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Detoxification foot baths , also known as foot detox , ionic cleansing , ionic foot bath and aqua/water detox are pseudoscientific alternative medical devices marketed as being able to remove toxins from the human body. They work by providing an electric current to an electrode array immersed in a salt water solution. When switched on, the electrodes rapidly rust in a chemical process called electrolysis which quickly turns the water brown. This reaction happens regardless of whether or not a person's feet are immersed in the water, and no toxins from the human body have ever been detected in the water after use.
Detoxification foot baths first became popular with consumers in the early 2000s and quickly became popular in spas due to the theatre of the visible brown water and sludge produced by the devices. [ 1 ] One manufacturer of the device, known as Aqua Detox, states that the concept is based on research from the 1920s to 1930s by Royal Rife , an inventor who claimed his Rife Devices could "devitalize disease organisms" by vibrating them at certain frequencies . [ 2 ] [ 3 ]
Detoxification foot baths consist of two major components, a simple container in which to place the feet and an electrode array. Usually a fragrant , warm salted water is used as the electrolyte and the customer's feet, along with the array, are immersed in this water. Inside the array are two metal electrodes, between which a current flows, causing the electrodes to rust rapidly due to electrolysis. [ 4 ] This reaction quickly turns the salt water solution brown, and flakes of rust may also be visible in the water. [ 5 ] Electrode arrays used in this application degrade quickly, and usually need to be replaced after roughly 16 hours of use. [ 3 ]
Proponents of detoxification foot baths claim they are capable of helping the human body in numerous ways. [ 5 ] Effects like "re-balancing the cellular energy" of the body, helping with headaches and sleeplessness, to kidney , liver , and immune system function are regularly stated. [ 6 ] More serious claims such as helping with heavy metal toxicity and autism spectrum disorder have been made by various proponents. [ 7 ] [ 8 ]
Some spas and manufacturers provide charts to show their customers the different areas of their bodies from which toxins originate. In these charts, the color of the water in the foot bath, after treatment, purportedly defines the source of toxins in the body. [ 7 ] [ 4 ] [ 9 ]
There is no scientific basis to the claims of these charts. [ 7 ] [ 4 ] [ 10 ]
Inside Edition visited several spas in New York City in 2011 to investigate detox foot treatments. At each spa they visited, they were told that the treatments would improve their overall health, and that the change in the color of the water was due to the release of toxins from their bodies. Inside Edition then purchased a detox foot bath and had it examined by electrical engineer Steve Fowler, at his lab. After examining the device, he concluded that "Everything you see here is just rust, this is nothing more than two pieces of metal rusting, it has nothing to do with toxins. It is just a simple chemistry experiment." [ 4 ]
In his 2008 book Bad Science , Ben Goldacre discussed his experiences investigating the science behind detox foot baths. After reading an article in The Daily Telegraph about them, he suspected the brown water could be rust. He then set up his experiment using a bucket of water, a car battery, and two large nails. His experiment quickly changed the color of the water in the bucket to a dark brown with a sludge on top. [ 1 ] [ 11 ]
With this information in mind, he sent a friend to a local spa to get a treatment and to collect water samples before and after. The samples were sent to the Medical Toxicology Unit at St Mary's Hospital in London to be analyzed. The water sampled before the detox foot bath was activated, contained only 0.54mg per liter of iron , and after the treatment was complete, it contained 23.6mg per liter. For reference, Goldacre's water sample from his original experiment contained 97mg per liter. [ 1 ] [ 11 ]
Goldacre approached several manufacturers of the devices regarding their claims about removing toxins from the body. None of them could explain which toxins were being removed from the body or if any were at all. With that information, he decided to have his water samples tested for creatinine and urea , two of the smallest breakdown molecules that the human body creates. Neither of these molecules was found in the samples, just the iron oxide rust. [ 1 ] [ 11 ]
Joe Schwarcz also explained that putting the iron and aluminum electrodes in water will produce iron oxide , showing as various shades of brownish residue. The magnesium and calcium naturally present in human sweat increase the electrolytic reaction. After trying the apparatus and getting the brown residue even when the bath is running without the presence of human feet, Timothy Caulfield concluded that "this is a really good example of what's ultimately nothing but a marketing scam ." [ 12 ]
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The Deutsche Gesellschaft für Kardiologie ( DGK ; German Cardiac Society in English) is a German medical research organization based in Düsseldorf . It is a member of the European Society of Cardiology , [ 1 ] and the World Heart Federation . [ citation needed ]
They award the Arthur Weber Prize for excellence in the field of cardiology . [ 2 ] [ 3 ]
This article about a medical organization or association is a stub . You can help Wikipedia by expanding it .
This article about an organisation based in Germany is a stub . You can help Wikipedia by expanding it .
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The fetal endocrine system is one of the first systems to develop during prenatal development of a human individual. The endocrine system arises from all three embryonic germ layers. The endocrine glands that produce the steroid hormones, such as the gonads and adrenal cortex, arise from the mesoderm. In contrast, endocrine glands that arise from the endoderm and ectoderm produce the amine, peptide, and protein hormones. [ 1 ]
The fetal adrenal cortex can be identified within four weeks of pregnancy . [ 2 ] The adrenal cortex originates from the thickening of the intermediate mesoderm . [ 3 ] At five to six weeks of gestation, the mesonephros differentiates into a tissue known as the gonadal ridge. The gonadal ridge produces the steroidogenic cells for both the gonads and the adrenal cortex. [ 4 ] The adrenal medulla is derived from ectodermal cells . Cells that will become adrenal tissue move retroperitoneally to the upper portion of the mesonephros. At seven weeks of gestation, the adrenal cells are joined by sympathetic cells that originate from the neural crest to form the adrenal medulla . At the end of the eighth week, the adrenal glands have been encapsulated and have formed a distinct organ above the developing kidneys. [ 4 ] At birth, the adrenal glands weigh approximately eight to nine grams (twice that of the adult adrenal glands) and are 0.5% of the total body weight. At 25 weeks, the adult adrenal cortex zone develops and is responsible for the primary synthesis of steroids during the early postnatal weeks. [ 2 ]
The thyroid gland develops from two different clusterings of embryonic cells. One part is from the thickening of the pharyngeal floor, which serves as the precursor of the thyroxine (T 4 ) producing follicular cells. The other part is from the caudal extensions of the fourth pharyngobranchial pouches which results in the parafollicular calcitonin-secreting cells. [ 5 ] These two structures are apparent by 16 to 17 days of gestation. Around the 24th day of pregnancy, the foramen cecum, a thin, flask-like diverticulum of the median anlage develops. At approximately 24 to 32 days of gestation, the median anlage develops into a bilobed structure. By 50 days of gestation, the medial and lateral anlage have fused together. [ 6 ] At 12 weeks of gestation, the fetal thyroid is capable of storing iodine for the production of TRH , TSH , and free thyroid hormone. At 20 weeks, the fetus is able to implement feedback mechanisms for the production of thyroid hormones. During fetal development, T 4 is the major thyroid hormone being produced while triiodothyronine (T 3 ) and its inactive derivative, reverse T 3 , are not detected until the third trimester. [ 2 ]
Once the embryo reaches four weeks of gestation, the parathyroid glands begins to develop. [ 7 ] The human embryo forms five sets of endoderm -lined pharyngeal pouches. The third and fourth pouch are responsible for developing into the inferior and superior parathyroid glands, respectively. [ 8 ] The third pharyngeal pouch encounters the developing thyroid gland and they migrate down to the lower poles of the thyroid lobes. The fourth pharyngeal pouch later encounters the developing thyroid gland and migrates to the upper poles of the thyroid lobes. At 14 weeks of gestation, the parathyroid glands begin to enlarge from 0.1 mm in diameter to approximately 1 – 2 mm at birth. [ 9 ] The developing parathyroid glands are physiologically functional beginning in the second trimester. [ citation needed ]
Studies in mice have shown that interfering with the HOX15 gene can cause parathyroid gland aplasia , which suggests the gene plays an important role in the development of the parathyroid gland. [ 9 ] The genes, TBX1 , CRKL , GATA3 , GCM2 , and SOX3 have also been shown to play a crucial role in the formation of the parathyroid gland. Mutations in TBX1 and CRKL genes are correlated with DiGeorge syndrome , while mutations in GATA3 have also resulted in a DiGeorge-like syndrome. [ 10 ] Malformations in the GCM2 gene have resulted in hypoparathyroidism. [ 11 ] Studies on SOX3 gene mutations have demonstrated that it plays a role in parathyroid development. These mutations also lead to varying degrees of hypopituitarism. [ 12 ]
The human fetal pancreas begins to develop by the fourth week of gestation. Five weeks later, the pancreatic alpha and beta cells have begun to emerge. Reaching eight to ten weeks into development, the pancreas starts producing insulin , glucagon , somatostatin , and pancreatic polypeptide . [ 13 ] During the early stages of fetal development, the number of pancreatic alpha cells outnumbers the number of pancreatic beta cells. The alpha cells reach their peak in the middle stage of gestation. From the middle stage until term, the beta cells continue to increase in number until they reach an approximate 1:1 ratio with the alpha cells. The insulin concentration within the fetal pancreas is 3.6 pmol/g at seven to ten weeks, which rises to 30 pmol/g at 16–25 weeks of gestation. Near term, the insulin concentration increases to 93 pmol/g. [ 14 ] The endocrine cells have dispersed throughout the body within 10 weeks. At 31 weeks of development, the islets of Langerhans have differentiated. [ citation needed ]
While the fetal pancreas has functional beta cells by 14 to 24 weeks of gestation, the amount of insulin that is released into the bloodstream is relatively low. In a study of pregnant women carrying fetuses in the mid-gestation and near term stages of development, the fetuses did not have an increase in plasma insulin levels in response to injections of high levels of glucose. [ 14 ] In contrast to insulin, the fetal plasma glucagon levels are relatively high and continue to increase during development. [ 15 ] At the mid-stage of gestation, the glucagon concentration is 6 μg/g, compared to 2 μg/g in adult humans. Just like insulin, fetal glucagon plasma levels do not change in response to an infusion of glucose. [ 16 ] However, a study of an infusion of alanine into pregnant women was shown to increase the cord blood and maternal glucagon concentrations, demonstrating a fetal response to amino acid exposure. [ 14 ]
As such, while the fetal pancreatic alpha and beta islet cells have fully developed and are capable of hormone synthesis during the remaining fetal maturation, the islet cells are relatively immature in their capacity to produce glucagon and insulin. This is thought to be a result of the relatively stable levels of fetal serum glucose concentrations achieved via maternal transfer of glucose through the placenta. On the other hand, the stable fetal serum glucose levels could be attributed to the absence of pancreatic signaling initiated by incretins during feeding. [ 16 ] In addition, the fetal pancreatic islets cells are unable to sufficiently produce cAMP and rapidly degrade cAMP by phosphodiesterase necessary to secrete glucagon and insulin. [ 14 ]
During fetal development, the storage of glycogen is controlled by fetal glucocorticoids and placental lactogen . Fetal insulin is responsible for increasing glucose uptake and lipogenesis during the stages leading up to birth. Fetal cells contain a higher amount of insulin receptors in comparison to adults cells and fetal insulin receptors are not downregulated in cases of hyperinsulinemia . [ 14 ] In comparison, fetal haptic glucagon receptors are lowered in comparison to adult cells and the glycemic effect of glucagon is blunted. [ 15 ] This temporary physiological change aids the increased rate of fetal development during the final trimester.
Poorly managed maternal diabetes mellitus is linked to fetal macrosomia , increased risk of miscarriage, and defects in fetal development. Maternal hyperglycemia is also linked to increased insulin levels and beta cell hyperplasia in the post-term infant. [ 16 ] Children of diabetic mothers are at an increased risk for conditions such as: polycythemia , renal vein thrombosis , hypocalcemia , respiratory distress syndrome , jaundice , cardiomyopathy , congenital heart disease , and improper organ development. [ 17 ]
The reproductive system begins development at four to five weeks of gestation with germ cell migration. The bipotential gonad results from the collection of the medioventral region of the urogenital ridge. At the five-week point, the developing gonads break away from the adrenal primordium. Gonadal differentiation begins 42 days following conception.
For males, the testes form at six fetal weeks and the sertoli cells begin developing by the eight week of gestation. SRY , the sex-determining locus, serves to differentiate the Sertoli cells . The Sertoli cells are the point of origin for anti-Müllerian hormone . Once synthesized, the anti-Müllerian hormone initiates the ipsilateral regression of the Müllerian tract and inhibits the development of female internal features. At 10 weeks of gestation, the Leydig cells begin to produce androgen hormones. The androgen hormone dihydrotestosterone is responsible for the development of the male external genitalia. [ 18 ]
The testicles descend during prenatal development in a two-stage process that begins at eight weeks of gestation and continues through the middle of the third trimester. During the transabdominal stage (8 to 15 weeks of gestation), the gubernacular ligament contracts and begins to thicken. The craniosuspensory ligament begins to break down. This stage is regulated by the secretion of insulin-like 3 (INSL3), a relaxin-like factor produced by the testicles, and the INSL3 G-coupled receptor, LGR8. During the transinguinal phase (25 to 35 weeks of gestation), the testicles descend into the scrotum. This stage is regulated by androgens, the genitofemoral nerve, and calcitonin gene-related peptide. During the second and third trimester, testicular development concludes with the diminution of the fetal Leydig cells and the lengthening and coiling of the seminiferous cords . [ 19 ]
For females, the ovaries become morphologically visible by the 8th week of gestation. The absence of testosterone results in the diminution of the Wolffian structures. The Müllerian structures remain and develop into the fallopian tubes, uterus, and the upper region of the vagina. The urogenital sinus develops into the urethra and lower region of the vagina, the genital tubercle develops into the clitoris, the urogenital folds develop into the labia minora, and the urogenital swellings develop into the labia majora. At 16 weeks of gestation, the ovaries produce FSH and LH/hCG receptors . At 20 weeks of gestation, the theca cell precursors are present and oogonia mitosis is occurring. At 25 weeks of gestation, the ovary is morphologically defined and folliculogenesis can begin. [ 19 ]
Studies of gene expression show that a specific complement of genes, such as follistatin and multiple cyclin kinase inhibitors are involved in ovarian development. [ 20 ] An assortment of genes and proteins - such as WNT4, [ 21 ] RSPO1, [ 22 ] FOXL2, [ 23 ] and various estrogen receptors [ 24 ] - have been shown to prevent the development of testicles or the lineage of male-type cells. [ 25 ]
The pituitary gland is formed within the rostral neural plate. The Rathke's pouch, a cavity of ectodermal cells of the oropharynx , forms between the fourth and fifth week of gestation [ 26 ] and upon full development, it gives rise to the anterior pituitary gland. [ 27 ] By seven weeks of gestation, the anterior pituitary vascular system begins to develop. During the first 12 weeks of gestation, the anterior pituitary undergoes cellular differentiation. At 20 weeks of gestation, the hypophyseal portal system has developed. The Rathke's pouch grows towards the third ventricle and fuses with the diverticulum. This eliminates the lumen and the structure becomes Rathke's cleft. The posterior pituitary lobe is formed from the diverticulum. Portions of the pituitary tissue may remain in the nasopharyngeal midline. In rare cases, this results in functioning ectopic hormone-secreting tumors in the nasopharynx. [ 28 ]
The functional development of the anterior pituitary involves spatiotemporal regulation of transcription factors expressed in pituitary stem cells and dynamic gradients of local soluble factors. [ 29 ] [ 30 ] The coordination of the dorsal gradient of pituitary morphogenesis is dependent on neuroectodermal signals from the infundibular bone morphogenetic protein 4 (BMP4). [ 27 ] This protein is responsible for the development of the initial invagination of the Rathke's pouch. Other essential proteins necessary for pituitary cell proliferation are fibroblast growth factor 8 (FGF8), [ 31 ] Wnt4, [ 32 ] and Wnt5. [ 32 ] Ventral developmental patterning and the expression of transcription factors is influenced by the gradients of BMP2 and sonic hedgehog protein (SHH). These factors are essential for coordinating early patterns of cell proliferation. [ 33 ]
Six weeks into gestation, the corticotroph cells can be identified. By seven weeks of gestation, the anterior pituitary is capable of secreting ACTH. Within eight weeks of gestation, somatotroph cells begin to develop with cytoplasmic expression of human growth hormone. Once a fetus reaches 12 weeks of development, the thyrotrophs begin expression of Beta subunits for TSH, while gonadotrophs being to express beta-subunits for LH and FSH. [ 34 ] Male fetuses predominately produced LH-expressing gonadotrophs, while female fetuses produce an equal expression of LH and FSH expressing gonadotrophs. [ 35 ] At 24 weeks of gestation, prolactin-expressing lactotrophs begin to emerge. [ 34 ]
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Developmental coordination disorder ( DCD ), also known as developmental motor coordination disorder , developmental dyspraxia , or simply dyspraxia (from Ancient Greek praxis 'activity'), is a neurodevelopmental disorder [ 1 ] characterized by impaired coordination of physical movements as a result of brain messages not being accurately transmitted to the body. Deficits in fine or gross motor skills movements interfere with activities of daily living. It is often described as disorder in skill acquisition, where the learning and execution of coordinated motor skills is substantially below that expected given the individual's chronological age. Difficulties may present as clumsiness, slowness and inaccuracy of performance of motor skills (e.g., catching objects, using cutlery, handwriting, riding a bike, use of tools or participating in team sports or swimming). It is often accompanied by difficulty with organisation and/or problems with attention, working memory and time management. [ citation needed ]
A diagnosis of DCD is reached only in the absence of other neurological impairments such as cerebral palsy , multiple sclerosis , or Parkinson's disease . The condition is lifelong and its onset is in early childhood. It is thought to affect about 5% of the population. Occupational therapy can help people with dyspraxia to develop their coordination and achieve things that they might otherwise find extremely challenging to accomplish. Dyspraxia has nothing to do with intelligence but people with dyspraxia may struggle with self-esteem because their peers can easily do things they struggle with on a daily basis. Dyspraxia is not often known as a disability in the general public.
The World Health Organization (WHO) recognizes DCD as a condition and have published their definition in the International Classification of Diseases . This describes DCD as:
Developmental motor coordination disorder is characterised by a significant delay in the acquisition of gross and fine motor skills and impairment in the execution of coordinated motor skills that manifest in clumsiness, slowness, or inaccuracy of motor performance. Coordinated motor skills are substantially below that expected given the individual's chronological age and level of intellectual functioning. Onset of coordinated motor skills difficulties occurs during the developmental period and is typically apparent from early childhood. Coordinated motor skills difficulties cause significant and persistent limitations in functioning (e.g., in activities of daily living, school work, and vocational and leisure activities). Difficulties with coordinated motor skills are not solely attributable to a Disease of the Nervous System, Disease of the Musculoskeletal System or Connective Tissue, sensory impairment, and not better explained by a Disorder of Intellectual Development.
The American Psychiatric Association (APA)'s Diagnostic and Statistical Manual, DSM-5 classifies Developmental Coordination Disorder (DCD) as a discrete motor disorder under the broader heading of neurodevelopmental disorders. [ 1 ] It is often described as a disorder in skill acquisition or motor learning, where the learning and execution of coordinated motor skills is substantially below that expected given the individual's chronological age. [ 3 ] Various areas of development can be affected by DCD and these may persist into adulthood. [ 4 ] [ 5 ] [ 6 ]
In children, DCD may exhibit as delays in early development of sitting, crawling, walking; poor ability or difficulties with childhood activities such as running, jumping, hopping, catching, sports and swimming; slowness; frequent tripping and bruising; poor handwriting skills; difficulties with self care; difficulties with skills such as using cutlery or tying shoelaces; poor spatial understanding; difficulty following instructions; poor time management; and often losing objects. [ 7 ]
In adulthood, in addition to a childhood history as above, the condition may manifest as a difficulty learning new motor skills or applying skills in a different or busy environment, poor organisation and time management skills, missed deadlines and lateness for appointments (or earliness as a coping strategy), and awkward pauses before answering in conversation. There is often a history of underachievement in education or the workplace. Although skills can be acquired, such as neat handwriting, handwriting speed will then be much lower than expected. [ 7 ]
Evidence from research and clinical practice indicates that DCD is not just a physical disorder, and there may be deficits in executive functions, behavioural organisation and emotional regulation that extend beyond the motor impairments and which are independent of diagnoses of co-morbidities. [ 8 ] In addition to the physical or motor impairments, developmental coordination disorder is associated with problems with memory, especially working memory . [ 9 ] This typically results in difficulty remembering instructions, difficulty organizing one's time and remembering deadlines, increased propensity to lose things or problems carrying out tasks which require remembering several steps in sequence (such as cooking). Whilst most of the general population experience these problems to some extent, they have a much more significant impact on the lives of dyspraxic people. [ 10 ] However, many dyspraxics have excellent long-term memories , despite poor short-term memory . [ 10 ] Many dyspraxic people benefit from working in a structured environment, as repeating the same routine minimises difficulty with time-management and allows them to commit procedures to long-term memory. [ citation needed ]
People with developmental coordination disorder sometimes have difficulty moderating the amount of sensory information that their body is constantly sending them, so as a result these dyspraxic people may be prone to sensory overload and panic attacks . [ 10 ]
Moderate to extreme difficulty doing physical tasks is experienced by some people with dyspraxia, and fatigue is common because so much energy is expended trying to execute physical movements correctly. Some dyspraxic people have hypotonia , low muscle tone, which can also detrimentally affect balance. [ 11 ]
Whole body movement and motor coordination issues mean that major developmental targets including walking, running, climbing and jumping can be affected. The difficulties vary from person to person and can include the following:
Fine-motor problems can cause difficulty with a wide variety of other tasks such as using a knife and fork, fastening buttons and shoelaces, cooking, brushing teeth, styling hair, shaving, [ 11 ] [ 15 ] applying cosmetics, opening jars and packets, locking and unlocking doors, and doing housework.
Difficulties with fine motor co-ordination lead to problems with handwriting, [ 11 ] [ 16 ] Problems associated with this area may include:
Developmental verbal dyspraxia (DVD) is a type of ideational dyspraxia, causing speech and language impairments . This is the favoured term in the UK; however, it is also sometimes referred to as articulatory dyspraxia, and in the United States the usual term is childhood apraxia of speech (CAS). [ 18 ] [ 19 ] [ 20 ]
Key problems include:
DCD is known to co-occur with other neurodevelopmental disorders. Most common is attention deficit hyperactivity disorder (ADHD), with an estimated 50% of people with ADHD also having DCD and vice versa. [ 21 ] Other co-occurring conditions are autism , [ 22 ] [ 23 ] [ 24 ] Developmental Language Disorder [ 25 ] , Prosopagnosia [ 26 ] and Developmental Learning Disorder. [ 2 ]
People who have developmental coordination disorder may also have one or more of these other co-morbid conditions:
However, a person with DCD is unlikely to have all of these conditions. The pattern of difficulty varies widely from person to person; an area of major weakness for one dyspraxic person can be an area of strength or gift for another. For example, while some dyspraxic people have difficulty with reading and spelling due to dyslexia, or with numeracy due to dyscalculia, others may have brilliant reading and spelling or mathematical abilities. Co-morbidity between ADHD and DCD is particularly high. [ 34 ] [ 35 ] [ 36 ]
Sensory processing disorder (SPD) concerns having oversensitivity or undersensitivity to physical stimuli, such as touch, light, sound, and smell. [ 37 ] This may manifest itself as an inability to tolerate certain textures such as sandpaper or certain fabrics such as wool, oral intolerance of excessively textured food (commonly known as picky eating), being touched by another individual (in the case of touch oversensitivity) or it may require the consistent use of sunglasses outdoors since sunlight may be intense enough to cause discomfort to a dyspraxic person (in the case of light oversensitivity). An aversion to loud music and naturally loud environments (such as clubs and bars) is typical behavior of individuals with dyspraxia who have auditory oversensitivity , while only being comfortable in unusually warm or cold environments is typical of a dyspraxic person with temperature oversensitivity. Undersensitivity to stimuli may also cause problems, as individuals do not receive the sensory input they need to understand where their bodies are in space. This can make it even more challenging to complete tasks. [ 38 ] Dyspraxic people who are undersensitive to pain may injure themselves without realising it. Some dyspraxic people may be oversensitive to some stimuli and undersensitive to others. [ 39 ]
Developmental Language Disorder ( DLD ) research has found that students with developmental coordination disorder and normal language skills still experience learning difficulties despite relative strengths in language. This means that, for students with developmental coordination disorder, their working memory abilities determine their learning difficulties. Any strength in language that they have is not able to sufficiently support their learning. [ 25 ]
Students with developmental coordination disorder struggle most in visual-spatial memory. When compared to their peers without motor difficulties, students with developmental coordination disorder are seven times more likely than typically developing students to achieve very poor scores in visual-spatial memory. [ 40 ] As a result of this working memory impairment, students with developmental coordination disorder have learning deficits as well. [ 41 ]
Physical consequences
Dyspraxic individuals face a higher prevalence of negative outcomes, including poor cardiovascular health, challenges with physical health and self-care (e.g., [ 42 ] [ 43 ] [ 44 ] ).
Psychological domain: Children with DCD may struggle with lower self-efficacy and lower self-perceived competence in peer and social relations. Some demonstrate greater aggressiveness and hyperactivity. [ 45 ] [ 46 ]
Social domain: Children may be more vulnerable to social rejection and bullying, possibly resulting in higher levels of loneliness [ 47 ] [ 48 ] [ 46 ] [ 49 ] .
Support domain: In the United Kingdom, dyspraxic adults are less likely to be awarded disability support for higher education than their dyslexic peers or those with co-occurring neurodivergence [ 50 ] [ 51 ] [ 52 ] . Consequently, misinterpretations and inadequate support in these settings are more likely to occur and are less likely to be included and supported.
Assessments for developmental coordination disorder typically require a developmental history, [ 53 ] detailing ages at which significant developmental milestones , such as crawling and walking , [ 54 ] [ 55 ] [ 56 ] occurred. Motor skills screening includes activities designed to indicate developmental coordination disorder, including balancing, physical sequencing, touch sensitivity, and variations on walking activities. [ citation needed ]
The American Psychiatric Association has four primary inclusive diagnostic criteria [ 56 ] for determining if a child has developmental coordination disorder.
The criteria are as follows:
Currently there is no single "gold standard" assessment test for DCD. [ 57 ] Various screening tests may be used, including the following.
A baseline motor assessment establishes the starting point for developmental intervention programs. Comparing children to normal rates of development may help to establish areas of significant difficulty.
However, research in the British Journal of Special Education has shown that knowledge is severely limited in many who should be trained to recognise and respond to various difficulties, including developmental coordination disorder, dyslexia and deficits in attention, motor control and perception (DAMP) . [ 56 ] The earlier that difficulties are noted and timely assessments occur, the quicker intervention can begin. A teacher or GP could miss a diagnosis if they are only applying a cursory knowledge.
"Teachers will not be able to recognise or accommodate the child with learning difficulties in class if their knowledge is limited. Similarly GPs will find it difficult to detect and appropriately refer children with learning difficulties." [ 71 ]
A diagnosis of DCD is reached only in the absence of other neurological impairments such as cerebral palsy , [ 72 ] [ 55 ] multiple sclerosis , or Parkinson's disease .
Developmental coordination disorder is classified in the fifth revision of the Diagnostic and Statistical Manual of Mental Disorders ( DSM-5 ) as a motor disorder , in the category of neurodevelopmental disorders . [ 1 ]
The exact proportion of people with the disorder is unknown since the disorder can be difficult to detect due to a lack of specific laboratory tests, thus making diagnosis of the condition one of elimination of all other possible causes/diseases. Approximately 5–10% of children and adults are affected by this condition. [ 73 ] [ 74 ] [ 54 ] [ 75 ] [ 76 ] [ 77 ] and approximately 2% are severely affected. [ 7 ]
Although dyspraxia affects roughly 10% of children and 5% of adults (Blank et al., 2019), the notion that individuals with dyspraxia ‘outgrow’ it, is misleading. While motor skills may improve with development and targeted interventions, dyspraxia itself is understood as a lifelong neurodivergence that has its onset in early childhood. The observed reduction in prevalence in adulthood likely reflects improved coping strategies, environmental adaptations, and potentially a lessening of the most overt motor difficulties in some individuals, rather than indicating a complete disappearance of the underlying neurological differences.
DCD is a lifelong neurological condition that is expected to be as common in males as it is in females . [ 4 ] [ 5 ] [ 6 ] Currently however, the diagnosis criteria favour males which results in over 80% of males being diagnosed before the age of 16 compared to only 22% for females. [ citation needed ]
There is no cure for the condition. Instead, it is managed through therapy. Physical therapy or occupational therapy can help those living with the condition. [ citation needed ] . Physical therapy for children with developmental coordination disorder focuses on improving motor skills, coordination, and efficiency of movements. This is done through task-oriented activities and neuromotor training. Research suggests that early and individualized PT programs may result in fundamental improvements in motor skills and daily functioning. [ 78 ]
Some people with the condition find it helpful to find alternative ways of carrying out tasks or organizing themselves, such as typing on a laptop instead of writing by hand, or using diaries and calendars to keep organized. [ 79 ] A review completed in 2017 by Cochrane of task-oriented interventions for DCD resulted in inconsistent findings and a call for further research and randomized controlled trials. [ 80 ]
Collier first described developmental coordination disorder as "congenital maladroitness". A. Jean Ayres referred to developmental coordination disorder as a disorder of sensory integration in 1972, [ 81 ] [ 82 ] while in 1975 Sasson Gubbay, MD, called it the "clumsy child syndrome". [ 53 ] [ 83 ] [ 84 ] Developmental coordination disorder has also been called "minimal brain dysfunction", although the two latter names are no longer in use.
Other names include developmental apraxia, [ 53 ] disorder of attention and motor perception (DAMP) [ 53 ] [ 83 ] dyspraxia, [ 55 ] developmental dyspraxia, [ 53 ] [ 85 ] [ 86 ] "motor learning difficulties", [ 53 ] [ 83 ] perceptuo-motor dysfunction, [ 53 ] [ 83 ] [ 82 ] and sensorimotor dysfunction. [ 53 ]
The World Health Organization currently lists developmental coordination disorder as "Specific Developmental Disorder of Motor Function". [ 55 ]
People who have publicly stated they have been diagnosed with developmental coordination disorder include:
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Developmental language disorder ( DLD ) is identified when a child has problems with language development that continue into school age and beyond. The language problems have a significant impact on everyday social interactions or educational progress, and occur in the absence of autism spectrum disorder , intellectual disability , or a known biomedical condition. The most obvious problems are difficulties in using words and sentences to express meanings, but for many children, understanding of language ( receptive language ) is also a challenge. This may not be evident unless the child is given a formal assessment.
The field of developmental language disorders has evolved significantly in recent years, with a move towards standardizing terminology to address confusion and improve communication. The CATALISE Consortium, composed of experts, endorsed the term "developmental language disorder" in 2017, recognizing it as a subset of language disorder within the broader spectrum of speech, language, and communication needs. This shift aimed to clarify understanding, increase public awareness, and improve access to services for affected children. [ 1 ] Previously, various terms like "developmental dysphasia" and "developmental aphasia" were used, causing confusion by implying similarities to adult language problems caused by brain damage. [ 2 ] Similarly, " specific language impairment " (SLI), commonly used in North America, was considered too narrow as it only focused on language issues without considering other potential difficulties children may face.
The term developmental language disorder (DLD) was endorsed in a consensus study involving a panel of experts (CATALISE Consortium) in 2017. [ 3 ] The study was conducted in response to concerns that a wide range of terminology was used in this area, with the consequence that there was poor communication, lack of public recognition, and in some cases children were denied access to services. Developmental language disorder is a subset of language disorder , which is itself a subset of the broader category of speech, language and communication needs.
The terminology for children's language disorders has been extremely wide-ranging and confusing, with many labels that have overlapping but not necessarily identical meanings. [ 2 ] In part this confusion reflected uncertainty about the boundaries of DLD, and the existence of different subtypes. Historically, the terms "developmental dysphasia" or "developmental aphasia" were used to describe children with the clinical picture of DLD. [ 4 ] These terms have, however, largely been abandoned, as they suggest parallels with adult-acquired aphasia . This is misleading, as DLD is not caused by brain damage . [ 5 ]
Although the term DLD has been used for many years, it has been less common than the term specific language impairment (SLI), [ 2 ] which has been widely adopted, especially in North America. [ 6 ] The definition of SLI overlaps with DLD, but was rejected by the CATALISE panel because it was seen as overly restrictive in implying that the child had relatively pure problems with language in the absence of any other impairments. Children with such selective problems are relatively rare, and there is no evidence that they respond differently to intervention, or have different causal factors, from other children with language problems. [ 1 ]
In the UK education system, the term "speech, language and communication needs" is widely used, but this is far broader than DLD, and includes children with speech, language and social communication difficulties arising from a wide range of causes. [ 7 ]
The question of whether to refer to children's language problems as a 'disorder' was a topic of debate among the CATALISE consortium, but the conclusion was that 'disorder' conveyed the serious nature and potential consequences of persistent language deficits. It is also parallel with other neurodevelopmental conditions and consistent with diagnostic frameworks such as the DSM-5 and ICD-11 . [ 3 ] Where there are milder or more transient difficulties, 'language difficulties' may be a more appropriate term.
DLD can affect a range of areas of language and the degree of impairment in different areas of language can vary from child to child. [ 8 ] However, although there have been attempts to define different subtypes, these have not generally resulted in robust categories. [ 9 ] The recommendation of the CATALISE panel was that the specific areas of impairment should be assessed and documented for individual children, while recognizing that different children might have different combinations of problems. The areas which can be affected are:
Speech is the act of articulating sounds, and this can be impaired for all kinds of reasons – a structural problem such as cleft lip and cleft palate , a neurological problem affecting motor control of the speech apparatus dysarthria , or inability to perceive distinctions between sounds because of hearing loss . Some distortions of speech sounds, such as a lisp , are commonly seen in young children. These misarticulations should not be confused with language problems, which involve the ability to select and combine linguistic elements to express meanings, and the ability to comprehend meanings. [ citation needed ]
Although speech disorders can be distinguished from language disorders, they can also co-occur. [ 31 ] When a child fails to produce distinctions between speech sounds for no obvious reason, this is typically regarded as a language problem affecting the learning of phonological contrasts. The classification of and terminology for disorders of speech sound production is a subject of considerable debate. [ 32 ] In practice, even for those with specialist skills, it is not always easy to distinguish between phonological disorders and other types of speech production problem. Speech sound disorder is any problem with speech production arising from any cause. [ 33 ]
Speech sound disorders of unknown cause that are not accompanied by other language problems are a relatively common reason for young children to be referred to speech-language therapy (speech-language pathology). [ 34 ] These often resolve by around 4–5 years of age with specialist intervention, [ 35 ] and so would not meet criteria for DLD. Where such problems continue beyond five years of age, they are usually accompanied by problems in broader language domains and have a poorer prognosis, [ 36 ] so a diagnosis of DLD with speech sound disorder is then appropriate.
