has to make a transition, it can be expected that the child will be more likely to have a tantrum because limit setting or unmet expectations may feel particularly overwhelming in these circumstances. In this case, it is advised that parents plan ahead and take a preventive stance by being aware of triggers and minimizing the potential for a tantrum. Parents should not make a tired or hungry child accompany them on an extended outing unless absolutely necessary. Additionally, depending on the childs devel opmental level, it is helpful to have a clear discussion ahead of time about the expectations in certain scenarios. An example of setting expectations to help prevent a tantrum is: When we go into the store I need you to (1) stay with me, (2) keep your hands to yourself, and (3) not whine for treats. If you can do these three things, we can pick one treat to bring home. When children are able to demonstrate good control, their behavior should be acknowledged, praised, and rewarded when appropriate. This will increase the likelihood that they will engage in the desired response more often, even in situa tions they find frustrating. When children tantrum as an expression of anger or sadness in not getting their way, parents may feel inclined to give in or respond to the negative behavior with yelling or threats. Unfortunately, these responses can reinforce and even escalate the oppositional behavior. Parents should attempt to avert
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defiance by giving the child choices (e.g., you can walk to the car on your own two feet or I can carry you). Active ignoring can be used for mild tantrum behaviors because pay ing attention, even negative attention, can be reinforcing. If a child is tantruming in a way that is unsafe, they can be removed from the unsafe situation and given a consequence by being placed in time out. If the tantrum was to avoid a task, the child should be required to com plete the task once time out is over. Breath holding spells occasionally occur during a tantrum and can be frightening to parents. These are reflexive events in which the crying child becomes apneic, pale, or cyanotic, may lose consciousness, and occasionally will have a brief seizure. Parents are best advised to ignore breath holding during a tantrum once it has started. Without reinforce ment, breath holding generally disappears. Subtypes of breath holding spells include cyanotic, pallid, or mixed episodes. Cyanotic spells are the dominant type. Pallid spells may be similar to vasovagal related syncopal events in older children and may be initiated by similar stimuli. Iron deficiency with or without anemia may be present, and some children with breath holding spells respond to iron therapy. There is no increased risk of seizure disorders in children who have had a short seizure during a breath holding spell. Medical conditions to rule out in breath holding spells (usually pallid) include seizures, Chiari crisis, familial dysautonomia, cardiac arrhyth mias, cataplexy, hereditary hyperekplexia, and other central nervous system lesions. The first key to the management of temper tantrums and breath holding spells is to help parents intervene before the child is highly distressed. The parent can be instructed to calmly remind the child of the expected behavior and the potential consequence if the expected behavior does not occur. In addition, distraction to another activity or conversation may help. If the child does not comply, he or she should be placed in time out for a period approximating 1 min for each year of age. Parents should state the reason the child is being placed in time out beforehand in a calm and neutral tone, but they should not discuss the reasons during time out. Once the time out is over and the child is calm, it may be helpful for parents to discuss with the child the reasons for the childs frustration and their expectations for how the child will respond in the future. Time out can be effectively used in children up to approximately 10 years of age. Parents should also be advised to be mindful of their own reactions to their childs tantrum behavior to avoid an escalation of the childs behavior caused by an angry parental response. If behavioral measures such as time out fail, pediatricians must assess other aspects of parentchild interactions, such as the frequency of positive interactions, the consistency of parental responses to child behavior, and the ways that parents handle anger,
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before making fur ther recommendations. In the absence of frequent positive parent child interactions, time out may not be effective, and inconsistent responding to problem behavior increases the likelihood of the nega tive behavior continuing. Children can be frightened by the intensity of their own angry feelings and by angry feelings they arouse in their par ents. Parents should model the anger control that they want their chil dren to exhibit. Some parents are unable to see that if they lose control themselves, their own angry behavior does not help their children to behave differently. Advising parents to calmly provide simple choices will help the child to feel more in control and to develop a sense of autonomy. Providing the child with options also typically helps reduce the childs feelings of anger and shame, which can later have adverse effects on social and emotional development. Providing choice also reduces power struggles between the parent and child and can aid in enhancing the parentchild relationship and building problem solving skills. When tantrum behavior, including breath holding, does not respond to parent coaching or is accompanied by head banging or high levels of aggression, referral for a mental health evaluation is indicated. Further evaluation is also recommended if tantrum behavior persists into the latency period and preteen years. Visit Elsevier eBooks at eBooks.Health.Elsevier.com for Bibliography. Chapter 43 Tantrums and Breath Holding Spells Keneisha R. Sinclair McBride, Erica H. Lee, David R. DeMaso, and Heather J. Walter Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. 282 Part III u Behavioral and Psychiatric Disorders Young children lie for a multitude of reasons. Lies for this age group can be considered developmentally normative attempts at understanding lan guage, communication, rules, and expectations. In early childhood, lying often occurs as a child experiments with language. By observing the reac tions of parents, preschoolers learn about expectations for honesty in com munication. Lying can also be a form of fantasy for children, who often describe things as they wish them to be rather than as they are. To avoid an unpleasant confrontation, a child who has not followed a rule or met an expectation may lie. At this stage, children often do not understand that lying only postpones a confrontation. Parents should keep in mind that lying behavior in this age group is rarely malicious or premeditated. In older children, lying is generally an effort to cover up actions that do not fit into the childs conceptualization of themselves. Children in this age group may lie as an attempt to maintain self esteem. Of course, lying is also often used to avoid a negative consequence for misbehavior. Older children are also more likely to intentionally leave out critical parts of a story in an attempt to deceive or avoid a negative consequence. Lying can also be promoted by poor adult modeling.
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Many children and adoles cents lie to avoid adults disapproval. If children and teens are responded to in harsh and punitive ways, they may lie to avoid this. Alternatively, lying may be used as a method of rebellion, especially in adolescence. Lying about forbidden activities, social media use, or other behaviors may be an attempt to continue to break the rules without detection. Chronic lying can occur in combination with several other antisocial behaviors and is a sign of underlying psychopathology or family dysfunction. Parents should address lying by giving the child a clear message of what is acceptable. Sensitivity and support combined with limit setting are nec essary for a successful intervention. Although habitual lying can become frustrating for parents, they should be discouraged from making accusa tions or focusing on catching their child in a lie and instead should work toward creating an atmosphere that makes it easier for their child to tell the truth. Parents should let the child know that telling the truth about a dif ficult situation will allow the parents to help them better problem solve the issue at hand. Should a situation arise where a child has lied and the parents are aware of the true details, the lie should be confronted while providing the facts of what is known and also stating the desired or expected behav ior. This should be done in a calm, neutral manner. For example, if a parent is aware that a child played video games instead of doing homework and the child denies it, the parent can state, I notice that your homework is incomplete and that you are playing without permission. Our rule is that you complete homework first. There will be no more video games for the rest of the week. This response reminds the child how he can meet his goals in an acceptable way and an appropriate consequence can then be given. Parents should be encouraged to address the expectations for their home and children in a family meeting or in regular discussions with their child outside the context of the childs lying. Regardless of age or developmental level, when lying becomes a common way of managing conflict, intervention is warranted. If this behavior cannot be resolved through the parents understanding of the situation and the childs understanding that lying is not a reasonable alternative, a mental health evaluation is indicated. STEALING Many children steal something at some point in their lives. Often, when very young children steal, the behavior is an impulsive action to acquire something they want. A common example is the child who takes candy or a toy from the store shelf. If a parent notices this behavior, they can use the situation as a teaching opportunity to explain that community and family expectations are that we have to pay for things at the store and not take them without permission. It should not be expected that a very young child will be aware of all the rules around shopping
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or stealing. It may also be difficult for a child who has been used to being able to freely take what ever she wants to be aware of all the expected behaviors across different set tings. When preschoolers and school age children begin to steal frequently even after they have been told not to, the behavior may be a response to stressful environmental circumstances and requires further exploration and evaluation. For some older children, stealing can be an expression of anger or revenge for perceived frustrations with parents or other authority figures. In such instances, stealing becomes one way the child and adolescent can manipulate and attempt to control their world. Stealing can also be learned from adults. Some children will report that the behavior is exciting for them, and they may also engage in the behavior for peer approval. In some cases, youth living in poverty may engage in the behavior as a survival mechanism. Kleptomania, an impulse control disorder, may begin in adoles cence and is characterized by an intense impulse to steal objects that may not be rationally needed by the patient. There are often comor bid disorders such as anxiety, eating disorders, substance misuse, and depression. Treatment includes cognitive behavioral therapy (CBT) in addition to various drugs such as lithium, naltrexone, and selective serotonin reuptake inhibitors (SSRIs). Parents should work with their children to rectify stealing through restitution. Parents should require that their child return stolen items or pay for them with their own money (i.e., allowance or gift money). When this is not possible, another reasonable consequence should be given, such as losing a privilege or completing additional chores. When stealing is part of a pattern of broader conduct problems, referral for a mental health evaluation is warranted. TRUANCY Truancy and running away are never developmentally appropriate. Truancy may represent an unsafe environment of disorganization within the home including lack of appropriate supervision or older children being required to caretake for younger siblings. Truancy can also be a sign of developing conduct problems or behavioral health problems including depression or anxiety. When truancy occurs in younger children, there are usually psychosocial concerns with the parents or adult caretakers in the home that prevent them from fol lowing through with the required demands of getting their children to school each day. Families struggling with housing and food insecurity may have difficulties having their children attend school regularly. Par ents with intellectual disability or their own mental health or substance abuse problems may become overwhelmed with managing the home and caring for their children; thus they might not consistently ensure their child gets to school. In addition, children might decide to remain at home to take care of parents who are impaired. Truancy is more common in preteens and adolescents and can be a function of multiple factors, including but not limited to learning dif ficulties, social anxiety, depression, traumatic exposure, bullying, peer pressure, and substance use. In any of these cases, the child should be referred
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for further evaluation to assess the barriers to returning to school. Best practices for dealing with truancy resulting from school avoidance and anxiety include addressing the underlying psychologic symptoms causing the school avoidance and empowering parents, chil dren, and school staff to work on a consistent plan for a return to school. Younger children may threaten running away out of frustration or a desire to get back at parents. Older children who run away are almost always expressing a serious underlying problem within themselves or their family, including violence, abuse, and neglect. Adolescent runaways are at high risk for substance abuse and other risk taking behaviors as well as at risk for being victims of abuse (e.g., sexual exploitation). Youth exhibiting truancy or running away should be referred for a mental health evaluation. Visit Elsevier eBooks at eBooks.Health.Elsevier.com for Bibliography. Chapter 44 Lying, Stealing, and Truancy Keneisha R. Sinclair McBride, Erica H. Lee, David R. DeMaso, and Heather J. Walter Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. Chapter 46 u SelfInjurious Behavior 283 Aggressive behavior is a serious symptom associated with signifi cant morbidity and mortality. Early intervention is indicated for persistent aggressive behavior given that children may not simply grow out of this pattern of behavior. Aggressive tendencies are heritable, although environmental factors can promote aggression in susceptible children. Both enduring and temporary stressors affecting a family can increase aggressive behavior in children. Aggression in childhood is correlated with both poverty and chaotic family situations, including chronic unemployment, family discord, and exposure to community and domestic violence, criminality, and psychiatric disorders. Children born to teenage mothers and parents with limited resources and support are also at risk. Males are reported to be more aggressive than females. A difficult tem perament and later aggressiveness are related. When children with temperament difficulties are responded to with punitive discipline strategies within the family environment, it can set up a cycle of increasing aggression. Aggressive children often misinterpret social cues in such a way that they perceive hostile intent in ambiguous or benign interactions, and then may react with verbal or physical aggression toward peers and parents. It is important to differentiate the causes and motives for child hood aggression. Intentional aggression may be primarily instru mental (i.e., to achieve an end), primarily hostile (i.e., to inflict physical or psychologic pain), or primarily impulsive. Impulsive aggression can often be effectively managed with simple behavioral interventions at home. Children who are callous, not empathetic, and more consistently aggressive require intervention in the spe cialty mental health setting (see Chapter 42). These children are at high risk for suspension from school and eventual school failure. Because learning disorders are common in this population, aggres sive children should be referred for screening. Aggressive behav ior is often present in a variety of other psychologic conditions, including attention deficithyperactivity and
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oppositional defiant, intermittent explosive, conduct, and disruptive mood dysregulation disorders (see Chapters 39 and 42). Aggressive behavior in males is relatively consistent from the pre school period through adolescence. Without effective intervention, a male with a high level of aggressive behavior between 3 and 6 years of age has a high probability of carrying this behavior into adolescence. The developmental progression of aggression among females is less well studied. Fewer females show physically aggres sive behavior in early childhood. However, interpersonal coercive behavior, especially in peer relationships, is seen in females. This behavior may be related to the development of physical aggression for females in adolescence (e.g., fighting) or other conduct prob lems (e.g., stealing). Children exposed to aggressive models on television, in video games, or in play have more aggressive behavior compared with children not exposed to these models. Parents anger and aggressive or harsh pun ishment can model behavior that children may imitate when they are physically or psychologically hurt. Parents abuse may be transmitted to the next generation by several modes: children imitate aggression Chapter 45 Aggression Keneisha R. Sinclair McBride, Erica H. Lee, David R. DeMaso, and Heather J. Walter that they have witnessed; abuse can cause neurologic damage, which itself predisposes the child to violence; and internalized rage often results from abuse. Aggressive behavior in youth is often oriented toward peers through bullying (see Chapter 15.1). Although it is developmentally normative for children to engage in some teasing behavior, bullying has a more serious tone. Bullying is defined as unwanted aggressive behavior in which there is a real or perceived imbalance of power or strength between the bully and the victim. Typically, it involves a pattern of behavior repeated over time. Although most often per ceived as physical aggression, bullying can take on a variety of forms, including relational bullying, the most common form engaged in by females. Cyberbullying is a particular risk during the middle and high school years because of increased exposure and access to mul tiple social media platforms at this developmental stage. Parents should be advised to closely monitor their childs social media and maintain open communication with their children. Children may bully others because of impulse control and social skills deficits, strong need for power and negative dominance, satisfaction in caus ing harm to others, or psychologic or material rewards. Children who bully are at risk for a variety of negative school and psychologic outcomes. Victims of bullying are particularly at risk for negative outcomes, especially if the behavior is not addressed by adults. Victimization experiences are associated with school avoidance and school drop out, social isolation, somatic symptoms, and increased psychologic problems such as depression and anxiety. There have been numer ous cases of suicide in children who reported a prior history of being bullied. Should a concern arise around bullying in the school setting, parents should be advised to reach out to their childs teacher, school counselor, and school administrative staff to have the bullying behavior addressed. Many
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schools also have a bullying intervention protocol that can be implemented, and state depart ments of education have antibullying policies with formal proto cols to address concerns. Given the significant psychologic risks for both victims and perpetrators of bullying, it is essential that all children who are persistently involved in these incidents be referred for mental health evaluation. Visit Elsevier eBooks at eBooks.Health.Elsevier.com for Bibliography. Self injurious behaviors, or deliberate engagement in self inflicted harm, comprise both suicidal behaviors and nonsuicidal self injury (NSSI) (see Chapter 40). NSSI, specifically, involves intentional self inflicted damage to bodily tissue without the intent to die, though it can unintentionally result in significant harm or even death. Suicidal behaviors and NSSI are both transdiagnostic behaviors occurring in the context of numerous psychiatry disorders as well as in the absence of any diagnosis at all. Nonetheless, the vast majority of youth who engage in NSSI meet diagnostic criteria for a psychiatry disorder. Self injurious behav ior may also be associated with developmental disabilities often as a manifes tation of stereotypic movement disorder (Chapter 37.2). Chapter 46 Self Injurious Behavior Kiera M. James and Molly C. Adrian Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. Chapter 46 u SelfInjurious Behavior 283 Aggressive behavior is a serious symptom associated with signifi cant morbidity and mortality. Early intervention is indicated for persistent aggressive behavior given that children may not simply grow out of this pattern of behavior. Aggressive tendencies are heritable, although environmental factors can promote aggression in susceptible children. Both enduring and temporary stressors affecting a family can increase aggressive behavior in children. Aggression in childhood is correlated with both poverty and chaotic family situations, including chronic unemployment, family discord, and exposure to community and domestic violence, criminality, and psychiatric disorders. Children born to teenage mothers and parents with limited resources and support are also at risk. Males are reported to be more aggressive than females. A difficult tem perament and later aggressiveness are related. When children with temperament difficulties are responded to with punitive discipline strategies within the family environment, it can set up a cycle of increasing aggression. Aggressive children often misinterpret social cues in such a way that they perceive hostile intent in ambiguous or benign interactions, and then may react with verbal or physical aggression toward peers and parents. It is important to differentiate the causes and motives for child hood aggression. Intentional aggression may be primarily instru mental (i.e., to achieve an end), primarily hostile (i.e., to inflict physical or psychologic pain), or primarily impulsive. Impulsive aggression can often be effectively managed with simple behavioral interventions at home. Children who are callous, not empathetic, and more consistently aggressive require intervention in the spe cialty mental health setting (see Chapter 42). These children are at high risk for suspension from school and eventual school failure. Because learning
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disorders are common in this population, aggres sive children should be referred for screening. Aggressive behav ior is often present in a variety of other psychologic conditions, including attention deficithyperactivity and oppositional defiant, intermittent explosive, conduct, and disruptive mood dysregulation disorders (see Chapters 39 and 42). Aggressive behavior in males is relatively consistent from the pre school period through adolescence. Without effective intervention, a male with a high level of aggressive behavior between 3 and 6 years of age has a high probability of carrying this behavior into adolescence. The developmental progression of aggression among females is less well studied. Fewer females show physically aggres sive behavior in early childhood. However, interpersonal coercive behavior, especially in peer relationships, is seen in females. This behavior may be related to the development of physical aggression for females in adolescence (e.g., fighting) or other conduct prob lems (e.g., stealing). Children exposed to aggressive models on television, in video games, or in play have more aggressive behavior compared with children not exposed to these models. Parents anger and aggressive or harsh pun ishment can model behavior that children may imitate when they are physically or psychologically hurt. Parents abuse may be transmitted to the next generation by several modes: children imitate aggression Chapter 45 Aggression Keneisha R. Sinclair McBride, Erica H. Lee, David R. DeMaso, and Heather J. Walter that they have witnessed; abuse can cause neurologic damage, which itself predisposes the child to violence; and internalized rage often results from abuse. Aggressive behavior in youth is often oriented toward peers through bullying (see Chapter 15.1). Although it is developmentally normative for children to engage in some teasing behavior, bullying has a more serious tone. Bullying is defined as unwanted aggressive behavior in which there is a real or perceived imbalance of power or strength between the bully and the victim. Typically, it involves a pattern of behavior repeated over time. Although most often per ceived as physical aggression, bullying can take on a variety of forms, including relational bullying, the most common form engaged in by females. Cyberbullying is a particular risk during the middle and high school years because of increased exposure and access to mul tiple social media platforms at this developmental stage. Parents should be advised to closely monitor their childs social media and maintain open communication with their children. Children may bully others because of impulse control and social skills deficits, strong need for power and negative dominance, satisfaction in caus ing harm to others, or psychologic or material rewards. Children who bully are at risk for a variety of negative school and psychologic outcomes. Victims of bullying are particularly at risk for negative outcomes, especially if the behavior is not addressed by adults. Victimization experiences are associated with school avoidance and school drop out, social isolation, somatic symptoms, and increased psychologic problems such as depression and anxiety. There have been numer ous cases of suicide in children who reported a prior history of being bullied. Should a concern
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arise around bullying in the school setting, parents should be advised to reach out to their childs teacher, school counselor, and school administrative staff to have the bullying behavior addressed. Many schools also have a bullying intervention protocol that can be implemented, and state depart ments of education have antibullying policies with formal proto cols to address concerns. Given the significant psychologic risks for both victims and perpetrators of bullying, it is essential that all children who are persistently involved in these incidents be referred for mental health evaluation. Visit Elsevier eBooks at eBooks.Health.Elsevier.com for Bibliography. Self injurious behaviors, or deliberate engagement in self inflicted harm, comprise both suicidal behaviors and nonsuicidal self injury (NSSI) (see Chapter 40). NSSI, specifically, involves intentional self inflicted damage to bodily tissue without the intent to die, though it can unintentionally result in significant harm or even death. Suicidal behaviors and NSSI are both transdiagnostic behaviors occurring in the context of numerous psychiatry disorders as well as in the absence of any diagnosis at all. Nonetheless, the vast majority of youth who engage in NSSI meet diagnostic criteria for a psychiatry disorder. Self injurious behav ior may also be associated with developmental disabilities often as a manifes tation of stereotypic movement disorder (Chapter 37.2). Chapter 46 Self Injurious Behavior Kiera M. James and Molly C. Adrian Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. 284 Part III u Behavioral and Psychiatric Disorders Although NSSI and suicidal behavior are distinct constructs based on the intent of the behavior, they are also highly comorbid. Research exploring the attitudes of youth who have engaged in NSSI indicates that there is a strong identification with suicide and death for this population, which makes NSSI a significant clinical issue and risk factor that cannot be ignored or minimized. Although some youth engage in repeated NSSI without ever attempting sui cide, studies suggest that 5075 of adolescents who have a history of NSSI will make a suicide attempt at some point. NSSI has been documented in children as young as 7 years of age, with rates increasing from childhood (8) to adolescents (18), and decreasing during adulthood (5.5). Although traditionally thought to be more prevalent in females than males, NSSI occurs in both sexes. Emerging research suggests that, if present at all, gender differences in rates of NSSI are more likely in clinical than commu nity populations. Notably, however, rates of NSSI are particularly high among transgender and gender nonconforming teens with up to 55 reporting past year engagement in NSSI. There are no sig nificant ethnicity or class differences among youth who engage in NSSI. Youth identified as those with the highest risk include females ages 15 19 and males 20 24. Cutting is the most commonly reported form of NSSI. For those youth who engage in NSSI for the first time, approximately
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20 will repeat the behavior within the same year; cutting is the most com monly repeated method of NSSI. Other methods of NSSI include scratching, burning, carving, piercing, hitting or punching, biting, picking at wounds, and digging nails into the skin. The most com mon areas of injury are the arms, legs, and torso, though NSSI may also occur on other parts of the body (e.g., breasts, genitals, groin, neck). Objects used in cutting include razors, scissors, broken glass, hard plastic, knives, staples, paper clips, or any other objects sharp enough to cause injury. Importantly, there are gender differences in methods such that females are more likely to engage in cutting, scratching, biting, hair pulling, and wound picking whereas males are more likely to engage in burning and self battery, including hit ting and head banging. Youth often report exposure to NSSI before engaging in the behavior. Some youth report that they have friends who self injure (e.g., cut) to attempt to alleviate negative emotions. Others may view stories of their peers engagement in NSSI on websites and social media. Impressionable youth have also reported learning about NSSI for the first time from celebrities who have engaged in the behavior. NSSI is associated with depression, anxiety, peer (bullying) victimiza tion, social isolation, low self esteem, substance abuse, eating disorders, impulsivity, poor school performance, delinquency, and neglectful or highly punitive parenting practices, as well as trauma, including a his tory of physical or sexual abuse. The behavior may begin as an impulsive response to internal distress for younger children, but for those who are older, the behavior can take on a self reinforcing function. Youth may feel a sense of relief or mastery over negative emotions once the behavior has been completed. Some youth report that they engage in NSSI when feel ing intense negative emotions, overwhelmed, or panicked to regulate their emotions. Others engage in the behavior when they are feeling numb, to feel something again. NSSI may also serve as a distraction from emo tional pain, provide a sense of control over the body, or be used as a form of self punishment for a perceived wrongdoing. NSSI may also function to communicate distress or strength or provide peer group affiliation. Youth often report that they are unable to resist the urge to engage in the behavior and will continue to feel increasing levels of distress until they engage in NSSI. Others plan or schedule the behavior, building it into their routine. Youth who view NSSI as an effective, private, and necessary coping strat egy tend to have more dependence on the behavior and more resistance to stopping it. Some adolescents and young adults engage in repeated NSSI for years without disclosing the behavior. Due to the shame associated with this stigmatized behavior, youth will often go to great lengths to keep it a secret. Some wear bracelets to cover scars on their arms or wear long sleeves in summer to hide the scarring. They report feeling ashamed of
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the behavior and fear rejection or disappoint ment from family and friends should they find out. At times, fear of being rejected or a disappointment to others can increase feelings of depression and anxiety and can serve to perpetuate the behavior. In contrast, others are more open about showing their scars and sharing their behavior with others. In either case, the behavior is a way to communicate or manage some level of distress. Many youth who engage in NSSI may never be seen in a hospital emergency department or by a mental health professional. Factors that pro tect against engagement in NSSI include a lack of awareness of, or exposure to, NSSI; an aversion to physical pain; an aversion to NSSI related stimuli (e.g., blood); a positive view of the self; the use of other more adaptive emotion regulation strategies; and social norms. Youth with repetitive NSSI should be referred to behavioral health services. Effective treatment strategies include conducting a functional analysis around NSSI behavior, identifying and teach ing alternative emotion regulation strategies, and reducing access to means to harm oneself. Reduction of NSSI has been observed with dialectical behavior therapy for adolescents, cognitive behavioral therapy, cognitive analytic therapy, and mentalization based ther apy for adolescents. There are no psychopharmacologic treatments that have demonstrated efficacy; thus behavioral approaches should be prioritized. Parents should be advised to monitor youth social media access and be aware of their peer group. Maintaining open communication can assist parents in recognizing an increase in concerning behav iors or patterns of behaviors. Parents should talk with their child about strategies for managing strong emotions and provide emotion coaching to support their child through experiences of distress. They should also be encouraged to talk with their child about their use of and exposure to drugs and alcohol as substance use can be associated with NSSI. Learning that their child has been engaging in self injury can be frightening for parents because they are unsure of what to do or why their child is engaging in this behavior. It is important that parents receive psychoeducation about NSSI to reduce common mis conceptions that make it difficult to understand their childs engage ment in NSSI and respond effectively. Such information should be digestible and accurate, including written suggestions and examples. Parents should also seek mental health services for their child. It is recommended that the child receive a full assessment for risk of suicide when NSSI is a concern. The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM 5) has classified NSSI as a condition requiring fur ther study before consideration for possible placement in forth coming editions of DSM. Proposed diagnostic criteria include self inflicted injury without suicidal intent occurring on 5 or more days in the past year, with lack of suicidal intent either stated by the individual or inferred by the individuals repeated engagement in a behavior not likely to result in death. The individual expects that the self injurious behavior will relieve a
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negative feeling or thought, resolve an interpersonal difficulty, or induce a positive feeling state. The self injurious behavior is associated with interpersonal dif ficulties or negative feelings or thoughts, preoccupation with the intended behavior that is difficult to control, or frequent thoughts about the intended behavior. The proposed criteria also specify that the behavior is not socially sanctioned (e.g., body piercing, tattooing) and is not restricted to skin picking or nail biting. The behavior must be associated with significant distress or functional impairment. Visit Elsevier eBooks at eBooks.Health.Elsevier.com for Bibliography. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. Chapter 47 u Childhood Psychoses 285 Chapter 47 Childhood Psychoses Jennifer A. Zaspel and Rosa K. Kim Table 47.1 DSM 5 Diagnostic Criteria for Brief Psychotic Disorder A. Presence of one (or more) of the following symptoms. At least one of these must be (1), (2), or (3): 1. Delusions 2. Hallucinations 3. Disorganized speech (e.g., frequent derailment or incoherence) 4. Grossly disorganized or catatonic behavior Note: Do not include a symptom if it is a culturally sanctioned response. B. Duration of an episode of the disturbance is at least 1 day but less than 1 mo, with eventual full return to premorbid level of functioning. C. The disturbance is not better explained by major depressive or bipolar disorder with psychotic features or another psychotic disorder such as schizophrenia or catatonia, and is not attributable to the physiologic effects of a substance (e.g., a drug of abuse, a medication) or another medical condition. Specify if: With marked stressor(s) (brief reactive psychosis): If symptoms occur in response to events that, singly or together, would be markedly stressful to almost anyone in similar circumstances in the individuals culture. Without marked stressor(s): If the symptoms do not occur in response to events that, singly or together, would be markedly stressful to almost anyone in similar circumstances in the individuals culture. With postpartum onset: If onset is during pregnancy or within 4 wk postpartum. From the Diagnostic and Statistical Manual of Mental Disorders, 5th ed. p 94. Copyright 2013. American Psychiatric Association. Psychosis is a severe disruption of thought, perception, and behav ior resulting in loss of reality testing. Psychosis can occur as part of a mood disorder, such as major depressive disorder or bipolar I disorder; between mood disorder episodes, as in schizoaffective disorder; or without mood disorder episodes, as in schizophrenia. Transient psychotic episodes can arise during times of psychologic or physiologic stress in patients who are vulnerable because of per sonality, developmental, or genetic disorders. Positive symptoms, including delusions, hallucinations, disorganized thinking, and grossly disorganized behavior, are key features that define psy choses across disorders, likely because of shared pathophysiologic mechanisms. Negative symptoms, on the other hand, are most typical of schizophrenia. Delusions are fixed, unchangeable, false beliefs held despite con flicting evidence. They may include a
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variety of themes, including persecutory, referential (the belief that irrelevant events or details in the world are related directly to oneself), somatic, religious, and grandiose. Delusions are considered bizarre if they are clearly implausible. Hallucinations are vivid, clear, perceptual distur bances that occur without external stimulus and have the full force and impact of normal perceptions. They may occur in any sensory modality; auditory hallucinations are the most common associated with psychosis. Disorganized thinking is inferred from an indi viduals speech by examining their thought process and thought content and is typically severe enough to impair ones ability to communicate. Grossly disorganized behavior may range from childlike silliness to unpredictable agitation to catatonic behavior. Negative symptoms include diminished emotional expression, avo lition (decreased drive to perform purposeful tasks), alogia (lack of speech), anhedonia, and social withdrawal. Negative symptoms account for a substantial portion of the long term morbidity associ ated with schizophrenia. Given the centrality of hallucinations and delusions in making a diagnosis of a psychotic illness, their differentiation from developmen tally normal fantasy is essential. When children are imagining, they control the fantasy and do not have the perceptual experience of see ing and hearing. When children are hallucinating, they do not control the hallucination. Almost two thirds of children will endorse at least one psychotic like experience, most often a hallucination. When not persistent or accompanied by distress, these experiences are not usu ally a cause for concern. The largest population based study to date evaluating psychotic symptoms and neurocognition in youth 11 21 years old found that those who endorsed more psychotic like experi ences than is typical for their age had reduced accuracy across neuro cognitive domains, reduced global functioning, and increased risk of depression, anxiety, behavioral disorders, substance use, and suicidal ideation. Thus psychotic like symptoms that are frequent, distressing, and cause impairment signal a need for further evaluation and moni toring; however, only a small minority of these children will develop persisting psychotic illnesses. 47.1 Schizophrenia Spectrum Disorders Jennifer A. Zaspel and Rosa K. Kim Schizophrenia spectrum and other psychotic disorders as described in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM 5) include brief psychotic disorder, schizophreni form disorder, schizophrenia, schizoaffective disorder, substance medication induced psychotic disorder, psychotic disorder caused by another medical condition, catatonia associated with another mental disorder, catatonic disorder due to another medical condi tion, unspecified catatonia, delusional disorder, schizotypal personal ity disorder, and other specifiedunspecified schizophrenia spectrum and other psychotic disorders. DESCRIPTION The schizophrenia spectrum and other psychotic disorders are pri marily characterized by the presence of symptoms of psychosis, spe cifically delusions, hallucinations, disorganized speech, or grossly disorganized or catatonic behavior, and negative symptoms. Brief psychotic disorder is characterized by the duration of one or more of these symptoms for at least 1 day but less than 1 month followed by complete resolution. Emergence of symptoms may or may not be preceded by an identifiable stressor (Table 47.1). Although brief, the level of impairment in
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this disorder may be severe enough that supervision is required to ensure that basic needs are met and that the individual is protected from the consequences of poor judgment and cognitive impairment. If two or more psychotic symptoms persist for between 1 and 6 months, the condition is called schizophreniform disorder (Table 47.2). To meet DSM 5 criteria for schizophrenia, two or more psy chotic symptoms must have been present for a significant portion of time for at least 1 month (unless suppressed by treatment), and the level of psychosocial functioning must either be markedly below the level achieved before the onset or there is failure to achieve the expected level of functioning. In addition, there must be continuous signs of the disturbance for at least 6 months (Table 47.3). Individuals with schizophrenia can display inappropriate affect, dysphoric mood, disturbed sleep patterns, and lack of interest in eating, or food refusal. Depersonalization, derealization, somatic concerns, and anxiety and phobias are common. Cognitive deficits are observed, including decrements in declarative memory, work ing memory, language function, and other executive functions, as well as slower processing speed. These individuals may have no Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. 286 Part III u Behavioral and Psychiatric Disorders insight or awareness of their disorder, which is a predictor of non adherence to treatment, higher relapse rates, and poorer progno sis. Hostility and aggression can be associated with schizophrenia, although spontaneous or random assault is uncommon. Aggression is more frequent for younger males and for individuals with a his tory of violence, nonadherence with treatment, substance abuse, and impulsivity. The essential features of schizophrenia are the same in childhood as in adulthood, but it is more difficult to make the diagnosis. In chil dren, delusions and hallucinations may be less elaborate, visual hal lucinations may be more common, and disorganized speech may be better attributed to an autism spectrum or communication disorder. In youth with schizophrenia, the most frequent psychotic symptoms are auditory hallucinations (82), delusions (78), thought disorder (66), disorganized or bizarre behavior (53), and negative symp toms (50). Childhood onset schizophrenia tends to represent a more severe form of the disorder spectrum, with more genetic risk factors, more brain abnormalities, and more prominent prepsychotic develop mental disorders. EPIDEMIOLOGY Brief psychotic disorder is reported to account for 9 of first onset psychosis in the United States and is more common in females than males. The incidence of schizophreniform disorders in the United States appears as much as fivefold less than that of schizophrenia. The lifetime prevalence of schizophrenia is approximately 0.30.7, although variations are reported by raceethnicity, across coun tries, and by geographic origin for immigrants. The male to female ratio is approximately 1.4:1. Males generally have poorer premor bid adjustment, lower educational achievement, more prominent negative symptoms, and more cognitive impairment than females. Childhood (preadolescent)