DLD often co-occurs with other, milder neurodevelopmental disorders of unknown origin, such as attention-deficit hyperactivity disorder , developmental dyslexia or developmental coordination disorder . [ 1 ] These do not preclude a diagnosis of DLD, but should be noted as co-occurring conditions. [ citation needed ]
It is generally accepted that DLD is strongly influenced by genetic factors. [ 37 ] The best evidence comes from the twin study method. Two twins growing up together are exposed to the same home environment, yet may differ radically in their language skills. Such different outcomes are, however, much more common in fraternal (non-identical) twins, who are genetically different. Identical twins share the same genes and tend to be much more similar in language ability. There can be some variation in the severity and persistence of DLD in identical twins, indicating that non-genetic factors affect the course of disorder, but it is unusual to find a child with DLD who has an identical twin with typical language. [ 38 ]
There was considerable excitement when a large, multigenerational family with a high rate of DLD were found to have a mutation of the FOXP2 gene just in the affected family members. [ 39 ] However, subsequent studies have found that, though DLD runs in families, it is not usually caused by a mutation in FOXP2 or another specific gene. [ 40 ] Current evidence suggests that there are many different genes that can influence language learning, and DLD results when a child inherits a particularly detrimental combination of risk factors, each of which may have only a small effect. [ 37 ] Nevertheless, study of the mode of action of the FOXP2 gene has helped identify other common genetic variants involved in the same neural pathways that may play a part in causing DLD. [ 41 ]
Language disorders are associated with aspects of home environment, and it is often assumed that this is a causal link, with poor language stimulation leading to weak language skills. Twin studies, however, show that two children in the same home environment can have very different language outcomes, suggesting we should consider other explanations for the link. Children with DLD often grow up into adults who have relatively low educational attainments, [ 42 ] and their children may share a genetic risk for language disorder. [ 2 ]
One non-genetic factor that is known to have a specific impact on language development is being a younger sibling in a large family. [ 43 ]
It has long been noted that males are more affected by DLD than females, with a sex ratio of affected males-to-females around 3 or 4:1. [ 44 ] However, the sex difference is much less striking in epidemiological samples, suggesting that similar problems may exist in females but are less likely to be detected. [ 45 ] The reason for the sex difference is not well understood. [ citation needed ]
Poor motor skills are commonly found in children with DLD. [ 46 ] Standardized measures of motor ability confirm that children with DLD exhibit deficits in fine and gross motor skill , both simple and complex. These difficulties also extend to speech-motor ability, particularly with the control of their articulatory movements. Children with DLD have difficulty with motor sequence learning and may show deficits in other procedural motor processes as well. [ 47 ]
Brain scans do not usually reveal any obvious abnormalities in children with DLD, although quantitative comparisons have found differences in brain size or relative proportions of white or grey matter in specific regions. In some cases, unusual brain gyri are found. To date, no consistent 'neural signature' for DLD has been found, although some studies have noted evidence for involvement of subcortical systems. [ 48 ] Differences in the brains of children with DLD versus typically developing children are subtle and may overlap with atypical patterns seen in other neurodevelopmental disorders. [ 49 ]
DLD is defined purely in behavioural terms: there is no biological test. There are three points that need to be met for a diagnosis of DLD: [ 3 ]
For research and epidemiological purposes, specific cutoffs on language assessments have been used to document the first criterion. Tomblin et al. [ 50 ] proposed the EpiSLI criterion, based on five composite scores representing performance in three domains of language (vocabulary, grammar, and narration) and two modalities (comprehension and production). Children scoring in the lowest 10% on two or more composite scores are identified as having language disorder.
The second criterion, persistence of language problems, can be difficult to judge in a young child, but longitudinal studies have shown that difficulties are less likely to resolve for children who have poor language comprehension, rather than difficulties confined to expressive language. [ 3 ] In addition, children with isolated difficulties in just one of the areas noted under 'subtypes' tend to make better progress than those whose language is impaired in several areas. [ 36 ]
The third criterion specifies that DLD is used for children whose language disorder is not part of another biomedical condition, such as a genetic syndrome, a sensorineural hearing loss, neurological disease, autism spectrum disorder or intellectual disability – these were termed 'differentiating conditions' by the CATALISE panel. [ 3 ] Language disorders occurring with these conditions need to be assessed and children offered appropriate intervention, but a terminological distinction is made so that these cases would be diagnosed as language disorder associated with the main diagnosis being specified: e.g. "language disorder associated with autism spectrum disorder." The reasoning behind these diagnostic distinctions is discussed further by Bishop (2017). [ 51 ]
Common signs at one year of age:
At two years of age:
At three years of age:
At four years of age:
At five years of age:
Assessment will usually include an interview with the child's caregiver, observation of the child in an unstructured setting, a hearing test, and standardized tests of language. [ 53 ] There is a wide range of language assessments in English. Some are restricted for use by experts in speech-language pathology : speech and language therapists (SaLTs/SLTs) in the UK, speech-language pathologists (SLPs) in the US and Australia. A commonly used test battery for diagnosis of DLD is the Clinical Evaluation of Language Fundamentals (CELF) .
Assessments that can be completed by a parent or teacher can be useful to identify children who may require more in-depth evaluation. The Children’s Communication Checklist (CCC–2) is a parent questionnaire suitable for assessing everyday use of language in children aged four years and above who can speak in sentences.
Informal assessments, such as language samples, are often used by speech-language therapists/pathologists to complement formal testing and give an indication of the child's language in a more naturalistic context. A language sample may be of a conversation or narrative retell. In a narrative language sample, an adult may tell the child a story using a wordless picture book (e.g. Frog Where Are You?, Mayer, 1969 ), then ask the child to use the pictures and tell the story back. Language samples can be transcribed using computer software such as the Systematic Analysis of Language Software , and then analyzed for a range of features: e.g., the grammatical complexity of the child's utterances, whether the child introduces characters to their story or jumps right in, whether the events follow a logical order, and whether the narrative includes a main idea or theme and supporting details. [ citation needed ]
There is, however, a large gap in assessment of developmental language disorder, specifically in bilingual and multilingual children. For a multilingual child to be diagnosed with DLD, they must be assessed in every language that they speak and show signs of DLD in each one. Current assessment practices for diagnosing DLD in multilingual children is inadequate. "Lack of knowledge about bilingual children and their needs is largely responsible for current referral and assessment practices." [ 54 ] SLPs do not speak every language and are unable to properly assess many children for language disorders as a result. The best practices for assessing multilingual children involves a combination of approaches including but not limited to questionnaires, parent/guardian interviews, and direct assessment.
Identifying Autism Spectrum Disorder can be broadened into three categories: sociability and empathy, imaginative play, and use of language. Sociability and Empathy: Search for limitations in the child's capacity to participate in social interactions, comprehend others' emotions, and deduce their viewpoints. Communicative Use of Language: Evaluate for challenges in utilizing language proficiently for communication. Imaginative Play: Assess the child’s capability to participate in inventive and imaginative play. Sensory Responses: Observe any uncommon or modified reactions to sensory stimuli.
Children with Speech-Language Impairment (SLI) have a higher likelihood of ASD compared to the general population. It is essential to conduct a detailed developmental history and a specific evaluation for autism characteristics. Use screening tools to help detect ASD. Verbal Children with Autism can be classified as follows: Impaired: They experience significant challenges with using language. Borderline: They have language abilities but with some impairments. Normal: Their language use falls within typical ranges, considering the context of autism.
Selective Mutism is an anxiety disorder where individuals are unable to speak in certain social situations despite being capable of speaking in other environments. This disorder is strongly linked to social anxiety. Children who have selective mutism do not speak in certain social situations, such as at school or with peers, but can speak normally in other contexts, like at home with their family. These children generally have good comprehension of language and can understand conversations and instructions, but they struggle to communicate verbally in specific scenarios. Research demonstrates that these children are capable of speaking normally or nearly normally in some settings, which emphasizes that their challenge lies not in their ability to speak, but in the anxiety related to speaking in particular situations. Compared to those with social phobia alone, children with selective mutism exhibit higher levels of social anxiety and internalizing symptoms. Some children with selective mutism may also have minor difficulties with speech and language, which may not be as obvious in kids with social phobia who mainly show social anxiety without significant language problems. Kids with selective mutism can improve with specific interventions that focus on both their anxiety and any speech and language challenges they may have. It is crucial to refer these children to the right services early on to ensure they receive effective treatment and support. [ 4 ]
Treatment is usually carried out by speech and language therapists/pathologists, who use a wide range of techniques to stimulate language learning. [ 55 ] In the past, there was a vogue for drilling children in grammatical exercises, using imitation and elicitation, but such methods fell into disuse when it became apparent that there was little generalization to everyday situations. Contemporary approaches to enhancing development of language structure, for younger children at least, are more likely to adopt 'milieu' methods, in which the intervention is interwoven into natural episodes of communication, and the therapist builds on the child's utterances, rather than dictating what will be talked about. Interventions for older children, may be more explicit, telling the children what areas are being targeted and giving explanations regarding the rules and structures they are learning, often with visual supports. [ 56 ] [ 57 ]
In addition, there has been a move away from a focus solely on grammar and phonology toward interventions that develop children's social use of language, often working in small groups that may include typically developing as well as language-impaired peers. [ 58 ]
Another way in contemporary remediation differ from the past is that parents are more likely to be directly involved, but this approach is largely used with preschool children, rather than those whose problems persist into school age. [ 59 ] [ 60 ]
For school-aged children, teachers are increasingly involved in intervention, either in collaboration with speech and language therapists/pathologists, or as the main agents of delivery of the intervention. Evidence for the benefits of a collaborative approach is emerging, [ 61 ] but the benefits of asking education staff to be the main deliverers of SLT intervention (the "consultative" approach) are unclear. [ 62 ]
In this field, randomized controlled trial methodology has not been widely used, and this makes it difficult to assess clinical efficacy with confidence. Children's language will tend to improve over time, and without controlled studies, it can be hard to know how much of observed change is down to a specific treatment. There is, however, increasing evidence that direct 1:1 intervention with an SLT/P can be effective for improving vocabulary and expressive language. [ 63 ] There have been few studies of interventions that target receptive language, [ 64 ] though some positive outcomes have been reported. [ 65 ] [ 66 ] [ 67 ]
Longitudinal studies indicate that problems are largely resolved by five years of age in around 40% of four-year-olds with early language delays who have no other presenting risk factors. [ 36 ] However, for children who still have significant language difficulties at school entry, reading problems are common, even for children who receive specialist help, [ 69 ] and educational attainments are typically poor. [ 70 ] Poor outcomes are most common in cases where comprehension as well as expressive language is affected. [ 71 ] There is also evidence that scores on tests of nonverbal ability of children with DLD decrease over the course of development. [ 72 ]
DLD is associated with an elevated risk of social, emotional and mental health concerns. [ 73 ] For instance, in a UK survey, 64% of a sample of 11-year-olds with DLD scored above a clinical threshold on a questionnaire for psychiatric difficulties, and 36% were regularly bullied, compared with 12% of comparison children. [ 74 ] In the longer-term, studies of adult outcomes of children with DLD have found elevated rates of unemployment, social isolation and psychiatric disorder among those with early comprehension difficulties. [ 75 ] However, better outcomes are found for children who have milder difficulties and do not require special educational provision. [ 76 ]
Epidemiological studies of children in the US [ 77 ] and the UK [ 45 ] converge in estimating the prevalence of DLD in five-year-olds at around 7%. Recently, an Australian population-based study demonstrated comparable prevalence of DLD amongst 10 year-old children. [ 78 ] Therefore, the prevalence is about one in every 15 children. By these statistics, in a classroom of 30 students, 2 would have DLD. [ 27 ] In research by Tomblin et al., prevalence of DLD in racial/ethnic groups was highest in Native Americans, with African Americans being the next highest, followed by Hispanic people, and then White people. [ 79 ] No students of Asian descent presented with DLD; however, other research does indicate that DLD is present in children of Asian descent.
Much research has focused on trying to identify what makes language learning difficult for some children. [ 80 ] A major divide is between theories that attribute the difficulties to a low-level problem with auditory temporal processing, and those that propose there is a deficit in a specialised language-learning system. [ 81 ] [ 82 ] Other accounts emphasise deficits in specific aspects of learning and memory. [ 83 ] [ 84 ] It can be difficult to choose between theories because they do not always make distinctive predictions, and there is considerable heterogeneity among children with DLD. It has also been suggested that DLD may only arise when more than one underlying deficit is present. [ 85 ]
Research has also suggested that peer nominations reveal differences in social understanding between children with DLD and their typically developing peers, as evidenced by the unequal distribution of peer acknowledgments. Research on peer and friendship acknowledgments offers insight into the relationship between language development and peer interactions. Children with DLD experience lower levels of acceptance, particularly during the early school years, as indicated by peer nominations. Improvement in peer acknowledgments may not be solely attributed to language and communication interventions, suggesting that other factors influence friendships. Findings from social cognition tasks, the tendency for children with DLD to receive more positive peer nominations, and the discrepancies in their friendship acknowledgments collectively suggest that the ability to comprehend others and identify peers as friends may significantly impact social connections. [ 86 ]
Relatively little research has been conducted to test the outcomes of DLD in adults. In a study comparing 17 men with DLD to siblings without DLD, researchers found that the DLD men had normal intelligence with higher performance IQ than verbal IQ. The participants still exhibited a severe and persisting language disorder, severe literacy impairments, and significant deficits in theory of mind and phonological processing. Within the DLD cohort , higher childhood intelligence and language were associated with superior cognitive and language ability at final adult outcome. In their mid-thirties, the DLD cohort had significantly worse social adaptation (with prolonged unemployment and a paucity of close friendships and love relationships) compared with both their siblings and National Child Development Study control cohorts, matched on childhood IQ and social class. Self-reports showed a higher rate of schizotypal features but not schizoaffective disorder . Four DLD adults had serious mental health problems (two had developed schizophrenia ). [ 75 ]
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Developmental neuropsychology combines the fields of neuroscience and developmental psychology , while drawing from various other related disciplines. It examines the relationship of behavior and brain function throughout the course of an individual's lifespan, though often emphasis is put on childhood and adolescence when the majority of brain development occurs. [ 1 ] Research tends to focus on development of important behavioral functions like perception , language , and other cognitive processes . [ 2 ] Studies in this field are often centered around children or other individuals with developmental disorders or various kinds of brain related trauma or injury. A key concept of this field is that looks at and attempts to relate the psychological aspects of development, such as behavior, comprehension, cognition, etc., to the specific neural structures; it draws parallels between behavior and mechanism in the brain. [ 3 ] Research in this field involves various cognitive tasks and tests as well as neuroimaging . Some of the many conditions studied by developmental neuropsychologists include congenital or acquired brain damage , autism spectrum disorder , attention deficit disorder , executive dysfunction , seizures , intellectual disabilities , obsessive compulsive disorder , stuttering , schizophrenia , developmental aphasia , and other learning delays such as dyslexia , dysgraphia , and dyspraxia . [ 4 ]
Alexander Luria is considered by some to be a founding father of the field of neuropsychology. [ 5 ] Luria's work, much of which was related to speech rehabilitation, [ 6 ] provided much of the foundation for what we know today as child neuropsychology (developmental neuropsychology focusing only on beginning of lifespan). The Luria-Nebraska Neuropsychological Battery , a standardized test of neuropsychological functioning, was created based on his ideas. Lev Vygotsky , a student of Luria, also made significant contributions to child neuropsychology. Together, their methods have developed the basis for what is known as the Vygotsky-Luria approach. This approach is characterized by the idea that "higher psychological functions are characterized by three main features: (1) social genesis; (2) system structure; and (3) dynamic organization and localization" [ 7 ] [ 8 ] [ 9 ] and examines the neural organization and function structure behind these higher mental functions. [ 10 ]
Over time, completion of education to at least the high school level has become increasingly common as more and more jobs require skills such as reading and writing. As pressure to have children complete their schooling increases, so has the pressure to provide adequate education to all children. This has led to laws whose aim is to ensure education for disabled students. In order to accomplish this, research focus began to shift from adults who were skilled or struggled to read and write to the developmental processes behind them. [ 3 ]
Research in developmental neuropsychology can generally be divided into two categories that are based on two main goals of the field: educational and clinical . The educational approach aims to understand and aid in the education of developing children (or in some cases adults) whom have deficits learning certain skills, most commonly language related – reading and writing. While some studies do focus on children with brain damage, a lot can be learned from children without brain damage who struggle to learn specific skills and/or have learning disabilities. The goal of this research is to understand the neural causes of these problems and how they relate to the psychological aspects of it in order to improve education programs and treatments. The clinical approach has a greater focus on pathology and medical treatments and diagnoses. Often these studies evaluate and describe a patient's neural damage due to injury, brain tumors , seizures, or various congenital disorders . This type of research typically examines loss of certain functions due to damage and assesses to what extent if any can patients, usually children with still developing brains, can regain these functions. [ 3 ] The objective of a neuropsychological evaluation is to have a comprehensive view of a child's overall functioning, including how their brain operates, their strengths and limitations, their preferred learning style, and any potential abnormalities. This process is essential in the evaluation for the medical provider.
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Developmental origins of health and disease ( DOHaD ) is an approach to medical research factors that can lead to the development of human diseases during early life development. These factors include the role of prenatal and perinatal exposure to environmental factors, such as undernutrition , stress, environmental chemical, etc. [ 1 ] [ 2 ] This approach includes an emphasis on epigenetic causes of adult chronic non-communicable diseases . [ 1 ] [ 3 ] [ 4 ] As well as physical human disease, the psychopathology of the foetus can also be predicted by epigenetic factors. [ 5 ]
DOHaD has evolved into its modern understanding from several precursor concepts. In the 19th century the idea of "maternal impressions" was popular. Maternal impression is the idea that anything the mother did before giving birth could affect her offspring. [ 6 ] Our modern understanding of DOHaD was developed by several studies by David Barker and his colleagues, which showed a strong relationship between infant mortality rates from 1921 to 1925 and ischemic heart disease rates from 1968 to 1978. This led to the fetal origins hypothesis of the origins of adult diseases, which proposed that this relationship was caused by differences in early life nutrition, with a supporting theory that birthweight is connected to the development of chronic disease. [ 7 ]
During the Dutch Hunger Winter Famine (1944-1945) [ 8 ] mothers were not able to receive the proper nutrition needed to healthily carry a baby. The babies who were born during this time developed diseases (such as heart disease, schizophrenia, and type 2 diabetes) at increased levels. Researchers were able to determine, decades after the famine, that the babies born during Dutch famine had an increase in methylation in some genes and a decrease in methylation in other genes compared to their siblings who were not born during the famine. The methylation levels explain why these individuals were predisposed to certain diseases. Data collected from the Dutch famine and similar events, such as the one at Leningrad, provided a reliable source of information to scientists studying DOHaD. [ 6 ] [ 9 ] [ 10 ]
These studies in turn led to greater interest in the roles of developmental plasticity and early life environmental exposures in adult disease. The World Congress on Fetal Origins of Adult Disease held two meetings – one in 2001 and the other in 2003 – summarizing the new research in these areas. This congress later evolved into the International Society for Developmental Origins of Health and Disease . [ 1 ]
Between 1944 and 1945, in the western regions of the Netherlands and in Amsterdam, a famine broke out due to a railway strike and German control limiting supplies. The people of these countries were receiving extremely limited calories (around 400-800 a day [ 11 ] ) which had an extreme effect on pregnant women and their children. Researchers began studying a cohort of middle-aged individuals whose mothers had been pregnant with them during the famine. The Dutch Hunger Winter study provided significant data to support the DOHaD. Further studies indicated that older people had a resilience to the effects of malnutrition on physical health in late life, but a higher vulnerability to socioeconomic stunting. [ 12 ] Results concluded that the women with low caloric and nutritional intake during pregnancy had children that had greater rates of obesity as opposed to those who were not exposed to famine. [ 11 ] This is conclusive with the DOHaD theory. The study goes on to investigate at what points in development DOHaD stood true. It is thought that exposure to famine in early gestational periods has a greater effect on the foetus, however, these theories are still under investigation.
The thrifty phenotype hypothesis was proposed by C. Nicholas Hales and David Barker in a study published in 1992. [ 13 ] This hypothesis suggested that poor growth during the fetal and infant stages can cause a development of type 2 diabetes later in life. Hales and Barker suggested that this poor growth was due to maternal malnutrition which leads to low birth weight. As previously stated, low infant birth weight usually leads to an increased risk of obesity which, if not acted on, can lead to type 2 diabetes. [ 14 ]
The paper suggests that due to maternal malnutrition, infants can have lower birth weights. Since this is occurring during the plastic stage of development, this can cause the foetus to be "programmed" to conserve energy and store fat, thus leading to a lower metabolism. If there is a surplus of food during adulthood their body simply stores this abundance as more fat. This can then lead to not only diabetes but other metabolic diseases, too. [ 15 ]
There are two different types of plasticity responses when dealing with human development. The first is an immediate adaptive response. This response will alter the development that is needed to survive if there have been changes in the environment. [ 16 ] An example of this type of response is when oxygen deprivation causes a change in blood flow that would normally help with the expense of less critical tissues. Predictive adaptive response (PAR) is the second type of plasticity response. PARs are cues that happen in early life development that cause phenotype development to change that are normally adapted to environmental cues in later life. [ 16 ] This can be a benefit only when the predicted and actual postnatal environment match.
This is also referred to as the mismatch theory . Foetal malnutrition followed by excess nutrition in adults is a key example of environmental mismatches. This is very common among people born in impoverished societies. For pregnant women who are living in this type of circumstance the foetuses which are in utero are more likely to sense a low-protein condition and alter their development to survive. Therefore, the foetus will predict that getting food will be very difficult which then will set its metabolism for a "thrifty phenotype". [ 16 ] By doing this it will use every calorie to its most efficient use for survival. This can be the same cause for a society with plenty of food available. The embryo will develop insulin resistance and enzyme levels will convert the food that is not being used into fat, which in later life can lead to obesity and diabetes. Overall the environmental mismatch hypothesis is an advantage for human development but not without some disadvantage in later life.
Epigenetic alterations of gene expression are closely related with developmental origins of the health and disease hypothesis. DNA methylation, histone modifications and non-coding RNAs are altered by the environment in the womb and potentially go on to produce higher rates of adult disease later in life. [ 17 ]
The process of DNA methylation is the most studied epigenetic response as it relates to the developmental origins of health and disease. The methylation of chief regulatory cytosines changes the DNA's hydrophobicity and begins to inhibit interactions with transcription factors responsible for the expression of the gene. Certain metabolic disorders, cancer and neurodegenerative disorders can be attributed to DNA methylation events. [ 17 ]
Modifications of histones are important processes in developmental programming, with studies showing that maternal and paternal stress can induce histone modifications. These histone modifications alter phenotypes of organisms and can be the mechanism behind the predisposition of some metabolic disorders. [ 17 ] Unbalanced diets increase the thioredoxin-interacting protein expressions causing blastocysts to form incorrectly because of altered histone methylation. [ 17 ] High-fat diets are shown to alter histone methylation and acetylation and potentially lead to changes in gene expression within fetal adipose, liver, and skeletal muscle tissues. [ 17 ]
Recent studies have shown the importance in non-coding RNA's ability to regulate cell differentiation and organismal development. There are many types of non-coding RNA that are present and play a role in differentiating stem cells. There are many non-coding RNAs responsible for differentiating cells for human brain and muscle development. These RNA molecules have also been implicated in having a role in cardiovascular development. Long non-coding RNA called lncRNA Fendrr has shown to be an important regulator of heart development and it modifies chromatin and controls developmental signaling of genetically modified mice hearts. [ 18 ] [ 17 ] There is still a vast amount of research needed to fully understand this mechanism and its relation to DOHaD. [ 17 ]
In a study done by Barker, he found a strong connection between poor prenatal environments and increased possibilities of cardiovascular diseases in adults. He found a direct correlation between infant mortality in 1921-1925 and mortality rates in 1968-1978 because of heart diseases in England. In areas where pregnant mothers had to face poor nutritional states, their newborn children were at a high risk of death. If they survived the early stages of life, they developed a higher risk of cardiovascular diseases. [ 7 ]
Studies on rats found that maternal nutrient restriction resulted in damage to the cardiac renin-angiotensin system (which regulates blood pressure and volume). Additionally, these studies have shown a decrease in the number of nephrons produced by the offspring of these mothers. These differences have been found to affect males and females differently, at least in the early stages. [ 6 ] The exact mechanism of action is unknown but it is believed that it is epigenetic. [ 6 ]
A study done at UC Irvine looked at the impact that maternal stress has on foetal development and overall foetal health. The researchers determined that a mother's stress and adverse pregnancy outcomes (APOs) related to the length of gestation and growth of the foetus along with impacts on the endocrine and immune systems of the foetus. [ 19 ]
Early life influences, both prenatal and postnatal, have important effects on children later in life. It was determined that breastfed infants have significantly lower risks of obesity later in life than infants that were formula-fed. [ 20 ]
Nutrition and growth during the early years of life can be related to the growth of diseases in humans later in their lives. For example, a study done in Jamaica showed that the blood pressure of children was associated with the mother's hemoglobin levels and body fat during pregnancy. [ 21 ] Another example of this is shown in an article from the New England Journal of Medicine which took place during the Dutch famine. This study concluded that those who were in utero at the time of the famine were at a greater risk of obesity, hypertension, and heart disease than those who were born before or after the famine. [ 22 ]
A maternal high-fat diet was used to help investigate how saturated fats cause unrestrained gestational weight gain and maternal obesity of offspring. [ 23 ] When there is high-fat feeding during pregnancy, there are effects on the maternal metabolism and body composition. Some of the effects are insulin resistance, increased circulating lipids, increased adiposity, and hyperinsulinemia (high insulin in blood). When the fat intake was increased it started to adjust consumption of other macronutrients in the diet, which reduced the carbohydrate and protein consumption to match the increase of fatty acid. On another note, people who have obesity and a diet that is high in fat can develop a condition called dyslipidemia. It can lead to fibrosis of the liver, which is the cause for about 45% of deaths in the world. [ 24 ]
During the Dutch famine doctors found that under-nutrition during the gestation period related to reduced glucose tolerance and raised insulin concentrations between the ages 50 and 58. There were 120 minute glucose and insulin concentrations that were known to be higher in people that were exposed to the famine at any stage during foetal development than those who were not exposed. [ 14 ] The effect could be explained due to the lower birth rates of babies that were born during the famine and the low weight gain of their mothers. People that were born before the famine had a larger increase in glucose and insulin concentration. That was due to them experiencing starvation during the early stage of their life which might have impacted their postnatal growth pattern.
Autism spectrum disorder (ASD) is a condition that typically manifests during the first three years of a person's life. It is a developmental disorder that impairs the brain's ability to develop the typical social and communication skills that are necessary for everyday life. People with ASD may experience difficulties with social interactions, verbal and nonverbal communication, and repetitive or restricted behaviors. The degree to which ASD affects an individual can vary widely, with some people experiencing mild symptoms while others may face more significant challenges.
The precise cause of ASD is still unknown, but it is believed that a combination of factors may contribute to its development. Research suggests that genetics may play a role, as ASD can run in families. In addition, certain medications taken during pregnancy may increase the risk of a child developing ASD. While some theories have been proposed, they have yet to be proven. For instance, some scientists believe that damage to a specific region of the brain, the amygdala, may be linked to ASD, while others are examining the possibility that a viral infection may trigger the disorder.
There has been some controversy regarding whether vaccines can cause ASD, but numerous studies have shown that there is no evidence of a link between vaccines and ASD. Major medical and government organizations have also confirmed this finding. The increase in ASD diagnoses in recent years may be attributed to better awareness and more comprehensive definitions of the disorder. Treatment for ASD involves a highly structured schedule of constructive activities that build on the child's interests and various techniques. It is important to avoid unproven treatments and seek advice from ASD specialists. [ 25 ]
Large-scale famines offer insights into the effects prenatal malnutrition has on developing foetuses. A team led by Mingqing Xu investigated this possible connection between prenatal malnutrition and schizophrenia by analyzing medical records of people born between 1960 and 1961 during the Great Chinese Famine . This study found that there was a two-fold risk for someone who was born in a rural area during this period of famine to later develop schizophrenia than someone who was born either before or after. [ 26 ] However, being born in an urban area during this time was not associated with an increased risk of schizophrenia. [ 26 ] [ 27 ] This is probably due to factors that exacerbated the impact of the famine in rural areas such as grain procurement and lack of large-scale grain storage. [ 27 ]
Similar results have been found in studying the effects of the Dutch famine from 1944 to 1945. A study by Hoek compared the levels of schizophrenia for those born between August 15 and December 31, 1945, to those born after the famine had ended. This study found that those born during the time period were between two and two and a half times more likely to have schizophrenia than those born after the famine had ended. [ 28 ]
The exact mechanism which connects undernutrition to an increased chance of schizophrenia later in life is not fully understood. Famines may lead to an enhanced risk of schizophrenia because they deprive the developing foetus of key micronutrients. Some of the leading candidates are folate, essential fatty acids, retinoids, vitamin D, and iron. [ 29 ] Of these micronutrients, folate, iron and vitamin D seem to be the most promising. [ 29 ] [ 30 ] Folate jumps out as a key candidate as the occurrence of neural tube defects raised alongside schizophrenia during the Dutch famine. [ 29 ] A lack of folate could cause DNA methylation which may affect the expression of genes crucial to neurodevelopment, and it could impede the conversion of homocysteine to methionine, causing homocysteine to accumulate and cause problems in the developing brain. [ 31 ] Iron has been put forward as a leading candidate as low levels of hemoglobin, a molecule created by iron, during development was highly associated with developing schizophrenia later on in life. [ 32 ] This connection may be due to iron having a key role in the creation and function of dopamine transmission. [ 33 ]
Another, less accepted, theory that explains the connection between famine and schizophrenia is protein-calorie malnutrition. Protein-calorie malnutrition has been associated with increased dopamine and serotonin release and malfunctions in the hippocampus such as reduced dendritic branching and a lower cell count, which are also found in people with schizophrenia. [ 29 ]
The effect stress has on expecting women may not only affect them, but their child as well. Studies have shown a link between child mental health and behavioral problems to maternal stress during pregnancy. Stress in the body leads to an increase in the cortisol levels. Maternal stress, therefore, exposes the fetus to high cortisol levels. Additionally stress falls along the line of exposure to depression or anxiety within the mother. These factors have been found to been associated with emotional and cognitive issues within the child's later life. [ 34 ] These levels have been linked to neurological and behavioral regulation issues in the child later in life. [ 35 ] For example, cognitive performance at 5 years of age was impaired in kids who mother had experienced stress from a catastrophic ice storm. Investigators found that schizophrenia was frequent in offspring that mothers endured the ice storm during pregnancy. Prenatal stress has been shown to increase reactivity in infants. [ 35 ] Infants that are from pregnancy with a lot of stress are harder to soothe rather than those that mothers didn't experience any stress during pregnancy. Human and animal studies did show that infants from stressed pregnancies have a poor immune function and are more likely to contract childhood illnesses as well as mental disorders. [ 35 ]
There was a study published in the Journal of Pediatrics of August 19, 2020, which looked at how maternal recognition and stress can affect infant health after or during pregnancy. [ 36 ] The study consisted of women from low income areas, and those that were overweight which were at the age of 28 years old. The women had to rate how they felt during challenges they had to endure. The infants born during this study had to get their medical records looked at from the first year of their lives. There was a 38 percent increase for having infectious illnesses. There was a 73 percent increase from not having non-infectious illnesses with an increase of 53 percent in other illnesses amid the infants. [ 36 ] It seems that the effects were more likely later in the pregnancy, but after the study was completed they realized that stress and depression in mothers is not associated with increase in illnesses amongst the infants. [ 36 ]
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https://en.wikipedia.org/wiki/Developmental_origins_of_health_and_disease
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Developmental psychopathology is the study of the development of psychological disorders (e.g., psychopathy , autism , schizophrenia and depression ) with a life course perspective . [ 1 ] Researchers who work from this perspective emphasize how psychopathology can be understood as normal development gone awry. [ 2 ] Developmental psychopathology focuses on both typical and atypical child development in an effort to identify genetic, environmental, and parenting factors that may influence the longitudinal trajectory of psychological well-being.
Developmental psychopathology is a sub-field of developmental psychology and child psychiatry characterized by the following (non-comprehensive) list of assumptions: [ 3 ] [ 4 ]
In 1974, Thomas M. Achenbach authored a book entitled, "Developmental Psychopathology [ 5 ] ", which laid the foundations for the discipline of Developmental psychopathology. The book was an outgrowth of his research on relations between development and psychopathology.
Dante Cicchetti is acknowledged to have played a pivotal role in defining and shaping the field of developmental psychopathology. [ 6 ] While at Harvard University , Cicchetti began publishing on the development of conditions such as depression and borderline personality disorder , in addition to his own work on child maltreatment and mental retardation . In 1984, Cicchetti edited both a book and a special issue of Child Development on developmental psychopathology. In that special issue he himself wrote, "The emergence of developmental psychopathology". [ 7 ]
These efforts launched developmental psychopathology, [ 8 ] a subfield of developmental science . In 1989, nine volumes of the Rochester Symposium on Developmental Psychopathology were published, as was the first issue of the journal Development and Psychopathology .
One central concept of developmental psychopathology is homotypic and heterotypic continuity. [ 9 ] Some children will develop different symptoms across development (heterotypic continuity), while others will develop similar types of problems (homotypic continuity). [ 10 ] While homotypic continuity of emotional and behavioural problems tends to be the norm across development, [ 11 ] the transitions between early childhood and late childhood, and between preadolescence and adolescence are associated with higher heterotypic continuity. [ 10 ]
Gerald R. Patterson and colleagues take a functionalist view of conduct problems in line with a behavior analysis of child development . They have found considerable evidence that the improper use of reinforcement in childhood can lead to this form of pathology. [ 12 ]
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Developmental verbal dyspraxia ( DVD ), also known as childhood apraxia of speech ( CAS ) and developmental apraxia of speech ( DAS ), [ 1 ] is a condition in which an individual has problems saying sounds, syllables and words. This is not because of muscle weakness or paralysis. The brain has problems planning to move the body parts (e.g., lips, jaw, tongue) needed for speech. The individual knows what they want to say, but their brain has difficulty coordinating the muscle movements necessary to say those words. [ 2 ]
The exact cause of this disorder is usually unknown. [ 1 ] Many observations suggest a genetic cause of DVD, as many with the disorder have a family history of communication disorders. [ 1 ] [ 3 ] [ 4 ] [ 5 ] The gene FOXP2 has been implicated in many studies of the condition, and when this is the cause, the condition is inherited in an autosomal dominant manner, however roughly 75% of these cases are de novo . [ 6 ]
There is no cure for DVD, but with appropriate, intensive intervention, people with this motor speech disorder can improve significantly. [ 7 ]
"Childhood apraxia of speech (CAS) is a neurological childhood (pediatric) speech sound disorder in which the precision and consistency of movements underlying speech are impaired in the absence of neuromuscular deficits (e.g., abnormal reflexes, abnormal tone). CAS may occur as a result of known neurological impairment, in association with complex neurobehavioral disorders of known or unknown origin, or as an idiopathic neurogenic speech sound disorder. The core impairment in planning and/or programming spatiotemporal parameters of movement sequences results in errors in speech sound production and prosody." American Speech-Language-Hearing Association (ASHA) Ad Hoc Committee on Apraxia of Speech in Children (2007) [ 7 ]
There are three significant features that differentiate DVD/CAS from other childhood speech sound disorders. These features are:
Even though DVD/CAS is a developmental disorder, it will not simply disappear when children grow older. Children with this disorder do not follow typical patterns of language acquisition and will need treatment in order to make progress. [ 7 ]
DVD/CAS is a motor disorder , which means that the problem is located in the brain and its signals, and not in the mouth. [ 8 ] In most cases, the cause is unknown. Possible causes include genetic syndromes and disorders . [ 8 ]
Recent research has focused on the significance of the FOXP2 gene [ 9 ] [ 10 ] [ 11 ] [ 12 ] [ 13 ] in both species and individual development. [ 14 ] Research regarding the KE family , where half the members of the extended family, over three generations, exhibited heritable developmental verbal dyspraxia, were found to have a defective copy of the FOXP2 gene. [ 4 ] [ 15 ] and further studies suggest that the FOXP2 gene as well as other genetic issues could explain DVD/CAS. [ 9 ] [ 16 ] including 16p11.2 microdeletion syndrome. [ 17 ] [ 18 ]
New research suggests a role for the sodium channel SCN3A in the development of the perisylvian areas, which maintain key language circuits- Broca and Wernicke Area. [ 19 ] Patients with mutations in SCN3A had oral-motor speech disorders. [ 19 ]
Birth/prenatal injuries, as well as stroke, can also be causes of DVD/CAS. Furthermore, DVD/CAS can occur as a secondary characteristic to a variety of other conditions. These include autism , [ 1 ] some forms of epilepsy , [ 1 ] fragile X syndrome , galactosemia [ 1 ] [ 20 ] and chromosome translocations [ 14 ] [ 21 ] involving duplications or deletions . [ 16 ] [ 22 ]
Developmental verbal dyspraxia can be diagnosed by a speech–language pathologist (SLP) through specific exams that measure oral mechanisms of speech. The oral mechanisms exam involves tasks such as pursing lips, blowing, licking lips, elevating the tongue, and also involves an examination of the mouth. A complete exam also involves observation of the patient eating and talking. Tests such as the Kaufman Speech Praxis test, [ 23 ] a more formal examination, are also used in diagnosis. [ 23 ] A differential diagnosis of DVD/CAS is often not possible for children under the age of two years old. Even when children are between 2–3 years, a clear diagnosis cannot always occur, because at this age, they may still be unable to focus on, or cooperate with, diagnostic testing. [ 24 ]
There is no cure for DVD/CAS, but with appropriate, intensive intervention, people with the disorder can improve significantly. [ 7 ]
DVD/CAS requires various forms of therapy which varies with the individual needs of the patient. Typically, treatment involves one-on-one therapy with a speech–language pathologist (SLP). [ 8 ] In children with DVD/CAS, consistency is a key element in treatment. Consistency in the form of communication, as well as the development and use of oral communication are extremely important in aiding a child's speech learning process. [ citation needed ]
Many therapy approaches are not supported by thorough evidence; however, the aspects of treatment that do seem to be agreed upon are the following:
Although these aspects of treatment are supported by much clinical documentation, they lack evidence from systematic research studies. In ASHA's position statement on DVD/CAS, [ 7 ] ASHA states there is a critical need for collaborative, interdisciplinary, and programmatic research on the neural substrates, behavioral correlates, and treatment options for DVD/CAS.