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onset is exceedingly rare, with an inci dence of less than 0.04, and 2:1 ratio in males versus females. CLINICAL COURSE Brief psychotic disorder most often appears in adolescence or early adulthood, with the average age of onset in the mid 30s but can occur throughout the life span. A diagnosis of brief psychotic dis order requires full remission within 1 month of onset and gradual return to premorbid level of function. The age of onset of schizo phreniform disorder is similar to that of schizophrenia. Recov ery from an episode of the disorder is within 6 months; however, about 65 of patients relapse and eventually receive a diagnosis of schizophrenia or schizoaffective disorder. Abrupt onset, confusion, absence of blunted affect, and good premorbid functioning predict a better outcome in schizophreniform disorder. Schizophrenia typically develops between the late teens and the mid 30s; onset before adolescence is rare. The peak age at onset for the first psychotic episode is in the early to mid 20s for males and in the late 20s for females. The onset may be abrupt or insidious, but most individuals manifest a slow and gradual development of symptoms, with about 50 of individuals complaining of depres sive symptoms. The predictors of course and outcome are largely unexplained. The course is favorable in approximately 20 of cases; a small number of individuals are reported to recover com pletely. However, many remain chronically ill, with exacerbations and remissions of active symptoms, whereas others experience Table 47.2 DSM 5 Diagnostic Criteria for Schizophreniform Disorder A. Two (or more) of the following, each present for a significant portion of time during a 1 mo period (or less if successfully treated). At least one of these must be (1), (2), or (3): 1. Delusions 2. Hallucinations 3. Disorganized speech (e.g., frequent derailment or incoherence) 4. Grossly disorganized or catatonic behavior 5. Negative symptoms (i.e., diminished emotional expression or avolition) B. An episode of the disorder lasts at least 1 mo but less than 6 mo. When the diagnosis must be made without waiting for recovery, it should qualified as provisional. C. Schizoaffective disorder and depressive or bipolar disorder with psychotic features have been ruled out because either (1) no major depressive or manic episodes have occurred concurrently with the active phase symptoms or (2) if mood episodes have occurred during active phase symptoms, they have been present for a minority of the total duration of the active and residual periods of the illness. D. The disturbance is not attributable to the physiologic effects of a substance (e.g., a drug of abuse, a medication) or another medical condition. Specify if: With good prognostic features: This specifier requires the presence of at least two of the following features: onset of prominent psychotic symptoms within 4 wk of the first noticeable change in usual behavior or functioning; confusion or perplexity; good premorbid social and occupational functioning; and absence of blunted or flat affect. Without good prognostic features: This specifier is applied if two or
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more of the previous features have not been present. From the Diagnostic and Statistical Manual of Mental Disorders, 5th ed. pp 9697. Copyright 2013. American Psychiatric Association. Table 47.3 DSM 5 Diagnostic Criteria for Schizophrenia A. Two (or more) of the following, each present for a significant portion of time during a 1 mo period (or less if successfully treated). At least one of these must be (1), (2), or (3): 1. Delusions 2. Hallucinations 3. Disorganized speech (e.g., frequent derailment or incoherence) 4. Grossly disorganized or catatonic behavior 5. Negative symptoms (i.e., diminished emotional expression or avolition) B. For a significant portion of the time since the onset of the disturbance, level of functioning in one or more major areas, such as work, interpersonal relations, or self care, is markedly below the level achieved before the onset (or when the onset is in childhood or adolescence, there is failure to achieve expected level of interpersonal, academic, or occupational functioning). C. Continuous signs of the disturbance persist for at least 6 mo. This 6 mo period must include at least 1 mo of symptoms (or less if successfully treated) that meet Criterion A (i.e., active phase symptoms) and may include periods of prodromal or residual symptoms. During these prodromal or residual periods, the signs of the disturbance may be manifested by only negative symptoms or by two or more symptoms listed in Criterion A present in an attenuated form (e.g., odd beliefs, unusual perceptual experiences). D. Schizoaffective disorder and depressive or bipolar disorder with psychotic features have been ruled out because either (1) no major depressive or manic episodes have occurred concurrently with the active phase symptoms or (2) if mood episodes have occurred during active phase symptoms, they have been present for a minority of the total duration of the active and residual periods of the illness. E. The disturbance is not attributable to the physiologic effects of a substance (e.g., a drug of abuse, a medication) or another medical condition. F. If there is a history of autism spectrum disorder or a communication disorder of childhood onset, the additional diagnosis of schizophrenia is made only if prominent delusions or hallucinations, in addition to the other required symptoms of schizophrenia, are also present for at least a month (or less if successfully treated). From the Diagnostic and Statistical Manual of Mental Disorders, 5th ed. pp 99100. Copyright 2013. American Psychiatric Association. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. Chapter 47 u Childhood Psychoses 287 progressive deterioration. Most individuals diagnosed with schizo phrenia require some form of daily living support. Positive symp toms tend to diminish over time, and negative symptoms are the most persistent, along with cognitive deficits. It is important to recognize hallmark phases in the assessment and management of schizophrenia. In the prodrome phase, most patients experience functional deterioration over
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the course of months (e.g., social withdrawal, idiosyncratic preoccupations, unusual behaviors, academic failure, deteriorating self care skills, andor dysphoria) before the onset of overt psychotic symptoms. The acute phase is characterized by prominent positive symp toms and deterioration in functioning and is the phase in which most patients present for care. During the recovery phase, nega tive symptoms and disorganization may persist as active psychosis remits. The residual phase has minimal to no positive symptoms, although negative symptoms may cause continued impairment. Some patients will experience chronic impairment despite ade quate treatment. DIFFERENTIAL DIAGNOSIS The differential diagnosis for the psychotic disorders is broad and includes reactions to substancesmedications (dextromethorphan, LSD, hallucinogenic mushrooms, psilocybin, peyote, cannabis, stimulants, inhalants, corticosteroids, anesthetics, anticholiner gics, antihistamines, amphetamines); medical conditions causing psychotic like symptoms (Table 47.4; see Table 32.4); and other psy chiatric disorders (depressive, bipolar, obsessive compulsive, facti tious, body dysmorphic, posttraumatic stress, autism spectrum, communication, personality). The differential diagnosis can be dif ficult because many conditions that can be mistaken for psychosis also increase the risk for it. There are many indications that suggest psychotic symptoms may be related to a physical illness rather than a primarily psychiatric ill ness (Table 47.5). When psychotic symptoms are caused by identifi able medical conditions, there are often impairments in attention, orientation, recent memory, and intellectual function. Hallucina tions associated with medical illness are more often tactile or visual, whereas auditory hallucinations are more common in primary psy chotic disorders. Patients whose hallucinations are caused by medi cal illness are more likely to recognize that they do represent reality. A positive family or prior personal history of psychosis or other serious psychiatric illnesses is less likely to be present. Autoimmune encephalitis caused by antiN methyl d aspartate (NMDA) receptor or other autoantibodies may manifest with psychosis, anxiety, depression, agitation, aggression, delusions, catatonia, visual or auditory hallucinations, disorientation, and paranoia in combination with sleep disturbances, autonomic dys function, dyskinesias, movement disorders, seizures, memory loss, and a depressed level of consciousness (Fig. 47.1; see Table 32.5). The cerebrospinal fluid (CSF) and MRI are usually, but not always, abnormal. The constellation of a relatively rapid onset psychosis and encephalitic features should suggest the diagnosis, although at presentation, behavioral problems may be the dominant feature (see Chapter 638.4; Table 47.6). A small number of patients present with purely psychiatric symptoms without other neurologic findings. Determining when identifiable medical conditions are caus ing delirium with prominent psychotic symptoms may be difficult Table 47.4 Possible Causes of Secondary Psychosis EXAMPLES INVESTIGATIONS Trauma Traumatic head injury CT, MRI Autoimmune disorders Systemic lupus erythematosus, NMDA receptor encephalitis and others Autoantibody titers Cytogeneticcongenital disorders Velocardiofacial syndrome, agenesis of corpus callosum Karyotyping, MRI Toxicsubstance induced disorders PCP, MDMA, LSD, cannabis, alcohol, cocaine, synthetic cannabinoids (bath salts) Lead, mercury or arsenic poisoning, ginseng, St. Johns Wort, ma huang Careful medication history; urine screen for drugs, heavy metal screen; trial off the offending agent Iatrogenic disorders Antimalarials, steroids, isoniazid Careful medication history; trial off the offending agent Cerebrovascular
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disorders Stroke, subdural hematomas CT, MRI Space occupying disorders Cerebral tumors CT, MRI Metabolic disorders Pheochromocytoma, metachromatic leukodystrophy, Wilson disease, adult Tay Sachs disease, acute intermittent porphyria Urinary catecholamines; arylsulfatase A levels, copper and ceruloplasmin levels Dietary disorders Pellagra, B12 deficiency; thiamine deficiency B12, folate, thiamine levels Sepsisinfectious disorders Neurosyphilis, toxoplasmosis, HIV disease, encephalitis RPR to rule out syphilis; HIV antibody titers; glucose, protein in CSF Unknown causedegenerative demyelinating disorders Lewy body dementia, Parkinson disease, Huntington disease, multiple sclerosis, Friedreich ataxia MRI, CT, EEG, evoked potentials Seizure disorders Partial complex seizures, temporal lobe epilepsy EEG, including sleep deprivation; telemetric EEG as indicated Endocrine disorders Hyperthyroidism, hypothyroidism, hyperparathyroidism Serum calcium, thyroidparathyroid hormone levels CSF, Cerebrospinal fluid; EEG, electroencephalography; LSD, lysergic acid diethylamide; MDMA, 3,4 methylenedioxy N methylamphetamine; NMDA, N methyl d aspartate; PCP, phencyclidine; RPR, rapid plasma reagin. Modified from Keshavan MS, Kaneko Y. Secondary psychoses: An update. World Psychiatry. 2013;12(1):415:Table 1, p 5. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. 288 Part III u Behavioral and Psychiatric Disorders and is more fully explored in Chapter 48. In general, delirium is hallmarked by fluctuating levels of consciousness and is often asso ciated with abnormalities in the neurologic exam and vital signs. Psychosis may be present in patients with delirium, but it will be accompanied by clear signs and symptoms of physical illness. The diagnosis of a psychotic disorder should be made only after other explanations for the observed symptoms have been thor oughly considered. Mistakenly diagnosing psychosis when it is not present can lead to inappropriate use of antipsychotics with their attendant risks. The persistence, frequency, and form of possible psychotic symptoms, as well as the degree of accompanying distress and functional regression, need to be considered in determining the likelihood of an underlying psychotic pathophysiology. Table 47.5 Red Flags and Features Suggesting Secondary Etiologies of Psychosis ATYPICAL FEATURES Normal before event Very early (13 yr) age of onset Acute or subacute onset (days, 1 mo) Catatonia Dyskinesias Isolated misidentification delusion (Capgras syndrome) Depressed level of consciousness; disorientation; somnolence Cognitive and recent memory decline Poor orientation Intractability despite adequate therapy Rapidly progressive andor fluctuating (polymorphic) symptoms Multimodal hallucinations: visual, auditory, olfactory, gustatory Poor response to antipsychotics HISTORY Infectious prodrome (fever) New or worsening headache; change in headache pattern Paresthesias Past, current substance misuse Recent onset incontinence Anorexiaweight loss Risk factors for cerebrovascular disease or central nervous system infections Malignancy Immunocompromised status Head trauma Seizures Hepatobiliary disorders Systemic lupus erythematosusother autoimmune diseases Biologic relatives with similar medical complaints Aphasia, mutism, dysarthria PHYSICAL EXAMINATION Autonomic hyperactivity: tachycardia, hypertension, mydriasis, sleep disturbance Incoordination, or gait difficulty; nystagmus Toxidrome Abnormal neurologic exam: upper and lower motor neuron focal findings Movement disorder Neuroendocrine changes DIAGNOSTIC ABNORMALITIES Abnormal electroencephalogram (extreme delta brush, diffuse slowing) Abnormal cerebrospinal fluid (pleocytosis: greater than 5 lymphocytes) Positive urine toxicology Screening laboratory tests including N
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methyl d aspartate receptor and other antibodies Abnormal neuroimaging studies (unilateral or bilateral hippocampal medial temporal lobe hyperdensities: limbic encephalitis) Hyponatremia Modified from Kliegman RM, Toth H, Bordini BJ, Basel D, eds. Nelson Pediatric Symptom Based Diagnosis. 2nd ed. Elsevier, 2023: Table 31.9, p 526 0 1 2 3 Time (wk) 4 5 Paranoid thoughts, visual or auditory hallucinations! Headache, lowgrade fever, nonspecific virallike illness (86 of patients) Bizarre personality changes, memory problems (all patients) Unresponsiveness (decreased consciousness) Dyskinesia, movement disorders Seizures Autonomic instability Central hypoventilation Cardiac dysrhythmias Symptom presentationhospital admission (77 psychiatric, 23 neuropsychiatric) Prodromal symptoms Fig. 47.1 Clinical characteristics of patients with antiNMDA receptor encephalitis. (Modified from Wandinger KP, Saschenbrecker S, Stoecker W, Dalmau J. Anti NMDA receptor encephalitis: A severe, multi stage, treatable disorder presenting with psychosis. J Neuroimmunol. 2011;231:8691. Fig 2.) Table 47.6 Proposed Diagnostic Criteria for Autoimmune Psychosis For a diagnosis of possible autoimmune psychosis: The patient must have current psychotic symptoms of abrupt onset (rapid progression of 3 months) with at least one of the following: Currently or recently diagnosed with a tumor Movement disorder (catatonia or dyskinesia) Adverse response to antipsychotics, raising suspicion of neuroleptic malignant syndrome (rigidity, hyperthermia, or raised creatine kinase) Severe or disproportionate cognitive dysfunction A decreased level of consciousness The occurrence of seizures that are not explained by a previously known seizure disorder A clinically significant autonomic dysfunction (abnormal or unexpectedly fluctuant blood pressure, temperature, or heart rate) If a patient has possible autoimmune psychosis, they should be investigated as per section 5 (Consensus multimodal approach to the systematic investigation of patients with suspected autoimmune psychosis), including electroencephalography, MRI, serum autoantibodies, and CSF analysis (including CSF autoantibodies). The results should lead to a diagnosis of non autoimmune psychosis or probabledefinite autoimmune psychosis. For a diagnosis of probable autoimmune psychosis: The patient must have current psychotic symptoms of abrupt onset (rapid progression of 3 mo) with at least one of the seven clinical criteria listed previously for possible autoimmune psychosis and at least one of the following: CSF pleocytosis of 5 white blood cellsL Bilateral brain abnormalities on T2 weighted fluid attenuated inversion recovery MRI highly restricted to the medial temporal lobes Or two of the following: Electroencephalogram encephalopathic changes (i.e., spikes, spike wave activity, or rhythmic slowing intermittent rhythmic delta or theta activity focal changes, or extreme delta brush CSF oligoclonal bands or increased IgG index The presence of a serum antineuronal antibody detected by cell based assay After exclusion of alternative diagnoses. For a diagnosis of definite autoimmune psychosis: The patient must meet the criteria for probable autoimmune psychosis with IgG class antineuronal antibodies in CSF. Note that these criteria do not exclude a diagnosis being made in a patient with an acute onset (3 mo) of psychosis, even if that patient has had a previous psychotic, other psychiatric, or encephalopathic episode that resolved. From Pollak TA, Lennox BR, Mller S, et al. Autoimmune psychosis: an international consensus on an approach to the diagnosis and management of psychosis
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of suspected autoimmune origin published correction appears in Lancet Psychiatry. 2019 Dec;6(12):e31. Lancet Psychiatry. 2020;7(1):93108: Panel 1, p 100. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. Chapter 47 u Childhood Psychoses 289 COMORBIDITY Among youth with schizophrenia, rates of comorbidity are approxi mately 34 for posttraumatic stress disorder, 34 for attention deficithyperactivity andor disruptive behavior disorders, and 32 for substance abusedependence. At least 1020 of children diag nosed with schizophrenia have intellectual delays; it is unclear if this is related to the impact of the illness on cognitive testing. Chil dren with schizophrenia also demonstrate impairments in language, communication, and information processing. Cooccurring rates of schizophrenia and autism spectrum disorder (ASD) are higher than would be expected in general populations; childhood onset schizo phrenia has been linked to ASD, with an estimated 3050 of cases preceded by a diagnosis of an ASD. SEQUELAE Follow up studies of early onset schizophrenia suggest moderate to severe impairment across the life span. Poor outcome is predicted by low pre morbid functioning, insidious onset, higher rates of negative symptoms, childhood onset, and low intellectual functioning. When followed into adulthood, youth with schizophrenia demonstrated greater social deficits, lower levels of employment, and lower likelihood of independent living, relative to those with other childhood psychotic disorders. Approximately 510 of individuals with schizophrenia die by suicide or accidental death directly related to behaviors caused by psychotic thinking, approximately 20 attempt suicide on one or more occasions, and many more have suicidal ideation. Life expec tancy is reduced in individuals with schizophrenia because of asso ciated medical conditions; a shared vulnerability for psychosis and medical disorders may explain some of the medical comorbidity of schizophrenia. ETIOLOGY AND RISK FACTORS Etiologic evidence for schizophrenia supports a neurodevelopmental and neurodegenerative model, with multiple genetic and environmen tal risks having important roles. It has been hypothesized that although psychotic disorders have their origins in early development, it is not until youth are in their mid teens that the underlying neural struc tures manifest the disabling functional deficits and resultant psychotic symptoms. Genetic Factors The lifetime risk of developing schizophrenia is 5 20 times higher in first degree relatives of affected probands than the general popula tion. Concordance rates of 4060 and 515 have been reported in monozygotic and dizygotic twins, respectively. Genome wide association studies have implicated variants in 100 different genes that are statistically significant but individually only demonstrate small increases in the risk for schizophrenia. The risk for schizo phrenia increases with increasing burden of these risk alleles; approximately 30 of the risk is attributable to common genetic variants. Rare variants of larger effect have also been implicated as increasing risk. Some rare copy number variants, where segments of the genome encompassing many genes are either duplicated or deleted, increase the risk of schizophrenia more markedly, with odds ratios of 2 25.