One technique that is frequently used to treat DVD/CAS is integral stimulation. Integral stimulation is based on cognitive motor learning, focusing on the cognitive motor planning needed for the complex motor task of speech. It is often referred to as the "watch me, listen, do as I do" approach and is founded on a multi-step hierarchy of strategies for treatment. This hierarchy of strategies allows the clinician to alter treatment depending upon the needs of the child. It uses various modalities of presentation, emphasizing the auditory and visual modes. Experts suggest that extensive practice and experience with the new material is key, so hundreds of target stimuli should be elicited in a single session. Furthermore, distributed (shorter, but more frequent) and random treatment, which mix target and non-target utterances, produces greater overall learning. [ citation needed ]
The six steps of the hierarchy upon which integral stimulation therapy for children is loosely organized are:
Another treatment strategy that has been shown to have positive effects is an integrated phonological approach. This approach "incorporates targeted speech production practice into phonological awareness activities and uses letters and phonological cues to prompt speech production". [ 26 ] McNeill, Gillon, & Dodd studied 12 children ages 4–7 with DVD/CAS who were treated with this approach two times a week for two six-week blocks of time (separated by a six-week withdrawal block). They found positive effects for most of the children in the areas of speech production , phonological awareness , word decoding, letter knowledge, and spelling . These results show that it is clinically productive to target speech production, phonological awareness, letter knowledge, spelling, and reading all at once. This is particularly important since children with DVD/CAS often have continuous problems with reading and spelling, even if their production of speech improves. [ 26 ]
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Devon colic was a condition that affected people in the English county of Devon during parts of the 17th and 18th centuries, before it was discovered to be lead poisoning .
The first written account of the colic comes from 1655. Symptoms began with severe abdominal pains and the condition was occasionally fatal. Cider is a traditional drink of Devonians, and the connection between the colic and cider drinking had been observed for many years. The condition was commonly attributed to the acidity of the beverage.
William Musgrave 's publication De arthritide symptomatica (2nd edn, 1715) included the first scientific description of "Devonshire colic" – it was later referred to by John Huxham and Sir George Baker . [ 1 ]
However, the precise cause was not discovered until the 1760s when Dr George Baker put forward the hypothesis that poisoning from lead in cider was to blame. He observed that the symptoms of the colic were similar to those of lead poisoning. He pointed out that lead was used in the cider making process both as a component of the cider presses and in the form of lead shot which was used to clean them. He also conducted chemical tests to demonstrate the presence of lead in Devon apple juice.
The publication of his results met with some hostile reaction from cider manufacturers, keen to defend their product. Once Baker's conclusions became accepted and the elimination of lead from the cider presses was undertaken, the colic declined. By 1818, Baker's son reported that it was "hardly known to exist" in Devon.
An illness with identical symptoms was described from Poitou in western France in a work of 1616 by François Citois. [ 2 ] It was known in English sources as Poitou colic . It was likewise demonstrated to be a form of lead poisoning in a 1757 publication by Théodore Tronchin of Geneva . [ 3 ]
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https://en.wikipedia.org/wiki/Devon_colic
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The dexamethasone suppression test ( DST ) is used to assess adrenal gland function by measuring how cortisol levels change in response to oral doses or an injection of dexamethasone . [ 1 ] It is typically used to diagnose Cushing's syndrome .
The DST was historically used for diagnosing depression, but by 1988 it was considered to be "at best, severely limited in its clinical ability" for this purpose. [ 2 ]
Dexamethasone is an exogenous steroid that provides negative feedback to the pituitary gland to suppress the secretion of adrenocorticotropic hormone (ACTH). Specifically, dexamethasone binds to glucocorticoid receptors in the anterior pituitary gland, which lie outside the blood–brain barrier , resulting in regulatory modulation. [ 3 ]
There are several types of DST procedures: [ 1 ]
Low-dose and high-dose variations of the test exist. [ 4 ] The test is given at low (usually 1–2 mg) and high (8 mg) doses of dexamethasone, and the levels of cortisol are measured to obtain the results. [ 5 ]
A low dose of dexamethasone suppresses cortisol in individuals with no pathology in endogenous cortisol production. A high dose of dexamethasone exerts negative feedback on pituitary neoplastic ACTH-producing cells (Cushing's disease), but not on ectopic ACTH-producing cells or adrenal adenoma (Cushing's syndrome). [ citation needed ]
A normal result is a decrease in cortisol levels upon administration of low-dose dexamethasone. Results indicative of Cushing's disease involve no change in cortisol on low-dose dexamethasone, but inhibition of cortisol on high-dose dexamethasone. If the cortisol levels are unchanged by low- and high-dose dexamethasone, then other causes of Cushing's syndrome must be considered with further work-up necessary.
After the high-dose dexamethasone, it may be possible to make further interpretations. [ 6 ]
†ACTH as measured prior to dosing of dexamethasone [ 7 ]
Equivocal results should be followed by a corticotropin-releasing hormone stimulation test , with inferior petrosal sinus sampling .
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The Dextroscope is a medical equipment system that creates a virtual reality (VR) environment in which surgeons can plan neurosurgical and other surgical procedures. [ 1 ]
The Dextroscope is designed to show a patient's 3D anatomical relationships and pathology in great detail. Although its main purpose is for planning surgery, the dextroscope has also proven useful in research in cardiology , [ 2 ] [ 3 ] radiology and medical education. [ 4 ]
The Dextroscope started as a research project in the mid-90s at the Kent Ridge Digital Labs research institute (part of Singapore's Agency for Science, Technology and Research (A*STAR)). It was initially named the Virtual Workbench [ 5 ] and underwent commercialization in 2000 by the company Volume Interactions Pte Ltd with the name Dextroscope. The Dextroscope was selected in 2021 by A*STAR as one of the 30 innovations and inventions that pushed scientific boundaries, made an economic impact or improved lives over its 30 years history ( A*STAR@30: 30 Innovations and Inventions Over Three Decades ).
The Dextroscope was designed to be a practical variation of Virtual Reality which introduced an alternative to the prevalent trend of full immersion of the 1990s. Instead of immersing the whole user into a virtual reality, it just immersed the neurosurgeon into the patient data.
The Dextroscope allows its user to interact intuitively with a Virtual Patient . This Virtual Patient is composed of computer-generated 3D multi-modal images obtained from any DICOM tomographic data including CT , MRI , MRA , MRV , functional MRI and CTA , PET , SPECT and Tractography . The Dextroscope can work with any multi-modality combination, supporting polygonal meshes as well. [ 6 ]
The surgeon sits at the Dextroscope 3D interaction console and manipulates the Virtual Patient using both hands, similar to real life. Using stereoscopic visualisations displayed via a mirror, the surgeon sees the Virtual Patient floating behind the mirror but within easy reach of the hands. The surgeon uses flexible 3D hand movements to rotate and manipulate the object of interest. The Dextroscope allows virtual segmentation of organs and structures, making accurate 3D measurements, etc.
In one hand the surgeon holds a handle with a switch that, when pressed, allows the 3D image to be moved freely as if it were an object held in real space. The other hand holds a pencil shaped stylus that the surgeon uses to select tools from a virtual control panel and perform detailed manipulations on the 3D image.
The surgeon does not see the stylus, handle or his/her hands directly, as they are hidden behind the surface of the mirror. Instead he/she sees a virtual handle and stylus calibrated to appear in exactly the same position as the real handle and stylus. The virtual handle can serve as a drill tool, measurement tool, cutter, etc. [ 5 ]
The Dextroscope allows surgeons to interact with and manipulate the Virtual Patient, such as simulating inter-operative viewpoints or the removal of bone and soft tissue. The surgeon is able to reach inside and manipulate the image interior.
The Dextroscope provides virtual tools to manipulate the 3D image. The surgeon can use them within the virtual person to extract surgically relevant structures like the cortex or a tumor , [ 7 ] extract blood vessels , [ 8 ] or to adjust the color and transparency of displayed structures to see deep inside the patient. The surgeon can simulated the removal of bone using a simulated skull drilling tool.
Typical structures that can be segmented are tumors, blood vessels, aneurysms , parts of the skull base, and organs . Segmentation is done either automatically (when the structures are demarcated clearly by their outstanding image intensity - such as the cortex) or through user interaction (using for example an outlining tool to define the extent of the structure manually).
A virtual ‘pick’ tool allows the user to pick a segmented object and uncouple it from its surroundings for closer inspection. A measurement tool provides accurate measurement of straight and curving 3D structures such as the scalp , and measure angles, such as those between vessels or bony structures (for example, when planning the insertion of a screw into the spine).
The use of the Dextroscope has been reported for several neurosurgical clinical scenarios; [ 1 ] [ 9 ] [ 10 ]
- cerebral arteriovenous malformations [ 11 ] [ 12 ]
- aneurysms [ 13 ] [ 14 ] [ 15 ]
- cranial nerve decompression (in cases of trigeminal neuralgia and hemifacial spasm) [ 16 ] [ 17 ] [ 18 ]
- meningiomas (convexity, falcine or parasagittal) [ 19 ] [ 20 ] [ 21 ]
- ependymomas or subependymomas [ 13 ] [ 22 ]
- craniopagus twin separation [ 23 ] [ 24 ]
- transnasal approaches [ 25 ] [ 26 ] [ 27 ]
- key-hole approaches [ 28 ] [ 29 ] [ 30 ]
- epilepsy [ 31 ]
- and a great variety of deep-brain and skull base tumors [ 32 ] [ 33 ] ( pituitary adenomas , craniopharyngiomas , arachnoid cysts , colloid cysts , cavernomas [ 34 ] , [ 35 ] hemangioblastomas , chordomas , epidermoids , gliomas , [ 36 ] jugular schwannomas , aqueductal stenosis, stenosis of Monro foramen, hippocampal sclerosis ). [ 13 ] [ 37 ] [ 38 ]
Brain and spine pathology, such as cervical fractures of the spine, syringomyelia , and sacral nerve root neurinomas have been evaluated. [ 39 ]
For other uses of the Dextroscope in neurosurgery refer to [ 40 ] [ 41 ] [ 42 ] [ 43 ] [ 44 ] [ 45 ] [ 46 ] [ 47 ] [ 48 ] [ 49 ] [ 50 ] [ 51 ] . [ 52 ]
The Dextroscope has been applied also outside of neurosurgery to benefit any patient presenting a surgical challenge: an anatomical or structural complexity that requires planning of the surgical (or interventional) approach, for example, ENT [ 53 ] orthopedic, trauma and cranio-facial surgery , [ 54 ] [ 55 ] [ 56 ] [ 57 ] [ 58 ] [ 59 ] cardiac surgery [ 60 ] and liver resection . [ 61 ] [ 62 ]
Dextroscope is not just for surgeons – radiologists use it, too. The rapid growth in multi-modal diagnostic imaging data routinely available has increased their workload tremendously. Using the Dextroscope, radiologists can reconstruct multimodal models from high volumes of 2D slices – hence facilitating a better understanding of the 3D anatomical structures and helping with the diagnosis.
Furthermore, the Dextroscope virtual reality environment helps bridge the gap between radiology and surgery - by allowing the radiologist to easily demonstrate to surgeons important 3D structures in a way that surgeons are familiar with. This demonstration capability makes it also useful as a base for medical educators in which to convey 3D information to students. [ 63 ] In order to reach a larger group of people in a classroom or auditorium, a version was manufactured called Dextrobeam . [ 64 ]
The Dextroscope was installed, (among other medical and research institutions) at:
The Dextroscope was a pre-operative planning system which created 3D patient-specific virtual models. To bring the patient data into the operating room, in particular to neurosurgery, the DEX-Ray [ 65 ] augmented reality neurosurgical navigation system was developed in 2006-2008. DEX-Ray overlaid 3D virtual patient information over a video stream obtained from a proprietary handheld tracked video probe designed by the company. This allowed image guidance by displaying co-registered planning data over the real images of the patient seen by the video camera, so that the clinician had 'see-through' visualization on the patient's head, and helped plan the craniotomy and guide during the intervention. The DEX-Ray was clinically tested at the Singapore National Neuroscience Institute (Singapore) and at the Hospital Clinic Barcelona (Spain). It was not released as a commercial product.
The Dextroscope and Dextrobeam were products of Volume Interactions Pte Ltd (a member of the Bracco Group ), a company spun-off from the Kent Ridge Digital Labs research institute in Singapore. They received USA FDA 510(K) - class II (2002) clearance, CE Marking - class I (2002), China SFDA Registration - class II (2004) and Taiwan Registration - type P (Radiology) (2007). For a comprehensive overview of the Dextroscope refer to the Springer International Publishing book chaper. [ 66 ]
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Diabetes insipidus ( DI ) is a condition characterized by large amounts of dilute urine and increased thirst . [ 1 ] The amount of urine produced can be nearly 20 liters per day. [ 1 ] Reduction of fluid has little effect on the concentration of the urine. [ 1 ] Complications may include dehydration or seizures . [ 1 ]
There are four types of DI, each with a different set of causes. [ 1 ]
Diagnosis is often based on urine tests , blood tests and the fluid deprivation test . [ 1 ] Despite the name, diabetes insipidus is unrelated to diabetes mellitus and the conditions have a distinct mechanism, though both can result in the production of large amounts of urine. [ 1 ]
Treatment involves drinking sufficient fluids to prevent dehydration. [ 1 ] Other treatments depend on the type. [ 1 ] In central and gestational DI, treatment is with desmopressin . [ 1 ] Nephrogenic DI may be treated by addressing the underlying cause or by the use of a thiazide , aspirin or ibuprofen . [ 1 ] The number of new cases of diabetes insipidus each year is 3 in 100,000. [ 4 ] Central DI usually starts between the ages of 10 and 20 and occurs in males and females equally. [ 2 ] Nephrogenic DI can begin at any age. [ 3 ] The term "diabetes" is derived from the Greek word meaning siphon . [ 6 ]
Excessive urination and extreme thirst and increased fluid intake (especially for cold water and sometimes ice or ice water) are typical for DI. [ 7 ] The symptoms of excessive urination and extreme thirst are similar to what is seen in untreated diabetes mellitus , with the distinction that the urine does not contain glucose. Blurred vision is a rarity. Signs of dehydration may also appear in some individuals since the body cannot properly regulate the amount of the water it takes in. [ 8 ]
Extreme urination continues throughout the day and the night. In children, DI can interfere with appetite, eating, weight gain and growth , as well. They may present with fever , vomiting or diarrhea . Adults with untreated DI may remain healthy for decades as long as enough water is consumed to offset the urinary losses. However, there is a continuous risk of dehydration and loss of potassium that may lead to hypokalemia . [ citation needed ] [ 9 ]
The several forms of diabetes insipidus are:
Central (or Neurogenic ) DI has many possible causes. According to the literature, the principal causes of central DI and their oft-cited approximate frequencies are as follows: [ citation needed ]
Nephrogenic diabetes insipidus is due to the inability of the kidney to respond normally to vasopressin. [ 10 ]
Dipsogenic DI or primary polydipsia results from excessive intake of fluids as opposed to deficiency of arginine vasopressin. It may be due to a defect or damage to the thirst mechanism, located in the hypothalamus , [ 11 ] or due to mental illness. Treatment with desmopressin may lead to water intoxication . [ 12 ]
Gestational DI occurs only during pregnancy and the postpartum period. During pregnancy, women produce vasopressinase in the placenta , which breaks down antidiuretic hormone (ADH). Gestational DI is thought to occur with excessive production and/or impaired clearance of vasopressinase. [ 13 ]
Most cases of gestational DI can be treated with desmopressin (DDAVP), but not vasopressin. In rare cases, however, an abnormality in the thirst mechanism causes gestational DI, and desmopressin should not be used. [ 14 ]
Diabetes insipidus is also associated with some serious diseases of pregnancy, including pre-eclampsia , HELLP syndrome and acute fatty liver of pregnancy . These cause DI by impairing hepatic clearance of circulating vasopressinase. [ citation needed ]
Electrolyte and volume homeostasis is a complex mechanism that balances the body's requirements for blood pressure and the main electrolytes sodium and potassium . In general, electrolyte regulation precedes volume regulation. When the volume is severely depleted, however, the body will retain water at the expense of deranging electrolyte levels. [ 15 ]
The regulation of urine production occurs in the hypothalamus , which produces ADH in the supraoptic and paraventricular nuclei. After synthesis, the hormone is transported in neurosecretory granules down the axon of the hypothalamic neuron to the posterior lobe of the pituitary gland , where it is stored for later release. In addition, the hypothalamus regulates the sensation of thirst in the ventromedial nucleus by sensing increases in serum osmolarity and relaying this information to the cortex . [ citation needed ]
Neurogenic/central DI results from a lack of ADH; occasionally it can present with decreased thirst as regulation of thirst and ADH production occur in close proximity in the hypothalamus. It is encountered as a result of hypoxic encephalopathy, neurosurgery, autoimmunity or cancer, or sometimes without an underlying cause (idiopathic). [ citation needed ]
The main effector organ for fluid homeostasis is the kidney . ADH acts by increasing water permeability in the collecting ducts and distal convoluted tubules; specifically, it acts on proteins called aquaporins and more specifically aquaporin 2 in the following cascade. When released, ADH binds to V2 G-protein coupled receptors within the distal convoluted tubules, increasing cyclic AMP , which couples with protein kinase A , stimulating translocation of the aquaporin 2 channel stored in the cytoplasm of the distal convoluted tubules and collecting ducts into the apical membrane. These transcribed channels allow water into the collecting duct cells. The increase in permeability allows for the reabsorption of water into the bloodstream, thus concentrating the urine. [ citation needed ]
Nephrogenic DI results from a lack of aquaporin channels in the distal collecting duct (decreased surface expression and transcription). It is seen in lithium toxicity , hypercalcemia , hypokalemia , or the release of ureteral obstruction. Therefore, a lack of ADH prevents water reabsorption and the osmolarity of the blood increases. With increased osmolarity, the osmoreceptors in the hypothalamus detect this change and stimulate thirst. With increased thirst, the person now experiences a polydipsia and polyuria cycle. [ citation needed ]
Hereditary forms of diabetes insipidus account for less than 10% of the cases of diabetes insipidus seen in clinical practice. [ 16 ]
To distinguish DI from other causes of excess urination, blood glucose levels, bicarbonate levels, and calcium levels need to be tested. Measurement of blood electrolytes can reveal a high sodium level ( hypernatremia as dehydration develops). Urinalysis demonstrates a dilute urine with a low specific gravity . Urine osmolarity and electrolyte levels are typically low. [ 17 ]
A fluid deprivation test is another way of distinguishing DI from other causes of excessive urination. If there is no change in fluid loss, giving desmopressin can determine if DI is caused by: [ citation needed ]
This test measures the changes in body weight, urine output, and urine composition when fluids are withheld to induce dehydration. The body's normal response to dehydration is to conserve water by concentrating the urine. Those with DI continue to urinate large amounts of dilute urine in spite of water deprivation. In primary polydipsia , the urine osmolality should increase and stabilize at above 280 mOsm/kg with fluid restriction, while a stabilization at a lower level indicates diabetes insipidus. [ 18 ] Stabilization in this test means, more specifically, when the increase in urine osmolality is less than 30 Osm/kg per hour for at least three hours. [ 18 ] Sometimes measuring blood levels of ADH toward the end of this test is also necessary, but is more time-consuming to perform. [ 18 ]
To distinguish between the main forms, desmopressin stimulation is also used; desmopressin can be taken by injection, a nasal spray, or a tablet. While taking desmopressin, a person should drink fluids or water only when thirsty and not at other times, as this can lead to sudden fluid accumulation in the central nervous system. If desmopressin reduces urine output and increases urine osmolarity, the hypothalamic production of ADH is deficient, and the kidney responds normally to exogenous vasopressin (desmopressin). If the DI is due to kidney pathology, desmopressin does not change either urine output or osmolarity (since the endogenous vasopressin levels are already high). [ medical citation needed ]
Whilst diabetes insipidus usually occurs with polydipsia, it can also rarely occur not only in the absence of polydipsia but in the presence of its opposite, adipsia (or hypodipsia). "Adipsic diabetes insipidus" is recognised [ 19 ] as a marked absence of thirst even in response to hyperosmolality. [ 20 ] In some cases of adipsic DI, the person may also fail to respond to desmopressin. [ 21 ]
If central DI is suspected, testing of other hormones of the pituitary , as well as magnetic resonance imaging , particularly a pituitary MRI, is necessary to discover if a disease process (such as a prolactinoma , or histiocytosis , syphilis , tuberculosis or other tumor or granuloma ) is affecting pituitary function. Most people with this form have either experienced past head trauma or have stopped ADH production for an unknown reason. [ medical citation needed ]
Treatment involves drinking sufficient fluids to prevent dehydration. [ 1 ] Other treatments depend on the type. [ 1 ] In central and gestational DI treatment is with desmopressin . [ 1 ] Nephrogenic DI may be treated by addressing the underlying cause or the use of a thiazide , aspirin , or ibuprofen . [ 1 ]
Central DI and gestational DI respond to desmopressin which is given as intranasal or oral tablets. Carbamazepine , an anticonvulsive medication, has also had some success in this type of DI. Also, gestational DI tends to abate on its own in four to six weeks following labor, though some women may develop it again in subsequent pregnancies. In dipsogenic DI, desmopressin is not usually an option. [ citation needed ]
Desmopressin will be ineffective in nephrogenic DI which is treated by reversing the underlying cause (if possible) and replacing the free water deficit. A thiazide diuretic , such as chlorthalidone or hydrochlorothiazide , can be used to create mild hypovolemia which encourages salt and water uptake in proximal tubule and thus improve nephrogenic diabetes insipidus. [ 22 ] Amiloride has additional benefit of blocking Na uptake. Thiazide diuretics are sometimes combined with amiloride to prevent hypokalemia caused by the thiazides. It seems paradoxical to treat an extreme diuresis with a diuretic, and the exact mechanism of action is unknown but the thiazide diuretics will decrease distal convoluted tubule reabsorption of sodium and water, thereby causing diuresis. This decreases plasma volume, thus lowering the glomerular filtration rate and enhancing the absorption of sodium and water in the proximal nephron. Less fluid reaches the distal nephron, so overall fluid conservation is obtained. [ 23 ]
Lithium-induced nephrogenic DI may be effectively managed with the administration of amiloride, a potassium-sparing diuretic often used in conjunction with thiazide or loop diuretics. Clinicians have been aware of lithium toxicity for many years, and traditionally have administered thiazide diuretics for lithium-induced polyuria and nephrogenic diabetes insipidus. However, amiloride has recently been shown to be a successful treatment for this condition. [ 24 ]
The word "diabetes" ( / ˌ d aɪ . ə ˈ b iː t iː z / or / ˌ d aɪ . ə ˈ b iː t ɪ s / ) comes from Latin diabētēs , which in turn comes from Ancient Greek : διαβήτης , romanized : diabētēs , which literally means "a passer through; a siphon ". [ 25 ] Ancient Greek physician Aretaeus of Cappadocia ( fl. in the first century CE ) used that word, with the intended meaning "excessive discharge of urine", as the name for the disease. [ 26 ] [ 27 ] Ultimately, the word comes from Greek διαβαίνειν ( diabainein ), meaning "to pass through", [ 25 ] which is composed of δια - ( dia -), meaning "through" and βαίνειν ( bainein ), meaning "to go". [ 26 ] The word "diabetes" is first recorded in English, in the form "diabete", in a medical text written around 1425.
"Insipidus" comes from Latin language insipidus (tasteless), from Latin: in- "not" + sapidus "tasty" from sapere "have a taste"—the full meaning is "lacking flavor or zest; not tasty". Application of this name to DI arose from the fact that diabetes insipidus does not cause glycosuria (excretion of glucose into the urine).
In a large survey conducted amongst patients with central diabetes insipidus, the majority were in favor of changing the disease's name to "vasopressin deficiency" to avoid confusion with diabetes mellitus. [ 6 ]
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Diadochokinesia or diadochokinesis is the ability to make antagonistic movements in quick succession, alternately bringing a limb into opposite positions, as of flexion and extension or of pronation and supination . [ 1 ] Speech-language pathology defines it as the speed necessary to stop a determined motor impulse and substitute it with its opposite. The relative timing of this kind of movements is also called alternate motion rates ( AMR ) or sequential motor rates ( SMR ). [ 2 ]
Loss of this ability, called dysdiadochokinesia , is a characteristic sign of cerebellar diseases . Many clinical tests may be employed to test for such disturbances. [ 3 ]
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Diagnosis ( pl. : diagnoses ) is the identification of the nature and cause of a certain phenomenon. Diagnosis is used in a lot of different disciplines , with variations in the use of logic , analytics , and experience, to determine " cause and effect ". In systems engineering and computer science , it is typically used to determine the causes of symptoms, mitigations, and solutions. [ 1 ]
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Diagnosis-related group ( DRG ) is a system to classify hospital cases into one of originally 467 groups, [ 1 ] with the last group (coded as 470 through v24, 999 thereafter) being "Ungroupable". This system of classification was developed as a collaborative project by Robert B Fetter, PhD, of the Yale School of Management , and John D. Thompson , MPH, of the Yale School of Public Health . [ 2 ] The system is also referred to as "the DRGs", and its intent was to identify the "products" that a hospital provides. One example of a "product" is an appendectomy. The system was developed in anticipation of convincing Congress to use it for reimbursement, to replace "cost based" reimbursement that had been used up to that point. DRGs are assigned by a "grouper" program based on ICD (International Classification of Diseases) diagnoses, procedures, age, sex, discharge status, and the presence of complications or comorbidities . DRGs have been used in the US since 1982 to determine how much Medicare pays the hospital for each "product", since patients within each category are clinically similar and are expected to use the same level of hospital resources. [ 3 ] DRGs may be further grouped into Major Diagnostic Categories (MDCs). DRGs are also standard practice for establishing reimbursements for other Medicare related reimbursements such as to home healthcare providers. [ 4 ]
The original objective of diagnosis-related groups (DRG) was to develop a classification system that identified the "products" that the patient received. Since the introduction of DRGs in the early 1980s, the healthcare industry has evolved and developed an increased demand for a patient classification system that can serve its original objective at a higher level of sophistication and precision. [ 5 ] To meet those evolving needs, the objective of the DRG system had to expand in scope.
Several different DRG systems have been developed in the United States. They include: [ 6 ]
Other DRG systems have been developed for markets such as Latin America and ASIA, for example:
As of 2003, the top 10 DRGs accounted for almost 30% of acute hospital admissions. [ 7 ] : 6
In 1991, the top 10 DRGs overall were: normal newborn ( vaginal delivery ), heart failure , psychoses , Caesarean section , neonate with significant problems, angina pectoris , specific cerebrovascular disorders, pneumonia , and hip / knee replacement . These DRGs comprised nearly 30 percent of all hospital discharges . [ 8 ]
In terms of geographic variation, as of 2011 hospital payments varied across 441 labor markets. [ 9 ]
The system was created in the early 1970s by Robert Barclay Fetter and John D. Thompson at Yale University with the material support of the former Health Care Financing Administration (HCFA), now called the Centers for Medicare & Medicaid Services (CMS). [ 2 ] [ 10 ]
DRGs were first implemented in New Jersey , beginning in 1980 at the initiative of NJ Health Commissioner Joanne Finley [ 7 ] : 13 with a small number of hospitals partitioned into three groups according to their budget positions — surplus, breakeven, and deficit — prior to the imposition of DRG payment. [ 11 ] The New Jersey experiment continued for three years, with additional cadres of hospitals being added to the number of institutions each year until all hospitals in New Jersey were dealing with this prospective payment system . [ 11 ]
DRGs were designed to be homogeneous units of hospital activity to which binding prices could be attached. A central theme in the advocacy of DRGs was that this reimbursement system would, by constraining the hospitals, oblige their administrators to alter the behaviour of the physicians and surgeons comprising their medical staffs. Hospitals were forced to leave the "nearly risk-free world of cost reimbursement" [ 12 ] and face the uncertain financial consequences associated with the provision of health care. [ 13 ] DRGs were designed to provide practice pattern information that administrators could use to influence individual physician behaviour. [ 11 ]
DRGs were intended to describe all types of patients in an acute hospital setting. DRGs encompassed elderly patients as well as new born, pediatric and adult populations. [ 14 ]
The prospective payment system implemented as DRGs had been designed to limit the share of hospital revenues derived from the Medicare program budget. [ 11 ] In 1982 the US Congress passed Tax Equity and Fiscal Responsibility Act with provisions to reform Medicare payment, and in 1983, an amendment was passed to use DRGs for Medicare, [ 7 ] : 16 with HCFA (now CMS) maintaining the definitions.
In 1988, New York state passed legislation instituting DRG-based payments for all non-Medicare patients. [ 15 ] [ 16 ] [ 17 ] This legislation required that the New York State Department of Health (NYS DOH) evaluate the applicability of Medicare DRGs to a non-Medicare population. This evaluation concluded that the Medicare DRGs were not adequate for a non-Medicare population. Based on this evaluation, the NYS DOH entered into an agreement with 3M to research and develop all necessary DRG modifications. The modifications resulted in the initial APDRG, which differed from the Medicare DRG in that it provided support for transplants, high-risk obstetric care, nutritional disorders, and pediatrics along with support for other populations. One challenge in working with the APDRG groupers is that there is no set of common data/formulas that is shared across all states as there is with CMS. Each state maintains its own information. [ citation needed ]
The history, design, and classification rules of the DRG system, as well as its application to patient discharge data and updating procedures, are presented in the CMS DRG Definitions Manual (Also known as the Medicare DRG Definitions Manual and the Grouper Manual ). A new version generally appears every October. The 20.0 version appeared in 2002. [ citation needed ]
In 2007, author Rick Mayes described DRGs as:
...the single most influential postwar innovation in medical financing: Medicare's prospective payment system (PPS). Inexorably rising medical inflation and deep economic deterioration forced policymakers in the late 1970s to pursue radical reform of Medicare to keep the program from insolvency. Congress and the Reagan administration eventually turned to the one alternative reimbursement system that analysts and academics had studied more than any other and had even tested with apparent success in New Jersey: prospective payment with diagnosis-related groups (DRGs). Rather than simply reimbursing hospitals whatever costs they charged to treat Medicare patients, the new model paid hospitals a predetermined, set rate based on the patient's diagnosis. The most significant change in health policy since Medicare and Medicaid's passage in 1965 went virtually unnoticed by the general public. Nevertheless, the change was nothing short of revolutionary. For the first time, the federal government gained the upper hand in its financial relationship with the hospital industry. Medicare's new prospective payment system with DRGs triggered a shift in the balance of political and economic power between the providers of medical care (hospitals and physicians) and those who paid for it - power that providers had successfully accumulated for more than half a century. [ 18 ]
DRGs were originally developed in New Jersey before the federal adoption for Medicare in 1983. [ 7 ] : 16 After the federal adoption, the system was adopted by states, including in Medicaid payment systems, with twenty states using some DRG-based system in 1991; however, these systems may have their own unique adjustments. [ 7 ] : 17
In 1992, New Jersey repealed the DRG payment system after political controversy. [ 7 ] : 21
Before the introduction of version 25, many CMS DRG classifications were "paired" to reflect the presence of complications or comorbidities (CCs). A significant refinement of version 25 was to replace this pairing, in many instances, with a trifurcated design that created a tiered system of the absence of CCs, the presence of CCs, and a higher level of presence of Major CCs. As a result of this change, the historical list of diagnoses that qualified for membership on the CC list was substantially redefined and replaced with a new standard CC list and a new Major CC list. [ citation needed ]
Another planning refinement was not to number the DRGs in strict numerical sequence as compared with the prior versions. In the past, newly created DRG classifications would be added to the end of the list. In version 25, there are gaps within the numbering system that will allow modifications over time, and also allow for new MS-DRGs in the same body system to be located more closely together in the numerical sequence. [ citation needed ]
DRGs and similar systems have expanded internationally; for example, in Europe some countries imported the scheme from US or Australia, and in other cases they were developed independently. [ 28 ] In England, a similar set of codes exist called Health Resource Groups. [ 29 ] : 199 As of 2018, Asian countries such as South Korea, Japan, and Thailand have limited adoption of DRGs. [ 30 ] Latin American countries use a DRG system adapted to regionally extended medical classifications and nomenclatures. This DRG system is called AVEDIAN DRG GROUPER (LAT-GRC).
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A diagnosis of exclusion or by exclusion ( per exclusionem ) is a diagnosis of a medical condition reached by a process of elimination , which may be necessary if presence cannot be established with complete confidence from history, examination or testing. Such elimination of other reasonable possibilities is a major component in performing a differential diagnosis . [ 1 ]
Diagnosis by exclusion tends to occur where scientific knowledge is scarce, specifically where the means to verify a diagnosis by an objective method is absent. It can also commonly occur where objective diagnostic tests do exist, but extensive diagnostic testing or sufficient exploration of differential diagnosis by a multidisciplinary team is not undertaken due to financial constraints or assessment bias ( health inequity ). [ 2 ] [ 3 ] [ 4 ] [ 5 ] [ 6 ]
The largest category of diagnosis by exclusion is seen among psychiatric disorders where the presence of physical or organic disease must be excluded as a prerequisite for making a functional diagnosis. [ 7 ] [ 8 ]
An example of such a diagnosis is " fever of unknown origin ": to explain the cause of elevated temperature the most common causes of unexplained fever (infection, neoplasm , or collagen vascular disease) must be ruled out.
Other examples include:
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Identification of a hearing loss is usually conducted by a general practitioner medical doctor , otolaryngologist , certified and licensed audiologist , school or industrial audiometrist , or other audiometric technician. Diagnosis of the cause of a hearing loss is carried out by a specialist physician (audiovestibular physician) or otorhinolaryngologist .
Difference between subjective and objective hearing test .
Subjective:
Objective:
A case history (usually a written form, with questionnaire) can provide valuable information about the context of the hearing loss, and indicate what kind of diagnostic procedures to employ. Case history will include such items as:
In case of infection or inflammation, blood or other body fluids may be submitted for laboratory analysis.
Hearing loss is generally measured by playing generated or recorded sounds, and determining whether the person can hear them. Hearing sensitivity varies according to the frequency of sounds. To take this into account, hearing sensitivity can be measured for a range of frequencies and plotted on an audiogram .
Other method for quantifying hearing loss is a hearing test using a mobile application or hearing aid application , which includes a hearing test . [ 1 ] [ 2 ] Hearing diagnosis using mobile application is similar to the audiometry procedure. As a result of hearing test , hearing thresholds at different frequencies ( audiogram ) are determined. Despite the errors in the measurements, application can help to diagnose hearing loss. [ 1 ] Audiogram , obtained using mobile application, can be used to adjust hearing aid application . [ 2 ]
An alternative approach to assessing hearing impairment is through the utilization of a speech-in-noise test. This evaluation method assesses an individual's ability to comprehend speech amidst background noise. Individuals with hearing loss typically experience difficulty in understanding speech, particularly in environments with high levels of noise. This is especially true for people who have a sensorineural loss – which is by far the most common type of hearing loss. As such, speech-in-noise tests can provide valuable information about a person's hearing ability, and can be used to detect the presence of a sensorineural hearing loss. A recently developed digit-triple speech-in-noise test may be a more efficient screening test. [ 3 ]
Otoacoustic emissions test is an objective hearing test that may be administered to toddlers and children too young to cooperate in a conventional hearing test. The test is also useful in older children and adults and is an important measure in diagnosing auditory neuropathy described above.
Auditory brainstem response testing is an electrophysiological test used to test for hearing deficits caused by pathology within the ear, the cochlear nerve and also within the brainstem. This test can be used to identify delay in the conduction of neural impulses due to tumours or inflammation but can also be an objective test of hearing thresholds. Other electrophysiological tests, such as cortical evoked responses, can look at the hearing pathway up to the level of the auditory cortex.
MRI and CT scans can be useful to identify the pathology of many causes of hearing loss. They are only needed in selected cases. [ vague ]
Hearing loss is categorized by type, severity, and configuration. Furthermore, a hearing loss may exist in only one ear (unilateral) or in both ears (bilateral). Hearing loss can be temporary or permanent, sudden or progressive.
The severity of a hearing loss is ranked according to ranges of nominal thresholds in which a sound must be so it can be detected by an individual. It is measured in decibels of hearing loss, or dB HL. The measurement of hearing loss in an individual is conducted over several frequencies , mostly 500 Hz, 1000 Hz, 2000 Hz and 4000 Hz. The hearing loss of the individual is the average of the hearing loss values over the different frequencies. Hearing loss can be ranked differently according to different organisations; and so, in different countries different systems are in use.
Hearing loss may be ranked as slight, mild, moderate, moderately severe, severe or profound as defined below: [ medical citation needed ]
The 'Audiometric Classifications of Hearing Impairment' according to the International Bureau Audiophonology (BIAP) in Belgium is as follows: [ 5 ]
Hearing loss may affect one or both ears. If both ears are affected, then one ear may be more affected than the other. Thus it is possible, for example, to have normal hearing in one ear and none at all in the other, or to have mild hearing loss in one ear and moderate hearing loss in the other.
For certain legal purposes such as insurance claims, hearing loss is described in terms of percentages. Given that hearing loss can vary by frequency and that audiograms are plotted with a logarithmic scale, the idea of a percentage of hearing loss is somewhat arbitrary, but where decibels of loss are converted via a legally recognized formula, it is possible to calculate a standardized "percentage of hearing loss", which is suitable for legal purposes only.
There are three main types of hearing loss, conductive hearing loss , sensorineural hearing loss . Combinations of conductive and sensorineural hearing losses are called a mixed hearing loss. [ 4 ] An additional problem which is increasingly recognised is auditory processing disorder which is not a hearing loss as such but a difficulty perceiving sound.
Conductive hearing loss is present when the sound is not reaching the inner ear, the cochlea . This can be due to external ear canal malformation, dysfunction of the eardrum or malfunction of the bones of the middle ear. The eardrum may show defects from small to total resulting in hearing loss of different degree. Scar tissue after ear infections may also make the eardrum dysfunction as well as when it is retracted and adherent to the medial part of the middle ear.
Dysfunction of the three small bones of the middle ear – malleus, incus, and stapes – may cause conductive hearing loss. The mobility of the ossicles may be impaired for different reasons including a boney disorder of the ossicles called otosclerosis and disruption of the ossicular chain due to trauma, infection or ankylosis may also cause hearing loss.
Sensorineural hearing loss is one caused by dysfunction of the inner ear, the cochlea or the nerve that transmits the impulses from the cochlea to the hearing centre in the brain. The most common reason for sensorineural hearing loss is damage to the hair cells in the cochlea. Depending on the definition it could be estimated that more than 50% of the population over the age of 70 has impaired hearing. [ 6 ]
Damage to the brain can lead to a central deafness. The peripheral ear and the auditory nerve may function well but the central connections are damaged by tumour, trauma or other disease and the patient is unable to process speech information.
Mixed hearing loss is a combination of conductive and sensorineural hearing loss. Chronic ear infection (a fairly common diagnosis) can cause a defective ear drum or middle-ear ossicle damages, or both. In addition to the conductive loss, a sensory component may be present.
This is not an actual hearing loss but gives rise to significant difficulties in hearing. One kind of auditory processing disorder is King-Kopetzky syndrome , which is characterized by an inability to process out background noise in noisy environments despite normal performance on traditional hearing tests. An auditory processing disorders is sometimes linked to language disorders in persons of all ages.
The shape of an audiogram shows the relative configuration of the hearing loss, such as a Carhart notch for otosclerosis, 'noise' notch for noise-induced damage, high frequency rolloff for presbycusis, or a flat audiogram for conductive hearing loss. In conjunction with speech audiometry, it may indicate central auditory processing disorder, or the presence of a schwannoma or other tumor. There are four general configurations of hearing loss:
People with unilateral hearing loss or single-sided deafness (SSD) have difficulty in:
In quiet conditions, speech discrimination is approximately the same for normal hearing and those with unilateral deafness; however, in noisy environments speech discrimination varies individually and ranges from mild to severe.
One reason for the hearing problems these patients often experience is due to the head shadow effect . Newborn children with no hearing on one side but one normal ear could still have problems. [ 7 ] Speech development could be delayed and difficulties to concentrate in school are common. More children with unilateral hearing loss have to repeat classes than their peers. Taking part in social activities could be a problem. Early aiding is therefore of utmost importance. [ 8 ] [ 9 ]
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A diagnosis of myocardial infarction is created by integrating the history of the presenting illness and physical examination with electrocardiogram findings and cardiac markers ( blood tests for heart muscle cell damage ). [ 1 ] [ 2 ] A coronary angiogram allows visualization of narrowings or obstructions on the heart vessels, and therapeutic measures can follow immediately. At autopsy , a pathologist can diagnose a myocardial infarction based on anatomopathological findings.
A chest radiograph and routine blood tests may indicate complications or precipitating causes and are often performed upon arrival to an emergency department . New regional wall motion abnormalities on an echocardiogram are also suggestive of a myocardial infarction. Echo may be performed in equivocal cases by the on-call cardiologist. [ 3 ] In stable patients whose symptoms have resolved by the time of evaluation, Technetium (99mTc) sestamibi (i.e. a "MIBI scan"), thallium-201 chloride or Rubidium-82 Chloride can be used in nuclear medicine to visualize areas of reduced blood flow in conjunction with physiologic or pharmacologic stress. [ 3 ] [ 4 ] Thallium may also be used to determine viability of tissue, distinguishing whether non-functional myocardium is actually dead or merely in a state of hibernation or of being stunned. [ 5 ]
According to the WHO criteria as revised in 2000, [ 6 ] a cardiac troponin rise accompanied by either typical symptoms, pathological Q waves, ST elevation or depression or coronary intervention are diagnostic of MI.
Previous WHO criteria [ 7 ] formulated in 1979 put less emphasis on cardiac biomarkers; according to these, a patient is diagnosed with myocardial infarction if two (probable) or three (definite) of the following criteria are satisfied:
The general appearance of patients may vary according to the experienced symptoms; the patient may be comfortable, or restless and in severe distress with an increased respiratory rate . A cool and pale skin is common and points to vasoconstriction . Some patients have low-grade fever (38–39 °C). Blood pressure may be elevated or decreased, and the pulse can become irregular . [ 8 ] [ 9 ] : 1444
If heart failure ensues, elevated jugular venous pressure and hepatojugular reflux , or swelling of the legs due to peripheral edema may be found on inspection. Rarely, a cardiac bulge with a pace different from the pulse rhythm can be felt on precordial examination . Various abnormalities can be found on auscultation , such as a third and fourth heart sound , systolic murmurs , paradoxical splitting of the second heart sound, a pericardial friction rub and rales over the lung. [ 8 ] [ 9 ] : 1450
The primary purpose of the electrocardiogram is to detect ischemia or acute coronary injury in broad, symptomatic emergency department populations. A serial ECG may be used to follow rapid changes in time. The standard 12 lead ECG does not directly examine the right ventricle , and is relatively poor at examining the posterior basal and lateral walls of the left ventricle . In particular, acute myocardial infarction in the distribution of the circumflex artery is likely to produce a nondiagnostic ECG. [ 10 ] The use of additional ECG leads like right-sided leads V3R and V4R and posterior leads V7, V8, and V9 may improve sensitivity for right ventricular and posterior myocardial infarction. [ citation needed ]
The 12 lead ECG is used to classify patients into one of three groups: [ 11 ]
A normal ECG does not rule out acute myocardial infarction. Mistakes in interpretation are relatively common, and the failure to identify high risk features has a negative effect on the quality of patient care. [ 12 ]
It should be determined if a person is at high risk for myocardial infarction before conducting imaging tests to make a diagnosis. [ 13 ] People who have a normal ECG and who are able to exercise, for example, do not merit routine imaging. [ 13 ] Imaging tests such as stress radionuclide myocardial perfusion imaging or stress echocardiography can confirm a diagnosis when a person's history, physical exam, ECG and cardiac biomarkers suggest the likelihood of a problem. [ 13 ]
Cardiac markers or cardiac enzymes are proteins that leak out of injured myocardial cells through their damaged cell membranes into the bloodstream. Until the 1980s, the enzymes SGOT and LDH were used to assess cardiac injury. Now, the markers most widely used in detection of MI are MB subtype of the enzyme creatine kinase and cardiac troponins T and I as they are more specific for myocardial injury. The cardiac troponins T and I which are released within 4–6 hours of an attack of MI and remain elevated for up to 2 weeks, have nearly complete tissue specificity and are now the preferred markers for assessing myocardial damage. [ 14 ] Heart-type fatty acid binding protein is another marker, used in some home test kits.
Elevated troponins in the setting of chest pain may accurately predict a high likelihood of a myocardial infarction in the near future. [ 15 ] New markers such as glycogen phosphorylase isoenzyme BB are under investigation. [ 16 ] Note that only the cardiac troponins are used clinically for myocardial infarction as creatine kinase adds little value in diagnosing MI while adding to system cost. [ 17 ] [ 18 ] [ 19 ]
The diagnosis of myocardial infarction requires two out of three components (history, ECG, and enzymes). When damage to the heart occurs, levels of cardiac markers rise over time, which is why blood tests for them are taken over a 24-hour period. Because these enzyme levels are not elevated immediately following a heart attack, patients presenting with chest pain are generally treated with the assumption that a myocardial infarction has occurred and then evaluated for a more precise diagnosis. [ 20 ]
In difficult cases or in situations where intervention to restore blood flow is appropriate, coronary angiography can be performed. A catheter is inserted into an artery (typically the radial or femoral artery [ 21 ] ) and pushed to the vessels supplying the heart. A radio-opaque dye is administered through the catheter and a sequence of x-rays (fluoroscopy) is performed. Obstructed or narrowed arteries can be identified, and angioplasty applied as a therapeutic measure (see below). Angioplasty requires extensive skill, especially in emergency settings. It is performed by a physician trained in interventional cardiology . [ citation needed ]
Histopathological examination of the heart may reveal infarction at autopsy . Gross examination may reveal signs of myocardial infarction. [ citation needed ]
Under the microscope, myocardial infarction presents as a circumscribed area of ischemic, coagulative necrosis (cell death). On gross examination, the infarct is not identifiable within the first 12 hours. [ 22 ]
Although earlier changes can be discerned using electron microscopy , one of the earliest changes under a normal microscope are so-called wavy fibers . [ 23 ] Subsequently, the myocyte cytoplasm becomes more eosinophilic (pink) and the cells lose their transversal striations, with typical changes and eventually loss of the cell nucleus . [ 24 ] The interstitium at the margin of the infarcted area is initially infiltrated with neutrophils , then with lymphocytes and macrophages , who phagocytose ("eat") the myocyte debris. The necrotic area is surrounded and progressively invaded by granulation tissue , which will replace the infarct with a fibrous ( collagenous ) scar (which are typical steps in wound healing ). The interstitial space (the space between cells outside of blood vessels) may be infiltrated with red blood cells . [ 22 ]
These features can be recognized in cases where the perfusion was not restored; reperfused infarcts can have other hallmarks, such as contraction band necrosis . [ 25 ]
These tables gives an overview of the histopathology seen in myocardial infarction by time after obstruction. [ citation needed ]
Differential diagnoses for myocardial fibrosis:
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The Diagnostic Interview for Genetic Studies (DIGS) is a structured interview for psychiatric disorders designed by researchers from the National Institute of Mental Health , first published in 1991. Although most of the diagnoses were based on DSM-III-R criteria, the instrument was also able to generate diagnoses for certain disorders in other systems including DSM-IV , Research Diagnostic Criteria , ICD-10 and Feighner Criteria . This was possible because the instrument records symptoms in sufficient detail to allow different criteria to be applied. [ 1 ] [ 2 ] The DIGS interview has gone through a number of revisions since being published. [ 3 ] The latest version is DIGS 4.0/BP which was published in 2005. All DIGS versions are available to download from the NIMH Center for Collaborative Genomic Studies on Mental Disorders
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The Diagnostic and Statistical Manual of Mental Disorders ( DSM ; latest edition: DSM-5-TR , published in March 2022 [ 1 ] ) is a publication by the American Psychiatric Association (APA) for the classification of mental disorders using a common language and standard criteria. It is an internationally accepted manual on the diagnosis and treatment of mental disorders, though it may be used in conjunction with other documents. Other commonly used principal guides of psychiatry include the International Classification of Diseases (ICD), Chinese Classification of Mental Disorders (CCMD), and the Psychodynamic Diagnostic Manual . However, not all providers rely on the DSM-5 as a guide, since the ICD's mental disorder diagnoses are used around the world, [ 2 ] and scientific studies often measure changes in symptom scale scores rather than changes in DSM-5 criteria to determine the real-world effects of mental health interventions. [ 3 ] [ 4 ] [ 5 ] [ 6 ]
It is used by researchers, psychiatric drug regulation agencies, health insurance companies, pharmaceutical companies , the legal system, and policymakers. Some mental health professionals use the manual to determine and help communicate a patient's diagnosis after an evaluation. Hospitals, clinics, and insurance companies in the United States may require a DSM diagnosis for all patients with mental disorders. Health-care researchers use the DSM to categorize patients for research purposes.
The DSM evolved from systems for collecting census and psychiatric hospital statistics, as well as from a United States Army manual. Revisions since its first publication in 1952 have incrementally added to the total number of mental disorders , while removing those no longer considered to be mental disorders.
Recent editions of the DSM have received praise for standardizing psychiatric diagnosis grounded in empirical evidence, as opposed to the theory-bound nosology (the branch of medical science that deals with the classification of diseases ) used in DSM-III. [ citation needed ] However, it has also generated controversy and criticism , including ongoing questions concerning the reliability and validity of many diagnoses; the use of arbitrary dividing lines between mental illness and " normality "; possible cultural bias ; and the medicalization of human distress. [ 7 ] [ 8 ] [ 9 ] [ 10 ] [ 11 ] The APA itself has published that the inter-rater reliability is low for many disorders in the DSM-5, including major depressive disorder and generalized anxiety disorder . [ 12 ]
An alternate, widely used classification publication is the International Classification of Diseases (ICD), produced by the World Health Organization (WHO). [ 13 ] The ICD has a broader scope than the DSM, covering overall health as well as mental health; chapter 6 of the ICD specifically covers mental, behavioral and neurodevelopmental disorders. Moreover, while the DSM is the most popular diagnostic system for mental disorders in the US, the ICD is used more widely in Europe and other parts of the world, giving it a far larger reach than the DSM. An international survey of psychiatrists in sixty-six countries compared the use of the ICD-10 and DSM-IV. It found the former was more often used for clinical diagnosis while the latter was more valued for research. [ 14 ] This may be because the DSM tends to put more emphasis on clear diagnostic criteria, while the ICD tends to put more emphasis on clinician judgement and avoiding diagnostic criteria unless they are independently validated. That is, the ICD descriptions of psychiatric disorders tend to be more qualitative information, such as general descriptions of what various disorders tend to look like. The DSM focuses more on quantitative and operationalized criteria; e.g., to be diagnosed with X disorder, one must fulfill 5 of 9 criteria for at least 6 months. [ 15 ]
Since 1980, every code that has been listed in the DSM has been an ICD-9 code. However, DSM-5, unlike previous versions of DSM, contains both ICD-9 and ICD-10 codes. [ 16 ] [ 17 ] Though recent editions of the DSM and ICD have become more similar due to collaborative agreements, each one contains information absent from the other. [ 18 ] For instance, the two manuals contain overlapping but substantially different lists of recognized culture-bound syndromes . [ 19 ] [ needs update ] The ICD also tends to focus more on primary-care and low and middle-income countries, as opposed to the DSM's focus on secondary psychiatric care in high-income countries. [ 15 ]
The initial impetus for developing a classification of mental disorders in the United States was the need to collect statistical information. The first official attempt was the 1840 census , which used a single category: " idiocy / insanity ". Three years later, the American Statistical Association made an official protest to the U.S. House of Representatives , stating that "the most glaring and remarkable errors are found in the statements respecting nosology , prevalence of insanity, blindness, deafness, and dumbness, among the people of this nation", pointing out that in many towns African Americans were all marked as insane, and calling the statistics essentially useless. [ 20 ]
The Association of Medical Superintendents of American Institutions for the Insane ("The Superintendents' Association") was formed in 1844. [ 21 ]
In 1860, during the international statistical congress held in London, Florence Nightingale made a proposal that was to result in the development of the first international model of systematic collection of hospital data. [ citation needed ]
In 1872, the American Medical Association (AMA) published its Nomenclature of Diseases , which included various "Disorders of the Intellect". [ 22 ] Its use was short-lived however. [ 23 ]
Edward Jarvis and later Francis Amasa Walker helped expand the census, from two volumes in 1870 to twenty-five volumes in 1880. [ 24 ]
In 1888, the Census Office published Frederick H. Wines' 582-page volume called Report on the Defective, Dependent, and Delinquent Classes of the Population of the United States, As Returned at the Tenth Census (June 1, 1880) . Wines used seven categories of mental illness, which were also adopted by the Superintendents: dementia , dipsomania (uncontrollable craving for alcohol), epilepsy , mania , melancholia , monomania , and paresis . [ 25 ]
In 1892, the Superintendents' Association expanded its membership to include other mental health workers, and renamed to the American Medico-Psychological Association (AMPA). [ 26 ]
In 1893, a French physician, Jacques Bertillon , introduced the Bertillon Classification of Causes of Death at a congress of the International Statistical Institute (ISI) in Chicago. [ 27 ] [ 28 ] (The ISI had commissioned him to create it in 1891). [ 28 ] A number of countries adopted the ISI's system. In 1898, the American Public Health Association (APHA) recommended that United States registrars also adopt the system. [ 28 ]
In 1900, an ISI conference in Paris reformed the Bertillion Classification, and created the International List of Causes of Death (ILCD) . [ 28 ] Another conference would be held every ten years, and a new edition of the ILCD would be released. Five were ultimately issued. Non-fatal conditions were not included.
In 1903, New York's Bellevue Hospital published "The Bellevue Hospital nomenclature of diseases and conditions", which included a section on "Diseases of the Mind". Revisions were released in 1909 and 1911. It was produced with the assistance of the AMA and Bureau of the Census. [ 29 ]
In 1917, together with the National Commission on Mental Hygiene (now Mental Health America ), the American Medico-Psychological Association developed a new guide for mental hospitals called the Statistical Manual for the Use of Institutions for the Insane . This guide included twenty-two diagnoses. It would be revised several times by the Association, and by the tenth edition in 1942, was titled Statistical Manual for the Use of Hospitals of Mental Diseases . [ 30 ] [ 31 ]
In 1921, the AMPA became the present American Psychiatric Association (APA). [ 32 ]
The first edition of the DSM notes in its foreword: "In the late twenties, each large teaching center employed a system of its own origination, no one of which met more than the immediate needs of the local institution." [ 33 ]
In 1933, the AMA's general medical guide the Standard Classified Nomenclature of Disease , (referred to as the Standard), was released. [ 34 ] Along with the New York Academy of Medicine , the APA provided the psychiatric nomenclature subsection. [ 35 ] It became well adopted in the US within two years. [ 33 ] A major revision of the Statistical Manual was made in 1934, to bring it in line with the new Standard. [ 33 ] A number of revisions of the Standard were produced, with the last in 1961. [ 36 ]
World War II saw the large-scale involvement of U.S. psychiatrists in the selection, processing, assessment, and treatment of soldiers. [ 37 ] This moved the focus away from mental institutions and traditional clinical perspectives. The U.S. armed forces initially used the Standard, but found it lacked appropriate categories for many common conditions that troubled troops. The United States Navy made some minor revisions but "the Army established a much more sweeping revision, abandoning the basic outline of the Standard and attempting to express present-day concepts of mental disturbance." [ 33 ]
Under the direction of James Forrestal , [ 38 ] a committee headed by psychiatrist Brigadier General William C. Menninger , with the assistance of the Mental Hospital Service, [ 39 ] developed a new classification scheme in 1944 and 1945.
Issued in War Department Technical Bulletin, Medical, 203 (TB MED 203); Nomenclature and Method of Recording Diagnoses was released shortly after the war in October 1945 under the auspices of the Office of the Surgeon General . [ 40 ] It was reprinted in the Journal of Clinical Psychology for civilian use in July 1946 with the new title Nomenclature of Psychiatric Disorders and Reactions . [ 41 ] This system came to be known as "Medical 203".
This nomenclature eventually was adopted by all the armed forces, and "assorted modifications of the Armed Forces nomenclature [were] introduced into many clinics and hospitals by psychiatrists returning from military duty." [ 33 ] The Veterans Administration also adopted a slightly modified version of the standard in 1947. [ 38 ]
The further developed Joint Armed Forces Nomenclature and Method of Recording Psychiatric Conditions was released in 1949. [ 42 ]
In 1948, the newly formed World Health Organization took over the maintenance of the ILCD. They greatly expanded it, included non-fatal conditions for the first time, and renamed it the International Statistical Classification of Diseases (ICD). The foreword to the DSM-I states the ICD-6 "categorized mental disorders in rubrics similar to those of the Armed Forces nomenclature." [ 33 ]
The APA Committee on Nomenclature and Statistics was empowered to develop a version of Medical 203 specifically for use in the United States, to standardize the diverse and confused usage of different documents. In 1950, the APA committee undertook a review and consultation. It circulated an adaptation of Medical 203, the Standard ' s nomenclature, and the VA system's modifications of the Standard to approximately 10% of APA members. 46% of members replied, with 93% approving the changes. After some further revisions, the Diagnostic and Statistical Manual of Mental Disorders was approved in 1951 and published in 1952. The structure and conceptual framework were the same as in Medical 203, and many passages of text were identical. [ 40 ] The manual was 130 pages long and listed 106 mental disorders. [ 43 ] These included several categories of "personality disturbance", generally distinguished from "neurosis" (nervousness, egodystonic ). [ 44 ]
The foreword to this edition describes itself as being a continuation of the Statistical Manual for the Use of Hospitals of Mental Diseases. [ 33 ] Each item was given an ICD-6 equivalent code, where applicable.
The DSM-I centers on three classes of symptoms: psychotic, neurotic, and behavioral. [ 45 ] Within each class of mental disorder, classifying information is provided to differentiate conditions with similar symptoms. Under each broad class of disorder (e.g. "Psychoneurotic Disorders" or "Personality Disorders"), all possible diagnoses are listed, generally from least to most severe. [ 45 ] The 1952 DSM version also includes sections detailing how to record patients' disorders along with their demographic details. [ 45 ] The form includes information like a patient's area of residence, admission status, discharge date/condition, and severity of disorder. [ 45 ] See Figure 1. for the form that psychiatrists were asked to utilize for recording preliminary diagnostic information. [ 45 ]
Furthermore, the APA listed homosexuality in the DSM as a sociopathic personality disturbance. Homosexuality: A Psychoanalytic Study of Male Homosexuals , a large-scale 1962 study of homosexuality by Irving Bieber and other authors, was used to justify inclusion of the disorder as a supposed pathological hidden fear of the opposite sex caused by traumatic parent–child relationships. This view was influential in the medical profession. [ 46 ] In 1956, however, the psychologist Evelyn Hooker performed a study comparing the happiness and well-adjusted nature of self-identified homosexual men with heterosexual men and found no difference. [ 46 ] Her study stunned the medical community and made her a heroine to many gay men and lesbians, [ 47 ] but homosexuality remained in the DSM until May 1974. [ 48 ]
In the 1960s, there were many challenges to the concept of mental illness itself. These challenges came from psychiatrists like Thomas Szasz , who argued mental illness was a myth used to disguise moral conflicts; from sociologists such as Erving Goffman , who said mental illness was another example of how society labels and controls non-conformists; from behavioural psychologists who challenged psychiatry's fundamental reliance on unobservable phenomena; and from gay rights activists who criticised the APA's listing of homosexuality as a mental disorder.
The APA was closely involved in the next significant revision of the mental disorder section of the ICD (version 8 in 1968). It decided to go ahead with a revision of the DSM, which was published in 1968. DSM-II was similar to DSM-I, listed 182 disorders, and was 134 pages long. The term "reaction" was dropped, but the term " neurosis " was retained. Both the DSM-I and the DSM-II reflected the predominant psychodynamic psychiatry, [ 49 ] although both manuals also included biological perspectives and concepts from Kraepelin 's system of classification. Symptoms were not specified in detail for specific disorders. Many were seen as reflections of broad underlying conflicts or maladaptive reactions to life problems that were rooted in a distinction between neurosis and psychosis (roughly, anxiety/depression broadly in touch with reality, as opposed to hallucinations or delusions disconnected from reality). Sociological and biological knowledge was incorporated, under a model that did not emphasize a clear boundary between normality and abnormality. [ 50 ] The idea that personality disorders did not involve emotional distress was discarded. [ 44 ]
A study published in Science in 1973, the Rosenhan experiment , received much publicity and was viewed as an attack on the efficacy of psychiatric diagnosis. [ 51 ] An influential 1974 paper by Robert Spitzer and Joseph L. Fleiss demonstrated that the second edition of the DSM (DSM-II) was an unreliable diagnostic tool. [ 52 ] Spitzer and Fleiss found that different practitioners using the DSM-II rarely agreed when diagnosing patients with similar problems. In reviewing previous studies of eighteen major diagnostic categories, Spitzer and Fleiss concluded that "there are no diagnostic categories for which reliability is uniformly high. Reliability appears to be only satisfactory for three categories: mental deficiency, organic brain syndrome (but not its subtypes), and alcoholism. The level of reliability is no better than fair for psychosis and schizophrenia and is poor for the remaining categories". [ 51 ]
As described by Ronald Bayer, a psychiatrist and gay rights activist, specific protests by gay rights activists against the APA began in 1970, when the organization held its convention in San Francisco . The activists disrupted the conference by interrupting speakers and shouting down and ridiculing psychiatrists who viewed homosexuality as a mental disorder. In 1971, gay rights activist Frank Kameny worked with the Gay Liberation Front collective to demonstrate at the APA's convention. At the 1971 conference, Kameny grabbed the microphone and yelled: "Psychiatry is the enemy incarnate. Psychiatry has waged a relentless war of extermination against us. You may take this as a declaration of war against you." [ 53 ]
This gay activism occurred in the context of a broader anti-psychiatry movement that had come to the fore in the 1960s and was challenging the legitimacy of psychiatric diagnosis. Anti-psychiatry activists protested at the same APA conventions, with some shared slogans and intellectual foundations as gay activists. [ 54 ] [ 55 ]
Taking into account data from researchers such as Alfred Kinsey and Evelyn Hooker , the seventh printing of the DSM-II, in 1974, no longer listed homosexuality as a category of disorder. [ a ] After a vote by the APA trustees in 1973, and confirmed by the wider APA membership in 1974, the diagnosis was replaced with the category of "sexual orientation disturbance". [ 56 ] [ 57 ]
The emergence of DSM-III represented a "quantum leap" in terms of the scale and reach of the manual. [ 58 ] In 1974, the decision to revise the DSM was made, and psychiatrist Robert Spitzer was selected as chair of the task force. The initial impetus was to make the DSM nomenclature consistent with that of the International Classification of Diseases (ICD). The revision took on a far wider mandate under the influence and control of Spitzer and his chosen committee members. [ 59 ] One added goal was to improve the uniformity and validity of psychiatric diagnosis in the wake of a number of critiques, including the famous Rosenhan experiment . There was also felt a need to standardize diagnostic practices within the United States and with other countries, after research showed that psychiatric diagnoses differed between Europe and the United States. [ 60 ] The establishment of consistent criteria was an attempt to facilitate the pharmaceutical regulatory process.
The criteria adopted for many of the mental disorders were influenced by the Research Diagnostic Criteria (RDC) and Feighner Criteria , which had just been developed by a group of research-orientated psychiatrists based primarily at Washington University School of Medicine and the New York State Psychiatric Institute . However, the influence of clinical psychiatrists, themselves often working with psychoanalytic ideas, were still strong. [ 61 ] Other criteria, and potential new categories of disorder, were established by debate, argument and consensus during meetings of the committee chaired by Spitzer. A key aim was to base categorization on colloquial English (which would be easier to use by federal administrative offices), rather than by assumption of cause, although its categorical approach still assumed each particular pattern of symptoms in a category reflected a particular underlying pathology (an approach described as " neo-Kraepelinian "). The psychodynamic view was marginalised, although still influential, in favor of a regulatory or legislative model that emphasised observable symptoms. [ 61 ] A new "multiaxial" system attempted to yield a picture more amenable to a statistical population census, rather than a simple diagnosis . Spitzer argued "mental disorders are a subset of medical disorders", but the task force decided on this statement for the DSM: "Each of the mental disorders is conceptualized as a clinically significant behavioral or psychological syndrome." [ 49 ] Personality disorders were placed on axis II along with "mental retardation". [ 44 ]
The first draft of DSM-III was ready within a year. It introduced many new categories of disorder, while deleting or changing others. A number of unpublished documents discussing and justifying the changes have recently come to light. [ 62 ] Field trials sponsored by the U.S. National Institute of Mental Health (NIMH) were conducted between 1977 and 1979 to test the reliability of the new diagnoses. A controversy emerged regarding deletion of the concept of neurosis, a mainstream of psychoanalytic theory and therapy but seen as vague and unscientific by the DSM task force. Faced with enormous political opposition, DSM-III was in serious danger of not being approved by the APA Board of Trustees unless "neurosis" was included in some form; a political compromise reinserted the term in parentheses after the word "disorder" in some cases. Additionally, the diagnosis of ego-dystonic homosexuality replaced the DSM-II category of "sexual orientation disturbance". The gender identity disorder in children (GIDC) diagnosis was introduced in the DSM-III; prior to the DSM-III's publication in 1980, there was no diagnostic criteria for gender dysphoria . [ 63 ] [ 64 ]
Finally published in 1980, DSM-III listed 265 diagnostic categories and was 494 pages long. It rapidly came into widespread international use and has been termed a revolution, or transformation, in psychiatry. [ 49 ] [ 50 ]
When DSM-III was published, the developers made extensive claims about the reliability of the radically new diagnostic system they had devised, which relied on data from special field trials. However, according to a 1994 article by Stuart A. Kirk :
Twenty years after the reliability problem became the central focus of DSM-III, there is still not a single multi-site study showing that DSM (any version) is routinely used with high reliably by regular mental health clinicians. Nor is there any credible evidence that any version of the manual has greatly increased its reliability beyond the previous version. There are important methodological problems that limit the generalizability of most reliability studies. Each reliability study is constrained by the training and supervision of the interviewers, their motivation and commitment to diagnostic accuracy, their prior skill, the homogeneity of the clinical setting in regard to patient mix and base rates, and the methodological rigor achieved by the investigator ... [ 51 ]
In 1987, DSM-III-R was published as a revision of the DSM-III, under the direction of Spitzer. Categories were renamed and reorganized, with significant changes in criteria. Six categories were deleted while others were added. Controversial diagnoses, such as Premenstrual Dysphoric Disorder and Masochistic Personality Disorder , were considered and discarded. (Premenstrual Dysphoric Disorder was later reincorporated in the DSM-5, published in 2013). [ 65 ] "Ego-dystonic homosexuality" was also removed and was largely subsumed under "sexual disorder not otherwise specified", which could include "persistent and marked distress about one's sexual orientation." [ 49 ] [ 66 ] Altogether, the DSM-III-R contained 292 diagnoses and was 567 pages long. Further efforts were made for the diagnoses to be purely descriptive, although the introductory text stated for at least some disorders, "particularly the Personality Disorders, the criteria require much more inference on the part of the observer"[page xxiii]. [ 44 ]
In 1994, DSM-IV was published, listing 410 disorders in 886 pages. The task force was chaired by Allen Frances and was overseen by a steering committee of twenty-seven people, including four psychologists. The steering committee created thirteen work groups of five to sixteen members, each work group having about twenty advisers in addition. The work groups conducted a three-step process: first, each group conducted an extensive literature review of their diagnoses; then, they requested data from researchers, conducting analyses to determine which criteria required change, with instructions to be conservative; finally, they conducted multi-center field trials relating diagnoses to clinical practice. [ 67 ] [ 68 ] A major change from previous versions was the inclusion of a clinical-significance criterion to almost half of all the categories, which required symptoms causing "clinically significant distress or impairment in social, occupational, or other important areas of functioning". Some personality-disorder diagnoses were deleted or moved to the appendix. [ 44 ]
The DSM-IV characterizes a mental disorder as "a clinically significant behavioral or psychological syndrome or pattern that occurs in an individual and that is associated with present distress or disability or with a significant increased risk of suffering death, pain, disability, or an important loss of freedom". [ 69 ] It also notes that "although this manual provides a classification of mental disorders it must be admitted that no definition adequately specifies precise boundaries for the concept of 'mental disorder." [ 70 ]
The DSM-IV is a categorical classification system. The categories are prototypes, and a patient with a close approximation to the prototype is said to have that disorder. DSM-IV states, "there is no assumption each category of mental disorder is a completely discrete entity with absolute boundaries" but isolated, low-grade, and non-criterion (unlisted for a given disorder) symptoms are not given importance. [ 71 ] Qualifiers are sometimes used: for example, to specify mild, moderate, or severe forms of a disorder. For nearly half the disorders, symptoms must be sufficient to cause "clinically significant distress or impairment in social, occupational, or other important areas of functioning", although DSM-IV-TR removed the distress criterion from tic disorders and several of the paraphilias due to their egosyntonic nature. Each category of disorder has a numeric code taken from the ICD coding system , used for health service (including insurance) administrative purposes.