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Although these copy number variants may be responsible for 0.51.0 of typical adolescentadult onset schizo phrenia, data indicate that they are responsible for about 12 of schizophrenia cases with onset before age 13 years. Environmental Factors In utero exposure to maternal famine, advanced paternal age, pre natal infections, obstetric complications, marijuana use, and immi gration have been hypothesized to contribute to the development of schizophrenia. Cannabis use in teens is associated with a higher risk of eventually developing psychosis, but it is difficult to determine whether this is related to drug effects or an unmasking of underlying disease potential. Environmental exposures may mediate disease risk through direct neurologic damage, gene environment interac tions, epigenetic effects, or de novo mutations. There is no evidence that psychologic or social factors alone cause schizophrenia. Rather, environmental factors potentially interact with biologic risk factors to mediate the timing of onset, course, and severity of an acute epi sode. Expressed emotion within the family setting can influence the onset and exacerbation of acute episodes and relapse rates. NEUROANATOMIC ABNORMALITIES Increased lateral ventricle volumes, along with reductions in hippo campus, thalamus, and frontal lobe volumes, have been reported in schizophrenia. Youth with schizophrenia have reductions in gray mat ter volumes and reduced cortical folding. Neurotransmitter systems, particularly central nervous system dopamine circuits, are hypoth esized to have a key role in the pathophysiology of schizophrenia. The dopamine hypothesis is derived in part from the identification of D2 receptor blockade as the mechanism for the action of antipsychotic medications. On neurologic exam, those with schizophrenia are often found to have deficits in smooth pursuit eye movements and auto nomic responsivity. PREVENTION There has been significant interest in prospectively identifying youth at risk for schizophrenia spectrum and other psychotic dis orders to provide early intervention before the development of a chronic psychotic disorder. Those considered to be at clinically high risk may express a variety of unusual or odd beliefs. They may have unusual perceptual experiences, including frank hallucinations, but retain insight into their unreality. Their speech and behavior may be unusual, but not overtly disorganized. Individuals who had been socially active may become withdrawn. The symptoms are described as present at least once per week for the past month and have begun or worsened over the past year. Although the symp toms are less severe and more transient than in a psychotic disorder, 2040 of patients with these attenuated symptoms appear to go on to a psychotic disorder within several years of symptom presenta tion. There is evidence that premorbid lower cognitive and social skills as well as a history of substance abuse contribute to the risk of developing a schizophrenia spectrum disorder. Some evidence indicates that antipsychotic medication may delay conversion to a psychotic disorder and ameliorate attenuated symp toms in active treatment, yet there appear to be no lasting effects after the medication is withdrawn. Additionally, the known adverse effects of antipsychotics argue against their being used broadly to prevent psy chosis in these patients,
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given that about 65 do not go on to develop a psychotic disorder. Antidepressants have been associated with symptomatic improvement in adolescents who are at risk of developing a schizo phrenia spectrum disorder. Psychologic interventions, including social skills, cognitive, and interaction training programs, as well as educational family interventions and cognitive behavioral therapy (CBT), are reported to improve symptoms and psychosocial func tioning in youth with early symptoms and decrease the rate of con version to psychosis. Despite improvements in diagnostic predictive validity, significant concern remains regarding a high false positive rate that may cause individuals to be stigmatized or exposed to unnecessary treatment. In this context, youth with early symptoms suggestive of psychosis should be referred to a child and adolescent psychiatrist or other qualified mental health specialist. SCREENING There are no validated tools for screening for schizophrenia spectrum disorders in children or adolescents. A widely accepted premorbid phenotype for childhood onset schizophrenia has yet to be established. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. 290 Part III u Behavioral and Psychiatric Disorders Of children with childhood onset schizophrenia, 67 show distur bances in social, motor, and language functioning, as well as learning disabilities. Many meet criteria for comorbid ASDs, mood disorders, and anxiety disorders. Pediatric practitioners can make general inquiries of youth and their parents regarding problems with thinking or perceptions, including hallucinations and delusions. For younger children, the clinician must ensure that the child understands the questions. True psychotic symptoms are generally confusing to the individual. Highly descriptive, detailed, organized, and situation specific reports are less likely to represent true psychosis. Overt evidence of psychosis is not always present on mental status examination, but in the absence of this, the validity of symptom reports should be scrutinized. Given the strong genetic component of schizophrenia spectrum disorders, a thorough family history is key in supporting the workup of psychosis in children. Youth presenting with possible psychosis warrant assess ment and treatment by a child and adolescent psychiatrist or other qualified mental health specialist. ASSESSMENT The diagnostic assessment of schizophrenia in youth is uniquely complicated; misdiagnosis is common. Most children who report hallucinations do not meet criteria for schizophrenia, and many do not have a psychotic illness. The persistence, frequency, and form of possible psychotic symptoms; the presence of distress; functional impairment; and insight need to be considered in arriving at a diag nosis. Expertise in childhood psychopathology and experience in assessing reports of psychotic symptoms in youth are important prerequisite skills for clinicians evaluating youth for psychosis. Comprehensive diagnostic assessments, which reconcile mental status findings with the rigorous application of diagnostic criteria, help improve accuracy. All children who present with psychotic symptoms should receive a thorough pediatric and neurologic evaluation to focus on ruling out nonpsychiatric causes of psychosis (see Tables 47.4 and 32.4). There is no neuroimaging or laboratory test
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that establishes a diag nosis of schizophrenia spectrum disorders; these diagnostic tests are instead used to further assist with the medical evaluation while also establishing baseline laboratory parameters for monitoring medication therapy. Routine laboratory testing typically includes blood counts; basic metabolic panel; and assessment of liver, renal, and thyroid function. More extensive evaluation is indicated for atypical presentations, such as a gross deterioration in cognitive and motor abilities, focal neurologic symptoms, or delirium (see Table 47.5). Neuroimaging may be indicated when neurologic deficits are present, or EEG may be indicated for a clinical history suggestive of seizures or encephalopathy. Toxicology screens are indicated for acute onset or exacerbations of psychosis when exposure to drugs of abuse cannot be ruled out. Genetic testing is indicated if there are associated dysmorphic or syndromic features. Tests to rule out specific syndromes or diseases are indicated for clinical presenta tions suggestive of a specific syndrome (e.g., amino acid screens for inborn errors of metabolism, ceruloplasmin for Wilson disease, porphobilinogen for acute intermittent porphyria, neuronal anti bodies for autoimmune encephalitis). Neuropsychologic testing cannot establish the diagnosis but may be important for document ing cognitive deficits for academic planning. TREATMENT Treatment goals include decreasing psychotic symptomatology, direct ing the child toward a developmentally typical trajectory, and reinte grating the child into the home and community. Children and families facing schizophrenia spectrum disorders require an array of mental health services to address their psychologic, social, educational, and cultural needs. Given the insidious onset and chronic course of these disorders, the patient must be followed longitudinally, with periodic reassessment to hone diagnostic accuracy and tailor services to meet the patients and familys needs. Integrated psychopharmacologic, psy chotherapeutic, psychoeducational, and case management services are often necessary. Psychoeducation about the illness with an assessment of the potential role of stigma in treatment participation is critical for improving adherence with treatment recommendations. Assessing a childs strengths and vulnerabilities as well as available environ mental resources is critical in devising an effective treatment plan. School and community liaison work to develop and maintain a day to day schedule for the patient is important. Specialized educational programs should be considered within the school system. Cogni tive remediation has led to some promising gains in planning ability and cognitive flexibility. Effective and collaborative communication among the family, the pediatrician, a child and adolescent psychia trist, and other mental health providers increases the potential for the patients optimal functioning. Pharmacotherapy First generation (typical) and second generation (atypical) antipsy chotic medications are effective in reducing psychotic symptoms. Antipsychotics appear to outperform placebo and to have approxi mately equal effectiveness, except for ziprasidone and clozapine, which may be less and more effective than the others, respectively. Risperidone, aripiprazole, quetiapine, olanzapine, and lurasidone are FDA approved second generation antipsychotics for treating schizophrenia in patients 13 years and older, and paliperidone for those 12 years and older. Several first generation antipsychotics are also FDA approved for children and adolescents. The choice of which agent to use first is typically
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based on FDA approval status, side effect profile, patient and family preference, clinician famil iarity, and cost. Although clozapine is effective in treating both positive and negative symptoms, it has a risk for agranulocytosis and seizures, which limits its use to those patients with treatment resistant disorders. Ziprasidone and paliperidone are associated with QT prolongation; this finding along with the inferior effective ness of ziprasidone limits its use with children and adolescents. All antipsychotics carry some degree of risk of sedation, weight gain, and extrapyramidal symptoms (see Chapter 33). Most patients require long term treatment and are at significant risk of relapse if their medication is discontinued. However, more than 75 of youth with schizophrenia discontinue their medica tion within 6 months. Common reasons for discontinuation include lack of efficacy, intolerable side effects, and general lack of adher ence with treatment plan. Many patients will continue to experience some degree of positive or negative symptoms, requiring ongoing treatment. Patients should maintain regular physician contact to monitor symptom course, side effects, and adherence. Depot or long acting injectable antipsychotics have not been studied well in pediatric age groups and have inherent risks with long term expo sure to adverse side effects. They are typically only considered when there is a well documented history of psychotic symptoms as well as poor medication adherence. Electroconvulsive Therapy Electroconvulsive therapy (ECT) may be used with severely impaired adolescents if medications are either not helpful or cannot be toler ated. It has not been systematically studied in children, but its use is supported in adults with schizophrenia, typically in combination with antipsychotic therapy. Visit Elsevier eBooks at eBooks.Health.Elsevier.com for Bibliography. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. Chapter 47 u Childhood Psychoses 291 47.2 NonSchizophrenia Spectrum Psychotic Disorders Jennifer A. Zaspel and Rosa K. Kim Beyond the schizophrenia spectrum of psychotic disorders, substance medication induced psychotic disorder (Table 47.7) and psychotic dis order due to another medical condition (Table 47.8) can be seen in pediatric populations. The hallmark features of substancemedication induced psy chosis are delusions and hallucinations that develop within the context of substance exposure: typically a drug of abuse, a medica tion, or a toxin exposure (see Tables 47.4 and 32.4 for a brief list). Synthetic cannabinoids (bath salts) are a common drug producing psychotic effects. A substance induced psychosis is distinguished from a primary psychotic disorder by examining the onset and course of symptoms; the onset of a primary psychosis may precede substance exposure and may occur during periods of sustained abstinence. Once they arise, psychotic symptoms may be present as long as substance exposure is continued. Although the prevalence of substancemedication induced psychotic disorder in the general population is unknown, it is estimated that 725 of individuals presenting with a first episode of psychosis meet criteria for this diagnosis. Symptoms can be managed with antipsychotics
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until they remit, which often happens shortly after the offending substance is removed. Patients can develop a schizophrenia spectrum disorder following substance exposure, but this tends to occur in individuals who are at high risk for developing a primary psychotic disorder regardless of substance exposure. Psychosis due to another medical condition (see Table 47.8) is also characterized by prominent hallucinations or delusions, but history, physical exam, and laboratory findings support a direct pathophysiologic connection between these symptoms and another medical condition (see Tables 32.4, 47.4, 47.5, and 47.8). Any sen sory modality can be affected by hallucinations. The hallucinations vary in complexity depending on their etiology, and their descrip tion may be highly suggestive of a particular diagnosis, like olfac tory hallucinations in temporal lobe epilepsy. Associations between delusions and medical conditions tend to be less specific. The list of medical conditions that can cause psychosis is long, and includes epilepsy, strokes, neoplasms, endocrine disorders, genetic syn dromes like velocardiofacial syndrome, autoimmune disorders, and the permanent sequelae of toxic exposures (see Tables 32.4 and 47.4). Notably, delirium is excluded from psychosis due to another medical condition. When narrowing the differential between schizophrenia spectrum disorders, psychosis due to another medi cal condition, and any other etiology, it is important to consider the timeline of symptoms, the presence of features that are atypical for a primary psychosis, and the possibility of substance or medica tion exposure. Treatment of the underlying medical condition may or may not require adjunctive antipsychotic treatment for manage ment of psychosis, and the course and prognosis of the psychosis will likely depend on the etiology. A notable example of psychosis due to another medical condi tion is psychosis associated with epilepsy. The disorder manifests with delusions or hallucinations associated with poor insight, and can be further differentiated into ictal, interictal, and postictal psy chosis. Ictal induced psychosis is a form of nonconvulsive status epilepticus, usually a complex partial status that can last for hours to days and is associated with periods of impaired consciousness. Brief interictal psychosis can last days to weeks and is associated with paranoia, delusions, and auditory hallucinations. Chronic interictal psychosis resembles schizophrenia and manifests with paranoia, visual hallucinations, and catatonia. Postictal psychosis is the most common type (observed in 27 of patients with epilepsy) and lasts up to 1 week and then spontaneously remits. The diagnosis requires a strong index of suspicion and EEG monitoring. Treat ment requires appropriate anticonvulsant drugs and, if the psycho sis persists, initiating low dose antipsychotic medication. Visit Elsevier eBooks at eBooks.Health.Elsevier.com for Bibliography.. 47.3 Catatonia in Children and Adolescents Jennifer A. Zaspel and Rosa K. Kim Catatonia is a constellation or syndrome of psychomotor features, the most notable of which are decreased purposeful motor activity, decreased engagement in interviews and physical exams, or exces sive and peculiar motor activity. The most characteristic symptoms are waxy flexibility and bizarre poses, but these may or may not be present (Table 47.9). Diagnosis can be challenging, as psycho motor disturbances can
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range from unresponsiveness to agitation. Catatonia has been associated with a broad array of conditions affecting children, adolescents, and adults, including psychotic, affective, drug related, autoimmune, encephalitic, and neurodevel opmental conditions (Table 47.10). Autoimmune encephalitis may be the most common etiology in childhood. In addition, catatonia (autism shut down syndrome) may complicate ASD (Chapter 58). Table 47.8 DSM 5 Diagnostic Criteria for Psychotic Disorder Due to Another Medical Condition A. Prominent hallucinations or delusions. B. There is evidence from the history, physical examination, or laboratory findings that the disturbance is the direct pathophysiologic consequence of another medical condition. C. The disturbance is not better explained by another mental disorder. D. The disturbance does not occur exclusively during the course of a delirium. E. The disturbance causes clinically significant distress or impairment in social, occupational, or other important areas of functioning. Specify whether: With delusions: If delusions are the predominant symptom. With hallucinations: If hallucinations are the predominant symptom. From the Diagnostic and Statistical Manual of Mental Disorders, 5th ed. pp 115116. Copyright 2013. American Psychiatric Association. . Table 47.7 DSM 5 Diagnostic Criteria for Substance Medication Induced Psychotic Disorder A. Presence of one or both of the following symptoms: 1. Delusions 2. Hallucinations B. There is evidence from the history, physical examination, or laboratory findings of both (1) and (2): 1. The symptoms of Criterion A developed during or soon after substance intoxication or withdrawal or after exposure to a medication. 2. The involved substancemedication is capable of producing the symptoms in Criterion A. C. The disturbance is not better explained by a psychotic disorder that is not substancemedication induced. D. The disturbance does not occur exclusively during the course of a delirium. E. The disturbance causes clinically significant distress or impairment in social, occupational, or other important areas of functioning. Specify if: With onset during intoxication: If the criteria are met for intoxication with the substance and the symptoms develop during intoxication. With onset during withdrawal: If the criteria are met for withdrawal from the substance and the symptoms develop during, or shortly after, withdrawal. From the Diagnostic and Statistical Manual of Mental Disorders, 5th ed. pp 110115. Copyright 2013. American Psychiatric Association. . Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. 292 Part III u Behavioral and Psychiatric Disorders The exact pathophysiology of catatonia is unknown, but neuroana tomic, neuroendocrine, immunologic, and neurotransmitter based theories have all been proposed based on the various underlying etiologies of catatonia. Morbidity and mortality are high in adults who have experienced catatonia and are presumed to be high in pediatric populations based on limited data primarily because of the severity of an underlying illness that could cause catatonia. Patients with schizophrenia spectrum disorders and catatonia tend to be more impaired than those who do not experience catatonia, and suicide rates are estimated to be 500 fold
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higher than in the general population. Catatonia is defined as 3 or more of the 12 symptoms listed in Table 47.11 and can be described by both etiology and presenta tion. The DSM 5 broadly splits etiology into presentations related to mental disorders and presentations related to another medical condition, the diagnosis of which must be supported by the patients history, physical exam, and any accompanying laboratory findings. Pediatric prevalence rates range from 0.617 in child psychiatric inpatients and up to 17 in medically hospitalized children, but rates are difficult to determine due to underdiagnosis of the condi tion. Catatonia can be further subdivided into three presentation categories: stuporous, excited, and malignant. Stuporous presenta tions are characterized by immobility, mutism, staring, and rigid ity, whereas excited presentations include prolonged periods of psychomotor agitation. Malignant catatonia is an emergent condi tion, presenting with hyperthermia, hypertension, rhabdomyolysis, and psychomotor agitation in addition to the psychiatric and motor Table 47.10 Conditions Associated with Catatonia Psychotic Disorders Paranoid schizophrenia, catatonic schizophrenia, psychosis, autism, Prader Willi syndrome, intellectual impairment Mood Disorders Bipolar disorder: manic or mixed episodes Major Depressive Disorder Medical Conditions Hyper hypothyroidism, euthyroid autoimmune thyroiditis, Addison disease, infections, electrolyte imbalances, pathogenic variants in SCN2A gene, systemic lupus erythematosus Neurologic Conditions Epilepsy, strokes, traumatic brain injury, multiple sclerosis, infectious and autoimmune encephalitis, acute disseminated encephalomyelitis, neuromyelitis optica spectrum Drugs Withdrawal: benzodiazepines, l dopa, gabapentin Overdose: LSD, PCP, cocaine, MDMA (Ecstasy), disulfiram, levetiracetam LSD, Lysergic acid; MDMA, 3,4 methylenedioxy N methylamphetamine; PCP, phencyclidine. Adapted from Weder ND, Muralee S, Penland H, Tampi RR. Catatonia: A review. Ann Clin Psychiatry. 2008;20(2):97107:Table 2. Table 47.11 DSM 5 Criteria for Catatonia Due to Another Medical Condition A. The clinical picture is dominated by three (or more) of the following symptoms: 1. Stupor (i.e., no psychomotor activity; not actively relating to environment). 2. Catalepsy (i.e., passive induction of a posture held against gravity). 3. Waxy flexibility (i.e., slight, even resistance to positioning by examiner). 4. Mutism (i.e., no, or very little, verbal response Note: not applicable if there is an established aphasia). 5. Negativism (i.e., opposing or not responding to instructions or external stimuli). 6. Posturing (i.e., spontaneous and active maintenance of a posture against gravity). 7. Mannerism (i.e., odd, circumstantial caricature of normal actions). 8. Stereotypy (i.e., repetitive, abnormally frequent, nongoal directed movements). 9. Agitation, not influenced by external stimuli. 10. Grimacing. 11. Echolalia (i.e., mimicking anothers speech). 12. Echopraxia (i.e., mimicking anothers movements). B. There is evidence from the history, physical examination, or laboratory findings that the disturbance is the direct pathophysiologic consequence of another medical condition. C. The disturbance is not better explained by another mental disorder (e.g., a manic episode). D. The disturbance does not occur exclusively during the course of a delirium. E. The disturbance causes clinically significant distress or impairment in social, occupational, or other areas of functioning. Coding note: Include the name of the medical condition in the name of the mental disorder (e.g., F06.1 catatonic disorder due to hepatic encephalopathy). The