The DSM-IV was organized into a five-part axial system: [ 72 ]
The DSM-IV does not specifically cite its sources, but there are four volumes of "sourcebooks" intended to be APA's documentation of the guideline development process and supporting evidence, including literature reviews, data analyses, and field trials. [ 73 ] [ 74 ] [ 75 ] [ 76 ] The sourcebooks have been said to provide important insights into the character and quality of the decisions that led to the production of DSM-IV, and the scientific credibility of contemporary psychiatric classification. [ 77 ] [ 78 ]
A text revision of DSM-IV, titled DSM-IV-TR, was published in 2000. The diagnostic categories were unchanged as were the diagnostic criteria for all but nine diagnoses. [ 79 ] The majority of the text was unchanged; however, the text of two disorders, pervasive developmental disorder not otherwise specified and Asperger's disorder, had significant and/or multiple changes made. The definition of pervasive developmental disorder not otherwise specified was changed back to what it was in DSM-III-R and the text for Asperger's disorder was practically entirely rewritten. Most other changes were to the associated features sections of diagnoses that contained additional information such as lab findings, demographic information, prevalence, and course. Also, some diagnostic codes were changed to maintain consistency with ICD-9-CM. [ 80 ]
The fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM), the DSM-5 , was approved by the Board of Trustees of the APA on December 1, 2012. [ 81 ] Published on May 18, 2013, [ 82 ] the DSM-5 contains extensively revised diagnoses and, in some cases, broadens diagnostic definitions while narrowing definitions in other cases. [ 83 ] The DSM-5 is the first major edition of the manual in 20 years. [ 84 ] DSM-5, and the abbreviations for all previous editions, are registered trademarks owned by the American Psychiatric Association. [ 8 ] [ 85 ]
A significant change in the fifth edition is the deletion of the subtypes of schizophrenia : paranoid , disorganized , catatonic , undifferentiated , and residual . [ 86 ] The deletion of the subsets of autistic spectrum disorder – namely, Asperger's syndrome , classic autism , Rett syndrome , childhood disintegrative disorder and pervasive developmental disorder not otherwise specified – was also implemented, with specifiers regarding intensity: mild, moderate, and severe.
Severity is based on social communication impairments and restricted, repetitive patterns of behavior, with three levels:
During the revision process, the APA website periodically listed several sections of the DSM-5 for review and discussion. [ 87 ]
The National Board of Medical Examiners (NBME), which is responsible for creating and publishing board exams for medical students around the United States, conforms to the use of DSM-5 criteria. [ 88 ]
After the release of the fifth edition, the APA communicated that they intended to add subsequent revisions more often, to keep up with research in the field. [ 89 ] It is notable that DSM-5 uses Arabic rather than Roman numerals . Beginning with DSM-5, the APA planned to use decimals to identify incremental updates (e.g., DSM-5.1, DSM-5.2) [ b ] and whole numbers for new editions (e.g., DSM-5, DSM-6), [ 90 ] similar to the scheme used for software versioning .
A revision of DSM-5, titled DSM-5-TR, was published in March 2022, updating diagnostic criteria and ICD-10-CM codes. [ 91 ] The diagnostic criteria for avoidant/restrictive food intake disorder was changed, [ 92 ] along with adding entries for prolonged grief disorder , unspecified mood disorder and stimulant-induced mild neurocognitive disorder . [ 93 ] [ 94 ] Prolonged grief disorder, which had been present in the ICD-11, had criteria agreed upon by consensus in a one day in-person workshop sponsored by the APA. [ 92 ] A 2022 study found that higher rates of diagnosis of prolonged grief disorder in the ICD-11 could be explained by the DSM-5-TR criteria requiring symptoms persist for 12 months, and the ICD-11 requiring only 6 months. [ 95 ]
Three review groups for sex and gender, culture and suicide, along with an "ethnoracial equity and inclusion work group" were involved in the creation of the DSM-5-TR which led to additional sections for each mental disorder discussing sex and gender, racial and cultural variations, and adding diagnostic codes for specifying levels of suicidality and nonsuicidal self-injury for mental disorders. [ 93 ] [ 92 ]
Other changed disorders included: [ 96 ]
The APA have supplemented the DSM with supporting works, collectively forming the "DSM Library." [ 97 ] As of 2022, the other books in the library are "DSM-5 Handbook of Differential Diagnosis", "DSM-5 Clinical Cases", "DSM-5 Handbook on the Cultural Formulation Interview" and "Guía De Consulta De Los Criterios Diagnósticos Del DSM-5". [ 97 ]
Many criticisms have been leveled against the DSM and its usefulness as a diagnostic manual.
The revisions of the DSM from the 3rd Edition forward have been mainly concerned with diagnostic reliability – the degree to which different diagnosticians agree on a diagnosis. Henrik Walter argued that psychiatry as a science can only advance if diagnosis is reliable. If clinicians and researchers frequently disagree about the diagnosis of a patient, then research into the causes and effective treatments of those disorders cannot advance. Hence, diagnostic reliability was a major concern of DSM-III. When the diagnostic reliability problem was thought to be solved, subsequent editions of the DSM were concerned mainly with "tweaking" the diagnostic criteria. Neither the issue of reliability or validity was settled. [ 98 ] [ 99 ]
In 2013, shortly before the publication of DSM-5, the director of the National Institute of Mental Health (NIMH), Thomas R. Insel , declared that the agency would no longer fund research projects that relied exclusively on DSM diagnostic criteria, due to its lack of validity. [ 100 ] Insel questioned the validity of the DSM classification scheme because "diagnoses are based on a consensus about clusters of clinical symptoms" as opposed to "collecting the genetic, imaging, physiologic, and cognitive data to see how all the data – not just the symptoms – cluster and how these clusters relate to treatment response." [ 101 ] [ 102 ]
Field trials of DSM-5 brought the debate of reliability back into the limelight, as the diagnoses of some disorders showed poor reliability. For example, a diagnosis of major depressive disorder , a common mental illness, had a poor reliability kappa statistic of 0.28, indicating that clinicians frequently disagreed on diagnosing this disorder in the same patients. The most reliable diagnosis was major neurocognitive disorder, with a kappa of 0.78. [ 103 ]
By design, the DSM is primarily concerned with the signs and symptoms of mental disorders, rather than the underlying causes. It claims to collect these disorders based on statistical or clinical patterns. As such, it has been compared to a naturalist's field guide to birds, with similar advantages and disadvantages. [ 104 ] The lack of a causative or explanatory basis, however, is not specific to the DSM, but rather reflects a general lack of pathophysiological understanding of psychiatric disorders. Proponents argue this absence of explanatory classification is necessary, but it presents a problem for researchers as it results in the grouping of individuals who may have little in common except superficial criteria. [ 8 ] [ 105 ] As DSM-III chief architect Robert Spitzer and DSM-IV editor Michael First outlined in 2005, "little progress has been made toward understanding the pathophysiological processes and cause of mental disorders. If anything, the research has shown the situation is even more complex than initially imagined, and we believe not enough is known to structure the classification of psychiatric disorders according to etiology." [ 106 ]
While there is generally a lack of consensus on underlying causation for most psychiatric disorders, some proponents of specific psychopathological paradigms have faulted the DSM for failing to incorporate evidence from other disciplines. For instance, evolutionary psychology distinguishes between genuine cognitive malfunctions and malfunctions due to psychological adaptations (that is learned behaviors may be adaptive in one context but maladaptive in another). However, this distinction is one that is challenged within general psychology. [ 107 ] [ 108 ] [ 109 ]
There is also criticism of the strong operationalist viewpoint of the DSM. The DSM relies on operational definitions , which means that intuitive concepts like depression are defined by specific measurable criteria (observable behavior, specific timelines). Some have argued that instead of replacing metaphysical terms like "desire" or "purpose" the DSM chose to legitimize them by giving them operational definitions. However, this may have served only to provide a "reassurance fetish" for mainstream methodological practice, rather than representing a substantial and meaningful alteration of mainstream psychiatric practice. [ 110 ]
A central problem with the use of superficial symptoms is that psychiatry deals with the phenomena of consciousness , which adds much more complexity than the somatic symptoms and signs used by most of medicine. A 2013 review published in the European Archives of Psychiatry and Clinical Neuroscience gives the example of the problem of superficial characterization of psychiatric signs and symptoms. If a patient says they "feel depressed, sad, or down" there are actually a wide variety of underlying experiences they could be referencing: "not only depressed mood but also, for instance, irritation , anger , loss of meaning, varieties of fatigue , ambivalence , ruminations of different kinds, hyper-reflectivity, thought pressure, psychological anxiety , varieties of depersonalization , and even voices with negative content, and so forth." This criticism is especially pertinent to the structured interview , as simple "yes or no" questions may not be specific enough to truly confirm or deny the diagnostic criterion at issue. That is, whether a patient says yes or no will rely on their own understanding of the meaning of the various words in the question as well as their own interpretation of their experience. There is thus danger in being overconfident in the face value of the answers. The authors of the 2013 review give an example: A patient who was being administered the Structured Clinical Interview for the DSM-IV Axis I Disorders denied thought insertion , but during a "conversational, phenomenological interview", a semi-structured interview tailored to the patient, the same patient admitted to experiencing thought insertion , along with a delusional elaboration . The authors suggested 2 reasons for this discrepancy: either the patient did not "recognize his own experience in the rather blunt, implicitly either/or formulation of the structured-interview question", or the experience did not "fully articulate itself" until the patient started talking about his experiences. [ 111 ]
The DSM-5 has been criticized for overlooking capitalism ’s interconnectivity with pathology. [ 112 ] One example is the development and treatment of diagnoses: around 69% of psychiatrists involved in the development of the DSM-5 were reported to have financial ties to the pharmaceutical industry . [ 113 ] These ties situate many care services within the medical-industrial complex , a framework that prioritizes profit instead of the care of individuals. [ 114 ] Lane found the medical-industrial complex intertwined with setting the parameters to diagnose conditions such as social anxiety disorder . [ 115 ] Other authors have supported similar findings. [ 116 ] [ 117 ] Kincaid and Sullivan estimate that the cost of the industry surrounding diagnosis will rise to around six trillion dollars by 2030. [ 118 ]
Scholars differ in the extent of capitalism 's influence on diagnosis. Davies supports the social model of disability in explaining that diagnosis at present relies on considering conditions a consequence of a “broken brain.” [ 119 ] His wider logic on mental illness in response to societal issues problematizes diagnosis as a tool of the medical-industrial complex . [ 119 ] His previous book, Cracked , demonstrates the market interactions within the medical-industrial complex , as diagnosis becomes a source for monetization. [ 120 ]
Others find that the dependency of patients on their psychiatric care providers makes the industry vulnerable to economic exploitation under capitalism . [ 121 ] These individuals argue that diagnosis is manipulated, but not caused, by capitalistic forces. [ 121 ] Academics have critiqued the directness of the association between the medical model , capitalism , and diagnosis, but generally agree that characteristics of the capitalist system contribute to poor mental health . [ 122 ]
Diagnoses of mental conditions have been used to obscure institutional practices of discrimination . [ 123 ] Late nineteenth-century diagnoses of white women with hysteria , for instance, were said to be caused by “overcivilization,” shaped by racially discriminatory Social Darwinism . [ 124 ] Similarly, American physician Samuel Cartwright coined " drapetomania " in 1851 as a mental condition which "caused" slaves to escape captivity. [ 125 ] In the present day, Brinkmann finds that “contemporary diagnostic cultures,” whereby humans assess their conditions through a psychiatric lens, can “risk losing sight of the larger historical and social forces that affect [their] lives.” [ 126 ] Contemporary diagnostic cultures help explain how diagnosis reflect larger historical biases. [ 126 ] [ 127 ]
Critics have argued that the DSM-5's criteria pathologize a wide range of people with distress or impairment. Chapman et al. discuss the implications for obscuring distress in the incarceration and confinement of "intellectually disabled" populations; they argue that "differentiation based on psychiatric and intellectual disability " is arbitrarily set and altered based on capitalism 's needs for "mobile and free workers." [ 128 ] Metzl demonstrates that the shifting diagnostic parameters of schizophrenia became a method for institutionalizing Black men during the Civil Rights Movement . [ 127 ] In sum, those who have experienced “domination” or “exploitation” based on an identity trait are more likely to be pathologized through diagnosis. [ 129 ]
Allen Frances , an outspoken critic of DSM-5, states that "normality is an endangered species," because of "fad diagnoses" and an "epidemic" of over-diagnosing, and suggests that the "DSM-5 threatens to provoke several more [epidemics]." [ 130 ] [ 131 ] Some researchers state that changes in diagnostic criteria, following each published version of the DSM, reduce thresholds for a diagnosis, which results in increases in prevalence rates for ADHD and autism spectrum disorder . [ 132 ] [ 133 ] [ 134 ] [ 135 ] Bruchmüller, et al. (2012) suggest that as a factor that may lead to overdiagnosis are situations when the clinical judgment of the diagnostician regarding a diagnosis (ADHD) is affected by heuristics . [ 133 ]
Despite caveats in the introduction to the DSM, it has long been argued that its system of classification makes unjustified categorical distinctions between disorders and uses arbitrary cut-offs between normal and abnormal. A 2009 psychiatric review noted that attempts to demonstrate natural boundaries between related DSM syndromes , or between a common DSM syndrome and normality, have failed. [ 8 ] Some argue that rather than a categorical approach, a fully dimensional, spectrum or complaint-oriented approach would better reflect the evidence. [ 136 ] [ 137 ] [ 138 ]
In addition, it is argued that the current approach based on exceeding a threshold of symptoms does not adequately take into account the context in which a person is living, and to what extent there is internal disorder of an individual versus a psychological response to adverse situations. [ 139 ] The DSM does include a step ("Axis IV") for outlining "Psychosocial and environmental factors contributing to the disorder" once someone is diagnosed with that particular disorder.
Because an individual's degree of impairment is often not correlated with symptom counts and can stem from various individual and social factors, the DSM's standard of distress or disability can often produce false positives. [ 140 ] On the other hand, individuals who do not meet symptom counts may nevertheless experience comparable distress or disability in their life.
Psychiatrists have argued that published diagnostic standards rely on an exaggerated interpretation of neurophysiological findings and so understate the scientific importance of social-psychological variables. [ 141 ] Advocating a more culturally sensitive approach to psychology, critics such as Carl Bell and Marcello Maviglia contend that researchers and service-providers often discount the cultural and ethnic diversity of individuals. [ 142 ] In addition, current diagnostic guidelines have been criticized [ 143 ] as having a fundamentally Euro-American outlook. Although these guidelines have been widely implemented, opponents argue that even when a diagnostic criterion-set is accepted across different cultures, it does not necessarily indicate that the underlying constructs have any validity within those cultures; even reliable application can only demonstrate consistency, not legitimacy. [ 141 ] Cross-cultural psychiatrist Arthur Kleinman contends that Western bias is ironically illustrated in the introduction of cultural factors to the DSM-IV: the fact that disorders or concepts from non-Western or non-mainstream cultures are described as "culture-bound", whereas standard psychiatric diagnoses are given no cultural qualification whatsoever, is to Kleinman revelatory of an underlying assumption that Western cultural phenomena are universal. [ 144 ] Other cross-cultural critics largely share Kleinman's negative view toward the culture-bound syndrome , common responses included both disappointment over the large number of documented non-Western mental disorders still left out, and frustration that even those included were often misinterpreted or misrepresented. [ 145 ] [ page needed ]
Mainstream psychiatrists have also been dissatisfied with these new culture-bound diagnoses, although not for the same reasons. Robert Spitzer, a lead architect of DSM-III, has held the opinion that the addition of cultural formulations was an attempt to placate cultural critics, and that they lack any scientific motivation or support. Spitzer also posits that the new culture-bound diagnoses are rarely used in practice, maintaining that the standard diagnoses apply regardless of the culture involved. In general, the mainstream psychiatric opinion remains that if a diagnostic category is valid, cross-cultural factors are either irrelevant or are only significant to specific symptom presentations. [ 141 ]
Historically, the DSM tended to avoid issues involving religion ; the DSM-5 relaxed this attitude somewhat. [ 146 ]
There was extensive analysis and comment on DSM-IV (published in 1994) in the years leading up to the 2013 publication of DSM-5. It was alleged that the way the categories of DSM-IV were structured, as well as the substantial expansion of the number of categories within it, represented increasing medicalization of human nature, very possibly attributable to disease mongering by psychiatrists and pharmaceutical companies , the power and influence of the latter having grown dramatically in recent decades. [ 147 ] In 2005, then APA President Steven Sharfstein released a statement in which he conceded that psychiatrists had "allowed the biopsychosocial model to become the bio-bio-bio model". [ 148 ] It was reported that of the authors who selected and defined the DSM-IV psychiatric disorders, roughly half had financial relationships with the pharmaceutical industry during the period 1989–2004, raising the prospect of a direct conflict of interest . The same article concluded that the connections between panel members and the drug companies were particularly strong involving those diagnoses where drugs are the first line of treatment, such as schizophrenia and mood disorders, where 100% of the panel members had financial ties with the pharmaceutical industry.
William Glasser referred to DSM-IV as having "phony diagnostic categories", arguing that "it was developed to help psychiatrists – to help them make money". [ 149 ] A 2012 article in The New York Times commented sharply that DSM-IV (then in its 18th year), through copyrights held closely by the APA, had earned the Association over $100 million. [ 150 ]
However, although the number of identified diagnoses had increased by more than 200% (from 106 in DSM-I to 365 in DSM-IV-TR), psychiatrists such as Zimmerman and Spitzer argued that this almost entirely represented greater specification of the forms of pathology, thereby allowing better grouping of similar patients. [ 8 ]
A core function of the DSM is the categorization of people's experiences into diagnoses based on symptoms. However, there is disagreement about the use of diagnoses as labels. Some individuals are relieved to find they have a recognized condition that they can apply a name to, and this has led to many people self-diagnosing . [ 151 ] Others, however, question the accuracy of diagnosis, or feel they have been given a label that invites social stigma and discrimination (the terms " mentalism " and "sanism" have been used to describe such discriminatory treatment). [ 152 ]
Diagnoses can become internalized and affect an individual's self-identity , and some psychotherapists have found that the healing process can be inhibited and symptoms can worsen as a result. [ 153 ] Some members of the psychiatric survivors movement (more broadly the consumer/survivor/ex-patient movement) actively campaign against their diagnoses, or the assumed implications, or against the DSM system in general. [ 154 ] [ 155 ] Additionally, it has been noted that the DSM often uses definitions and terminology that are inconsistent with a recovery model , and such content can erroneously imply excess psychopathology (e.g. multiple " comorbid " diagnoses) or chronicity . [ 155 ]
Psychiatrist Allen Frances has been critical of proposed revisions to the DSM–5. In a 2012 New York Times editorial, Frances warned that if this DSM version is issued unamended by the APA, "it will medicalize normality and result in a glut of unnecessary and harmful drug prescription." [ 156 ]
In a December 2012, blog post on Psychology Today , Frances provides his "list of DSM 5's ten most potentially harmful changes:" [ 157 ]
A group of 25 psychiatrists and researchers, among whom were Frances and Thomas Szasz , have published debates on what they see as the six most essential questions in psychiatric diagnosis: [ 158 ]
In 2011, psychologist Brent Robbins co-authored a national letter for the Society for Humanistic Psychology that has brought thousands into the public debate about the DSM. Over 15,000 individuals and mental health professionals have signed a petition in support of the letter. [ 159 ] Thirteen other APA divisions have endorsed the petition. [ 159 ] Robbins has noted that under the new guidelines, certain responses to grief could be labeled as pathological disorders, instead of being recognized as being normal human experiences. [ 160 ]
There are several works written in recent years by scholars of the disabled community that specifically critique the cultural impact of the DSM-5. These pieces criticize the DSM-5 from different cultural perspectives, integrating the experiences of disabled people identifying as crip , feminists , Asian Americans , Black Americans and other marginalized viewpoints.
DSM CRIP is a collection of essays by various authors that explore the critiques of the DSM-5 from feminist and crip perspectives. These essays tackle the critiques of the DSM using specific diagnoses such as gender dysphoria , transvestic disorder , complex somatic symptom disorder , hypoactive sexual desire disorder, schizophrenia and autism. These are used as case studies to tackle the topics of the potential harm of labels, overmedicalization , overdiagnosis , pathologizing normality and various other critiques informed by the feminist and crip lens. [ 161 ]
Open in Emergency is a multimedia collaborative project of the Asian American Literary Review that takes the lens of an Asian American Experience and redefines wellness in terms of care instead of focusing on diagnosis, unlike the original DSM V. This included mock versions of DSM diagnoses such as gender dysphoria, social anxiety disorder and cannabis use disorder that mean to recharacterize the disorders under the lens of wellness and care. [ 162 ] The project was said [ by whom? ] to contextualize mental disorders with their relationship to structures of power like patriarchy , colonialism and violence (here). [ citation needed ]
The Protest Psychosis: How Schizophrenia became a Black disease is a critically acclaimed book that was written to analyze the history of schizophrenia and how perceptions of the condition have changed. In this book, Metzl shows how the condition of schizophrenia was experienced against the backdrop of the Civil Rights Movement . [ 127 ] This book was recognized by the Disability Studies Quarterly academic journal as an excellent analysis of schizophrenia's link to black history. [ 163 ]
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Diagnostic greed is a medical term coined by physician Maurice Pappworth to describe the rigidity of physicians in insisting on every classic symptom and physical sign be present before making a diagnosis . Pappworth explained that “overwhelming evidence is not essential for correct diagnosis, and the absence of some expected symptom or sign often does not invalidate an otherwise reasonable diagnosis.” [ 1 ] [ 2 ]
Where a diagnosis may have considerable impact, additional tests providing supporting evidence might be required, making diagnostic greed advantageous. [ 3 ]
The term "diagnostic greed" was coined by physician Maurice Pappworth to describe the rigidity of physicians in insisting on every classic symptom and physical sign be present before making a diagnosis. Pappworth explained that “overwhelming evidence is not essential for correct diagnosis, and the absence of some expected symptom or sign often does not invalidate an otherwise reasonable diagnosis.” [ 1 ] [ 4 ] [ 5 ] He recorded that the correct question was "wherefore is this disease different from all other disease?" [ 6 ] Coming to a correct diagnosis "is not like a jury's verdict. It does not have to be proved beyond a reasonable doubt." [ 7 ]
Where a person presents with a classic history associated with clearly recognisable symptoms and signs of a condition, a diagnosis can be confidently made with ease. However, clinical scenarios of the same disease frequently vary and insisting on an exact match before making the diagnosis may miss the diagnosis and therefore be considered a "sin of greed". [ 1 ] One example is of kidney cancer , which classically presents with flank pain , blood in urine and a mass felt in the abdomen ; a triad of features which present in less than 10% of cases. In practice, all "essential" features are rarely present and a person may reveal just a few classic features, which is where the request for testing plays a role in confirming or ruling out the suspected diagnosis. [ 1 ]
In dermatology , every textbook feature of a lesion need not be present to make the diagnosis. [ 8 ] Likewise, in cardiology , the expectation to explain every change on an ECG to conclude a diagnosis may represent diagnostic greed. [ 9 ] Another example has been of lead poisoning , where toxicology results have failed to support the diagnosis despite other features of heavy metal poisoning being present. [ 10 ]
Arguments for the need, on occasion, to have diagnostic greed, have also been made. Where a diagnosis may have considerable impact, additional tests providing supporting evidence might be required, making diagnostic greed advantageous. [ 3 ]
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Diagnostic microbiology is the study of microbial identification. Since the discovery of the germ theory of disease , scientists have been finding ways to harvest specific organisms. Using methods such as differential media or genome sequencing , physicians and scientists can observe novel functions in organisms for more effective and accurate diagnosis of organisms. Methods used in diagnostic microbiology are often used to take advantage of a particular difference in organisms and attain information about what species it can be identified as, which is often through a reference of previous studies. New studies provide information that others can reference so that scientists can attain a basic understanding of the organism they are examining.
Anaerobic organisms require an oxygen-free environment. When culturing anaerobic microbes, broths are often flushed with nitrogen gas to extinguish oxygen present, and growth can also occur on media in a chamber without oxygen present. [ 1 ] Sodium resazurin can be added to indicate redox potential. [ 2 ] Cultures are to be incubated in an oxygen-free environment for 48 hours at 35 °C before growth is examined. [ 3 ]
Anaerobic bacteria collection can come from a variety of sources in patient samples, including blood, bile, bone marrow, cerebrospinal fluid , direct lung aspirate, tissue biopsies from a normally sterile site, fluid from a normally sterile site (like a joint), dental, abscess, abdominal or pelvic abscess, knife, gunshot, or surgical wound, or severe burn. [ 4 ]
Incubation times vary based upon the microbe that requires culturing. Traditional culturing techniques, for example, require less than 24 hours culture time for Escherichia coli but 6–8 weeks for successful culturing of Mycobacterium tuberculosis before definitive results are expressed. [ 5 ] A benefit of non-culture tests is that physicians and microbiologists are not handicapped by waiting periods.
Incubation follows a growth curve variable for every microorganism. Cultures follow a lag, log, stationary, and finally death phase. [ 6 ] The lag phase is not well known in microbiology, but it is speculated that this phase consists of the microorganism adjusting to its environment by synthesizing proteins specific for the surrounding habitat. [ 6 ] The log phase is the period where a culture experiences logarithmic growth until nutrients become scarce. The stationary phase is when culture concentration is the highest and cells stop reproducing. When nutrients in the environment are depleting, organisms enter the death phase where toxic metabolites become abundant and nutrients are depleted to the point where cell death exceeds reproduction. [ 5 ]
Automatic cell culturing systems are becoming popular because of their ability to maintain a sterile growth environment and remove strain on the laboratory staff involving repetitive experimentation. [ 7 ] Laboratories can also set incubation times to adjust for the lag period involved in bacterial growth.
Blood cultures can allow for diagnostic results after culture. Recent development of DNA based PCR diagnostics have provided faster diagnostic results as opposed to overnight biochemical tests. DNA diagnostic test can diagnose with near the same specificity as biochemical test, resulting in the same diagnostic result in 90% of cases. [ 8 ]
Breath test for microbial diagnosis on patients has been used in a clinical setting for bacteria, including Helicobacter pylori . [ 9 ] Diagnostic test using the breath of patients look for metabolites excreted that were manufactured by the infectious microorganism. H. pylori is tested by testing patients for CO 2 concentration, increased because of the organism’s ability to convert urea into other derivatives. [ 10 ]
A benefit of antibody detection ( ELISA ) is that protein identification on a microorganism becomes faster than a western blot . Antibody detection works by attaching an indicator to an antibody with a known specificity and observing whether the antibody attaches. [ 11 ] ELISA can also indicate viral presence and is highly specific, having a detection specificity of 10 −9 -10 −12 moles per litre detection. By knowing the epitope sequence of the antibody, ELISA can also be used for antigen detection in a sample. [ 12 ]
Histological methods used for microbiology are useful because of their ability to quickly identify a disease present in a tissue biopsy .
Staining used in microbiology identification include: Gram stain , Acid-fast stain , Giemsa stain , India ink stain , Ziehl–Neelsen stain .
Immunofluorescence is performed by the production of anti-antibodies with a fluorescent molecule attached, making it a chemiluminescent molecule, which provides a glow when subject to ultraviolet light. [ 13 ] Antibodies are added to a bacterial solution, providing an antigen for the binding of fluorescent anti-antibody adherence.
MALDI-TOF ( Matrix-assisted laser desorption/ionization - time of flight) is a specific type of mass spectrometry that is able to identify microorganisms. A pure culture is isolated and spread directly on a stainless steel or disposable target. The cells are lysed and overlaid with a matrix, which forms protein complexes with the bacterial proteins. The MALDI fires a laser and ionizes the protein complexes, which break off and travel up the vacuum where they are detected based on mass and charge. The resulting protein spectra is compared to a known database of previously catalogued organisms, resulting in rapid diagnosis of microorganisms. [ 14 ] Recent studies have suggested that these tests can become specific enough to diagnose down to the sub-species level by observing novel biomarkers . [ 14 ]
The MALDI-TOF identification method requires pure cultures that are less than 72 hours old. This places the organism in log phase with an abundance of ribosomal proteins, which are the most common proteins detected in the spectra. Identifications with this technology can also be impacted if the culture is exposed to cold temperatures, as this would change the typical protein distribution.
Phenotypic tests are used to identify microbes based on metabolic and biochemical pathways present in those microbes. [ 15 ] There are many automated and semi-automated commercial systems available. These methods can be very informative but are not as accurate as MALDI-TOF or genotypic methods.
The 6.5% salt broth test is used to analyze the tolerance level of various bacteria under halophilic conditions. This test is used because most organisms cannot survive in high salt concentrations while Staphylococci , Enterococci , and Aerococci are all expected to tolerate 6.5% NaCl concentrations. [ 16 ]
The acetate utilization test is used primarily to differentiate between Escherichia coli from members of the genus Shigella . Many of the Escherichia coli strains have the capability of the utilization of acetate for a sole carbon and energy source, while Shigella does not. Since acetate utilization results in an increase in pH, an indicator is added that changes color under conditions of acetate utilization.
An ALA ( delta-aminolevulinic acid ) test is used to test for the presence of porphyrin and cytochrome compounds. Finding hemin synthesis indicates that the organism is likely Haemophilus . [ 17 ]
The aminopeptidase test analyzes bacteria for the production of the enzyme L-alanine-aminopeptidase, an enzyme found in many gram-negative bacteria . Adding L-Alanine-4-nitroanilide hydrochloride to a bacterial culture works as an indicator, changing to a yellow color in the presence of L-alanine-aminopeptidase. [ 18 ]
An analytical profile index is a fast identification system based on biochemical incubation tests. Usually, this test is used to quickly diagnose clinically relevant bacteria by allowing physicians to run about 20 tests at one time. [ 19 ]
Antibiotic disks are used to test the ability for an antibiotic to inhibit growth of a microorganism. This method, which is commonly used with Mueller–Hinton agar , is used by evenly seeding bacteria over a petri dish and applying an antibiotic treated disk to the top of the agar. By observing the ring formed around the disk formed due to the lack of bacterial growth, the zone of inhibition can be found, which is used to find the susceptibility of an organism to an antibiotic. [ 19 ]
The bile esculin test is used to differentiate members of the genus Enterococcus from Streptococcus . [ citation needed ]
Bile solubility is used to test for Streptococcus Pneumoniae due to their unique ability to be lysed by sodium deoxycholate . Lysis indicates S. Pneumoniae while no lysis does not. [ 20 ]
A CAMP test is used to differentiate between Streptococcus agalactiae and other species of beta-hemolytic Streptococcus. This biochemical test uses the fact that Streptococcus agalactiae excretes a CAMP substance, making it slightly more hemolytic, which can be observed on blood agar media. [ 21 ]
The catalase test tests whether a microbe produces the enzyme catalase, which catalyzes the breakdown of hydrogen peroxide. Smearing a colony sample onto a glass slide and adding a solution of hydrogen peroxide (3% H 2 O 2 ) will indicate whether the enzyme is present or not. Bubbling is a positive test while nothing happening is a negative result. [ 22 ]
Cetrimide agar slants is a selective agar used to isolate Pseudomonas aeruginosa .
The CLO test is used to diagnose H. Pylori in patient biopsies. A sample of the biopsy is places in a medium containing urea , which H. Pylori can use in some of its biochemical pathways. Consumption of urea indicates a positive test result. [ 23 ]
The coagulase test determines whether an organism can produce the enzyme coagulase, which causes the fibrin to clot. Inoculating a plasma test tube with the microbe indicates whether coagulase is produced. A clot indicates the presence of coagulase, while no clot indicates the lack of coagulase. [ 24 ]
DNase agar is used to test whether a microbe can produce the exoenzyme deoxyribonuclease (DNase), which hydrolyzes DNA. Methyl green is used as an indicator in the growth medium because it is a cation that provides an opaqueness to a medium with the presence of negatively charged DNA strands. When DNA is cleaved, the media becomes clear, showing the presence of DNase activity. DNA hydrolysis is tested by growing an organism on a DNase Test Agar plate (providing nutrients and DNA) and then checking the plate for hydrolysis. The agar plate has DNA-methyl green complex, and if the organism on the agar does hydrolyze DNA then the green color fades and the colony is surrounded by a colorless zone. [ 25 ]
The gelatin test is used to analyze whether a microbe can hydrolyze gelatin with the enzyme gelatinase . The gelatin makes the agar solid, so if an organism can produce gelatinase and consume gelatin as an energy and carbon source, the agar will become liquid during growth. [ 26 ]
The Gonochek II test, a commercial biochemical test, is used to differentiate between Neisseria lactamica , Neisseria meningitidis , N. gonorrhoeae and Moraxella catarrhalis. The principle behind this test is to use enzymes native to the organism to create a colored product in the presence of foreign molecules. The chemical 5-bromo-4-chloro-3-indolyl-beta-D-galactoside is used in the test because N. lactamica can hydrolyze it with the production of β- galactosidase , turning the solution into a blue color. Gamma-glutamyl-p-nitroanilide is added to the solution to indicate whether the bacteria is N. meningitides, which hydrolyzes the molecule with the enzyme gamma-glutamylaminopeptidase, producing a yellow end-product. Prolyl-4-methoxynaphthylamide is in the solution to identify N. gonorrhoeae because of its ability to hydrolyze the molecule with the enzyme hydroxyprolylaminopeptidase, creating a red-pink derivative. M. catarrhalis contains none of these enzymes, rendering the solution colorless. This process of identification takes approximately 30 minutes in total. [ 27 ]
The Hippurate diagnostic test is used to differentiate between Gardnerella vaginalis , Campylobacter jejuni , Listeria monocytogenes and group B streptococci using the chemical Hippurate. The Hippurate hydrolysis pathway, capable by organisms with the necessary enzymes, produces glycine as a byproduct. Using the indicator ninhydrin , which changes color in the presence of glycine, will display either a colorless product, a negative result, of a dark blue color, a positive result. [ 28 ]
An indole butyrate disc is used to differentiate between Neisseria gonorrhoeae (negative result) and Moraxella catarrhalis (positive result). This test involves a butyrate disk, which when smeared with a culture, will change color for a positive result after 5 minutes of incubation. A blue color is the result of a positive test. [ 29 ]
The lysine iron agar slant test is used to tell whether an organism can decarboxylate lysine and/or produce hydrogen sulfide .
The lysostaphin test is used to differentiate between Staphylococcus and Micrococcus bacteria. Lysostaphin can lyse Staphylococcus, but Micrococcus bacteria are resistant to the chemical. [ 30 ]
The methyl red test is used to analyze whether a bacterium produces acids through sugar fermentation. [ citation needed ]
Microdase is a modified oxidase test used to differentiate Micrococcus from Staphylococcus by testing for the presence of cytochrome c . A positive result produces a dark color around the inoculant while negative result produces no color change. [ 31 ]
The nitrite test is commonly used to diagnose urinary tract infections by measuring the concentrations of nitrite in solution, indicating the presence of a gram-negative organism. A simple nitrite test can be performed by adding 4 M sulfuric acid to the sample until acidic, and then adding 0.1 M iron (II) sulfate to the solution. A positive test for nitrite is indicated by a dark brown solution, arising from the iron-nitric oxide complex ion. [ citation needed ]
The oxidase test indicates whether a microbe is aerobic. By using the chemical N,N,N,N-tetramethyl-1,4-phenylendiamin , an electron acceptor that changes color when oxidized by cytochrome c oxidase , one can deduce whether a microbe can perform aerobic respiration. A color change to purple indicates oxidative respiration while no color change provides evidence that the organism does not have cytochrome c oxidase. [ 22 ]
The phenylalanine deaminase test is used to tell whether an organism can produce the enzyme deaminase. Deaminase is the enzyme that can deaminate the amino acid phenylalanine into the products ammonia and phenylpyruvic acid . The test is performed by adding phenylalanine to the growth medium and allowing growth to occur. After incubation, 10% ferric chloride is added to the solution, which will react with phenylpyruvic acid in solution to make a dark green color, resulting in a positive test result. [ 32 ]
The PYR test is used to check if an organism has enzymes to hydrolyze L-pyrrolidonyl- β-napthylamide. A positive result indicates that the organism is either group A streptococcus and/or group D enterococcus . [ 33 ]
The reverse CAMP test utilizes the synergetic hemolytic abilities of the CAMP factor produced by Streptococcus agalactiae with the α-toxin produced by Clostridium perfringens . Streaking these two organisms perpendicular to each other on a blood agar plate will yield a “bow-tie” clearing of the blood agar by the hemolytic capabilities of the two organisms’ toxins. Incubation requires 24 hours at 37 °C. [ 34 ]
Simmons' citrate agar is used to test whether an organism can utilize citrate for its sole carbon source. [ citation needed ]
The spot indole test is used to determine if a microbe can deaminate tryptophan to produce indole . This test is performed by saturating a piece of filter paper with Indole Kovacs Reagent and scraping a portion of microbe onto the paper. A color to a pink-red color indicates a positive result while no color change indicates the lack of tryptophanase . [ 35 ]
The sulfide indole motility medium is a three-part test for an organism’s ability to reduce sulfates, produce indoles, and motile ability. [ citation needed ]
The triple sugar iron (TSI) test is a differential media used to tell whether an organism can ferment glucose, sucrose, and/or lactose and whether an organism can produce hydrogen sulfide gas. [ 36 ]
The urease agar slant is used to measure an organism’s ability to produce urease , an enzyme capable to digesting urea in carbon dioxide and ammonia through hydrolysis. Because ammonia is alkaline, the media contains phenol red, an indicator that changes from orange to pink when a pH increases above 8.1. When ammonia is increased to high enough concentrations, the media will change to a pink color, indicating the presence of urease production. [ 37 ]
The Voges-Proskauer test detects whether a bacterium is producing the product acetoin from the digestion of glucose. [ 38 ]
Mycolic acid analysis has been an evolving field of study for gas-liquid chromatography , as it offers a solution to slow growth rates in Mycobacterium . Mycolic acid is a fatty acid found in the disease tuberculosis , offering a chemical target for diagnosticians to look for. [ 39 ]
With high speed buoyant density ultracentrifugation , a density gradient is created with caesium chloride in water. DNA will go to the density that reflects its own, and ethidium bromide is then added to enhance the visuals the nucleic acid band provides. [ 40 ]
New extraction techniques have been developed using magnetic beads for the purification of nucleic acids by taking advantage of the charged and polymeric nature of long strand of DNA. Beads are both uncoated to increase surface are and yield, while others are more selective by being coated with functional groups that interact with the polymers present in microbes. [ 41 ] One common method is to use polyethylene glycol to drive DNA binding to the magnetic beads. The molecular weight and concentration of the PEG will control what molecular weight DNA binds.
Phenol-Chloroform extraction is a liquid-liquid method used by biochemists to separate nucleic acids from proteins and lipids after cells have been lysed. [ 42 ] [ citation needed ] This method has fallen out of favor with scientists and microbiologists as there are easier methods available which require less hazardous chemicals.
Solid phase extraction which separates long polymers like DNA from other substances found in the cells. This is similar to magnetic beads, where the solid phase is fixed and selectively binds a cellular component, allowing for its isolation.
Gel electrophoresis is a technique to separate macromolecules by taking advantage of the charge on many of the molecules found in nucleic acids and protein. This is also the key method for Sanger sequencing. Fluorescent-labeled DNA fragments move through a polymer and are separated with one base precision. A laser excites the fluorescent tag and is captured by a camera. The result is an electropherogram which reads the DNA sequence.
Optical mapping is a technique using multiple restriction enzymes to create a genomic “barcode” which can be referenced back to diagnose an unknown microbe.
Pulsed-field gel electrophoresis is a technique used to separate large DNA in an electric field that periodically changes direction. By cutting segments of the DNA with restriction enzymes , pulse-field can be used to separate out the segments of DNA.
Restriction enzymes are first used to recognize and then cut specific nucleic acid sequences. These cut pieces of DNA can be run through a gel electrophoresis to allow diagnostics of the organism by referencing back to previous gel electrophoresis results.
Ribotyping is a rapid automated method for microbial diagnostics, testing for rRNA in bacteria using restriction enzyme digestion and Southern blot technology. [ 43 ]
Multiple-locus VNTR analysis is a test used to detect variable number tandem repeats , which act as a DNA fingerprint in microbial diagnostics. [ 44 ]
Multilocus sequence typing (MLST) is the sequencing of numerous loci to diagnose an organism by comparing DNA sequences to a database of known organisms. [ 45 ] [ 46 ] This method is often used to compare isolates or strains of the same species to see if they are indistinguishable or different from each other. This is common for tracking food-borne illnesses and public health outbreaks. Most MLST assays are published in scientific journals so consistent methods are used worldwide. There are also public databases available for tracking and comparisons.
Single-locus sequence typing (SLST) is the sequencing of a single locus of an organism to produce data that can be used for strain-level comparisons between isolates of the same species. [ 47 ]
For bacterial identifications, microbiologists sequence the 16S rRNA gene and for fungal identifications, sequence the ITS regions. Both regions are part of the ribosomal operon so they are well-conserved but provide enough variation to allow for speciation. Accurate identifications require high quality sequence data, a robust data analysis, and a broad microbial database of known organisms. It is also useful to use a Neighbor Joining tree or some other phylogenetic approach to make the identification.
Whole genome sequencing and genomics applications can be used for large-scale alignment and comparative analysis with both bacteria and fungi. WGS can be used to diagnose, identify, or characterize an organism down to the individual base pairs by sequencing the entire genome. [ 48 ] WGS can also be used to compare the genomes or average nucleotide identity (ANI) of the shared genes between two strains and can be a robust way to compare genetic relatedness and if often used for investigating organisms involved in foodborne illness and other outbreaks.
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In dentistry , diagnostic wax-up is used to visualize the results of a prosthetic case prior to the treatment being executed.
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Dialogues in Clinical Neuroscience is a quarterly peer-reviewed medical journal covering neurology and clinical neuropsychiatry . It was established in 1999 and was originally published by Laboratoires Servier . Starting 2022, the journal is published by Taylor & Francis on behalf of the World Federation of Societies of Biological Psychiatry . The editor-in-chief is Florence Thibaut ( Hospital Cochin ).
The journal is abstracted and indexed in:
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Dialysis disequilibrium syndrome ( DDS ) is the collection of neurological signs and symptoms , attributed to cerebral edema , during or following shortly after intermittent hemodialysis [ 1 ] or CRRT. [ 2 ]
Classically, DDS arises in individuals starting hemodialysis due to end-stage chronic kidney disease and is associated, in particular, with "aggressive" (high solute removal) dialysis. [ 3 ] However, it may also arise in fast onset, i.e. acute kidney failure in certain conditions.
Diagnosis of mild DDS is often complicated by other dialysis complications such as malignant hypertension, uremia, encephalopathy, subdural hemorrhage, hyper- and hypoglycaemia, or electrolyte imbalances. Presentation of moderate and severe DDS requires immediate identification and treatment as the condition can result in severe neurological issues and death. [ citation needed ]
The cause of DDS is currently not well understood. There are two theories to explain it; the first theory postulates that urea transport from the brain cells is slowed in chronic kidney disease, leading to a large urea concentration gradient , which results in reverse osmosis . The second theory postulates that organic compounds are increased in uremia to protect the brain and result in injury by, like in the first theory, reverse osmosis . [ 1 ] More recent studies on rats noted that brain concentrations of organic osmolytes were not increased relative to baseline after rapid dialysis. Cerebral edema was thus attributed to osmotic effects related to a high urea gradient between plasma and brain. [ 4 ]
Clinical signs of cerebral edema, such as focal neurological deficits , papilledema [ 5 ] and decreased level of consciousness , if temporally associated with recent hemodialysis, suggest the diagnosis. A computed tomography of the head is typically done to rule-out other intracranial causes. [ citation needed ]
MRI of the head has been used in research to better understand DDS. [ 6 ]
Avoidance is the primary treatment. Better alternatives are Nocturnal or Daily Dialysis , which are far more gentle processes for the new dialysis patient. Dialysis disequilibrium syndrome is a reason why hemodialysis initiation should be done gradually, i.e. it is a reason why the first few dialysis sessions are shorter and less aggressive than the typical dialysis treatment for end-stage renal disease patients. [ citation needed ]
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In pathology , diastasis is the separation of parts of the body that are normally joined, such as the separation of certain abdominal muscles during pregnancy, or of adjacent bones without fracture. [ 1 ]
Compare with:
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https://en.wikipedia.org/wiki/Diastasis_(pathology)
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In physiology , diastasis is the middle stage of diastole during the cycle of a heartbeat , where the initial passive filling of the heart's ventricles has slowed, but before the atria contract to complete the active filling.
Diastasis is the longest phase of cardiac cycle. [ 1 ]
This cardiovascular system article is a stub . You can help Wikipedia by expanding it .
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https://en.wikipedia.org/wiki/Diastasis_(physiology)
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A diastema ( pl. : diastemata , from Greek διάστημα , 'space') is a space or gap between two teeth . Many species of mammals have diastemata as a normal feature, most commonly between the incisors and molars . More colloquially, the condition may be referred to as gap teeth or tooth gap .
In humans, the term is most commonly applied to an open space between the upper incisors (front teeth). It happens when there is an unequal relationship between the size of the teeth and the jaw . Diastemata are common for children and can exist in adult teeth as well.
1. Oversized Labial Frenulum : Diastema is sometimes caused or exacerbated by the action of a labial frenulum (the tissue connecting the lip to the gum), causing high mucosal attachment and less attached keratinized tissue. This is more prone to recession or by tongue thrusting, which can push the teeth apart. [ 1 ]
2. Periodontal Disease : Periodontal disease, also known as gum disease , can result in bone loss that supports the teeth. If a person loses enough bone, the teeth can become loose and cause gaps to form. [ 2 ]
3. Mesiodens : Mesiodens is an extra tooth that grows behind the front teeth. A mesiodens may push the front teeth apart to make room for itself thus creating a gap between the front teeth. [ 3 ]
4. Skeletal discrepancy : Dental skeletal discrepancy can be a cause behind gap teeth. If the upper jaw grows more than the lower jaw, teeth on the upper jaw will have more space to cover thus leaving gaps between them.
5. Proclination : If the front teeth are angled forward, a small gap between them may appear large. This is called proclination; it may be a result of aggressive tongue thrusting. [ 4 ]
A diastema is not a pathology and doesn't require treatment. Any interventions to modify a diastema are purely cosmetic.
1. Determine the cause of the diastema, then treat the cause.
2. Diastema treatment options can differ from one patient to another, but generally it is treated by orthodontics , [ 5 ] or composite fillings , or a combination of veneers or crowns .
In The Canterbury Tales , Geoffrey Chaucer wrote of the " gap-toothed wife of Bath ". [ 6 ] As early as this time period, the gap between the front teeth, especially in women, was associated with lustful characteristics. [ 7 ] Thus, the implication in describing "the gap-toothed wife of Bath" is that she is a middle-aged woman with insatiable lust. [ 7 ]
In Ghana , Namibia and Nigeria , as well as throughout many communities in Kenya, diastemata are regarded as being attractive and a sign of fertility, and some people have even had them created through cosmetic dentistry . [ 8 ] [ 9 ]
In France, they are called dents du bonheur (lucky/happiness teeth). [ 10 ] This expression originated in Napoleon 's time: when the Napoleonic army recruited, it was imperative that soldiers had incisors in perfect condition because they had to open the paper cartridges (containing gunpowder) with their teeth when loading their muskets. All those who had teeth apart were then classified as unfit to fight. Some men broke their own teeth to avoid going to war. [ citation needed ]
Les Blank 's Gap-Toothed Women (1987) is a 30-minute documentary film about diastematic women. [ 11 ]
Some well-known people noted for having diastema include:
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https://en.wikipedia.org/wiki/Diastema
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In mammals , cardiac electrical activity originates from specialized myocytes of the sinoatrial node (SAN) which generate spontaneous and rhythmic action potentials (AP). The unique functional aspect of this type of myocyte is the absence of a stable resting potential during diastole. Electrical discharge from this cardiomyocyte may be characterized by a slow smooth transition from the Maximum Diastolic Potential (MDP, -70 mV) to the threshold (-40 mV) for the initiation of a new AP event. The voltage region encompassed by this transition is commonly known as pacemaker phase, or slow diastolic depolarization or phase 4.
The duration of this slow diastolic depolarization (pacemaker phase) thus governs the cardiac chronotropism. It is also important to point out that the modulation of the cardiac rate by the autonomic nervous system also acts on this phase. Sympathetic stimuli induce the acceleration of rate by increasing the slope of the pacemaker phase, while parasympathetic activation exerts the opposite action.
The amount of net inward current required to move the cell membrane potential during the pacemaker phase is extremely small, in the order of few pAs, but this net flux arises from the time to time changing contribution of several currents that flow with different voltage and time dependence. Evidence in support of the active presence of K + , Ca 2+ , Na + channels and Na + /K + exchanger during the pacemaker phase have been variously reported in the literature, but several indications point to the funny current (I f ) as one of the most important. [ 1 ] [ 2 ] There is now substantial evidence that also sarcoplasmic reticulum (SR) Ca 2+ -transients participate in the generation of the diastolic depolarization via a process involving the Na–Ca exchanger.
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https://en.wikipedia.org/wiki/Diastolic_depolarization
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In clinical cardiology the term "diastolic function" is most commonly referred as how the heart fills. [ 1 ] Parallel to "diastolic function", the term " systolic function" is usually referenced in terms of the left ventricular ejection fraction (LVEF), which is the ratio of stroke volume and end-diastolic volume . [ 2 ] Due to the epidemic of heart failure , [ 3 ] particularly the cases determined as diastolic heart failure , it is increasingly urgent and crucial to understand the meaning of “diastolic function”. Unlike "systolic function", which can be simply evaluated by LVEF, there are no established dimensionless parameters for "diastolic function" assessment. [ 4 ] Hence to further study "diastolic function" the complicated and speculative physiology must be taken into consideration.
How the heart works during its filling period still has many misconceptions remaining. To better understand diastolic function, it is crucial to realize that the left ventricle is a mechanical suction pump at, and for a little while after, the mitral valve opening. [ 5 ] In other words, when mitral valve opens, the atrium does not push blood into the ventricle, instead, it is the ventricle that mechanically "sucks" in blood from the atrium . [ 6 ] [ 7 ] The energy that drives the suction process is generated from phase of systole . During systole, to overcome the peripheral arterial load at ejection, ventricle contracts, which also compresses elastic tissues internal to and external to the myocardium . Then, when cardiac muscle relaxes, the energy captured by compressed elements releases, driving the recoil of ventricular wall until a new balanced equilibrium state is reached. [ 8 ]
During diastole , the ventricle of heart must remain elastic or compliant enough and have capacity to hold incoming blood to guarantee effectiveness of the filling phase. Hence stiffness and relaxation are ventricle's intrinsic feature parameters that are practical in evaluating and quantifying diastolic function. [ 9 ] In addition, volumetric load [ 10 ] serves as an extrinsic indicating parameter that modulates diastolic function.
The most established index to describe left ventricular diastolic function is Tau, left ventricular diastolic time constant. Measurement of Tau is traditionally delivered in a catheter lab by an invasive method. Recently, non-invasive measurement of Tau is available for mitral regurgitation or aortic regurgitation patients in an Echo lab. [ 11 ]
There have been many attempts intending for extracting both intrinsic and extrinsic properties. Early attempts concentrated on pulse-wave Doppler-echo measured trans-mitral flow velocity contours. [ citation needed ]
In terms of filling, diastolic intervals consist of early rapid filling E-waves followed by diastasis and followed by atrial systole-generated A-waves. Empirically, E- and A- wave contours were simplified as triangles. Nowadays, triangle-based indexes, such as the peak velocities of the E- and A-waves and ratio of them, the deceleration time and time duration of the E-wave, and the velocity time integral of both E- and A- waves, are usually measured and evaluated. [ citation needed ]
The triangular approach applies to E-wave shape conveniently, especially in the past when the images rendered by technology back in days are of poor resolution quality. Nevertheless, with rapidly improving temporal resolution and image processing capabilities, the curvature of E-wave contours can be clearly identified with detailed information revealed.
Due to advancement of modern medical imaging technology, the measurement of even smaller (i.e. tissue) velocities are possible to be made, which even leads to capability to measure the longitudinal displacements of the mitral annulus . The shapes of mitral annular velocity contours used to be approximated to be triangles, whose peak height is label to be E’. E’ proved useful in selected patient populations for estimation of end-diastolic pressure (EDP). [ 9 ]
Other innovative imaging modalities consist of techniques such as speckle tracking . Speckle tracking enables strain and strain-rate measurements. It is a relatively recent instance of technological progress, due to the fact that it relies on the information content inherent in the seemingly random arrangement of bright speckles present in all echocardiographic images. [ 12 ] Even though a variety of echo-based imaging technologies represent multiple levels of research innovation, much remains to be studied in relation to how to interpret the recorded data embedded in images.
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https://en.wikipedia.org/wiki/Diastolic_function
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In medicine and allied fields, diathesis (from Greek διάθεσις) is a hereditary or constitutional predisposition to a group of diseases, an allergy, or other disorder. [1] [ 1 ] There are many types of diathesis. Some including strumous diathesis, sthenic diathesis, and many more.
Atopic diathesis is a predisposition to develop one or more of hay fever , allergic rhinitis , bronchial asthma , or atopic dermatitis . [ 2 ]
[ 1 ]
This medical article is a stub . You can help Wikipedia by expanding it .
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https://en.wikipedia.org/wiki/Diathesis_(medicine)
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Dichotic listening is a psychological test commonly used to investigate selective attention and the lateralization of brain function within the auditory system . It is used within the fields of cognitive psychology and neuroscience .
In a standard dichotic listening test, a participant is presented with two different auditory stimuli simultaneously (usually speech ), directed into different ears over headphones. [ 1 ] In one type of test, participants are asked to pay attention to one or both of the stimuli; later, they are asked about the content of either the stimulus they were instructed to attend to or the stimulus they were instructed to ignore. [ 1 ] [ 2 ]
Donald Broadbent is credited with being the first scientist to systematically use dichotic listening tests in his work. [ 3 ] [ 4 ] In the 1950s, Broadbent employed dichotic listening tests in his studies of attention, asking participants to focus attention on either a left- or right-ear sequence of digits. [ 5 ] [ 6 ] He suggested that due to limited capacity, the human information processing system needs to select which channel of stimuli to attend to, deriving his filter model of attention . [ 6 ]
In the early 1960s, Doreen Kimura used dichotic listening tests to draw conclusions about lateral asymmetry of auditory processing in the brain. [ 7 ] [ 8 ] She demonstrated, for example, that healthy participants have a right-ear superiority for the reception of verbal stimuli, and left-ear superiority for the perception of melodies. [ 9 ] From that study, and others studies using neurological patients with brain lesions, she concluded that there is a predominance of the left hemisphere for speech perception, and a predominance of the right hemisphere for melodic perception. [ 10 ] [ 11 ]
In the late 1960s and early 1970s, Donald Shankweiler [ 12 ] and Michael Studdert-Kennedy [ 13 ] of Haskins Laboratories used a dichotic listening technique (presenting different nonsense syllables) to demonstrate the dissociation of phonetic (speech) and auditory (nonspeech) perception by finding that phonetic structure devoid of meaning is an integral part of language and is typically processed in the left cerebral hemisphere . [ 14 ] [ 15 ] [ 16 ] A dichotic listening performance advantage for one ear is interpreted as indicating a processing advantage in the contralateral hemisphere . In another example, Sidtis (1981) [ 17 ] found that healthy adults have a left-ear advantage on a dichotic pitch recognition experiment. He interpreted this result as indicating right-hemisphere dominance for pitch discrimination.
An alternative explanation of the right-ear advantage in speech perception is that most people being right-handed, more of them put a telephone to their right ear. [ 18 ] [ 19 ] The two explanations are not necessarily incompatible, in that telephoning behavior could be partly to do with hemispheric asymmetry. Some of the converse findings for nonspeech (e.g. environmental sounds [ 20 ] [ 21 ] ) are readily interpretable in this framework too.
During the early 1970s, Tim Rand demonstrated dichotic perception at Haskins Laboratories . [ 22 ] [ 23 ] In his study, the first stimuli: formant (F1), was presented to one ear while the second and third stimuli:(F2) and (F3) formants, were presented to the opposite ear. F2 and F3 varied in low and high intensity. Ultimately, in comparison to the binaural condition, "peripheral masking is avoided when speech is heard dichotically." [ 23 ] This demonstration was originally known as "the Rand effect" but was later renamed "dichotic release from masking". The name for this demonstration continued to evolve and was finally named "dichotic perception" or "dichotic listening." Around the same time, Jim Cutting (1976), [ 24 ] an investigator at Haskins Laboratories , researched how listeners could correctly identify syllables when different components of the syllable were presented to different ears. The formants of vowel sounds and their relation are crucial in differentiating vowel sounds. Even though the listeners heard two separate signals with neither ear receiving a 'complete' vowel sound, they could still identify the syllable sounds.
The "dichotic fused words test" (DFWT) is a modified version of the basic dichotic listening test. It was originally explored by Johnson et al. (1977) [ 25 ] but in the early 80's Wexler and Hawles (1983) [ 26 ] modified this original test to ascertain more accurate data pertaining to hemispheric specialization of language function. In the DFWT, each participant listens to pairs of monosyllabic rhyming consonant-vowel-consonant (CVC) words. Each word varies in the initial consonant. The significant difference in this test is "the stimuli are constructed and aligned in such a way that partial interaural fusion occurs: subjects generally experience and report only one stimulus per trial." [ 27 ] According to Zatorre (1989), some major advantages of this method include "minimizing attentional factors, since the percept is unitary and localized to the midline" and "stimulus dominance effects may be explicitly calculated, and their influence on ear asymmetries assessed and eliminated." [ 27 ] Wexler and Hawles study obtained a high test-retest reliability (r=0.85). [ 26 ] High test-retest reliability is good, because it proves that the data collected from the study is consistent.
An emotional version of the dichotic listening task was developed. In this version individuals listen to the same word in each ear but they hear it in either a surprised, happy, sad, angry, or neutral tone. Participants are then asked to press a button indicating what tone they heard. Usually dichotic listening tests show a right-ear advantage for speech sounds. Right-ear/left-hemisphere advantage is expected, because of evidence from Broca's area and Wernicke's area , which are both located in the left hemisphere. In contrast, the left ear (and therefore the right hemisphere) is often better at processing nonlinguistic material. [ 28 ] The data from the emotional dichotic listening task is consistent with the other studies, because participants tend to have more correct responses to their left ear than to the right. [ 29 ] It is important to note that the emotional dichotic listening task is seemingly harder for the participants than the phonemic dichotic listening task, meaning more incorrect responses were submitted by individuals.
The manipulation of voice onset time (VOT) during dichotic listening tests has given many insights regarding brain function. [ 30 ] To date, the most common design is the utilisation of four VOT conditions: short-long pairs (SL), where a Consonant-Vowel (CV) syllable with a short VOT is presented to the left ear and a CV syllable with a long VOT is presented to the right ear, as well as long-short (LS), short-short (SS) and long-long (LL) pairs. In 2006, Rimol, Eichele, and Hugdahl [ 31 ] first reported that, in healthy adults, SL pairs elicit the largest REA while, in fact, LS pairs elicit a significant left ear advantage (LEA). A study of children 5–8 years old has shown a developmental trajectory whereby long VOTs gradually start to dominate over short VOTs when LS pairs are being presented under dichotic conditions. [ 32 ] Converging evidence from studies of attentional modulation of the VOT effect shows that, around age 9, children lack the adult-like cognitive flexibility required to exert top-down control over stimulus-driven bottom-up processes. [ 33 ] [ 34 ] Arciuli et al.(2010) further demonstrated that this kind of cognitive flexibility is a predictor of proficiency with complex tasks such as reading. [ 30 ] [ 35 ]
Dichotic listening tests can also be used as lateralized speech assessment task. Neuropsychologists have used this test to explore the role of singular neuroanatomical structures in speech perception and language asymmetry. For example, Hugdahl et al. (2003), investigated dichotic listening performance and frontal lobe function [ 36 ] in left and right lesioned frontal lobe nonaphasiac patients compared to healthy controls. In the study, all groups were exposed to 36 dichotic trials with pairs of CV syllables and each patient was asked to state which syllable he or she heard best. As expected, the right lesioned patients showed a right ear advantage like the healthy control group but the left hemisphere lesioned patients displayed impairment when compared to both the right lesioned patients and control group. From this study, researchers concluded "dichotic listening as into a neuronal circuitry which also involves the frontal lobes, and that this may be a critical aspect of speech perception." [ 36 ] Similarly, Westerhausen and Hugdahl (2008) [ 37 ] analyzed the role of the corpus callosum in dichotic listening and speech perception. After reviewing many studies, it was concluded that "...dichotic listening should be considered a test of functional inter-hemispheric interaction and connectivity, besides being a test of lateralized temporal lobe language function" and "the corpus callosum is critically involved in the top-down attentional control of dichotic listening performance, thus having a critical role in auditory laterality." [ 37 ]
Dichotic listening can also be used to test the hemispheric asymmetry of language processing . In the early 60s, Doreen Kimura reported that dichotic verbal stimuli (specifically spoken numerals) presented to a participant produced a right ear advantage (REA). [ 38 ] She attributed the right-ear advantage "to the localization of speech and language processing in the so-called dominant left hemisphere of the cerebral cortex." [ 39 ] : 115 According to her study, this phenomenon was related to the structure of the auditory nerves and the left-sided dominance for language processing. [ 40 ] It is important to note that REA doesn't apply to non-speech sounds. In "Hemispheric Specialization for Speech Perception," by Studdert-Kennedy and Shankweiler (1970) [ 14 ] examine dichotic listening of CVC syllable pairs. The six stop consonants (b, d, g, p, t, k) are paired with the six vowels and a variation in the initial and final consonants are analyzed. REA is the strongest when the sound of the initial and final consonants differ and it is the weakest when solely the vowel is changed. Asbjornsen and Bryden (1996) state that "many researchers have chosen to use CV syllable pairs, usually consisting of the six stop consonants paired with the vowel \a\. Over the years, a large amount of data has been generated using such material." [ 41 ]
In selective attention experiments, the participants may be asked to repeat aloud the content of the message they are listening to. This task is known as shadowing . As Colin Cherry (1953) [ 42 ] found, people do not recall the shadowed message well, suggesting that most of the processing necessary to shadow the attended to message occurs in working memory and is not preserved in the long-term store . Performance on the unattended message is worse. Participants are generally able to report almost nothing about the content of the unattended message. In fact, a change from English to German in the unattended channel frequently goes unnoticed. However, participants are able to report that the unattended message is speech rather than non-verbal content. In addition to this, if the content of the unattended message contains certain information, such as the listener's name, then the unattended message is more likely to be noticed and remembered. [ 43 ] A demonstration of this was done by Conway, Cowen, and Bunting (2001) in which they had subjects shadow words in one ear while ignoring words in the other ear. At some point, the subject's name was spoken in the ignored ear, and the question was whether the subject would report hearing their name. Subjects with a high working memory (WM) span were more capable of blocking out the distracting information. [ 44 ] Also if the message contains sexual words then people usually notice them immediately. [ 45 ] This suggests that the unattended information is also undergoing analysis and keywords can divert attention to it.
Some data gathered from dichotic listening test experiments suggests that there is possibly a small-population sex difference in perceptual and auditory asymmetries and language laterality. According to Voyer (2011), [ 46 ] "Dichotic listening tasks produced homogenous effect sizes regardless of task type (verbal, non-verbal), reflecting a significant sex difference in the magnitude of laterality effects, with men obtaining larger laterality effects than women." [ 46 ] : 245–246 However, the authors discuss numerous limiting factors ranging from publication bias to small effect size. Furthermore, as discussed in "Attention, reliability, and validity of perceptual asymmetries in the fused dichotic words test," [ 47 ] women reported more "intrusions" or words presented to the uncued ear than men when presented with exogenous cues in the Fused Dichotic Word Task which suggests two possibilities: 1) Women experience more difficulty paying attention to the cued word than men and/or 2) regardless of the cue, women spread their attention evenly as opposed to men who may possibly focus in more intently on exogenous cues. [ 46 ]
A study conducted involving the dichotic listening test, with emphasis on subtypes of schizophrenia (particularly paranoid and undifferentiated), demonstrated that people with paranoid schizophrenia have the largest left hemisphere advantage – whereas people with undifferentiated schizophrenia (where psychotic symptoms are present but the criteria for paranoid, disorganized, or catatonic types have not been met) having the smallest. [ 48 ] The application of the dichotic listening test helped to further the beliefs that preserved left hemisphere processing is a product of paranoid schizophrenia, and in contrast, that the left hemisphere's lack of activity is a symptom of undifferentiated schizophrenia. In 1994, M.F. Green and colleagues tried to relate "the functional integration of the left hemisphere in hallucinating and nonhallucinating psychotic patients" using a dichotic listening study. The study showed that auditory hallucinations are connected to a malfunction in the left hemisphere of the brain. [ 49 ]
Dichotic listening can also be found in the emotion-oriented parts of the brain. Further study on this matter was done by Phil Bryden and his dichotic listening research focused on emotionally loaded stimuli (Hugdahl, 2015). [ 50 ] More research, focused on how lateralization and the identification of the cortical regions of the brain created inquiries on how dichotic listening is implicated whenever two dichotic listening tasks are provided. In order to obtain results, a Functional magnetic resonance imaging (fMRI) was used by Jancke et al. (2001) to determine the activation of parts of the brain in charge of attention, auditory stimuli to a specific emotional stimuli. Following results on this experiment clarified that the dependability of the provided stimuli (Phonetic, emotion) had a significant presence on activating the different parts of the brain in charge of the specific stimuli. However, no concerning difference in cortical activation was found. [ 51 ]
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https://en.wikipedia.org/wiki/Dichotic_listening
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Dichotic listening is a psychological test commonly used to investigate selective attention and the lateralization of brain function within the auditory system . It is used within the fields of cognitive psychology and neuroscience .
In a standard dichotic listening test, a participant is presented with two different auditory stimuli simultaneously (usually speech ), directed into different ears over headphones. [ 1 ] In one type of test, participants are asked to pay attention to one or both of the stimuli; later, they are asked about the content of either the stimulus they were instructed to attend to or the stimulus they were instructed to ignore. [ 1 ] [ 2 ]
Donald Broadbent is credited with being the first scientist to systematically use dichotic listening tests in his work. [ 3 ] [ 4 ] In the 1950s, Broadbent employed dichotic listening tests in his studies of attention, asking participants to focus attention on either a left- or right-ear sequence of digits. [ 5 ] [ 6 ] He suggested that due to limited capacity, the human information processing system needs to select which channel of stimuli to attend to, deriving his filter model of attention . [ 6 ]
In the early 1960s, Doreen Kimura used dichotic listening tests to draw conclusions about lateral asymmetry of auditory processing in the brain. [ 7 ] [ 8 ] She demonstrated, for example, that healthy participants have a right-ear superiority for the reception of verbal stimuli, and left-ear superiority for the perception of melodies. [ 9 ] From that study, and others studies using neurological patients with brain lesions, she concluded that there is a predominance of the left hemisphere for speech perception, and a predominance of the right hemisphere for melodic perception. [ 10 ] [ 11 ]
In the late 1960s and early 1970s, Donald Shankweiler [ 12 ] and Michael Studdert-Kennedy [ 13 ] of Haskins Laboratories used a dichotic listening technique (presenting different nonsense syllables) to demonstrate the dissociation of phonetic (speech) and auditory (nonspeech) perception by finding that phonetic structure devoid of meaning is an integral part of language and is typically processed in the left cerebral hemisphere . [ 14 ] [ 15 ] [ 16 ] A dichotic listening performance advantage for one ear is interpreted as indicating a processing advantage in the contralateral hemisphere . In another example, Sidtis (1981) [ 17 ] found that healthy adults have a left-ear advantage on a dichotic pitch recognition experiment. He interpreted this result as indicating right-hemisphere dominance for pitch discrimination.
An alternative explanation of the right-ear advantage in speech perception is that most people being right-handed, more of them put a telephone to their right ear. [ 18 ] [ 19 ] The two explanations are not necessarily incompatible, in that telephoning behavior could be partly to do with hemispheric asymmetry. Some of the converse findings for nonspeech (e.g. environmental sounds [ 20 ] [ 21 ] ) are readily interpretable in this framework too.
During the early 1970s, Tim Rand demonstrated dichotic perception at Haskins Laboratories . [ 22 ] [ 23 ] In his study, the first stimuli: formant (F1), was presented to one ear while the second and third stimuli:(F2) and (F3) formants, were presented to the opposite ear. F2 and F3 varied in low and high intensity. Ultimately, in comparison to the binaural condition, "peripheral masking is avoided when speech is heard dichotically." [ 23 ] This demonstration was originally known as "the Rand effect" but was later renamed "dichotic release from masking". The name for this demonstration continued to evolve and was finally named "dichotic perception" or "dichotic listening." Around the same time, Jim Cutting (1976), [ 24 ] an investigator at Haskins Laboratories , researched how listeners could correctly identify syllables when different components of the syllable were presented to different ears. The formants of vowel sounds and their relation are crucial in differentiating vowel sounds. Even though the listeners heard two separate signals with neither ear receiving a 'complete' vowel sound, they could still identify the syllable sounds.
The "dichotic fused words test" (DFWT) is a modified version of the basic dichotic listening test. It was originally explored by Johnson et al. (1977) [ 25 ] but in the early 80's Wexler and Hawles (1983) [ 26 ] modified this original test to ascertain more accurate data pertaining to hemispheric specialization of language function. In the DFWT, each participant listens to pairs of monosyllabic rhyming consonant-vowel-consonant (CVC) words. Each word varies in the initial consonant. The significant difference in this test is "the stimuli are constructed and aligned in such a way that partial interaural fusion occurs: subjects generally experience and report only one stimulus per trial." [ 27 ] According to Zatorre (1989), some major advantages of this method include "minimizing attentional factors, since the percept is unitary and localized to the midline" and "stimulus dominance effects may be explicitly calculated, and their influence on ear asymmetries assessed and eliminated." [ 27 ] Wexler and Hawles study obtained a high test-retest reliability (r=0.85). [ 26 ] High test-retest reliability is good, because it proves that the data collected from the study is consistent.
An emotional version of the dichotic listening task was developed. In this version individuals listen to the same word in each ear but they hear it in either a surprised, happy, sad, angry, or neutral tone. Participants are then asked to press a button indicating what tone they heard. Usually dichotic listening tests show a right-ear advantage for speech sounds. Right-ear/left-hemisphere advantage is expected, because of evidence from Broca's area and Wernicke's area , which are both located in the left hemisphere. In contrast, the left ear (and therefore the right hemisphere) is often better at processing nonlinguistic material. [ 28 ] The data from the emotional dichotic listening task is consistent with the other studies, because participants tend to have more correct responses to their left ear than to the right. [ 29 ] It is important to note that the emotional dichotic listening task is seemingly harder for the participants than the phonemic dichotic listening task, meaning more incorrect responses were submitted by individuals.