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other medical condition should be coded and listed separately immediately before the catatonic disorder due to the medical condition (e.g., K71.90 hepatic encephalopathy; F06.1 catatonic disorder due to hepatic encephalopathy) Adapted from Weder ND, Muralee S, Penland H, Tampi RR. Catatonia: A review. Ann Clin Psychiatry. 2008;20(2):97107:Table 2. Table 47.9 Catatonia Excitement: Extreme hyperactivity; constant motor unrest, which is apparently nonpurposeful Immobilitystupor: Extreme hypoactivity, immobility; minimally responsive to stimuli Mutism: Verbally unresponsive or minimally responsive Staring: Fixed gaze, little or no visual scanning of environment, decreased blinking Posturingcatalepsy: Maintains posture(s), including mundane (e.g., sitting or standing for hours without reacting) Grimacing: Maintenance of odd facial expressions Echopraxiaecholalia: Mimics of examiners movementsspeech Stereotypy: Repetitive, nongoal directed motor activity (e.g., finger play; repeatedly touching, patting, or rubbing self) Mannerisms: Odd, purposeful movements (hopping or walking tiptoe, saluting passersby, exaggerated caricatures of mundane movements) Verbigeration: Repetition of phrases or sentences Rigidity: Maintenance of a rigid posture despite efforts to be moved Negativism: Apparently motiveless resistance to instructions or to attempts to moveexamine the patient; contrary behavior does the opposite of the instruction Waxy flexibility: During reposturing of the patient, offers initial resistance before allowing themselves to be repositioned (similar to that of bending a warm candle) Withdrawal: Refusal to eat, drink, or make eye contact Impulsivity: Suddenly engaging in inappropriate behavior (e.g., runs down the hallway, starts screaming, or takes off clothes) without provocation; afterward, cannot explain Automatic obedience: Exaggerated cooperation with examiners request, or repeated movements that are requested once Passive obedience (mitgehen): Raising arm in response to light pressure of finger, despite instructions to the contrary Negativism (gegenhalten): Resistance to passive movement that is proportional to strength of the stimulus; response seems automatic rather than willful Ambitendency: Appears stuck in indecisive, hesitant motor movements Grasp reflex: Striking the patients open palm with two extended fingers of the examiners hand results in automatic closure of the patients hand Perseveration: Repeatedly returns to the same topic or persists with the same movements Combativeness: Belligerence or aggression, usually in an undirected manner, without explanation Autonomic abnormality: Abnormality of body temperature (fever), blood pressure, pulse rate, respiratory rate, inappropriate sweating From Dhossche DM, Wachtel LE. Catatonia is hidden in plain sight among different pediatric disorders: A review article. Pediatr Neurol. 2010;43:307315. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. Chapter 47 u Childhood Psychoses 293 symptoms seen in catatonia. The differential diagnosis for this type includes neuroleptic malignant syndrome or serotonin syndrome (see Chapter 33). Most children will present with a stuporous clini cal picture, whereas the remaining cases present as excited or malig nant, 19 and 5, respectively. The severity of symptoms can be measured and tracked using the Bush Francis Catatonia Rating Scale, a validated tool that accompanies a standardized physical examination and observation of patient behavior (Table 47.12). The diagnostic approach is driven by the search
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for the underlying cause for catatonia and the monitoring of its potentially dangerous effects on the body. Beyond supportive care and discontinuation of any precipitating agents, treatment of catatonia should be expeditious to reduce the medical sequelae of prolonged symptoms. Benzodiazepines, in par ticular lorazepam, are typically first line pharmacologic treatment for catatonia. Low dose lorazepam is often trialed as a confirmatory challenge for patients with suspected catatonia, where a positive result is improvement or even resolution of symptoms within hours of administration of the medication. If the initial challenge test does reverse symptoms, increasing doses of lorazepam are indicated, with careful monitoring to avoid side effects (Fig. 47.2). Rapid withdrawal of benzodiazepines can, in turn, precipitate catatonia in those who are susceptible. The use of antipsychotics in catatonia is controversial, as they have been associated with an increased inci dence of malignant catatonia or neuroleptic malignant syndrome. ECT has also been used in both adults and children, though it is underutilized due to caretaker and ethical concerns. Its use is typi cally recommended when other viable treatment options have either not been successful or cannot be safely administered. It has been successful in treating refractory catatonia in children with autism. Visit Elsevier eBooks at eBooks.Health.Elsevier.com for Bibliography. 47.4 Hallucinations of Childhood Jennifer A. Zaspel and Rosa K. Kim Hallucinations are perceptions that occur in the absence of identifi able external stimuli. Nondiagnostic hallucinations are those that fall within the realm of normal human experience, such as hear ing footsteps, knocking, or ones name being called. Hypnogogic and hypnopompic hallucinations are experienced as one transi tions into and out of sleep, respectively, and on their own carry no psychopathologic implications. In younger children, reported hallucinations can reflect a developmentally appropriate blurring between fantasy and reality, especially regarding dreams and imagi nary friends. Children are also more susceptible to perceptual dis tortions or illusions (misinterpretations of external stimuli) but may communicate these phenomena to adults in a way that most would interpret as hallucinations. The first clinical task in evaluat ing youth who report hallucinations is to sort out those associated with severe mental illness from those derived from other causes (Fig. 47.3). Acute phobic hallucinations are benign, common, and typically occur in otherwise healthy preschool children. The hallucinations are often visual or tactile, last 10 60 minutes, and most often occur at night. The children are quite frightened and might complain that bugs or snakes are crawling over themselves and attempt to remove them. The childs fear is not alleviated by reassurance by the parents or phy sician, and the child is not amenable to reason. Findings on physical and mental status examinations are otherwise normal, and the cause is unknown. Symptoms can persist for 1 3 days, slowly abating over 1 2 weeks. In children with nonpsychotic hallucinations, all other symptoms of psychosis are absent. Nonpsychotic hallucinations typically occur in the context of severe traumatic stress, developmental difficulties, social and emotional deprivation, parents whose own psychopathol ogy promotes a
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breakdown in the childs sense of reality, cultural beliefs in mysticism, and unresolved mourning. Auditory hallucinations of voices telling the child to do bad things may be associated with disruptive behavior disorders in an unconscious attempt to distance oneself from undesirable behaviors. Hearing a voice invoking suicide is often associated with depression. Trauma related hallucinations are commonly associated with posttraumatic stress disorder and are likely a representation of flashbacks. Auditory and visual hallucinations may similarly be endorsed in complex bereavement. The content of the hal lucinations is often relevant in understanding the underlying psycho pathology and developmental issues. Table 47.12 Standard Examination of Catatonia The method described here is used to complete the 23 item Bush Francis Catatonia Rating Scale (BFCRS) and the 14 item Bush Francis Catatonia Screening Instrument (BFCSI). Item definitions on the two scales are the same. The BFCSI measures only the presence or absence of the first 14 signs. Ratings are based solely on observed behaviors during the examination, with the exception of completing the items for withdrawal and autonomic abnormality, which may be based on directly observed behavior or chart documentation. As a general rule, only items that are clearly present should be rated. If the examiner is uncertain as to the presence of an item, rate the item as 0. PROCEDURE 1. Observe the patient while trying to engage in a conversation. 2. The examiner should scratch his or her head in an exaggerated manner. 3. The arm should be examined for cogwheeling. Attempt to reposture and instruct the patient to keep your arm loose. Move the arm with alternating lighter and heavier force. 4. Ask the patient to extend his or her arm. Place one finger beneath his or her hand and try to raise it slowly after stating, Do not let me raise your arm. 5. Extend the hand stating, Do not shake my hand. 6. Reach into your pocket and state, Stick out your tongue. I want to stick a pin in it. 7. Check for grasp reflex. 8. Check the chart for reports from the previous 24 hour period. Check for oral intake, vital signs, and any incidents. 9. Observe the patient indirectly, at least for a brief period each day, regarding the following: Activity level Abnormal movements Abnormal speech Echopraxia Rigidity Negativism Waxy flexibility Gegenhalten Mitgehen Ambitendency Automatic obedience Grasp reflex Gegenhalten, Resistance to movements that is equal and opposite to the pressure exerted by examiner; mitgehen, extreme mitmachen where even slightest pressure moves limb; mitmachen, passive movement of extremity despite instruction not to move. From Bush G, Fink M, Petrides G, Dowling F, Francis A. Catatonia. I. Rating scale and standardized examination. Acta Psychiatr Scand. 1996;93(2):129136. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. 294 Part III u Behavioral and Psychiatric Disorders Fig. 47.2 Algorithm for the eval uation, diagnosis, and treatment
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of catatonia in children and ado lescents. ECT, Electroconvulsive therapy; LZP, lorazepam. (From Dhossche DM, Wilson C, Wach tel LE. Catatonia in childhood and adolescents: Implications for the DSM 5. Prim Psychiatry. 2010;17:2326.) Medical workup urine toxicology Search and eliminate culprit substances or medications Possible catatonia Catatonia Improved When relapsing, maintenance LZP ECT LZP Bilateral ECT Somewhat improved When relapsing, maintenanceECT Bilateral ECT Not improved When relapsing, maintenanceECT Bilateral ECT Not improved When relapsing, LZP maintenance LZP continuation Much improved 3day LZP trial LZP challenge test Apply catatonia criteria Assess severity of catatonia (e.g., using rating scales) Mental status examination Hallucinations History of seizures Complex partial epilepsy Idiopathic occipital epilepsy of Gastaut Delusions Psychosis Schizophrenia Bipolar disorder Major depressive disorder Drug induced Delusional infestation Autoimmune encephalitis Normal Fantasy Culture Grief Hypnogogic hallucinations Night terrors Acute phobic hallucinations Fever Fig. 47.3 Algorithm for the evaluation of hallucinations. The evaluation of the underlying condition directs the type of treat ment needed. Diagnostic nonpsychotic hallucinations suggest the need for disorder specific psychotherapy and adjunctive medication, if indi cated. CBT focused on helping the youth understand the origin of the hallucinations and on developing coping strategies for stressful situa tions may be helpful for older children and adolescents. Visit Elsevier eBooks at eBooks.Health.Elsevier.com for Bibliography. Delirium is defined as a disorder of awareness and attention and is characterized by its waxing and waning nature. It is not a primary psy chiatric diagnosis and instead occurs secondary to an underlying med ical condition, though at the time of initial presentation the underlying cause is often unknown. The symptoms of delirium are similar between adults and children. Delirium in children carries risks of adverse out comes, including death, if it is not treated. Untreated delirium can serve to prolong the recovery course of comorbid and underlying conditions; the clinical features of delirium, including agitation, aggression, and confusion, can often interfere with necessary medical care. Delirium in children and adolescents is associated with a 12.529 mortality rate. Quick recognition, diagnosis, and treatment of delirium and its underlying cause is essential in ensuring the best outcome for patients. DIAGNOSIS Criteria for the diagnosis of delirium are included in the DSM 5 under Neurocognitive Disorders (Table 48.1). Delirium presents with an acute onset, developing quickly over the course of hours to days and symptoms tend to wax and wane. This fluctuation of symptoms can be dramatic over the course of a day, with a patient appearing Chapter 48 Delirium Colleen K. Manak and Rosa K. Kim Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. Chapter 48 u Delirium 295 relatively well from a cognitive perspective during one assessment, and then seeming acutely altered at the next. At the core of delirium is an alteration in attention and awareness, and a disturbance in cognition. Patients with delirium will struggle to focus and sustain attention.
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They are often disoriented, showing confusion about where they are, poor orientation to time, and sometimes disorientation to self. In addition to these core features, delirium often presents with symptoms that have the potential to be mistaken for psychosis or mania. People with delir ium may hallucinate, engage in bizarre or purposeless movements, and show alterations in their sleepwake cycles. Delirium can be further categorized into subtypes (Table 48.2). The hyperactive subtype is characterized by increased motor activity, loss of control of activity, restlessness, and wandering. The hypoactive subtype presents with reduction in activity, speed of actions, aware ness of surroundings, quantity and speed of speech, and alertness. It is possible for patients to present with both hyperactive and hypoactive symptoms over the course of 24 hours, classified as having a mixed motor subtype. There has been emerging evidence of a fourth group, identified as the no motor subtype, in which they do not show charac teristics of either hyper or hypoactive subtypes. Although these subtypes are often seen in both pediatric and adult delirium, diagnosing delirium in children can pose challenges not present in adult populations. Developmental differences, especially in young children, necessitate alternative approaches to assessing and diagnosing delirium. Bedside staff and caregivers can provide helpful insight into behaviors and cognitive changes, such as changes in atten tion, increased fussiness over baseline, and difficulty soothing, which might be missed by clinicians who are unable to evaluate symptoms of delirium using traditional methods (Fig. 48.1). EPIDEMIOLOGY The prevalence rate of pediatric delirium is an estimated to be 1344 among hospitalized children, with higher rates seen in patients who are admitted to the intensive care unit (ICU) andor those being mechani cally ventilated. Increased risk for delirium may be associated with the underlying medical condition, prolonged hospitalization (especially ICU admission), young age, neurocognitive and developmental disor ders, and a personal history of delirium. Potentially modifiable risk fac tors include polypharmacy, deep sedation, the use of benzodiazepines and anticholinergic medications, disrupted sleep, pain, sensory depri vation, and lack of familiar environment or caregivers. Delirium can occur at any age and has been observed in infants in the NICU. ETIOLOGY Although nearly any medical condition that requires hospitalization can lead to delirium, there are diagnoses that are more commonly asso ciated with delirium (Table 48.3). Similarly, there are several drugs that are associated with the development of delirium in children includ ing benzodiazepines, anticholinergic medications, sedatives, opiates, steroids, and some illicit substances (synthetic cathinone, synthetic cannabinoids). ASSESSMENT A thorough review of the medical record helps to identify predispos ing and precipitating factors including exposures, changes in behavior, recent illness, and surgeries. If a reasonable cause is unable to be found on history, a further medical work up is usually indicated. It is possible for children with known psychiatric illnesses to develop delirium in response to medical stress. Having a comorbid psychiatric diagnosis should not delay the diagnosis of delirium. Psychiatric ill nesses that can be confused with delirium include psychosis, mania, depression,
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and catatonia (Table 48.4). Key factors to look for in the history of patients with delirium are an acute onset without prodrome or other previous concern for worsening behavioral functioning, vari able symptoms from moment to moment, and deficits in attention and orientation. One of the factors that complicates assessment of delirium in chil dren is the developmental level of the child. A young child will be unable to answer some of the standard assessment questions (e.g., questions about orientation), which means that a fair amount of the assessment will come from the bedside staff and the childs primary caregivers. More standard assessment strategies can be utilized in older children and adolescents. In the patient interview, a good assessment will strive to evaluate affect, thought process, thought content, attention, and orientation to make the diagnosis of delirium. Because the nature of delirium is waxing and waning, it would not be atypical to have a seemingly normal exam in a patient one suspects to have delirium. Performing multiple assessments over the course of time is important to mak ing an accurate diagnosis. In delirium, patients can have a disrup tion in their normal affect and may appear restricted or dysthymic. Table 48.1 DSM 5 Diagnostic Criteria for Delirium A. A disturbance in attention (i.e., reduced ability to direct, focus, sustain, and shift attention) and awareness (reduced orientation to the environment). B. The disturbance develops over a short period of time (usually hours to a few days), represents a change from baseline attention and awareness, and tends to fluctuate in severity during the course of a day. C. An additional disturbance in cognition (e.g., memory deficit, disorientation, language, visuospatial ability, or perception). D. The disturbances in Criteria A and C are not explained by another preexisting, established, or evolving neurocognitive disorder and do not occur in the context of a severely reduced level of arousal, such as coma. E. There is evidence from the history, physical examination, or laboratory findings that the disturbance is a direct physiologic consequence of another medical condition, substance intoxication or withdrawal (i.e., due to a drug of abuse or to a medication), or exposure to a toxin, or is due to multiple etiologies. From the Diagnostic and Statistical Manual of Mental Disorders, 5th ed. p. 596. Copyright 2013. American Psychiatric Association. Table 48.2 DSM 5 Delirium Subtypes Hyperactive delirium Increased psychomotor activity and mood lability Confusion Psychosis Disorientation Agitation Hypervigilance Hyper alertness Combativeness Loud, pressured speech Behavioral dysregulation Pulling at linescatheters Hypoactive delirium Decreased psychomotor activity Sluggishness Lethargy Stupor Confusion Apathy Mixed delirium Normal level of psychomotor activity Poor attention Decreased awareness Rapid fluctuation of activity level Adapted from Meagher D, Moran M, Raju B, et al. A new data based motor subtype schema for delirium. J Neuropsychiatry Clin Neurosci. 2008;20(2):185193:Fig 1. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. 296
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Part III u Behavioral and Psychiatric Disorders RASS score (if 4 or 5 do not proceed) Please answer the following questions based on your interactions with the patient over the course of your shift: 1. Does the child make eye contact with the caregiver? Cornell Assessment of Pediatric Delirium (CAPD) The Preschool Confusion Assessment Method for the ICU (psCAMICU) Never 4 Rarely 3 Sometimes 2 Often 1 Always 0 Score Never 0 Rarely 1 Sometimes 2 TOTAL Often 3 Always 4 3. Is the child aware of hisher surroundings? 4. Does the child communicate needs and wants? 5. Is the child restless? 6. Is the child inconsolable? 7. Is the child underactivevery little movement while awake? 8. Does it take the child a long time to respond to interactions? A B 2. Are the childs actions purposeful? Is there an acute change from mental status baseline? (Y or N) Attends to 7 or less picturesmirrors? Does the patient currently have an altered LOC? (i.e. not alert and calm) Does the patient have a sleepwake cycle disturbance? (Any of the following) Sleeps mostly during the day Has difficulty getting to sleep Sleeps little at night Does not awaken easily to stimulation Patient does not maintain spontaneous eye opening in between verbal prompts Has the patients mental status fluctuated during the past 24 hours? (Y or N) If YES to EITHER question then Feature 1 is present Move on to Feature 2 Yes Yes No Yes Yes No No No If YES to EITHER question then Feature 2 is present Move on to Feature 3 If YES then Feature 3 is present DELIRIUM PRESENT If NO then Feature 3 is not present Move on to Feature 4 If YES then Feature 4 is present DELIRIUM PRESENT STOP Delirium absent Delirium absent Delirium present Acute change or fluctuating course of mental status Inattention Show alternating picturesmirrors and give verbal prompts 1 2 Altered level of consciousness (LOC)3 Disorganized brain4 Fig. 48.1 Screening tools for the assessment of delirium. A, Cornell Assessment of Pediatric Delirium (CAPD). B, The Preschool Confusion Assess ment Method for the ICU (psCAM ICU). The short form (clinical) psCAM ICU is used to assess for delirium in infants and children who are at least responsive to voice. RASS, Richmond Agitation and Sedation Scale. (A from Traube C, Silver G, Kearney J, et al. Cornell Assessment of Pediatric Delirium: A valid, rapid, observational tool for screening delirium in the PICU. Crit Care Med. 2014;42:656663; B from Smith HA, Gangopadhyay M, Goben CM, et al. The Preschool Confusion Assessment Method for the ICU: Valid and Reliable Delirium Monitoring for Critically Ill Infants and Children. Crit Care Med. 2016;44:592600:Fig. 2.) Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. Chapter 48 u Delirium 297 Thought processes are often disorganized, tangential, or circum stantial and may seem loosely associated
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with, or not at all related to, the reality of what is going on in the moment. Patient with delirium may also be perseverative in their thought content, with difficulty moving away from a subject or becoming highly fixated on, or pre occupied with, one thing. They may have altered thought content, with hallucinations. Visual hallucinations especially are one of the hallmark alterations of thought content associated with delirium. Attention is frequently impacted in delirium, with patients demon strating decreased attention, with an impaired ability to attend to a conversation or a situation. Orientation in people with delirium is often altered, especially with regards to orientation to place and time. Although all of these changes are observed to wax and wane during the course of delirium, changes in orientation can be the most striking, with patients sometimes going from being fully ori ented to quite confused in the span of hours. RATING SCALES There are multiple rating scales that have been created to help to screen for delirium, particularly in critical care or intensive care setting (see Fig. 48.1). The Cornell Assessment for Pediatric Delirium (CAPD), Pediatric Confusion Assessment Method for the Intensive Care Unit (pCAM ICU), Preschool Confusion Assessment Method for the ICU (psCAM ICU), and Richmond Agitation Sedation Scale (RASS) are all scales that are frequently used to help monitor for delirium. The CAPD, pCAM ICU, and psCAM ICU have all been validated for use in the pediatric population. Rating scales are not diagnostic on their own but can be useful for identifying patients at risk for delirium and for follow ing response to treatment. MEDICAL EVALUATION Delirium is a clinical diagnosis and can be made with history and phys ical exam alone. There are no tests that are routinely recommended in Table 48.3 Etiologies of Pediatric Delirium (CRITICAL CARE mnemonic) Cardiovascular Anemia, shock, vasculitis, hypertensive encephalopathy Respiratory Respiratory insufficiency, respiratory failure, pneumothorax Infection Sepsis, encephalitis, urinary tract infection, meningitis, fever, pneumonia, tracheitis, cellulitis, surgical site infection, COVID 19 Toxins Polypharmacy, heavy metals, drug:drug interactions Inflammatory process Autoimmune and rheumatologic disease CNS pathology Stroke, seizure, head trauma, intracranial bleed, tumor, anoxic brain injury Abuse, withdrawal, sedation Alcohol, benzodiazepines, opioids, barbiturates, prolongedexcessive sedation Liver Liver insufficiency, hepatic failure, hyperammonemia Catheters, central line infections Invasive device or procedure complications Alimentation Electrolyte imbalance, nutritional deficiencies, dehydration Renal Renal insufficiency or failure Endocrinopathies Glycemic disturbance, thyroid disease, parathyroid disease, adrenal disease Adapted from Malas N, Brahmbhatt K, McDermott C, Smith A, Ortiz Aguayo R, Turkel S. Pediatric delirium: Evaluation, management, and special considerations. Curr Psychiatry Rep. 2017;19(9):65. Table 48.4 Differential Diagnosis of Delirium CLINICAL FEATURE DELIRIUM PSYCHOSIS DEPRESSION CATATONIA Course Acute onset, hours, days or more Insidious onset over many months, prodrome Insidious onset, at least 2 wk, often over months Onset variable Attention Markedly impaired attention and arousal Normal to mild impairment Mild impairment Variable difficulty with attention and arousal Fluctuation Characterized by a waxing and waning course; disturbed daynight cycle Absent Absent Less likely to fluctuate, motor signs may show