The manipulation of voice onset time (VOT) during dichotic listening tests has given many insights regarding brain function. [ 30 ] To date, the most common design is the utilisation of four VOT conditions: short-long pairs (SL), where a Consonant-Vowel (CV) syllable with a short VOT is presented to the left ear and a CV syllable with a long VOT is presented to the right ear, as well as long-short (LS), short-short (SS) and long-long (LL) pairs. In 2006, Rimol, Eichele, and Hugdahl [ 31 ] first reported that, in healthy adults, SL pairs elicit the largest REA while, in fact, LS pairs elicit a significant left ear advantage (LEA). A study of children 5–8 years old has shown a developmental trajectory whereby long VOTs gradually start to dominate over short VOTs when LS pairs are being presented under dichotic conditions. [ 32 ] Converging evidence from studies of attentional modulation of the VOT effect shows that, around age 9, children lack the adult-like cognitive flexibility required to exert top-down control over stimulus-driven bottom-up processes. [ 33 ] [ 34 ] Arciuli et al.(2010) further demonstrated that this kind of cognitive flexibility is a predictor of proficiency with complex tasks such as reading. [ 30 ] [ 35 ]
Dichotic listening tests can also be used as lateralized speech assessment task. Neuropsychologists have used this test to explore the role of singular neuroanatomical structures in speech perception and language asymmetry. For example, Hugdahl et al. (2003), investigated dichotic listening performance and frontal lobe function [ 36 ] in left and right lesioned frontal lobe nonaphasiac patients compared to healthy controls. In the study, all groups were exposed to 36 dichotic trials with pairs of CV syllables and each patient was asked to state which syllable he or she heard best. As expected, the right lesioned patients showed a right ear advantage like the healthy control group but the left hemisphere lesioned patients displayed impairment when compared to both the right lesioned patients and control group. From this study, researchers concluded "dichotic listening as into a neuronal circuitry which also involves the frontal lobes, and that this may be a critical aspect of speech perception." [ 36 ] Similarly, Westerhausen and Hugdahl (2008) [ 37 ] analyzed the role of the corpus callosum in dichotic listening and speech perception. After reviewing many studies, it was concluded that "...dichotic listening should be considered a test of functional inter-hemispheric interaction and connectivity, besides being a test of lateralized temporal lobe language function" and "the corpus callosum is critically involved in the top-down attentional control of dichotic listening performance, thus having a critical role in auditory laterality." [ 37 ]
Dichotic listening can also be used to test the hemispheric asymmetry of language processing . In the early 60s, Doreen Kimura reported that dichotic verbal stimuli (specifically spoken numerals) presented to a participant produced a right ear advantage (REA). [ 38 ] She attributed the right-ear advantage "to the localization of speech and language processing in the so-called dominant left hemisphere of the cerebral cortex." [ 39 ] : 115 According to her study, this phenomenon was related to the structure of the auditory nerves and the left-sided dominance for language processing. [ 40 ] It is important to note that REA doesn't apply to non-speech sounds. In "Hemispheric Specialization for Speech Perception," by Studdert-Kennedy and Shankweiler (1970) [ 14 ] examine dichotic listening of CVC syllable pairs. The six stop consonants (b, d, g, p, t, k) are paired with the six vowels and a variation in the initial and final consonants are analyzed. REA is the strongest when the sound of the initial and final consonants differ and it is the weakest when solely the vowel is changed. Asbjornsen and Bryden (1996) state that "many researchers have chosen to use CV syllable pairs, usually consisting of the six stop consonants paired with the vowel \a\. Over the years, a large amount of data has been generated using such material." [ 41 ]
In selective attention experiments, the participants may be asked to repeat aloud the content of the message they are listening to. This task is known as shadowing . As Colin Cherry (1953) [ 42 ] found, people do not recall the shadowed message well, suggesting that most of the processing necessary to shadow the attended to message occurs in working memory and is not preserved in the long-term store . Performance on the unattended message is worse. Participants are generally able to report almost nothing about the content of the unattended message. In fact, a change from English to German in the unattended channel frequently goes unnoticed. However, participants are able to report that the unattended message is speech rather than non-verbal content. In addition to this, if the content of the unattended message contains certain information, such as the listener's name, then the unattended message is more likely to be noticed and remembered. [ 43 ] A demonstration of this was done by Conway, Cowen, and Bunting (2001) in which they had subjects shadow words in one ear while ignoring words in the other ear. At some point, the subject's name was spoken in the ignored ear, and the question was whether the subject would report hearing their name. Subjects with a high working memory (WM) span were more capable of blocking out the distracting information. [ 44 ] Also if the message contains sexual words then people usually notice them immediately. [ 45 ] This suggests that the unattended information is also undergoing analysis and keywords can divert attention to it.
Some data gathered from dichotic listening test experiments suggests that there is possibly a small-population sex difference in perceptual and auditory asymmetries and language laterality. According to Voyer (2011), [ 46 ] "Dichotic listening tasks produced homogenous effect sizes regardless of task type (verbal, non-verbal), reflecting a significant sex difference in the magnitude of laterality effects, with men obtaining larger laterality effects than women." [ 46 ] : 245–246 However, the authors discuss numerous limiting factors ranging from publication bias to small effect size. Furthermore, as discussed in "Attention, reliability, and validity of perceptual asymmetries in the fused dichotic words test," [ 47 ] women reported more "intrusions" or words presented to the uncued ear than men when presented with exogenous cues in the Fused Dichotic Word Task which suggests two possibilities: 1) Women experience more difficulty paying attention to the cued word than men and/or 2) regardless of the cue, women spread their attention evenly as opposed to men who may possibly focus in more intently on exogenous cues. [ 46 ]
A study conducted involving the dichotic listening test, with emphasis on subtypes of schizophrenia (particularly paranoid and undifferentiated), demonstrated that people with paranoid schizophrenia have the largest left hemisphere advantage – whereas people with undifferentiated schizophrenia (where psychotic symptoms are present but the criteria for paranoid, disorganized, or catatonic types have not been met) having the smallest. [ 48 ] The application of the dichotic listening test helped to further the beliefs that preserved left hemisphere processing is a product of paranoid schizophrenia, and in contrast, that the left hemisphere's lack of activity is a symptom of undifferentiated schizophrenia. In 1994, M.F. Green and colleagues tried to relate "the functional integration of the left hemisphere in hallucinating and nonhallucinating psychotic patients" using a dichotic listening study. The study showed that auditory hallucinations are connected to a malfunction in the left hemisphere of the brain. [ 49 ]
Dichotic listening can also be found in the emotion-oriented parts of the brain. Further study on this matter was done by Phil Bryden and his dichotic listening research focused on emotionally loaded stimuli (Hugdahl, 2015). [ 50 ] More research, focused on how lateralization and the identification of the cortical regions of the brain created inquiries on how dichotic listening is implicated whenever two dichotic listening tasks are provided. In order to obtain results, a Functional magnetic resonance imaging (fMRI) was used by Jancke et al. (2001) to determine the activation of parts of the brain in charge of attention, auditory stimuli to a specific emotional stimuli. Following results on this experiment clarified that the dependability of the provided stimuli (Phonetic, emotion) had a significant presence on activating the different parts of the brain in charge of the specific stimuli. However, no concerning difference in cortical activation was found. [ 51 ]
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Dichotic pitch (or the dichotic pitch phenomenon ) is a pitch heard due to binaural processing, when the brain combines two noises presented simultaneously to the ears. [ 1 ] In other words, it cannot be heard when the sound stimulus is presented monaurally (to one ear) but, when it is presented binaurally (simultaneously, to both ears) a sensation of a pitch can be heard. [ 2 ] The binaural stimulus is presented to both ears through headphones simultaneously, and is the same in several respects except for a narrow frequency band that is manipulated. [ 3 ] The most common variation is the Huggins Pitch, which presents white-noise that only differ in the interaural phase relation over a narrow range of frequencies. [ 3 ] For humans, this phenomenon is restricted to fundamental frequencies lower than 330 Hz and extremely low sound pressure levels. [ 4 ] Experts investigate the effects of the dichotic pitch on the brain. [ 4 ] For instance, there are studies that suggested it evokes activation at the lateral end of Heschl's gyrus . [ 5 ]
When continuous white noise (with a frequency content below about 2000 Hz) is presented by headphones to the left and right ear of a listener, binaurally, and given a particular interaural phase relationship between the left and right ear signals, a sensation of pitch (psychophysics) may be observed. [ 6 ] Thus, stimulation of either ear alone gives rise to the sensation of white noise only, but stimulation of both ears together produces pitch. Therefore, as a special case of dichotic listening , such a pitch is called dichotic pitch or binaural pitch. Generally, a dichotic pitch is perceived somewhere in the head amidst the noisy sound filling the binaural space. To be more specific, the dichotic pitch is characterized by three perceptual properties: pitch value, timbre, and in-head position (lateralization). Experiments on the dichotic pitch were motivated in the context of the study of the pitch in general, and of the binaural system in particular, relevant for sound localization and separation of competing for sound sources (see cocktail party effect ). In the past, various configurations of the dichotic pitch were studied and several auditory models were developed. However, no singular model has been developed that accounts for all aspects of the dichotic pitch, from how it is formed to the lateralization of the dichotic pitch. [ 7 ] The great challenge for psychophysical and physiological acoustics is to predict both the pitch value and pitch-image position in one model. For more information, references, audio demos etc. see more .
Huggins pitch and Binaural edge pitch elicit a pure-tone like sound at singular frequency and are generated by creating an interaural phase shift at a narrow frequency band. [ 8 ] This changes the point at which the sound wave that first reaches the ear, so the sound wave of the white noise stimulus reaches the ear at different points. In other words, the noise is decorrelated at that frequency. [ 9 ]
For HP to occur, the same white noise that is identical at all frequencies except for a narrow frequency band must be presented simultaneously to the ears. [ 2 ] An all-pass filter is used at this narrow frequency band to create an interaural phase shift from 0 to 2π radians (sometimes referred to as a 360-degree phase shift). [ 2 ] [ 10 ]
BEP is created by introducing an interaural phase shift from 0 to π radians (a 180-degree phase shift). It is best heard within the frequency range of 350–800 Hz. [ 10 ]
Both the Fourcin pitch and Dichotic repetition pitch are complex tones. They are generated by creating large interaural delays in the binaural stimulus but differ in where these large interaural delays are applied. [ 8 ]
The FP is similar to pure tones in the sense that an interaural phase shift is needed, however, it also presents different stimuli, differing in their interaural delays, to each ear at the same time. [ 8 ]
The DRP presents the same stimuli with a singular large interaural delay binaurally, simultaneously, to the ears. [ 8 ]
The equalization-cancellation (E-C) is a model that explains how the dichotic pitch is created, specifically, the Binaural edge pitch and the Huggins pitch, [ 10 ] and is related to binaural unmasking . [ 11 ]
The dichotic pitch stimulus is processed in a two-step process: equalization followed by the cancellation. [ 11 ] Equalization is the process in which the binaural system modifies the differences in the interaural time delay, level and phase. [ 12 ] [ 8 ] That is the differences in the time the stimulus reaches the ears, the difference in the loudness and frequency to each ear, and the different phase of the wave when it reaches each ear, respectively. This allows the binaural system to subtract out what was perfectly correlated in the broadband noise. What is left is the interaural phase shift created at the narrow frequency band, [ 10 ] the only part of the broadband noise that was decorrelated. [ 12 ] The results of E-C is what is heard as the HP and BEP. [ 8 ]
More specifically, the BEP is created as the E-C process creates a central spectrum with a sharp edge and a high-pass or low-pass sound where the BEP is heard. [ 8 ] [ 10 ]
It was found that the characteristics of the white noise stimulus influences where Huggins pitch is lateralized. This includes the centre frequency and interaural time delay of the white noise.
The half-period rule theorizes that the lateralization of the Huggins pitch depends on the difference in the time it takes for the noise to reach each ear, otherwise known as the interaural time delay. However, this model does not accurately account for the lateralization of the dichotic pitch under all circumstances. [ 7 ]
Using the dichotic pitch, pitch processing in relation to Heschl's gyrus in the brain was studied. Using various pitch evoking stimuli, fMRI scans in Hall & Plack's study found that multiple areas, including the Heschl's gyrus and, primarily, the planum temporale which is posterior of Heschl's gyrus, were activated by the pitch-evoking stimuli (the binaural stimulus) such as Huggins pitch. [ 9 ]
The activation of Heschl's gyrus and the planum temporale was replicated by another study that used 2 dichotic pitches (Huggins pitch and Binaural band pitch) and pure tones which sound the same as the dichotic pitch but have dissimilar characteristics to study whether the activation depended on the characteristics of the pitch. The fMRI scans showed that the dichotic pitch and its corresponding pure tone activated the same areas: the lateral end of Heschl's gyrus and the lateral border of the Planum temporal. This reflects how Heschl's gyrus activation may not depend on the characteristics of the pitch but on the pitch itself. Huggins pitch was also found to affect the region bilaterally. [ 13 ] The Planum temporale was also found to be more responsive to changes in the pitch such as those found in melodies. [ 13 ]
There have been many findings on the subject of dichotic pitch, showing that different disorders experience it in multiple different ways. Individuals with dyslexia seem to experience dichotic pitch in a similar way, too if they were trying to distinguish words and letters. Robert F. Dougherty and team, ran an experiment using both dyslexic and non-dyslexic children. The participants were given a melody to listen to and different tones were then played within the melody. The dyslexic children were able to decipher the higher-pitched tones but were unable to distinguish the lower notes from the background melody. It became apparent that the lower notes caused some sort of auditory and sensory problem for the dyslexic children that made it harder for their brain to sort out the information being sent to it. [ 1 ]
Santurette and Dau compared the ability for hearing-impaired individuals to hear the dichotic pitch to non-hearing-impaired listeners. It was found that most hearing-impaired individuals were able to hear the dichotic pitch, but had more difficulty hearing it compared to non-hearing-impaired listeners. However, not all hearing-impaired participants, such as those with central auditory processing deficits, were able to hear the dichotic pitch. While this is only preliminary research, the researchers suggested that due to the differential ability for hearing-impaired individuals to perceive the dichotic pitch, this may make the dichotic pitch a useful tool for diagnosing hearing-impaired individuals. [ 14 ]
A study done by Bianca Pinheiro Lanzetta-Valdo and the team looked at children with the diagnosis of Attention Deficit Hyperactivity Disorder (ADHD) and dichotic pitch. [ 15 ] At the beginning of the experiment, all of the children were at a base level of the medication methylphenidate, a stimulant that is used to try and calm individuals with ADHD. Over a 6-month period, the children were given auditory stimulation that consisted of white noise, and during this stimulation, they would be given physical, neurological, visual and auditory examinations, as well as biochemical tests to see if any improvement was made. Lanzetta-Valdo and collaborators did find any improvements in the participants over the 6 months in their different evaluations, but there are controversial results on this topic.
Frequency shift detectors (FSDs) are hypothesized to play a role in linking sounds together so that one can perceive words and melodies. They detect when the pitch in noise increases and decreases. [ 12 ]
Carcagno and colleagues studied whether FSDs could detect frequency changes in both dichotic pitches (binaural stimuli) and from the monaural stimulus. They used an up/down task which asked participants to discriminate between the direction of the frequency change. The dichotic pitch and monaural stimulus did not change the ability for participants to do the up/down task. The similar results obtained amongst the two trials led to the conclusion that FSDs are equally as sensitive to changes in frequency in the monaural and binaural stimulus. This also led to the conclusion that FSDs are located somewhere after the binaural convergence, the point where the auditory processing system combines the noise stimuli that has arrived at the ears. [ 12 ]
Dougherty, R.F., Cyander, M.S., Bjornson, B.H., Edgell, D., & Giaschi, D.E. (1998). Dichotic Pitch: A new stimulus distinguishes normal and dyslexic auditory function. NeruoReport.9(13) Retrieved from https://www.researchgate.net/profile/Robert_Dougherty/publication/13482828_Dichotic_pitch_A_new_stimulus_distinguishes_normal_and_dyslexic_auditory_function/links/00b4952dafbd0e7c3d000000/Dichotic-pitch-A-new-stimulus-distinguishes-normal-and-dyslexic-auditory-function.pdf
Lanzetta-Valdo, B. P., de Oliveira, G. A., Ferreira, J. C., & Palacios, E. N. (2017). Auditory Processing Assessment in Children with Attention Deficit Hyperactivity Disorder: An Open Study Examining Methylphenidate Effects. International Archives Of Otorhinolaryngology , 21 (1), 72–78. doi : 10.1055/s-0036-1572526
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The Dickson Prize in Medicine and the Dickson Prize in Science were both established in 1969 by Joseph Z. Dickson and Agnes Fischer Dickson.
The Dickson Prize in Medicine is awarded annually by the University of Pittsburgh and recognizes US citizens who have made "significant, progressive contributions" to medicine. [ 1 ] The award includes $50,000, a bronze medal, and the Dickson Prize Lecture . [ 2 ]
Source: University of Pittsburgh
The Dickson Prize in Science is awarded annually by Carnegie Mellon University and recognizes those who "have made the most progress in the scientific field in the United States for the year in question." [ 18 ] The award is dated by the year in which it was announced, which is often the year before the lecture occurs. [ 19 ]
Source: Carnegie Mellon University
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Diencephalic syndrome , or Russell's syndrome , is a rare neurological disorder seen in infants and children and characterised by failure to thrive and severe emaciation despite normal or slightly decreased caloric intake. Classically there is also locomotor hyperactivity and euphoria. Less commonly diencephalic syndrome may involve skin pallor without anaemia , hypoglycaemia , and hypotension . [ 1 ] The syndrome is a rare but potentially fatal cause of failure to thrive in children. Failure to thrive presents on average at seven months of age. [ 1 ] Of note the syndrome is not associated with developmental delay. [ 2 ] There may be associated hydrocephalus . [ citation needed ]
Diencephalic syndrome was first described by Dr. A. Russell in 1951. [ 3 ] It is usually caused by a brain tumor such as a low-grade glioma or astrocytoma located in the hypothalamic - optic chiasmatic region. [ 1 ] It is not yet understood how diencephalic syndrome causes the effects on appetite and metabolism which are seen, though inappropriately high growth hormone release has been proposed, [ 4 ] as has excessive β-lipotropin secretion [ 1 ] and overall increased metabolic demand. [ 5 ] It is treated with nutritional optimisation while the underlying lesion is treated with chemotherapy , surgery or radiotherapy . [ citation needed ]
This article about a medical condition affecting the nervous system is a stub . You can help Wikipedia by expanding it .
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Many dietary recommendations have been proposed to reduce the risk of cancer, few have significant supporting scientific evidence. [ 1 ] [ 2 ] [ 3 ] Obesity and drinking alcohol have been correlated with the incidence and progression of some cancers. [ 1 ] Lowering the consumption of sweetened beverages is recommended as a measure to address obesity. [ 4 ]
Some specific foods are linked to specific cancers. There is strong evidence that processed meat and red meat intake increases risk of colorectal cancer . [ 5 ] [ 6 ] [ 7 ] [ 8 ] Aflatoxin B 1 , a frequent food contaminant, increases risk of liver cancer , [ 9 ] while drinking coffee is associated with a reduced risk. [ 10 ] Betel nut chewing causes oral cancer . [ 9 ] Stomach cancer is more common in Japan due to its high-salt diet. [ 9 ] [ 11 ]
Dietary recommendations for cancer prevention typically include weight management and eating a healthy diet , consisting mainly of "vegetables, fruit, whole grains and fish, and a reduced intake of red meat, animal fat, and refined sugar." [ 1 ] A healthy dietary pattern may lower cancer risk by 10–20%. [ 12 ] There is no clinical evidence that diets or specific foods can cure cancer. [ 13 ] [ 14 ]
It is a popular misconception that cancer can be treated by "starving" a tumour or restricting carbohydrate intake, when in reality the health of people with cancer is best served by following a healthy diet . [ 15 ] A number of specific diets and diet-based regimes have been claimed to be useful against cancer, including the Breuss diet , Gerson therapy , the Budwig protocol and the macrobiotic diet . None of these diets has been found to be effective, and some of them have been found to be harmful. [ 16 ]
Nutritional epidemiologists use multivariate statistics , such as principal components analysis and factor analysis , to measure how patterns of dietary behavior influence the risk of developing cancer. [ 17 ] (The most well-studied dietary pattern is the Mediterranean diet .) Based on their dietary pattern score, epidemiologists categorize people into quantiles . To estimate the influence of dietary behavior on risk of cancer, they measure the association between quantiles and the distribution of cancer prevalence (in case–control studies ) and cancer incidence (in longitudinal studies ). They usually include other variables in their statistical model to account for the other differences between people with and without cancer ( confounders ). For breast cancer , there is a replicated trend for women with a more "prudent or healthy" diet, i.e. higher in fruits and vegetables , to have a lower risk of cancer. [ 18 ]
Unhealthy dietary patterns are associated with a higher body mass index suggesting a potential mediating effect of obesity on cancer risk. [ 19 ]
The Western pattern diet has been generally linked to increased risk for colorectal cancer . [ 20 ] Meta-analyses have found that diet patterns consistent with those of the Western pattern diet are positively correlated with risk for prostate cancer . [ 21 ] [ 22 ] Greater adherence to a Western pattern diet was also found to increase the overall risk of mortality due to cancer. [ 23 ]
Alcohol is associated with an increased risk of a number of cancers. [ 30 ] It has been reported that 3.6% of all cancer cases and 3.5% of cancer deaths worldwide are attributable to drinking of alcohol. [ 31 ] Breast cancer in women is linked with alcohol intake. [ 1 ] [ 32 ] Alcohol also increases the risk of cancers of the mouth, esophagus, pharynx and larynx, [ 33 ] colorectal cancer , [ 34 ] [ 35 ] liver cancer , [ 36 ] stomach [ 37 ] and ovaries . [ 38 ] The International Agency for Research on Cancer (Centre International de Recherche sur le Cancer) of the World Health Organization has classified alcohol as a Group 1 carcinogen . Its evaluation states, "There is sufficient evidence for the carcinogenicity of alcoholic beverages in humans. ... Alcoholic beverages are carcinogenic to humans (Group 1)." [ 39 ]
A 2015 meta-analysis found an association between higher egg consumption (five a week) with increased risk of breast cancer compared to no egg consumption. [ 40 ] Another meta-analysis found that egg consumption may increase ovarian cancer risk. [ 41 ]
A 2019 meta-analysis found an association between high egg consumption and risk of upper aero-digestive tract cancers in hospital-based case-control studies. [ 42 ]
There is strong evidence that processed meat and red meat intake increases risk of colorectal cancer. [ 45 ] [ 46 ] [ 47 ] The American Cancer Society in their "Diet and Physical Activity Guideline", stated "evidence that red and processed meats increase cancer risk has existed for decades, and many health organizations recommend limiting or avoiding these foods." [ 48 ]
On October 26, 2015, the International Agency for Research on Cancer of the World Health Organization reported that eating processed meat (e.g., bacon, ham, hot dogs, sausages) or red meat was linked to some cancers and classed them as Group 1 (carcinogenic to humans) and Group 2a (probably carcinogenic to humans) carcinogens respectively. [ 49 ] There is some evidence that suggests that heme and nitrite are involved in the processes linking red and processed meat intake with colorectal cancer. [ 49 ] Heme is present in particular in red meat and nitrite is used as curing salt in many processed meats.
Processed and unprocessed red meat intake is associated with an increased risk of breast cancer . [ 50 ] [ 51 ]
The World Health Organization has found that the consumption of processed meat , and potentially red meat , promote carcinogenesis and can increase the risk of colorectal cancer . [ 52 ] Colorectal cancer is the second most common cause of cancer death in the world. [ 53 ] A 2023 systematic review and meta analysis found that meat consumption was associated with an increased risk of colorectal cancer, colon cancer and rectal cancer. [ 54 ] A meta analysis reported in 2024, provided evidence that consumption of high levels of red meat increased the risk of developing esophageal , pancreatic , liver , colon, rectal and colorectal cancers, and that consumption of processed meat (as distinct from red meat) also increased the levels of pancreatic colon, rectal and colorectal cancers. [ 55 ] In contrast, high consumption of fish significantly reduced the risk of colon, rectal and colorectal cancers. [ 55 ]
A metabolic link has been suggested between a fat- and meat rich diet and cancer associated gut microbes that convert primary bile acids into secondary carcinogenic bile acids. [ 56 ]
There is strong evidence that consumption of dietary fiber reduces risk of colorectal cancer. [ 3 ] [ 62 ] [ 63 ] Two 2020 meta-analyses found that a high fiber intake was associated with a lower risk of both premenopausal and postmenopausal breast cancers [ 64 ] and a higher survival rate in patients with breast cancer. [ 65 ]
A 2021 review found that there is moderate-quality evidence 200g of fruit intake per day is associated with a lower risk of breast cancer. [ 66 ] Another review found that high total fruit and vegetable consumption are associated with reduced risk of breast cancer. [ 67 ] A 2024 review found convincing evidence for high dietary fiber intake associated with lower breast cancer risk. [ 68 ]
In 1993, the World Health Organization listed traditional Asian pickled vegetables as possible carcinogens , [ 69 ] and the British Journal of Cancer released an online 2009 meta-analysis of research on pickles as increasing the risks of esophageal cancer . The report, citing limited data in a statistical meta analysis, indicates a potential two-fold increased risk of esophageal cancer associated with Asian pickled vegetable consumption. Results from the research are described as having "high heterogeneity" and the study said that further well-designed prospective studies were warranted. [ 70 ] However, their results stated "The majority of subgroup analyses showed a statistically significant association between consuming pickled vegetables and Oesophageal Squamous Cell Carcinoma". [ 70 ]
Consuming pickled vegetables is also associated with a 28% increase in the risk of stomach cancer . [ 71 ]
The 2009 meta-analysis reported heavy infestation of pickled vegetables with fungi . Some common fungi can facilitate the formation of N-nitroso compounds , which are strong esophageal carcinogens in several animal models. [ 72 ] Roussin red methyl ester, [ 73 ] a non-alkylating nitroso compound with tumour-promoting effect in vitro, was identified in pickles from Linzhou, Henan (formerly Linxian) in much higher concentrations than in samples from low-incidence areas. Fumonisin mycotoxins have been shown to cause liver and kidney tumours in rodents. [ 70 ]
A 2017 study in Chinese Journal of Cancer [ 74 ] has linked salted vegetables ( pickled mustard green [ zh ] common in Chinese cuisine ) to a fourfold increase in nasopharynx cancer . The researchers believe possible mechanisms include production of nitrosamines (a type of N-nitroso compound) by fermentation and activation of Epstein–Barr virus by fermentation products. [ 75 ] [ 76 ]
Flavonoids (specifically flavonoids such as the catechins) are "the most common group of polyphenolic compounds in the human diet and are found ubiquitously in plants." [ 77 ] While some studies have suggested flavonoids may have a role in cancer prevention, others have been inconclusive or suggested they may be harmful. [ 78 ] [ 79 ]
Restriction of methionine has been suggested as a strategy in cancer growth control in cancers that depend on methionine for survival and proliferation. [ 80 ] According to a 2012 review, the effect of methionine restriction on cancer has yet to be studied directly in humans and "there is still insufficient knowledge to give reliable nutritional advice". [ 80 ]
Reviews of epidemiological studies have found no association between dietary methionine and breast or pancreatic cancer risk. [ 81 ] [ 82 ]
According to Cancer Research UK , "there is currently no evidence that any type of mushroom or mushroom extract can prevent or cure cancer", although research into some species continues. [ 83 ]
A 2020 review found that higher mushroom consumption is associated with lower risk of breast cancer . [ 84 ]
There is no scientific evidence that consuming dairy products causes cancer. [ 85 ] The British Dietetic Association have described the idea that milk promotes hormone related cancerous tumour growth as a myth, stating "no link between dairy containing diets and risk of cancer or promoting cancer growth as a result of hormones". [ 86 ] In 2024, Cancer Research UK stated "there is no reliable evidence that casein or hormones in dairy causes cancer in people". [ 85 ] The American Cancer Society (ACS) does not make specific recommendations on dairy food consumption for cancer prevention. [ 87 ] Higher-quality research is needed to characterise valid associations between dairy consumption and risk of and/or cancer-related mortality. [ 88 ]
There is strong evidence that consumption of whole grains decreases risk of colorectal cancer . [ 63 ] [ 92 ] [ 93 ] [ 94 ]
Several reviews of case–control studies have found that saturated fat intake is associated with breast cancer risk and mortality. [ 95 ] [ 96 ] [ 97 ] Observational studies have shown that a diet high in saturated fat is associated with increased prostate cancer risk. [ 98 ]
The American Cancer Society have stated that "there is some evidence from human and lab studies that consuming traditional soy foods such as tofu may lower the risk of breast and prostate cancer, but overall the evidence is too limited to draw firm conclusions". [ 100 ]
A 2023 review found that soy protein lowers breast cancer risk. [ 101 ]
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Diff-Quik is a commercial Romanowsky stain variant used to rapidly stain and differentiate a variety of pathology specimens. It is most frequently used for blood films and cytopathological smears, including fine needle aspirates . [ 1 ] [ 2 ] [ 3 ] The Diff-Quik procedure is based on a modification of the Wright-Giemsa stain pioneered by Harleco in the 1970s, [ 1 ] and has advantages over the routine Wright-Giemsa staining technique in that it reduces the 4-minute process into a much shorter operation and allows for selective increased eosinophilic or basophilic staining depending upon the time the smear is left in the staining solutions. [ 4 ]
There are generic brands of such stain, [ 1 ] [ 5 ] and the trade name is sometimes used loosely to refer to any such stain (much as "Coke" or "Band-Aid" are sometimes used imprecisely).
Diff-Quik may be utilized on material which is air-dried prior to alcohol fixation rather than immersed immediately (i.e. "wet-fixed"), although immediate alcohol fixation results in improved microscopic detail. [ 2 ] [ 3 ] [ 6 ]
The primary use of Romanowsky-type stains in cytopathology is for cytoplasmic detail , while Papanicolaou stain is used for nuclear detail. Diff-Quik stain highlights cytoplasmic elements such as mucins , fat droplets and neurosecretory granules. Extracellular substances, such as free mucin, colloid, and ground substance , are also easily stained, and appear metachromatic . Major applications include blood smears , bone marrow aspirates, semen analysis and cytology of various body fluids including urine and cerebrospinal fluid . [ 7 ] [ 8 ] Microbiologic agents, such as bacteria and fungi, also appear more easily in Diff-Quik. [ 3 ] This is useful for the detection of for example Helicobacter pylori from gastric and pyloric specimens. [ 5 ]
Due to its short staining time, Diff-Quik stain is often used for initial screening of cytopathology specimens. This staining technique allows the cytotechnologist or pathologist to quickly assess the adequacy of the specimen, identify possible neoplastic or inflammatory changes, and decide whether or not additional staining is required. [ 4 ] [ 9 ] [ 10 ]
The Diff-Quik stain consists of 3 solutions: [ 4 ]
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In healthcare, a differential diagnosis ( DDx ) is a method of analysis that distinguishes a particular disease or condition from others that present with similar clinical features. [ 1 ] Differential diagnostic procedures are used by clinicians to diagnose the specific disease in a patient , or, at least, to consider any imminently life-threatening conditions. Often, each possible disease is called a differential diagnosis (e.g., acute bronchitis could be a differential diagnosis in the evaluation of a cough, even if the final diagnosis is common cold ).
More generally, a differential diagnostic procedure is a systematic diagnostic method used to identify the presence of a disease entity where multiple alternatives are possible. This method may employ algorithms, akin to the process of elimination , or at least a process of obtaining information that decreases the "probabilities" of candidate conditions to negligible levels, by using evidence such as symptoms, patient history, and medical knowledge to adjust epistemic confidences in the mind of the diagnostician (or, for computerized or computer-assisted diagnosis, the software of the system).
Differential diagnosis can be regarded as implementing aspects of the hypothetico-deductive method , in the sense that the potential presence of candidate diseases or conditions can be viewed as hypotheses that clinicians further determine as being true or false.
A differential diagnosis is also commonly used within the field of psychiatry / psychology , where two different diagnoses can be attached to a patient who is exhibiting symptoms that could fit into either diagnosis. For example, a patient who has been diagnosed with bipolar disorder may also be given a differential diagnosis of borderline personality disorder , [ 2 ] given the similarity in the symptoms of both conditions.
Strategies used in preparing a differential diagnosis list vary with the experience of the healthcare provider. While novice providers may work systemically to assess all possible explanations for a patient's concerns, those with more experience often draw on clinical experience and pattern recognition to protect the patient from delays, risks, and cost of inefficient strategies or tests. Effective providers utilize an evidence-based approach, complementing their clinical experience with knowledge from clinical research . [ 3 ]
A differential diagnosis has four general steps. The clinician will:
A mnemonic to help in considering multiple possible pathological processes is VINDICATEM : [ citation needed ] [ clarification needed ]
There are several methods for differential diagnostic procedures and several variants among those. Furthermore, a differential diagnostic procedure can be used concomitantly or alternately with protocols, guidelines, or other diagnostic procedures (such as pattern recognition or using medical algorithms ). [ citation needed ]
For example, in case of medical emergency , there may not be enough time to do any detailed calculations or estimations of different probabilities, in which case the ABC protocol (airway, breathing and circulation) may be more appropriate. Later, when the situation is less acute, a more comprehensive differential diagnostic procedure may be adopted.
The differential diagnostic procedure may be simplified if a " pathognomonic " sign or symptom is found (in which case it is almost certain that the target condition is present) or in the absence of a sine qua non sign or symptom (in which case it is almost certain that the target condition is absent).
A diagnostician can be selective, considering first those disorders that are more likely (a probabilistic approach), more serious if left undiagnosed and untreated (a prognostic approach), or more responsive to treatment if offered (a pragmatic approach). [ 7 ] Since the subjective probability of the presence of a condition is never exactly 100% or 0%, the differential diagnostic procedure may aim at specifying these various probabilities to form indications for further action.
The following are two methods of differential diagnosis, being based on epidemiology and likelihood ratios, respectively.
One method of performing a differential diagnosis by epidemiology aims to estimate the probability of each candidate condition by comparing their probabilities to have occurred in the first place in the individual. It is based on probabilities related both to the presentation (such as pain) and probabilities of the various candidate conditions (such as diseases). [ citation needed ]
The statistical basis for differential diagnosis is Bayes' theorem . As an analogy, when a die has landed the outcome is certain by 100%, but the probability that it Would Have Occurred in the First Place (hereafter abbreviated WHOIFP ) is still 1/6. In the same way, the probability that a presentation or condition would have occurred in the first place in an individual (WHOIFPI) is not same as the probability that the presentation or condition has occurred in the individual, because the presentation has occurred by 100% certainty in the individual. Yet, the contributive probability fractions of each condition are assumed the same, relatively:
where:
When an individual presents with a symptom or sign, Pr(Presentation has occurred in individual) is 100% and can therefore be replaced by 1, and can be ignored since division by 1 does not make any difference:
The total probability of the presentation to have occurred in the individual can be approximated as the sum of the individual candidate conditions:
Also, the probability of the presentation to have been caused by any candidate condition is proportional to the probability of the condition, depending on what rate it causes the presentation:
where:
The probability that a condition would have occurred in the first place in an individual is approximately equal to that of a population that is as similar to the individual as possible except for the current presentation, compensated where possible by relative risks given by known risk factor that distinguish the individual from the population:
where:
The following table demonstrates how these relations can be made for a series of candidate conditions:
One additional "candidate condition" is the instance of there being no abnormality, and the presentation is only a (usually relatively unlikely) appearance of a basically normal state. Its probability in the population ( P(No abnormality in population) ) is complementary to the sum of probabilities of "abnormal" candidate conditions.