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more fluctuation Perception Misperceptions; hallucinations (visual, fleeting); paramnesia Hallucinations, auditory with personal reference May have mood congruent hallucinations May have hallucinations, especially if secondary to primary psychosis Speech and language Abnormal clarity, speed and coherence; disjointed and dysarthric; misnaming; characteristic dysgraphia Disorganized with bizarre theme Decreased amount of speech Mutism; echolalia Other cognition Disorientation to time, place; recent memory and visuo spatial abnormalities Disorientation to person; concrete interpretations Mental slowing; indecisiveness; memory retrieval difficulty Global disorientation Behavior Lethargy; nonsystematized delusions; emotional lability Systematized delusions; paranoia; bizarre behavior Depressed mood; anhedonia; lack of energy; sleep and appetite disturbance Stupor; catalepsy; negativism; posturing; stereotypy; agitation not influenced by external stimuli; grimacing; echopraxia Electroencephalogram Diffuse slowing; low voltage fast activity; specific patterns Normal Normal Normal, focal abnormalities or generalized slowing Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. 298 Part III u Behavioral and Psychiatric Disorders Table 48.5 Nonpharmacologic Management of Delirium Environmental modifications Maintain lighting consistent with the time of day Minimize noise Familiar objects Visible clock, calendar Sensory modifications Have appropriate sensory aides available (glasses, hearing aids) Soft, calming music Minimize lines, catheters, restraints Maintain comfortable position and body alignment Caregiver interventions Frequent reorientation Fewer care team providersdifferent faces Cluster cares to minimize interruptions Promote normal sleepwake schedule Presence of familiar caregivers the evaluation for delirium, rather clinicians should be guided by the history and medical concerns. There are times when laboratory, imag ing, and other testing modalities can be helpful particularly in patients with suspected delirium when the underlying medical etiology of delir ium is unknown. Central nervous system imaging may be recommended to help identify underlying processes that may be contributing to delirium; brain imaging on its own is not a tool that can diagnose delirium and is not recommended for the sole purpose of diagnosis. Electroencephalogram (EEG) is one of the few tools that can be used to help confirm a delirium diagnosis if there is diagnos tic ambiguity or uncertainty. Various studies have found 6586 of children with delirium have abnormal EEGs. Findings associated with delirium typically include some degree of diffuse background slowing and disorganization. This EEG finding has been shown to effectively discriminate between children with delirium and healthy controls. However, these EEG findings are nonspecific and are not sufficient to diagnose delirium. Another caveat when utilizing EEG in the evaluation of delirium is the reality that several of the underlying causes of delirium, including metabolic derangement, seizures, infections, and intoxication, can also lead to EEG changes in the absence of delirium (see Table 48.3). DIFFERENTIAL DIAGNOSIS Both medical and psychiatric disorders may share or mimic some of the symptoms of delirium and can sometimes lead to complications when trying to make the diagnosis. Catatonia, depression, and psychosis are some of the more frequently occurring diagnoses that can be confused for delirium in children and especially adolescents (see Table
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48.4; see Chapter 47). In particular, catatonia can be difficult to separate from delirium, espe cially because the two can co occur. It is important to attempt to clarify the diagnosis because treatment of delirium and catatonia is different; the treatment for one can exacerbate the other. To help distinguish between the two, it is often helpful to assess for motor signs seen in catatonia that are not typically present in delirium (see Chapter 47.3). Additionally, catatonia is less likely to present with a waxing and waning course. The Bush Francis Rating Scale can be used to help diagnose catatonia (see Table 47.12). Delirium can also mimic psychosis, frequently presenting with halluci nations and sometimes delusions. One of the most profound differences between the two is the onset; delirium has an acute onset compared with the prodromal nature of a first episode of psychosis. It would be unusual for primary psychosis to develop over the course of days. However, this is characteristic of delirium. Hallucinations in delirium are often visual, whereas primary psychotic illnesses typically present with predominantly auditory hallucinations. Delusional thought content in delirium often lacks any internal structure or interconnectedness, while delusions in primary psychotic disorders are frequently structured around a common theme. Patients with depression may have some characteristics of delirium. The course and onset can help to distinguish depression from delirium; with depression the timing of onset is often closer to that of delirium. Depression does not demonstrate a waxing and waning course, and while cognition can be affected, it is often slowed with some memory problems, whereas orientation remains intact. TREATMENT Nonpharmacologic Interventions Nonpharmacologic interventions are a mainstay in both delirium treatment and prevention. The goal behind these interventions is to provide a supportive environment and to provide sensory and envi ronmental modifications to help offset the challenges posed by the need for hospital based care and treatment. Strategies such as frequent reorientation, adherence to normal routines, clustering care, and main taining a normal sleepwake cycle are all frequently implemented to prevent or manage delirium (Table 48.5) Pharmacologic Treatment Pharmacologic management of delirium focuses on both utiliz ing medications to help manage the symptoms of delirium while the underlying process is being treated and removing medications that may precipitate or worsen delirium. Antipsychotics Medications for the behavioral symptoms of delirium target disruptive behaviors that pose a danger to the patient and caregivers and interfere with necessary medical care. Although these medications do not treat the underlying cause of delirium, they can help to decrease distress and lead to a shorter overall course. Antipsychotic medications are the mainstay of treatment for the behavioral and psychiatric symptoms of delirium. Both first and second generation antipsychotics are effective, and the choice of medication is based on what other medical needs are co occurring. It is recommended to start low and go slow to arrive at an effective dose. Although typically used only for a short course (days to weeks), it remains important to consider adverse effects of antipsy
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chotic medications (see Chapter 33). All antipsychotics can cause QTc prolongation; thus it is recommended that electrocardiogram (ECG) monitoring be considered at the onset of and throughout the treatment. For a patient who is unable to take medications by mouth, intramuscular (IM) or intravenous (IV) haloperidol can be used. IV haloperidol is more potent than IM or oral haloperidol; switching between formulations and modes of administration must be done carefully. For patients who can take medications by mouth, second generation antipsychotics are typi cally the preferred choice. Risperidone, quetiapine, and olanzapine have all been shown to be effective in treating children and adolescents with delirium. Risperidone and olanzapine are available in an oral disintegrat ing tablet, and quetiapine is available in a liquid solution, which makes them easy to administer for patients who are dependent on a nasogastric tube for nutrition. Choice of medication is often dependent on what is available in the treatment setting, and the preferred route of administra tion. In chronically ill medical patients, inquiring about a past history of delirium and treatment can be helpful in guiding medication choices. Other Medications Melatonin has some utility in the management of delirium as it can help to promote a normal circadian rhythm and the return to a healthy sleepwake cycle. Trazodone has also been shown to have some benefit for patients who are struggling with nocturnal sleep maintenance. Medications to Avoid In addition to adding medications for the treatment of delirium, elimi nating unnecessary or potentially deliriogenic medications is equally important. Benzodiazepines worsen delirium and should be avoided as much as possible in patients at risk of developing delirium. They should not be used to treat agitation in delirious patients. Anticholinergic medications are also known to potentiate delirium and should also be avoided. Minimizing polypharmacy to the extent possible can help to Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. Chapter 48 u Delirium 299 eliminate potentially deliriogenic medications and aid in the preven tion of delirium. Pain Medications Opiate pain medications can be associated with worsening delirium and should be used with care in patients at risk for delirium. Compli cating this is the reality that untreated or undertreated pain can also be associated with the development and perpetuation of delirium, so ensuring adequate pain control will help to manage, and in some cases, prevent delirium. Course and Sequelae Course The resolution of delirium can be variable. Some patients improve quickly once the underlying cause is identified and treated, while others may take weeks to months to show full resolution of symptoms. Patients who have delirium related to complex medical issues, such as autoimmune encephalitis, or prolonged hospital stays, may have longer lasting delirium. When symptoms improve, antipsychotic medications can be weaned; patients do not need to be on them long term. Sequelae Patients who have delirium are more likely to
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have subsequent episodes of delirium. There is evidence that patients with delirium go on to have impaired cognitive functioning compared to patients who have never had an episode of delirium. Visit Elsevier eBooks at eBooks.Health.Elsevier.com for Bibliography. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. 300 PART IV Learning and Developmental Disorders TERMINOLOGY AND EPIDEMIOLOGY A neurodevelopmental function is a basic brain process needed for learning and productivity and involves the following core neurode velopmental domains: sensory, motor, language, visual spatialvisual perceptual, intellectual, memory, social cognition, and executive function. Executive function (EF) is a broad term used to describe specific neurocognitive processes involved in the regulating, guid ing, organizing, and monitoring of thoughts and actions to achieve a specific goal. Processes considered to be executive in nature include inhibitionimpulse control, cognitivemental flexibility, emotional control, initiation skills, planning, organization, working memory, and self monitoring. Neurodevelopmental variation refers to differences in neurodevel opmental functioning. Wide variations in these functions exist within and between individuals. These differences can change over time and need not represent pathology or abnormality. Neurodevelopmental andor executive dysfunctions reflect any disruptions or weaknesses in these processes, which may result from neuroanatomic disturbance or neuropsychologic malfunctioning. Neurodevelopmental andor executive dysfunction places a child at risk for developmental, cognitive, emotional, behavioral, psychosocial, and adaptive challenges. Preschool age children with neurodevelop mental or executive dysfunction may manifest delays in developmen tal domains such as language, motor, self help, or social emotional development and self regulation. For the school age child, an area of particular focus is academic skill development. It is at this age that dis orders of learning are often diagnosed. The Diagnostic and Statistical Manual of Mental Disorder, Fifth Edition (DSM 5) classifies disorders of learning within the group of neurodevelopmental disorders as spe cific learning disorder (SLD), with separate specifiers recognizing impairments in reading, written expression, and mathematics. In the International Classification of Diseases, Tenth Edition (ICD 10), neu rodevelopmental disorders include specific developmental disorders of scholastic skills with specific reading disorder, mathematics disor der, and disorder of written expression. Dyslexia is a term used more frequently by neurologists and by some advocacy groups to describe reading disorders. Disorders of EF have traditionally been viewed as a component of attention deficithyperactivity disorder (ADHD), which is also classified in DSM 5 as a neurodevelopmental disorder. Frontal lobe and executive function deficit is a recognized diagnostic term used primarily by neuropsychologists. There are no prevalence estimates specifically for neurodevelopmen tal dysfunction, but overall estimates for learning disorders range from 5 to 10 or more with a similar range reported for ADHD. These disorders frequently co occur. The range in prevalence is related to differences in criteria used for classification and diagnosis, the over lap and interaction of neurodevelopmental variations, and differing methods of assessment. ETIOLOGY AND PATHOGENESIS Neurodevelopmental and executive dysfunction may result from a
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broad range of etiologic factors, including genetic, medical, psycho logic, environmental, and sociocultural influences. A high degree of heritability is reported in learning and attention dis orders, with estimates ranging from 45 to 80, but identification of specific gene associations is elusive. Neurodevelopmental dysfunctions generally fall along a continuum of traits with disorders becoming evi dent at extremes of dimensions or thresholds of dysfunction. The same genetic and early environmental risk factors that are associated with a disorder such as ADHD also predict trait levels in the general popula tion. Specific genes have been identified as associated with reading dis orders, including the DYX2 locus on chromosome 6p22 and the DYX3 locus on 2p12. Neuroimaging studies have confirmed links between gene variations and variations in cortical thickness in areas of the brain known to be associated with learning and academic performance, such as the temporal regions. Chromosomal abnormalities can lead to unique pat terns of dysfunction, such as visual spatial deficits in females diagnosed with Turner syndrome (see Chapter 99.4) or executive and language deficits in children with fragile X syndrome (see Chapter 99.6). Chromo some 22q11.2 deletion syndrome (see Chapter 99.3) has been associated with predictable patterns of neurodevelopmental and executive dysfunc tion that can be progressive, including a higher prevalence of intellectual disability and deficits in visual spatial processing, attention, working memory (e.g., the ability to hold and manipulate information over short periods), verbal learning, arithmetic, and language. Perinatal factors, including very low birthweight, severe intrauter ine growth restriction, perinatal hypoxic ischemic encephalopathy, and prenatal exposure to substances such as alcohol and drugs or infections, may independently disrupt neurodevelopment or exacerbate genetic vulnerabilities. Increased risk of neurodevelopmental and executive dys function has also been associated with environmental toxins, including lead (see Chapter 761); drugs such as cocaine; infections such as men ingitis, HIV, and Zika; and brain injury associated with intraventricular hemorrhage, periventricular leukomalacia, or head trauma. The negative academic impact of concussion in children and adolescents, although usually temporary, has been well characterized, including impaired con centration and slowed processing speed. Repeated injuries have a much higher likelihood of long term negative neurocognitive effects. Early psychologic trauma may result in both structural and neu rochemical changes in the developing brain, which may contribute to neurodevelopmental and executive dysfunction. Exposure to trauma, abuse, or other adverse experiences in early childhood in the absence of positive experiencesprimarily safe, stable, and nurturing relation shipscan lead to diminished regulatory influences mediated by key brain regions (hippocampus and prefrontal cortex) and may influ ence right hemisphere function with associated risk for problems with information processing, memory, focus, and self regulation. Environ mental and sociocultural deprivation can also lead to, or potentiate, neurodevelopmental and executive dysfunction, and numerous studies have indicated that parentcaregiver executive functioning affects the development of EFs in children. Investigations of neuroanatomic substrates have yielded important information about the underlying pathogenesis in neurodevelopmen tal and executive dysfunction. Differences have been demonstrated in the left parietotemporal and left occipitotemporal brain regions
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of indi viduals with dyslexia compared to those without reading difficulties (see Chapter 51). Studies have also described the neural circuitry, primar ily in the parietal cortex, underlying mathematical competencies such as the processing of numerical magnitude and mental arithmetic. The associations between executive dysfunction and the prefrontalfrontal cortex have been established, and injury to the frontal lobe regions often Chapter 49 Neurodevelopmental and Executive Function and Dysfunction Desmond P. Kelly and Darla H. McCain Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. Chapter 49 u Neurodevelopmental and Executive Function and Dysfunction 301 result in dysfunction of executive abilities (e.g., poor inhibitory con trol). Although the prefrontalfrontal cortex may be the primary control region for EFs, there is considerable interconnectivity between the brains frontal regions and other areas, such as arousal systems (reticular activat ing system), motivational and emotional systems (limbic system), corti cal association systems (posterioranterior; leftright hemispheres), and inputoutput systems (frontal motorposterior sensory areas). CORE NEURODEVELOPMENTAL FUNCTIONS The neurodevelopmental processes that are critical to a childs success ful functioning may best be understood as falling within core neuro developmental domains that are highly integrated. Sensory and Motor Function Sensory development begins well before birth in the primary visual, auditory, and somatosensory cortical regions along with the olfac tory and gustatory cortices. This neurodevelopmental process is cru cial in helping children experience, understand, and manipulate their environments. Sensory development progresses in association with environmental exposure and with the development of other cognitive processes, such as motor development. Through sensory experiences, childrens brains mature as new neuronal pathways are created and existing pathways are strengthened. There are three distinct, yet related, forms of neuromotor ability: fine motor, graphomotor, and gross motor coordination. Fine motor function reflects the ability to control the muscles that produce small, exact movements. Deficits in fine motor function can disrupt the abil ity to communicate in written form and to excel in artistic and crafts activities and can interfere with learning a musical instrument or mastering a computer keyboard. Graphomotor function refers to the specific motor aspects of written output. Several subtypes of graphomotor dysfunction can significantly impede writing. Children who harbor weaknesses of visualization dur ing writing have trouble picturing the configurations of letters and words as they write (orthographics), with poorly legible written output and inconsistent spacing between words. Others have weaknesses in orthographic memory and may labor over individual letters and prefer printing (manuscript) to cursive writing. Some exhibit signs of finger agnosia and have trouble localizing their fingers while they write, need ing to keep their eyes very close to the page and applying excessive pressure to the pencil. Others struggle to produce the highly coordi nated motor sequences needed for writing. It is important to empha size that a child may show excellent fine motor dexterity (as revealed in mechanical or artistic domains) but very
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poor graphomotor fluency (with labored or poorly legible writing). Gross motor function refers to control of large muscles. Children with gross motor incoordination often have problems in processing outer spatial information to guide gross motor actions. Affected chil dren may be inept at catching or throwing a ball because they cannot form accurate judgments about trajectories in space. Others demonstrate diminished body position sense. They do not efficiently receive or inter pret proprioceptive and kinesthetic feedback from peripheral joints and muscles. They are likely to evidence difficulties when activities demand balance and tracking of body position and movement. Others are unable to meet the motor planning demands of complex motor procedures such as those needed for dancing, gymnastics, or swimming. The term dyspraxia relates to difficulty in developing an ideomotor plan and activating coordinated and integrated visual motor actions to complete a task or solve a motor problem, such as assembling a model or learning a new movement. Developmental coordination disorder is categorized in DSM 5 as a motor disorder where the learning and execution of coordinated motor skills is below age level given the childs opportunity for skill learning, and the motor difficulties significantly interfere with activities of daily living, academic productivity, and play. Language Language is one of the most critical and complex cognitive functions and can be broadly divided into receptive (auditory comprehension understanding) and expressive (speech and language production and or communication) functions (see Chapter 53). Children who primar ily experience receptive language problems may have difficulty under standing verbal information, following instructions and explanations, and interpreting what they hear. Expressive language weaknesses can result from problems with speech production andor problems with higher level language development. Speech production difficulties include oromotor problems affecting articulation, verbal fluency, and naming. Some children have trouble with sound sequencing within words. Others find it difficult to regulate the rhythm or prosody of their verbal output. Their speech may be dysfluent, hesitant, and inappropri ate in tone. Problems with word retrieval can result in difficulty find ing exact words when needed (as in a class discussion) or substituting definitions for words (circumlocution). The basic components of language include phonology (ability to process and integrate the individual sounds in words), semantics (understanding the meaning of words), syntax (mastery of word order and grammatical rules), discourse (processing and producing para graphs and passages), metalinguistics (ability to think about and ana lyze how language works and draw inferences), and pragmatics (social understanding and application of language). Children who evidence higher level expressive language impediments have trouble formulat ing sentences, using grammar appropriately, and organizing spoken (and possibly written) narratives. To one degree or another, all academic skills are taught largely through language, and thus it is not surprising that children who expe rience language dysfunction often experience problems with academic performance. In fact, some studies suggest that up to 80 of children who present with a specific learning disorder also experience language based weaknesses. Additionally, the role of language in executive functioning cannot
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be understated, because language serves to guide cognition and behavior. Visual SpatialVisual Perceptual Function Important structures involved in the development and function of the visual system include the retina, the optic nerves, the brainstem (control of automatic responses, e.g., pupil dilation), the thalamus (e.g., lateral geniculate nucleus for form, motion, color), and the primary (visual space and orientation) and secondary (color percep tion) visual processing regions located in and around the occipital lobe. Other brain areas, although considered to be outside of the pri mary visual system, are also important to visual function, helping to process what is seen (temporal lobe) and where it is located in space (parietal lobe). Critical aspects of visual processing development in the child include appreciation of spatial relations (ability to perceive objects accurately in space in relation to other objects), visual discrimination (ability to differentiate and identify objects based on their individual attributes, e.g., size, shape, color, form, position), and visual closure (ability to recognize or identify an object when the entire object cannot be seen). Visual spatial processing dysfunctions are rarely the cause of reading disorders, but some investigations have established that defi cits in orthographic coding (visual spatial analysis of character based systems) can contribute to reading disorders. Spelling and writing can emerge as a weakness because children with visual processing problems usually have trouble with the precise visual configurations of words. In mathematics, these children often have difficulty with visual spatial orientation, with resultant difficulty aligning digits in columns when performing calculations and difficulty managing geometric material. In the social realm, intact visual processing allows a child to make use of visual or physical cues when communicating and interpreting the paralinguistic aspects of language. Secure visual functions are also necessary to process proprioceptive and kinesthetic feedback and to coordinate movements during physical activities. Intellectual Function A useful definition of intellectual function is the capacity to think in the abstract, reason, problem solve, and comprehend. Intelligence is viewed as a global construct composed of more specific cognitive Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. 302 Part IV u Learning and Developmental Disorders functions (e.g., auditory and visual perceptual processing, spatial abili ties, processing speed, and working memory). The expression of intellect is mediated by many factors, includ ing language development, sensorimotor abilities, genetics, heredity, environment, and neurodevelopmental function. When an individu als measured intelligence is 2 standard deviations below the mean (a standard score of 70 on most IQ tests) and accompanied by sig nificant weaknesses in adaptive skills, the diagnosis of intellectual disability may be warranted (see Chapter 56). Functionally, some common characteristics distinguish children with intellectual disabil ity from those with average or above average abilities. Typically, those at the lowest end of the spectrum (e.g., profound or severe intellec tual disability) are incapable of independent function and require a highly structured environment
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with constant aid and supervision. At the other end of the spectrum are those with unusually well developed intellect (gifted). Stronger intellect has been associated with better developed concept formation, critical thinking, problem solving, understanding and formulation of rules, brainstorming and creativity, and metacognition (ability to think about thinking). Although high levels of intellectual functioning offer many opportunities, they can also be associated with functional challenges related to socialization, learning, and communication style. Individuals whose intellect falls in the below average range (some times referred to as the borderline or slow learner range) tend to experience greater difficulty processing and managing information that is abstract, making connections between concepts and ideas, and generalizing information (e.g., may be able to comprehend a concept in one setting but be unable to carry it over and apply it in different situ ations). In general, these individuals tend to do better when informa tion is presented in more concrete and explicit terms (with repetition) and when working with rote information (e.g., memorizing specific material). Memory Memory is a term used to describe the complex, cognitive mechanism by which information is acquired, retained, and recalled. Major brain areas involved in memory processing include the hippocampus, fornix, temporal lobes, and cerebellum, with connections in and between most brain regions. Memory consists of multiple distinct and interconnected subsystems that are categorized based on the length of time informa tion is stored (e.g., short term memory, long term memory), type of information stored (e.g., events, facts, procedures, emotional associa tions, conditioned reflexes), modality of the information (e.g., visual, auditory, olfactory), and whether memories are consciously recalled (explicit memory) or unconsciously recalled (implicit memory). Information processing models also include working memory as a distinct component. Memory formation begins with sensory input (e.g., auditory, visual, tactile) that is identified, or registered, and subsequently encoded. Encoding is a mental process that transforms perceptual input into a representational code for the memory system. Information in short term memory is transferred into long term memory through the pro cess of consolidation and storage. Information capacity in short term memory is limited and brief, lasting for seconds to minutes, whereas information in long term memory is potentially unlimited in terms of capacity and can be available for hours or as long as a life span. Once information finds its way into long term memory, it must be accessed. In general, information can be retrieved spontaneously (a process known as free recall) or with the aid of cues (cued or recogni tion recall). With deliberate, repeated practice, children can develop automaticity, the ability to instantaneously and effortlessly access information that has been learned in the past. Automaticity frees cog nitive resources to process other information and promote learning. For example, automaticity in decoding words allows a child to focus on the meaning of the text. Social Cognition The development of effective social skills is heavily dependent on secure social cognition, which consists of mental processes that allow an individual to understand and interact with the
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social environment. Although some evidence shows that social cognition exists as a discrete area of neurodevelopmental function, multiple cognitive processes are involved with social cognition. These include the ability to recognize, interpret, and make sense of the thoughts, communications (verbal and nonverbal), and actions of others; the ability to understand that oth ers perceptions, perspectives, and intentions might differ from ones own (commonly referred to as theory of mind); the ability to use lan guage to communicate with others socially (pragmatic language); and the ability to make inferences about others and the environment based on contextual information. It can also be argued that social cognition involves processes associated with memory and EFs, such as flexibility and shifting. Children with autism spectrum disorder harbor deficits in social cognition (see Chapter 58). Executive Function EF involves multiple skills (Table 49.1) that begin development early in life (early indications of inhibitory control and even working memory have been found in infancy), mature significantly during the preschool years, and continue to develop through adolescence and well into adult hood. Some studies suggest that secure EF may be more important than intellectual ability for academic success and have revealed that a childs ability to delay gratification early in life predicts competency, attention, self regulation, frustration tolerance, aptitude, physical and mental health, and even risk for substance dependency in adolescence and adulthood. Conversely, deficits in other areas of neurodevelopment, such as language development, affect EF. Attention is far from a unitary, independent, or specific brain func tion. This may be best illustrated through the phenotype associated with ADHD (see Chapter 50). Disordered attention can result from faulty mechanisms in and across subdomains of attention. These sub domains include selective attention (ability to focus attention on a particular stimulus and to discriminate relevant from irrelevant infor mation), divided attention (ability to orient to more than one stimulus at a given time), sustained attention (ability to maintain ones focus), and alternating attention (capacity to shift focus between stimuli). Attention problems in children can manifest at any point, from arousal through output. Children with diminished alertness and Table 49.1 Symptom Expression of Executive Dysfunction EXECUTIVE FUNCTION DEFICIT SYMPTOM EXPRESSION Inhibitory control Impulsivitypoor behavioral regulation Interrupts Blurts things out Shifting Problems with transitioning from one taskactivity to another Unable to adjust to unexpected change Repeats unsuccessful problem solving approaches Initiation Difficulty independently beginning tasksactivities Lacks initiative Difficulty developing ideas or making decisions Working memory Challenges following multistep instruction (e.g., only completes one of three steps) Forgetfulness Organization and planning Fails to plan ahead Work is often disorganized Procrastinates and does not complete tasks Messy child Self monitoring Fails to recognize errors and check work Does not appreciate impact of actions on others Poor self awareness Emotional control Experiences behavioral and emotional outbursts (e.g., tantrums) Easily upsetfrustrated Frequent mood changes Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc.
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All rights reserved. Chapter 49 u Neurodevelopmental and Executive Function and Dysfunction 303 arousal can exhibit signs of mental fatigue in a classroom or when engaged in any activity requiring sustained focus. They are apt to have difficulty directing and sustaining their concentration, and their efforts may be erratic and unpredictable, with extreme performance incon sistency. Weaknesses in determining saliency often result in allocat ing cognitive resources to the wrong stimuli, at home, in school, and socially, and missing important information. Distractibility can take the form of listening to extraneous noises instead of a teacher, staring out the window, or constantly thinking about the future. Attention dys function can affect the output of work, behavior, and social activity. It is important to appreciate that most children with attentional dysfunc tion also have other forms of neurodevelopmental dysfunction that can be associated with academic disorders (with some estimates suggesting up to 60 comorbidity). Inhibitory control (IC) can be described as ones ability to restrain, resist, and not act (cognitively or behaviorallyemotionally) on a thought. IC may also be seen as ones ability to stop thoughts or ongo ing actions. Deficits in this behavioralimpulse regulation mechanism are a core feature of the combined or hyperactive impulsive presenta tion of ADHD and have a significant adverse impact on a childs overall functioning. In everyday settings, children with weak IC may exhibit difficulties with self control and self monitoring of their behavior and output (e.g., impulsivity), may not recognize their own errors or mistakes, and often act prematurely and without consideration of the potential consequences of their actions. In the social context, disin hibited children may interrupt others and demonstrate other impul sive behaviors that often interfere with interpersonal relationships. The indirect consequences of poor IC can include challenges with behav ior, emotional regulation, and academic functioning and have adverse impacts on social interactions and safety. Shifting is the ability to transition from one activity, topic, or aspect of a problem to another when needed. Effective shifting allows a child to flexibly move through their day, tolerating changes in schedule and routine. Additionally, shifting allows a child to change strategies when working a problem and adjust to changes in topics when conversing with others. Children with difficulties in shifting can become quickly upset in novel situations (e.g., when presented with a substitute teacher) and show marked resistance to change in routine. They can get stuck on one problem solving strategy, which compromises their work efficiency. Socially, problems with shifting can result in one sided conversations, negatively affecting a childs ability to build and maintain friendships. Initiation refers to the ability to independently begin an activity, a task, or thought process (e.g., problem solve). Children who pres ent with initiation difficulties often have trouble getting started. This can be exhibited behaviorally, such that the child struggles to start on physical activities like getting out of bed or beginning chores. Cogni tively, weaknesses in initiation may manifest as difficulty coming up with ideas or generating plans.
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In school, children who have poor ini tiation abilities may be slow or unable to start homework assignments or tests. In social situations, initiation challenges may cause a child to have difficulty beginning conversations, calling on friends, or going out with friends. Deficits in primary initiation are relatively rare and are often asso ciated with significant neurologic conditions and treatments (e.g., trau matic brain injury, anoxia, effects of radiation treatment in childhood cancer). More often, initiation deficits are secondary to other execu tive problems (e.g., disorganization) or behavioral (e.g., oppositional defiant behaviors), developmental (e.g., autism spectrum disorder), or emotional (e.g., depression, anxiety) disorders. Working memory (WM) can be defined as the ability to hold, manipulate, and store information for short periods. In its simplest form, WM involves the interaction of short term verbal and visual processes (e.g., memory, phonologic awareness, and spatial skills) with a centralized control mechanism that is responsible for coordinating all the cognitive processes involved (e.g., temporarily suspending infor mation in memory while manipulating it). Ultimately, this function enables new information arriving in short term memory to be linked to prior knowledge or procedures held in long term memory. As such, working memory is critical to be able to complete multistep problems and more complex instructions and tasks. WM capacity can double or triple between the preschool years and adolescence. In the classroom, a child with a weakness in working memory might appear inattentive or careless when completing their work. When doing math, a child with WM dysfunction might have difficulty carrying a number and follow ing the expected procedure. When reading a paragraph, a child might not recall key facts or be able to integrate information when reading, particularly long paragraphs. For writing tasks, a child might leave out ideas they intended to express while they are recalling grammar rules, such as placing a comma, and working on spelling a word correctly. Planning refers to the ability to effectively generate, sequence, and put into motion the steps and procedures necessary to realize a specific goal. In real world settings, children who struggle with planning are typically described by caregivers and teachers as being inept at inde pendently gathering what is required to solve a problem or as unable to complete more weighty assignments. These children commonly exhibit poor time management skills. Organization is an ability that represents a childs proficiency in arranging, ordering, classifying, and categorizing information. Plan ning and organizing depend on discrimination ability, which refers to the childs ability to determine what is and is not valuable when trying to problem solve or organize. Common daily life challenges associated with organizational difficulties in childhood include problems with gathering and managing materials or items. When children struggle with organization, indirect consequences may include becoming over whelmed with information and being unable to complete a task or activity. Effective organization is a vital component in learning (more specifically, in memoryretention); many studies, along with clinical experience, have shown that poor organization significantly affects how well a
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child recalls information. Self monitoring involves awareness and assessment of ones actions, whether it be a work product (e.g., writing an essay) or social interac tion with another. This EF allows one to evaluate and make necessary corrections. Children with difficulty in self monitoring fail to recognize errors in their work and struggle with editing. When interacting with others, they may not realize how their verbal and nonverbal behaviors are being perceived, ultimately missing opportunities to correct their behavior and resulting in poor social interactions. Emotional control is the ability to regulate emotions in order to realize goals and direct ones behavior, thoughts, and actions. It has been well established that affectiveemotional states have an impact on many aspects of functioning. Conversely, executive function or dys function often contributes to modulation of affect. Although emotional control is highly interrelated with different EFs (e.g., disinhibition, self monitoring), separating it conceptually facilitates an appreciation for and recognition of the often overlooked role that a childs emotional state plays in cognitive and behavioral functioning. Children with weak emotional control may exhibit explosive outbursts, poor temperanger control, and oversensitivity. Understanding a childs emotional state is vital to understanding its impact not only on executive functioning but also on functioning as a whole (e.g., socially, mentally, behaviorally, academically). Any discussion involving emotional control should also recognize motivation. Motivationeffort may be defined as the reason or reasons one acts or behaves in a certain way. Less motivated children are less likely to engage and utilize all their abilities. Such a disposition not only interferes with application of executive skills but also results in less than optimal performance and functioning. The less success a child feels, the less likely the child is to put forth effort and to persevere when things become more challenging. If a childs initial efforts are met with a negative reaction, the likelihood that the child will continue put ting forth adequate effort diminishes. If left unchecked, a childs over all level of functioning will likely be compromised. More importantly, the childs sense of personal efficacy (e.g., self esteem) and competence may suffer. CLINICAL MANIFESTATIONS The symptoms and clinical manifestations of neurodevelopmental and executive dysfunction differ with age. Preschool age children Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. 304 Part IV u Learning and Developmental Disorders might present with delayed language development, including prob lems with articulation, vocabulary development, word finding, and rhyming. They often experience early challenges with learning colors, shapes, letters, numbers, the alphabet, and days of the week. Children with visual processing deficits may have difficulty learning to draw and write and have problems with art activities. These children might also have trouble discriminating between left and right. They might encounter problems recognizing letters and words. Difficulty following instructions, overactivity, and distractibility may be early symptoms of emerging executive dysfunction. Difficulties with fine
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motor devel opment (e.g., grasping crayonspencils, coloring, drawing) and social interaction may develop. These manifestations should be considered as potential red flags for future learning challenges (see Assessment and Diagnosis). School age children with neurodevelopmental and executive dys functions can vary widely in clinical presentations. Their specific pat terns of academic performance and behavior represent final common pathways of neurodevelopmental strengths and deficits interacting with environmental, social, or cultural factors; temperament; educa tional experience; and intrinsic resilience (Table 49.2). Children with language weaknesses might have problems integrating and associating letters and sounds, decoding words, deriving meaning, and being able to comprehend passages. Children with early signs of a mathematics weakness might have difficulty with concepts of quantity or with add ing or subtracting without using concrete representation (e.g., their fingers when calculating). Difficulty learning time concepts and con fusion with directions (rightleft) might also be observed. Poor fine motor control and coordination and poor planning can lead to writing problems. Attention and behavioral regulation weaknesses observed earlier can continue, and together with other EF weaknesses (e.g., organization, initiation skills), further complicate the childs ability to acquire and generalize new knowledge. Children with weaknesses in WM may struggle to remember the steps necessary to complete an activity or problem solve. In social settings, these children often have difficulty keeping up with more complex conversations. In middle school children the substantial increase in cognitive, aca demic, and regulatory demands can cause further difficulties for those with existing neurodevelopmental and executive challenges. In reading and writing, middle school children might present with transposition and sequencing errors; might struggle with root words, prefixes, and suffixes; might have difficulty with written expression; and might avoid reading and writing altogether. Challenges completing word problems in math are common. Difficulty with recall of information might also be experienced. Although observable in both lower and more advanced grades, behavioral, emotional, and social difficulties tend to become more salient in middle school children who experience cognitive or academic problems. High school students can present with deficient reading compre hension, written expression, and slower processing efficiency. Difficulty in answering open ended questions, dealing with abstract information, and deploying executive control (e.g., self monitoring, organization, planning, self starting) is often reported. Academic Problems Reading disorders (see Chapter 51) can stem from a number of neu rodevelopmental dysfunctions, as described earlier (see Table 49.2). Most often, language and auditory processing weaknesses are present, as evidenced by poor phonologic processing that results in deficiencies at the level of decoding individual words and, consequently, a delay in automaticity (e.g., acquiring a repertoire of words readers can iden tify instantly) that causes reading to be slow, laborious, and frustrat ing. Deficits in other core neurodevelopmental domains might also be present. Weak WM might make it difficult for a child to hold sounds and symbols in mind while breaking down words into their compo nent sounds, or might cause reading comprehension problems. Some children experience temporal ordering weaknesses and struggle with reblending phonemes into correct sequences.
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Memory dysfunction can cause problems with recall and summarization of what was read. Some children with higher order cognitive deficiencies have trouble understanding what they read because they lack a strong grasp of the concepts in a text. Although rare as a cause of reading difficulty, prob lems with visual spatial functions (e.g., visual perception) can cause children difficulty in recognizing letters. It is not unusual for children with reading problems to avoid reading practice, and a delay in read ing proficiency becomes increasingly pronounced and difficult to remediate. Spelling and writing impairments share many related underlying processing deficits with reading, so it is not surprising that the two disorders often occur simultaneously in school age children (see Table 49.2). Core neurodevelopmental weaknesses that underlie spelling dif ficulties include phonologic and decoding difficulties, orthographic problems (coding letters and words into memory), and morphologic deficits (use of suffixes, prefixes, and root words). Problems in these areas can manifest as phonetically poor, yet visually comparable, approximations to the actual word (faght for fight), spelling that is pho netically correct but visually incorrect (fite for fight), and inadequate spelling patterns (plade for played). Children with memory disorders might misspell words because of coding weaknesses. Others misspell because of poor auditory WM that interferes with their ability to pro cess letters. Sequencing weaknesses often result in transposition errors when spelling. Writing difficulties have been classified as disorder of written expression, or dysgraphia (see Table 49.2). Although many of the same dysfunctions described for reading and spelling can contribute to problems with writing, written expression is the most complex of the language arts, requiring synthesis of many neurodevelopmental functions (e.g., auditory, visual spatial, memory, executive; see Chap ter 52.2). Weaknesses in these functions can result in written output that is difficult to comprehend, disjointed, and poorly organized. The child with WM challenges can lose track of what the child intended to write. Attention deficits can make it difficult for a child to mobilize and sustain the mental effort, pacing, and self monitoring demands nec essary for writing. In many cases, writing is laborious because of an underlying graphomotor dysfunction (e.g., fluency does not keep pace Table 49.2 Neurodevelopmental Dysfunction Underlying Academic Disorders ACADEMIC DISORDER POTENTIAL UNDERLYING NEURODEVELOPMENTAL DYSFUNCTION Reading Language Phonologic processing Verbal fluency Syntactic and semantic skills Memory Working memory Sequencing Visual spatial Attention Written expression, spelling Language Phonologic processing Syntactic and semantic skills Graphomotor Visual spatial Memory Working memory Sequencing Attention Mathematics Visual spatial Memory Working memory Language Sequencing Graphomotor Attention Isolated neurodevelopmental dysfunction can lead to a specific academic disorder, but more often there is a combination of factors underlying weak academic performance. In addition to the dysfunction in neurodevelopmental domains as listed in the table, the clinician must also consider the possibility of limitations of intellectual and cognitive abilities or associated social and emotional problems. Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without
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permission. Copyright 2024. Elsevier Inc. All rights reserved. Chapter 49 u Neurodevelopmental and Executive Function and Dysfunction 305 with ideation and language production). Thoughts may also be forgot ten or underdeveloped during writing because the mechanical effort is so taxing. Weaknesses in mathematical ability, known as mathematics dis order or dyscalculia, involve the assimilation of both procedural knowledge (e.g., calculations) and higher order cognitive processes (e.g., WM) (see Table 49.2). There are many reasons why children struggle with mathematics (see Chapter 52.1). It may be difficult for some to grasp and apply math concepts effectively and systematically; good mathematicians are able to use both verbal and perceptual con ceptualization to understand such concepts as fractions, percentages, equations, and proportion. Children with language dysfunctions have difficulty in mathematics because they have trouble understand ing their teachers verbal explanations of quantitative concepts and operations and are likely to experience frustration in solving word problems and in processing the vast network of technical vocabulary in math. Mathematics also relies on visualization. Children who have difficulty forming and recalling visual imagery may be at a disadvan tage. They might experience problems writing numbers correctly, placing value locations, and processing geometric shapes or fractions. Children with executive dysfunction may be unable to focus on fine detail (e.g., operational signs), might take an impulsive approach to problem solving, engage in little or no self monitoring, forget com ponents of the problem, or commit careless errors. When a childs memory system is weak, the child might have difficulty recalling appropriate procedures and automatizing mathematical facts (e.g., multiplication tables). Moreover, children with mathematical dis abilities can have superimposed mathematics phobias; anxiety over mathematics can be especially debilitating. Nonacademic Problems The impulsivity and lack of effective self monitoring of children with executive dysfunction can lead to unacceptable actions that were unin tentional. Children struggling with neurodevelopmental dysfunction can experience excessive performance anxiety, sadness, or clinical depression; declining self esteem; and chronic fatigue. Some children may lose motivation and feel no need to exert effort and develop future goals. These children may be easily led toward dysfunctional interper sonal relationships, detrimental behaviors (e.g., delinquency, substance abuse), and the development of mental health disorders, such as mood disorders (see Chapter 39) or conduct disorder (see Chapter 42). ASSESSMENT AND DIAGNOSIS Pediatricians have a critical role in identifying and treating the child with neurodevelopmental or executive dysfunction (Fig. 49.1). They have knowledge of the childs medical and family history and social environmental circumstances and have the benefit of longitudinal contact over the course of routine health visits. Focused surveillance and screening will facilitate early identification of developmental behavioral and preacademic difficulties and interventions to facilitate optimal outcomes. A family history of a parent who still struggles with reading or time management or an older sibling who has failed at school should spur an increased level of monitoring. Risk factors in the medical history, such as extreme prematurity or chronic medical conditions, should likewise be flagged. Children with low birthweight and those born
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prematurely who appear to have been spared more serious neurologic problems might only manifest academic problems later in their school career. Nonspecific physical complaints or unexpected changes in behavior might be presenting symptoms. Warning signs might be sub tle or absent, and parents might have concerns about their childs learn ing progress but may be reluctant to share these with the pediatrician unless prompted, such as through completion of standardized devel opmental screening questionnaires or direct questioning regarding possible concerns. Concerns voiced to parents or caregivers by daycare, preschool, or early elementary teachers might be the first indicators of neurodevelopmental dysfunctions. There should be a low threshold for initiating further school performance screening and assessment if there are any concerns or red flags (see Clinical Manifestations). In elementary school, review of school report cards and teacher com ments can provide very useful information. In addition to patterns of grades in the various academic skill areas, it is also important to review ratings of classroom behavior and work habits. Group administered standardized tests provide further information, although interpre tation is required because poor scores could result from a learning disorder, ADHD, emotional problems, lack of motivation, or some combination. Conversely, a discrepancy between above average scores on standardized tests and unsatisfactory classroom performance could signal motivation, adjustment issues, or instructional mismatches. Challenges related to homework, such as excessive time to complete, can provide further insight regarding EFs, academic skill, and behav ioral factors or factors related to the home environment. Underlying or associated medical problems should be ruled out. Any suspicion of sensory difficulty should warrant referral for vision or hearing testing. The influence of chronic medical problems or poten tial side effects of medications should be considered. Sleep deprivation is increasingly being recognized as a contributor to academic problems, especially in middle and high school. Substance use must always be a consideration as well, especially in the adolescent previously achieving well who has shown a rapid decline in academic performance. The physician should be alert for dysmorphic physical features, minor congenital anomalies, or constellations of physical findings (e.g., cardiac and palatal anomalies in 22q11.2 deletion syndrome) and should perform a detailed neurologic examination, including an assessment of fine and gross motor coordination and any involuntary movements or soft neurologic signs. Genetic testing is often recom mended for children with intellectual disability or autism spectrum disorder; electroencephalogram and brain MRI are generally not indi cated in the absence of specific medical findings or a family history. Early signs of executive dysfunction can also be subtle and easily overlooked or misinterpreted. Informal inquiry might include ques tions about how children complete schoolwork or tasks, how organized or disorganized they are, how much guidance they need, whether they think through problems or respond and react too quickly, what cir cumstances or individuals affect their ability to employ EFs, how easily they begin tasks and activities, and how well they plan, manage belong ings, and control their emotions. Pediatricians who are interested in performing
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further assessment before referral, or who are practicing in areas where psychologic test ing resources are limited, can use standardized rating scales and inventories or brief, individually administered tests to narrow poten tial diagnoses and guide next steps in diagnosis and treatment. Such instruments, completed by the parents, teachers, and the child (if old enough), can provide information about emotions and behavior, pat terns of academic performance, and traits associated with specific neu rodevelopmental dysfunctions (see Chapter 32). Screening instruments such as the Pediatric Symptom Checklist and behavioral questionnaires such as the Child Behavior Checklist (CBCL) and Behavior Assessment System for Children, Third Edition (BASC 3) can aid in evaluation. EFs can be further assessed by instruments such as the Behavior Rat ing Inventory of Executive Function, Second Edition (BRIEF 2), which provides a comprehensive measure of real world behaviors that are closely tied to executive functioning in children age 5 18 years. Tests that can be directly administered to gauge intellectual and language functioning include the Kaufman Brief Intelligence Test, Second Edition (KBIT 2) and Peabody Picture Vocabulary Test, Fifth Edition (PPVT 5; assessing receptive vocabulary). A relatively brief test of academic skills is the Wide Range Achievement Test5 (WRAT5). It should be rec ognized that these are midlevel tests that can provide descriptive esti mates of function but are not diagnostic. Children who are struggling academically are entitled to evalua tions in school. Such assessments are guaranteed in the United States under Public Law 101 476, the Individuals with Disabilities Educa tion Act (IDEA). One increasingly common type of evaluation model supported by IDEA is referred to as a Response to Intervention (RtI) model (see Chapter 52.1). In this model, students who are struggling with academic skills are initially provided research based instruc tion. If a child does not respond to this instruction, an individualized Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. 306 Part IV u Learning and Developmental Disorders evaluation by a multidisciplinary team is conducted. Children found to have attentional dysfunction and other disorders might qualify for educational accommodations in the regular classroom under Section 504 of the Rehabilitation Act of 1973 (504 Plan) or might qualify for an individualized education program (IEP). The pediatrician should advise and support parents regarding steps to request evaluations by the school. Multidisciplinary evalua tions are focused primarily on determining whether a student meets the eligibility criteria for special education services and to assist in developing an IEP for those eligible for these services. Independent evaluations can provide second opinions outside the school setting. The multidisciplinary team should include a psychologist and prefer ably an educational diagnostician who can undertake a detailed analy sis of academic skills and subskills to pinpoint where breakdowns are occurring in the processes of reading, spelling, writing, and mathemat ics. Other professionals should become involved, as needed, such
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as a speech language pathologist, occupational therapist, and social worker. A mental health specialist can be valuable in identifying family based issues or psychiatric disorders that may be complicating or aggravating neurodevelopmental dysfunctions. In some cases, more in depth examination of a childs neurocog nitive status is warranted. This is particularly true for children who Fig. 49.1 Algorithm showing components of a primary care ap proach to identification, diagnosis, and comprehensive multidiscipli nary management of neurodevel opmental and executive dysfunc tion. Primary Care Approach to Neurodevelopmental and Executive Dysfunction Early Identification Medical Assessment Neurodevelopmental Emotional Assessment Abnormal movements; motor coordination; soft neurological signs; focal findings Questionnaires; interview; midlevel tests Report cards; teacher reports History and Examination Sleep Associated medical conditions Medications; substance abuse Growth; dysmorphic features; exam Medical Home Ensure adequate sleep, nutrition, exercise Optimize management of associated conditions Prescribe and manage medications if needed Support child and parents Explain test findings and demystify Advocate for appropriate services; advise on nonstandard therapies Developmental andor Psychosocial Assessment Speechlanguage; Physical and Occupational Therapy; Psychology; Social Work; Neuropsychology; Psychiatry; Neurology; Genetics Evaluation and Diagnosis Psychoeducational Assessment Intellectual ability Academic achievement Executive function Emotionalbehavioral function Treatment Surveillance Birth and perinatal history Medical and family history Parentcaregiver concerns School or behavioral problems Screening Standardized developmental screening Emotionalbehavioral screening tests School achievement test scores Educational, Developmental, Mental Health Accommodations: school and home Interventions: tutoring; special education resource services; developmental therapies Address executive dysfunction: modeling; games; strategies; programs Strengthen strengths and leverage affinities Counseling Referral School testing Psychologist; Educational Specialist DevelopmentalBehavioral Pediatrician Medical subspecialist; Developmental therapist Downloaded for mohamed ahmed (dr.mms2020gmail.com) at University of Southern California from ClinicalKey.com by Elsevier on April 20, 2024. For personal use only. No other uses without permission. Copyright 2024. Elsevier Inc. All rights reserved. Chapter 49 u Neurodevelopmental and Executive Function and Dysfunction 307 present with developmental or cognitive difficulties in the presence of a medical condition (e.g., epilepsy, traumatic brain injury, child hood cancersbrain tumors, genetic conditions). A neuropsychologic evaluation involves comprehensive assessment to understand brain functions across domains. Neuropsychologic data are often analyzed together with other tests, such as MRI, to look for supporting evidence of any areas of difficulty (e.g., memory weaknesses associated with temporal lobe anomalies). Neuropsychologists can also provide more in depth evaluation of EFs. Assessment of EFs is typically completed in an examination setting using tools specifically designed to identify any weaknesses in these functions. Although few tools are currently available to assess EF in preschool age children, the assessment of school age children is better established. Problems with EFs should be evaluated across measures and in different settings, particularly within the context of the childs daily demands. TREATMENT Treatment for neurodevelopmental and executive dysfunction involves a multimodal, multidisciplinary cross sector approach to fos ter optimal outcomes. This process begins with demystification, which involves educating the child and family about the nature of the childs delay or dysfunction while also identifying a childs strengths. The explanation of the dysfunction should be provided in nontechni cal
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language, communicating a sense of optimism for improvement with appropriate intervention. Children need to have their affinities, potentials, and talents identified clearly and emphasized as an inte gral component of the long term treatment plan. It is as important to augment strengths as it is to attempt to remedy deficiencies. Athletic skills, artistic inclinations, creative talents, and mechanical abilities are among the potential assets of certain students who are underachieving academically. Parents and school personnel need to create opportuni ties for such students to build on these assets. These well developed personal assets can ultimately have implications for the transition into young adulthood, including career or college selection. In the clinic setting, the pediatrician plays an important role as a consultant and advocate in overseeing and monitoring the imple mentation of a comprehensive multidisciplinary management plan for children with neurodevelopmental dysfunctions. The primary care provider should identify and treat any underlying or associated medical problems that might contribute to neurodevelopmental and EF dysfunction, such as iron deficiency, elevated lead levels, and sleep problems, including inadequate sleep related to poor sleep hygiene or poor quality of sleep (e.g., obstructive sleep apnea). Additionally, the pediatrician will need to monitor for conditions that often co occur with neurodevelopmental delays and executive dysfunction or that may develop over time, including anxiety, depression, and substance use disorder. Bypass Strategies (Accommodations) Numerous techniques can enable a child to circumvent neurodevelop mental dysfunctions. Such strategies are typically used in the regular classroom and can be incorporated into a 504 Plan or IEP. Accommo dations change how the child learns, allowing them to access material and meet the same expectations as their peers. Examples of accommo dations include using large print for those with visual impairment and using a frequency modulation (FM) system for students with hearing impairment. For children with learning disorders, accommodations may include using a calculator while solving mathematical problems, writing essays with a word processor and use of spellcheck, or present ing oral instead of written reports. Children with executive dysfunction might benefit from being seated near the teacher to minimize distrac tions and taking tests untimed. These bypass strategies do not cure neurodevelopmental dysfunctions, but they minimize their academic and nonacademic effects and can provide a scaffold for more successful academic achievement. Curriculum Modifications Many children with neurodevelopmental dysfunctions require altera tions in the school curriculum to succeed, especially as they progress through secondary school. A modification changes what the child is taught or expected to learn. Modifications include a student learning different material (e.g., continuing to work on addition and subtrac tion facts while peers move on to fractions) and instructors assigning grades using a different standard. In high school and college, students with memory weaknesses might need to work with an advisor to select courses that avoid an inordinate cumulative memory load in any single semester. For adolescents with learning disorders, the timing of for eign language learning and the selection of mathematics and science courses are critical to their academic
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success. RemediationTargeted Intervention Interventions can be implemented at home and in school to strengthen academic skills. Early identification is critical so that appropriate instructional interventions can be introduced to minimize the long term effects of academic disorders. Any interventions should be empirically supported (e.g., phonologically based reading intervention has been shown to significantly improve reading skills in school age children). Remediation may take place in a resource room or learn ing center at school and is usually limited to children who have met the educational criteria for special education services described earlier. Reading specialists, mathematics tutors, and other professionals can use diagnostic data to select techniques that use a students neurodevel opmental strengths to improve decoding skills, writing ability, or math ematical computation skills. Remediation need not focus exclusively on specific academic areas. Many students need assistance in acquiring study skills, cognitive strategies, and productive organizational habits. Speech language pathologists offer intervention for children with various forms of language disability. Occupational therapists focus on sensorimotor skills, including the motor skills of students with writing problems, and physical therapists address gross motor incoordination. Treatment of Executive Dysfunction Interventions to strengthen EFs can be implemented throughout child hood but are most effective if started at a young age. Preschool age children first learn EFs by way of the modeling, boundaries, and rules observed and put in place by their parentscaregivers, and this modeled behavior must gradually become internalized by the child. Early play has been shown to be effective in promoting executive skills in younger children with games such as peek a boo (WM); pat a cake (WM and IC); follow the leader, Simon Says, and Ring Around the Rosie (self control); imitation activities (attention and impulse control); matching and sorting games (organization and attention); and imaginary play (attention, WM, IC, self monitoring, cognitive flexibility). In school age children it is crucial to establish consistent cognitive and behavioral routines that foster and maximize independent, goal oriented problem solving and performance through mechanisms that include modification of the childs environment, modeling and guid ance with the child, and positive reinforcement strategies. Interven tions should promote generalization (teaching executive routines in the context of a problem, not as a separate skill) and should move from the external to the internal (from external support with active and directive modeling to an internal process). An intervention could proceed from external modeling of multistep problem solving rou tines and external guidance in developing and implementing everyday routines, to practicing application and use of routines in everyday situ ations, to a gradual fading of external support and cueing of internal generation and use of executive skills. Such approaches should make the child a part of intervention planning, should avoid labeling, reward effort not outcomes, make interventions positive, and hold the child responsible for his or her efforts. Studies have consistently shown that a combination of medication and behavioral treatments are most effective, although evidence for long term efficacy is lacking. It is important that any treatment plans aimed
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