This example case demonstrates how this method is applied but does not represent a guideline for handling similar real-world cases. Also, the example uses relatively specified numbers with sometimes several decimals , while in reality, there are often simply rough estimations, such as of likelihoods being very high , high , low or very low , but still using the general principles of the method. [ citation needed ]
For an individual (who becomes the "patient" in this example), a blood test of, for example, serum calcium shows a result above the standard reference range , which, by most definitions, classifies as hypercalcemia , which becomes the "presentation" in this case. A clinician (who becomes the "diagnostician" in this example), who does not currently see the patient, gets to know about his finding.
By practical reasons, the clinician considers that there is enough test indication to have a look at the patient's medical records . For simplicity, let's say that the only information given in the medical records is a family history of primary hyperparathyroidism (here abbreviated as PH), which may explain the finding of hypercalcemia. For this patient, let's say that the resultant hereditary risk factor is estimated to confer a relative risk of 10 (RR PH = 10).
The clinician considers that there is enough motivation to perform a differential diagnostic procedure for the finding of hypercalcemia. The main causes of hypercalcemia are primary hyperparathyroidism (PH) and cancer , so for simplicity, the list of candidate conditions that the clinician could think of can be given as:
The probability that 'primary hyperparathyroidism' (PH) would have occurred in the first place in the individual ( P(PH WHOIFPI) ) can be calculated as follows:
Let's say that the last blood test taken by the patient was half a year ago and was normal and that the incidence of primary hyperparathyroidism in a general population appropriately matches the individual (except for the presentation and mentioned heredity) is 1 in 4000 per year. Ignoring more detailed retrospective analyses (such as including speed of disease progress and lag time of medical diagnosis ), the time-at-risk for having developed primary hyperparathyroidism can roughly be regarded as being the last half-year because a previously developed hypercalcemia would probably have been caught up by the previous blood test. This corresponds to a probability of primary hyperparathyroidism (PH) in the population of:
With the relative risk conferred from the family history, the probability that primary hyperparathyroidism (PH) would have occurred in the first place in the individual given from the currently available information becomes:
Primary hyperparathyroidism can be assumed to cause hypercalcemia essentially 100% of the time (r PH → hypercalcemia = 1), so this independently calculated probability of primary hyperparathyroidism (PH) can be assumed to be the same as the probability of being a cause of the presentation:
For cancer , the same time-at-risk is assumed for simplicity, and let's say that the incidence of cancer in the area is estimated at 1 in 250 per year, giving a population probability of cancer of:
For simplicity, let's say that any association between a family history of primary hyperparathyroidism and risk of cancer is ignored, so the relative risk for the individual to have contracted cancer in the first place is similar to that of the population (RR cancer = 1):
However, hypercalcemia only occurs in, very approximately, 10% of cancers, [ 8 ] (r cancer → hypercalcemia = 0.1), so:
The probabilities that hypercalcemia would have occurred in the first place by other candidate conditions can be calculated in a similar manner. However, for simplicity, let's say that the probability that any of these would have occurred in the first place is calculated at 0.0005 in this example.
For the instance of there being no disease , the corresponding probability in the population is complementary to the sum of probabilities for other conditions:
The probability that the individual would be healthy in the first place can be assumed to be the same:
The rate at which the case of no abnormal condition still ends up in measurement of serum calcium of being above the standard reference range (thereby classifying as hypercalcemia) is, by the definition of standard reference range, less than 2.5%. However, this probability can be further specified by considering how much the measurement deviates from the mean in the standard reference range. Let's say that the serum calcium measurement was 1.30 mmol/L, which, with a standard reference range established at 1.05 to 1.25 mmol/L, corresponds to a standard score of 3 and a corresponding probability of 0.14% that such degree of hypercalcemia would have occurred in the first place in the case of no abnormality:
Subsequently, the probability that hypercalcemia would have resulted from no disease can be calculated as:
The probability that hypercalcemia would have occurred in the first place in the individual can thus be calculated as:
Subsequently, the probability that hypercalcemia is caused by primary hyperparathyroidism (PH) in the individual can be calculated as:
Similarly, the probability that hypercalcemia is caused by cancer in the individual can be calculated as:
and for other candidate conditions:
and the probability that there actually is no disease:
For clarification, these calculations are given as the table in the method description:
Thus, this method estimates that the probability that the hypercalcemia is caused by primary hyperparathyroidism, cancer, other conditions or no disease at all are 37.3%, 6.0%, 14.9%, and 41.8%, respectively, which may be used in estimating further test indications.
This case is continued in the example of the method described in the next section.
The procedure of differential diagnosis can become extremely complex when fully taking additional tests and treatments into consideration. One method that is somewhat a tradeoff between being clinically perfect and being relatively simple to calculate is one that uses likelihood ratios to derive subsequent post-test likelihoods.
The initial likelihoods for each candidate condition can be estimated by various methods, such as:
One method of estimating likelihoods even after further tests uses likelihood ratios (which is derived from sensitivities and specificities ) as a multiplication factor after each test or procedure. In an ideal world, sensitivities and specificities would be established for all tests for all possible pathological conditions. In reality, however, these parameters may only be established for one of the candidate conditions. Multiplying with likelihood ratios necessitates conversion of likelihoods from probabilities to odds in favor (hereafter simply termed "odds") by:
However, only the candidate conditions with known likelihood ratio need this conversion. After multiplication, conversion back to probability is calculated by:
The rest of the candidate conditions (for which there is no established likelihood ratio for the test at hand) can, for simplicity, be adjusted by subsequently multiplying all candidate conditions with a common factor to again yield a sum of 100%.
The resulting probabilities are used for estimating the indications for further medical tests , treatments or other actions. If there is an indication for an additional test, and it returns with a result, then the procedure is repeated using the likelihood ratio of the additional test. With updated probabilities for each of the candidate conditions, the indications for further tests, treatments, or other actions change as well, and so the procedure can be repeated until an endpoint where there no longer is any indication for currently performing further actions. Such an endpoint mainly occurs when one candidate condition becomes so certain that no test can be found that is powerful enough to change the relative probability profile enough to motivate any change in further actions. Tactics for reaching such an endpoint with as few tests as possible includes making tests with high specificity for conditions of already outstandingly high-profile-relative probability, because the high likelihood ratio positive for such tests is very high, bringing all less likely conditions to relatively lower probabilities. Alternatively, tests with high sensitivity for competing candidate conditions have a high likelihood ratio negative , potentially bringing the probabilities for competing candidate conditions to negligible levels. If such negligible probabilities are achieved, the clinician can rule out these conditions, and continue the differential diagnostic procedure with only the remaining candidate conditions.
This example continues for the same patient as in the example for the epidemiology-based method. As with the previous example of epidemiology-based method, this example case is made to demonstrate how this method is applied but does not represent a guideline for handling similar real-world cases. Also, the example uses relatively specified numbers, while in reality, there are often just rough estimations. In this example, the probabilities for each candidate condition were established by an epidemiology-based method to be as follows:
These percentages could also have been established by experience at the particular clinic by knowing that these are the percentages for final diagnosis for people presenting to the clinic with hypercalcemia and having a family history of primary hyperparathyroidism.
The condition of highest profile-relative probability (except "no disease") is primary hyperparathyroidism (PH), but cancer is still of major concern, because if it is the actual causative condition for the hypercalcemia, then the choice of whether to treat or not likely means life or death for the patient, in effect potentially putting the indication at a similar level for further tests for both of these conditions.
Here, let's say that the clinician considers the profile-relative probabilities of being of enough concern to indicate sending the patient a call for a clinician visit, with an additional visit to the medical laboratory for an additional blood test complemented with further analyses, including parathyroid hormone for the suspicion of primary hyperparathyroidism.
For simplicity, let's say that the clinician first receives the blood test (in formulas abbreviated as "BT") result for the parathyroid hormone analysis and that it showed a parathyroid hormone level that is elevated relative to what would be expected by the calcium level.
Such a constellation can be estimated to have a sensitivity of approximately 70% and a specificity of approximately 90% for primary hyperparathyroidism. [ 9 ] This confers a likelihood ratio positive of 7 for primary hyperparathyroidism.
The probability of primary hyperparathyroidism is now termed Pre-BT PH because it corresponds to before the blood test (Latin preposition prae means before). It was estimated at 37.3%, corresponding to an odds of 0.595. With the likelihood ratio positive of 7 for the blood test, the post- test odds is calculated as:
where:
An Odds(PostBT PH ) of 4.16 is again converted to the corresponding probability by:
The sum of the probabilities for the rest of the candidate conditions should therefore be:
Before the blood test for parathyroid hormone, the sum of their probabilities were:
Therefore, to conform to a sum of 100% for all candidate conditions, each of the other candidates must be multiplied by a correcting factor:
For example, the probability of cancer after the test is calculated as:
The probabilities for each candidate conditions before and after the blood test are given in following table:
These "new" percentages, including a profile-relative probability of 80% for primary hyperparathyroidism, underlie any indications for further tests, treatments, or other actions. In this case, let's say that the clinician continues the plan for the patient to attend a clinician visit for a further checkup, especially focused on primary hyperparathyroidism.
A clinician visit can, theoretically, be regarded as a series of tests, including both questions in a medical history , as well as components of a physical examination , where the post-test probability of a previous test, can be used as the pre-test probability of the next. The indications for choosing the next test are dynamically influenced by the results of previous tests.
Let's say that the patient in this example is revealed to have at least some of the symptoms and signs of depression, bone pain, joint pain or constipation of more severity than what would be expected by the hypercalcemia itself, supporting the suspicion of primary hyperparathyroidism, [ 10 ] and let's say that the likelihood ratios for the tests, when multiplied together, roughly results in a product of 6 for primary hyperparathyroidism.
The presence of unspecific pathologic symptoms and signs in the history and examination are often concurrently indicative of cancer as well, and let's say that the tests gave an overall likelihood ratio estimated at 1.5 for cancer. For other conditions, as well as the instance of not having any disease at all, let's say that it is unknown how they are affected by the tests at hand, as often happens in reality. This gives the following results for the history and physical examination (abbreviated as P&E):
These probabilities after the history and examination may make the physician confident enough to plan the patient for surgery for a parathyroidectomy to resect the affected tissue.
At this point, the probability of "other conditions" is so low that the physician cannot think of any test for them that could make a difference that would be substantial enough to form an indication for such a test , and the physician thereby practically regards "other conditions" as ruled out, in this case not primarily by any specific test for such other conditions that were negative, but rather by the absence of positive tests so far.
For "cancer", the cutoff at which to confidently regard it as ruled out maybe more stringent because of severe consequences of missing it, so the physician may consider that at least a histopathologic examination of the resected tissue is indicated.
This case is continued in the example of Combinations in the corresponding section below.
The validity of both the initial estimation of probabilities by epidemiology and further workup by likelihood ratios are dependent on the inclusion of candidate conditions that are responsible for a large part as possible of the probability of having developed the condition, and it is clinically important to include those where relatively fast initiation of therapy is most likely to result in the greatest benefit. If an important candidate condition is missed, no method of differential diagnosis will supply the correct conclusion. The need to find more candidate conditions for inclusion increases with the increasing severity of the presentation itself. For example, if the only presentation is a deviating laboratory parameter and all common harmful underlying conditions have been ruled out, then it may be acceptable to stop finding more candidate conditions, but this would much more likely be unacceptable if the presentation would have been severe pain.
If two conditions get high post-test probabilities, especially if the sum of the probabilities for conditions with known likelihood ratios becomes higher than 100%, then the actual condition is a combination of the two. In such cases, that combined condition can be added to the list of candidate conditions, and the calculations should start over from the beginning.
To continue the example used above, let's say that the history and physical examination were indicative of cancer as well, with a likelihood ratio of 3, giving an Odds(PostH&E) of 0.057, corresponding to a P(PostH&E) of 5.4%. This would correspond to a "Sum of known P(PostH&E)" of 101.5%. This is an indication for considering a combination of primary hyperparathyroidism and cancer, such as, in this case, a parathyroid hormone-producing parathyroid carcinoma . A recalculation may therefore be needed, with the first two conditions being separated into "primary hyperparathyroidism without cancer", "cancer without primary hyperparathyroidism" as well as "combined primary hyperparathyroidism and cancer", and likelihood ratios being applied to each condition separately. In this case, however, tissue has already been resected, wherein a histopathologic examination can be performed that includes the possibility of parathyroid carcinoma in the examination (which may entail appropriate sample staining ).
Let's say that the histopathologic examination confirms primary hyperparathyroidism, but also showed a malignant pattern. By an initial method by epidemiology, the incidence of parathyroid carcinoma is estimated at 1 in 6 million people per year, [ 11 ] giving a very low probability before taking any tests into consideration. In comparison, the probability that non-malignant primary hyperparathyroidism would have occurred at the same time as an unrelated non-carcinoma cancer that presents with malignant cells in the parathyroid gland is calculated by multiplying the probabilities of the two. The resultant probability is, however, much smaller than the 1 in 6 million. Therefore, the probability of parathyroid carcinoma may still be close to 100% after histopathologic examination despite the low probability of occurring in the first place.
Machine differential diagnosis is the use of computer software to partly or fully make a differential diagnosis. It may be regarded as an application of artificial intelligence . Alternatively, it may be seen as "augmented intelligence" if it meets the FDA criteria, namely that (1) it reveals the underlying data, (2) reveals the underlying logic, and (3) leaves the clinician in charge to shape and make the decision. Machine learning AI is generally seen as a device by the FDA, whereas augmented intelligence applications are not.
Many studies demonstrate improvement of quality of care and reduction of medical errors by using such decision support systems. Some of these systems are designed for a specific medical problem such as schizophrenia, [ 12 ] Lyme disease [ 13 ] or ventilator-associated pneumonia. [ 14 ] Others are designed to cover all major clinical and diagnostic findings to assist physicians with faster and more accurate diagnosis.
However, these tools all still require advanced medical skills to rate symptoms and choose additional tests to deduce the probabilities of different diagnoses. Machine differential diagnosis is also currently unable to diagnose multiple concurrent disorders. [ 15 ] Their usage by non-experts is therefore not a substitute for professional diagnosis.
The method of differential diagnosis was first suggested for use in the diagnosis of mental disorders by Emil Kraepelin . It is more systematic than the old-fashioned method of diagnosis by gestalt (impression). [ citation needed ]
"Differential diagnosis" is also used more loosely to refer simply to a list of the most common causes of a given symptom, to a list of disorders similar to a given disorder, or to such lists when they are annotated with advice on how to narrow the list down ( French's Index of Differential Diagnosis is an example). Thus, a differential diagnosis in this sense is medical information specially organized to aid in diagnosis.
Methods similar to those of differential diagnostic processes in medicine are also used by biological taxonomists to identify and classify organisms, living and extinct. For example, after finding an unknown species, there can first be a listing of all potential species, followed by ruling out of one by one until, optimally, only one potential choice remains.
Similar procedures may be used by plant and maintenance engineers and automotive mechanics and used to be used in diagnosing faulty electronic circuitry.
In the American television medical drama House , the main protagonist Dr. Gregory House leads a team of diagnosticians who regularly use differential diagnostics procedures.
Signs and symptoms Syndrome Disease
Medical diagnosis Differential diagnosis Prognosis
Acute Chronic Cure
Eponymous disease Acronym or abbreviation Remission
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Differential staining is a staining process which uses more than one chemical stain . [ 1 ] Using multiple stains can better differentiate between different microorganisms or structures/cellular components of a single organism.
Differential staining is used to detect abnormalities in the proportion of different white blood cells in the blood . The process or results are called a WBC differential . This test is useful because many diseases alter the proportion of certain white blood cells . By analyzing these differences in combination with a clinical exam and other lab tests, medical professionals can diagnose disease.
One commonly recognizable use of differential staining is the Gram stain . Gram staining uses two dyes: Crystal violet and Fuchsin or Safranin (the counterstain) to differentiate between Gram-positive bacteria (large Peptidoglycan layer on outer surface of cell) and Gram-negative bacteria.
Acid-fast stains are also differential stains.
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Differentiation therapy is a method to treating advanced cancers in which malignant cells are encouraged to differentiate into more mature forms using pharmacological agents. The basis of the therapy stems from the tendency of malignant tumor cells to assume a less specialized, stem cell -like dedifferentiated state. [ 1 ]
The approach was motivated by noticing that leukemia cells fail to differentiate and fully mature. [ 2 ]
By 2001 encouraging clinical results were seen. [ 3 ]
The first differentiation agent found to be successful was all-trans-retinoic acid (ATRA) in the treatment of acute promyelocytic leukemia (APL). [ 1 ]
The process of cancer spreading ( metastasis ) involves tumour cells undergoing an epithelial-to-mesenchymal transition (EMT) to invade and spread, followed by a mesenchymal-to-epithelial transition (MET) at remote sites.
Other agents investigated (pre-clinically) to encourage MET include cholera toxin (CTx) and forskolin (Fsk). [ 4 ]
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Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia ( DIPNECH ) is a diffuse parenchymal lung disease which often presents with symptoms of cough and shortness of breath. The pathological definition published by the World Health Organization is “a generalized proliferation of scattered single cells, small nodules (neuroendocrine bodies), or linear proliferations of pulmonary neuroendocrine (PNE) cells that may be confined to the bronchial and bronchiolar epithelium.” [ 1 ] The true prevalence of this disease is not known. To date, just under 200 cases have been reported in the literature. [ 2 ] However, with an increase in recognition of this disease by radiologists and pulmonologists, the number of cases has been increasing. DIPNECH predominantly affects middle-aged women [ 3 ] with slowly progressive lung obstruction. DIPNECH is usually discovered in one of two ways: 1) as an unexpected finding following a lung surgery; or 2) by evaluation of a patient in a pulmonary clinic with longstanding, unexplained symptoms. [ 4 ]
About 20% of DIPNECH patients are symptom free at the time they first present. The most common symptoms include: [ 5 ] [ 6 ] [ 7 ]
Symptoms may be present for many years prior to diagnosis and are often ascribed to other lung conditions. Erroneous initial diagnoses of asthma or chronic obstructive pulmonary disease often are made in patients with DIPNECH. [ 8 ]
The major criterion for diagnosis is typically a confirmed surgical biopsy . Minor diagnostic criteria have been proposed for DIPNECH. [ 8 ]
In most DIPNECH cases, upon examination of the lung tissue, the overgrowth of pulmonary neuroendocrine cells is seen along the small airways, with extension through the basement membrane of the bronchiolar epithelium leading to formation of carcinoid tumorlets. When the tumorlets become greater than 5mm in size they are considered bronchial carcinoids. Upon microscopic examination, the PNE cells have round, oval, or spindle nuclei with salt-and-pepper chromatin and clear or eosinophilic cytoplasm . [ 1 ]
Although no formal definition exists regarding the extent of PNE hyperplasia necessary for a DIPNECH diagnosis, this process is often seen throughout the small airways. Because the hyperplasia of PNE cells can be seen as a reaction to chronic lung disease, surrounding solitary bronchial carcinoids and adenocarcinoma of the lung, these causes must be excluded prior to a DIPENCH diagnosis. [ 1 ]
Obstructive bronchiolitis has been reported as a characteristic histopathologic finding in patients with DIPNECH. [ 8 ] The bronchiolitis is thought to be a response of the small airways to neuropeptides secreted by the PNE cells. [ citation needed ]
The findings on chest imaging in DIPNECH patients are bilateral and diffuse. The most frequent findings on a computed tomography (CT) of the chest are multiple primary nodules and/or masses, on a background of mosaic attenuation and airway wall thickening. [ 2 ] [ 9 ]
The nodules have an indolent pattern of growth and are found throughout the lungs. The nodules are typically rounded and well-defined. Upon surgical resection, histologically the nodules are found to be typical carcinoids or carcinoid tumorlets depending on size. [ citation needed ]
Although some patients present with normal lung function, pulmonary function tests generally demonstrate fixed airway obstruction with a decreased FEV1 and reduced FEV1/FVC ratio without bronchodilator response. Air trapping is common and leads to increased residual volumes. As the disease progresses, a mixed pattern of obstruction and restriction may develop. In general the obstructive lung disease is slowly progressive with periods of stability. [ 8 ]
To date there have been no clinical trials to determine effective treatment for this disease. Some patients have been treated with somatostatin analogs. Although the cough associated with DIPNECH tends to diminish on this treatment, improvement in pulmonary function has not been clearly demonstrated. [ 2 ] [ 8 ] There are also reports of symptomatic treatment with long- and short-acting beta agonists. Although steroids , both oral and inhaled, have been used in the setting of DIPNECH, there is no clear improvement with this treatment. [ citation needed ]
It is not uncommon for typical carcinoids to arise within DIPNECH. Due to presence of these tumors, DIPNECH is classified as a pre-malignant condition. [ 1 ] Although there have been reports of atypical carcinoids with local lymph node involvement, there are no reports of more aggressive neuroendocrine tumors, such as large cell neuroendocrine or small cell lung cancer, associated with DIPNECH. [ 3 ] When isolated bronchial carcinoids are diagnosed, oncology guidelines recommend surgical resection with lymph node sampling. [ 10 ] However, as multiple carcinoids may develop in the setting of DIPNECH, a more conservative approach is often considered to preserve lung function. [ citation needed ]
The morbidity associated with DIPNECH is due to the associated obstructive lung disease. The lung disease tends to be slowly progressive, but given enough time can lead to significant disability and require supplemental oxygen therapy. [ 8 ] There have been reports of lung transplantation in the setting of end-stage DIPNECH. [ 11 ]
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https://en.wikipedia.org/wiki/Diffuse_idiopathic_pulmonary_neuroendocrine_cell_hyperplasia
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Diffusing Alpha-emitters Radiation Therapy or DaRT is an alpha-particle -based radiation therapy for the treatment of solid tumors . [ 1 ] [ 2 ]
This therapy was developed at Tel Aviv University in Israel, by Professors Itzhak Kelson and Yona Keisari. The treatment is delivered by the intratumoral insertion of metal tubes called “seeds”, which have Radium-224 atoms fixed to their surface. When the radium decays, its short-lived daughter Radon-220 is released from the seed through recoil energy. [ 3 ] The daughters of Radon-220, in particular Pb-212, disperse in the tumor, and emit high-energy alpha particles, which destroy the tumor. Because the alpha-emitting atoms diffuse only a few millimeters in tissue, the DaRT eradicates the tumor cells and spares the surrounding healthy tissue. [ 3 ]
Alpha radiation is a nuclear phenomenon in which a heavy radionuclide emits an energetic alpha particle (consisting of two protons and two neutrons) and transmutes to a different radionuclide. The emitted alpha particle has a range in tissue of only 40-90 microns, which minimizes collateral damage when used for treatment purposes. However, this also limits its ability to destroy tumors that are many millimeters in diameter. Alpha radiation possesses a potent cell-killing capability because it has a high linear energy transfer (LET) which translates into a high Relative Biological Effectiveness (RBE). [ 4 ]
The invention of DaRT makes possible the use of alpha radiation for treating solid tumors, because it overcomes the range limitation of alpha particles in tissue. The daughter atoms of Radium-224 can each diffuse several millimeters in tumor tissue, while emitting alpha particles. The tumor-killing capability of DaRT comes mainly from the ability of alpha radiation to irreparably break the double stranded DNA in tumor cells. [ 5 ] This capability does not seem to be dependent on the stage of the cell cycle or the level of oxygenation of the cancer cell. [ citation needed ]
Preclinical studies have demonstrated that DaRT can effectively damage all solid tumor types. Studies of 10 different tumor types in mice demonstrated that all responded to DaRT. [ 6 ] [ 7 ] [ 8 ] [ 9 ] [ 10 ] [ 11 ] [ 12 ] [ excessive citations ]
In preclinical studies, DaRT effectiveness was enhanced when combined with standard chemotherapies such as 5-FU. In addition, DaRT was able to turn the tumor into its own vaccine and stimulate a systemic anti-tumor immune response. [ 13 ] This immune response was effectively augmented by addition of immunostimulants and/or inhibitors of immunosuppressive cells. This immune effect was observed not only as enhanced local tumor destruction at the primary tumor site, but also by elimination of tumor metastases in the lungs. [ 12 ] [ 14 ] These results suggest that DaRT combined with immunotherapy induces a tumor-specific systemic immune response. [ citation needed ]
The first results of the DaRT in human patients, from a pilot study of 28 patients by Prof. Popovtzer (Israel) and Dr. Bellia (Italy), were published in 2020. [ 15 ] From among this cohort of elderly patients (median age, 80.5 years), 61% had recurrent and previously treated tumors, including 42% who were radioresistant from prior therapy. Patients were diagnosed with histopathologically confirmed squamous cell carcinoma of the skin or head and neck . One-hundred percent of tumors responded to DaRT, with complete responses occurring in greater than 78% of cases, and no major toxicity was noted. Thirty days after treatment, there was no measurable radioactivity in the blood or urine of patients. Additional studies in larger populations are now ongoing to strengthen support regarding the safety and effectiveness of this technique of intratumoral alpha radiation-based tumor ablation. [ citation needed ]
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https://en.wikipedia.org/wiki/Diffusing_alpha_emitters_radiation_therapy
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Digestion chambers are a histologic finding in nerves that are undergoing Wallerian degeneration . [ 1 ]
Digestion chambers consist of small globular fragments, which represent degenerating myelin sheaths.
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https://en.wikipedia.org/wiki/Digestion_chambers
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Digestive system surgery , or gastrointestinal surgery , can be divided into upper GI surgery and lower GI surgery. [ 1 ]
Upper gastrointestinal surgery , often referred to as upper GI surgery , refers to a practise of surgery that focuses on the upper parts of the gastrointestinal tract . There are many operations relevant to the upper gastrointestinal tract that are best done only by those who keep constant practise, owing to their complexity. Consequently, a general surgeon may specialise in 'upper GI' by attempting to maintain currency in those skills.
Upper GI surgeons would have an interest in, and may exclusively perform, the following operations:
Lower gastrointestinal surgery includes colorectal surgery as well as surgery of the small intestine .
Academically, it refers to a sub-specialisation of medical practise whereby a general surgeon focuses on the lower gastrointestinal tract .
In the U.S., a student wanting to specialize and practice in adult lower GI surgery would generally have to go through four years of undergraduate college pre-medical education and get a bachelor's degree, then finish the four years of medical school, then finish a typically five-year-long residency in general surgery, and then perform a subsequent one-year-long (minimum) residency in surgery of the small intestine or large intestine (the colon - specifically, the cecum , the vermiform appendix , the ascending colon , the transverse colon , the hepatic flexure and the splenic flexure , the descending colon , and the sigmoid colon ; and also the rectum and the anus ).
A fellowship (in surgery of the small intestine or of the large bowel, or in pediatric/neonatal lower GI surgery, or in surgery of congenital abnormalities or rare disorders of the lower GI tract, or in emergency/trauma surgery or in cancer surgery of the area), would add on approximately one to three more years. [ 2 ]
A lower GI surgeon might specialise in the following operations:
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The Digital Pathology Association (DPA), is a non-profit organization of professionals in the field of pathology and related technologies. It has over 2,000 members and is headquartered in Carmel, Indiana .
Founded in 2009, the DPA's primary achievement has been to work with the FDA to develop a framework for clearance to market whole slide imaging systems. [ 1 ] [ 2 ] The DPA provides educational resources at its web site as well as hosting an annual scientific and educational conference, Pathology Visions. [ 3 ]
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https://en.wikipedia.org/wiki/Digital_Pathology_Association
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A Virtual Autopsy is a non-invasive autopsy in which digital imaging technology, such as with computerized tomography (CT) or magnetic resonance imaging (MRI) scans, is used to develop three-dimensional images for a virtual exploration of a human body.
Virtual Autopsy, simply, means conducting autopsy in computerized environment by digital tools. The first step of digitizing starts with the medical imaging modalities that provide the raw data images from the deceased. The most common modalities are computerized tomography (CT scan) and magnetic resonance imaging (MRI) scanner. Three dimensional medical visualization is the technical process that provide the digital environment for exploration of the 3D body and conducting the Virtual Autopsy.
The term cannot be found before 1980 in the literature. However, there are many other similar terms like: Postmortem CT scanning for individual organs, [ 1 ] volumetric radiologic scanning, [ 2 ] Virtual Autopsy [ 3 ] and Virtopsy . [ 4 ]
One of the first documented Virtual Autopsy studies was conducted at the department of Neuroradiology, University Hospital Mainz, Germany in the year 1980, where in 105 specimens of human stillborn and live-birth infants, ranging in age from gestational week 13 to postnatal month 18 were studied. [ 5 ] Since then the arena of 2D CT scan images has gradually evolved to present day technologies of Multi-planar reconstructions (MPR) and real to life high definition 3D rendering. In the year 1998 various aspects of human and animal anatomy and pathology were successfully studied by Digital 3D examination on the ancient mummified specimens at the Academic Medical Centre, Amsterdam. Similar studies have also since then been done at the British Museum. The digital 3D analysis of data obtained from CT scanning the mummies has helped in visualization of the faces of some of the mummies, including that of chanters from the Temple of Karnak. This technology has also given vast information about the embalming and burial processes. [ 6 ] In the year, 2009 CT scanning and digital analysis of DICOM data was successfully used by the VIFM, Australia during the phase 2 of the DVI process for the Victorian bushfires. All dead bodies and scattered remains were CT scanned in their body bags using specific protocols and analyzed. Digital examination helped not only in separating the presence of non-human remains, but also was useful at the time of autopsy to capture and analyze the identifying features in cases of severe disfiguration. [ 7 ]
Currently Virtual Autopsy is being successfully used in many countries like Switzerland, The United States of America, The United Kingdom, Malaysia, and Japan. Radiologists may call it Post-mortem Computed Tomography (PMCT) that does not provide colourful 3D views. In Switzerland, it is called Virtopsy (virtual autopsy). Pathologists (Forensic pathologists) know this procedure as Virtual Autopsy.
In a forensic autopsy or Post-mortem examination, body of deceased is examined to acquire information on the cause of death inclusive but not limited to manner of death in people dying sudden, unexpected, violent, drug-related, or otherwise suspicious deaths. [ 8 ] Virtual Autopsy tries to answer the same investigative questions without actual dissection as in a conventional autopsy.
The main concept of Virtual Autopsy came into existence to overcome some problems during conventional autopsies without losing the objectivity of post-mortem examination. The main problems in conventional autopsy are:
Virtual Autopsy would be a technical solution for above mentioned problems. Employing medical imaging modalities like CT or MRI scanners is the first step in order to examine the deceased visually without any destructive, contaminating and non-preservative procedures like dissection. Moreover, using these images with software processing in visualization is the second step toward acquiring data from difficult regions from anatomical perspective and dignity of the body. Digital bodies in the system can be examined multiple times and reported not only in text but also in variety of available media (photo, movie, etc.). In addition, quick evaluation of bodies and body parts in massive disasters is available in comparison to time-consuming procedure of conventional autopsy.
However, there are few limitations in Virtual Autopsy. The main constraint is the data that is provided by medical imaging modalities are based on X-Ray and Magnetic fields (CT and MRI) that limits the view to what can be recorded by these technologies. A very obvious difference is the real colour of internal body organs and their changes in the deceased, in comparison to what is simulated in the visualization software. The novelty of this technological solution has not given enough time for studies on the consistency of reports among different professionals on the same cases. Moreover, there are few articles about validity of Virtual Autopsy in action.
Computed tomography and MRI scanning are the most common imaging modalities employed for this Virtual Autopsy. Furthermore, CT Angiography has been used to provide the imaging data for analysing the deceased. The work output of these modalities are standard image files ( DICOM files). Each image may have a thickness of 5mm, which means after whole body scan (human average height of 175 cm) it would produce 3500 images (slices) of human body. Using volume rendering these two dimensional images are assembled to make a 3D projection of human body. The 3D model is painted through RGBA transfer function to a colourful model.
All visualization and image processing features for manipulating and navigating this 3D model make digital tools for conducting a Virtual Autopsy. These features enable pathologist to explore the entire body and examine interested regions and organs from different angles. Image processing algorithms help them to virtually remove layers of body tissues like skin, muscle and bones. Moreover, low density objects like air and high density objects like metallic foreign bodies can be marked and viewed in the three dimensional body. For instance, organs with air (inside) like sinuses or intestines can be separated from other parts or any remnants of bullet in body due to gunshot injuries.
The process starts with registration of the case with all corresponding meta-data in a Virtual Autopsy Facility. The best place for these facilities are in neighbourhood of mortuaries because of considerations about security, carriage and body condition. The body would be scanned according to the schedule with proper adjustments for deceased body. It means there are different configuration for emitting the ray in deceased in comparison to live bodies. This step may take 5 – 10 minutes depends on the abilities of scanner. The output is aforementioned DICOM files (around 3500 files for whole body scan) that would be sent for visualization process. The result is a colourful 3D body that can be explored and examined for positive or negative findings with the digital tools.
The process is not finished with 3D exploration. The findings would be reported digitally in a multimedia report. This report includes all textual results accompanied by images and recorded movie of Virtual Autopsy during examination. This report is not only for common submission to the court but also to be displayed in the court for attendance.
There are not many justice systems around the world who have accepted the Virtual Autopsy as their legal procedures of forensic investigations. While Switzerland is pioneering in the acceptance, [ 9 ] countries like Israel with strong religious background does not accept forensic imaging as a substitute or in conjunction with autopsy report. This might be due to lack of cases and documentation. [ 10 ] Some researchers tried to evaluate the reliability of Virtual Autopsy in comparison with conventional (standard) autopsy that reveals totally 68% accuracy of Virtual Autopsy regarding the pathogenetic mechanisms. [ 11 ]
In UK, the Department of Health is currently considering recommendations for an integrated national cross-sectional autopsy imaging service, based on a regional service provided by mortuary-based imaging centres. [ 12 ] Furthermore, Royal College of Radiologists and the Royal College of Pathologists prepared a document to standardize medico-legal post-mortem cross-sectional imaging in adults in the UK. [ 13 ]
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Diomid Gherman (10 April 1928 – 19 April 2014) was a professor and researcher from Moldova and a corresponding member of the Academy of Sciences of Moldova . [ 1 ] [ 2 ] He was a leader of the Democratic Forum of Romanians in Moldova . [ 3 ] [ 4 ]
Gherman was born on April 10, 1928, in the village Bocșa , Fălești district , in a family of teachers . After graduating the school of his village, he continued his studies at Commercial High School, then at General School no. 1 in Bălți , which he graduated successfully in 1946. Between 1946 and 1951 he studied at the State Medical Institute in Chișinău . After graduating from the Institute, he began his activity as head physician at the Chirileni village Hospital of Ungheni district (1951-1952). In 1952, he was admitted to clinical neurology at the Department of Neurology, under the leadership of renowned scholar Boris Șarapov. Consecutively, he served as the Head of Hospital of Congaz District (1954-1956), Inspector of the Ministry of Health and Chairman of the Central Committee of the Red Cross in Moldova.
Fully devoted to medicine and science, Gherman has continuously improved his knowledge and practical skills. In 1962, he held the Postgraduate diploma in medical sciences, and a decade later - the PhD degree. Since 1961, Gherman has served as assistant, then lecturer at the Department of Neurology . In 1973, he obtained his professorship. During 1969-1998, Gherman held the position of head of the Department of Neurology of the State University of Medicine and Pharmacy "Nicolae Testemitanu". Later, he worked as university professor at the same university and as a senior collaborator in the Vertebra-neurology Laboratory of the Institute of Neurology and Neurosurgery. Since 1993, Gherman is elected academician of the Academy of Sciences of Moldova. Professor Gherman is the founder of the National School of Neurology and Neurosurgery. Under his leadership, the priority directions of the native neurological school were drawn, including vascular medullary pathology. Academician Gherman is known in the medical and scientific world and as founder of the national vertebra-neurology school.
In over 55 years of teaching, Gherman trained several generations of specialists, who are working in the republic and abroad. Gherman is recognized as the patriarch of national neurology. His research in the field of neurology is recognized out of the borders of the Republic of Moldova, and the outcomes have been reflected in about 400 publications, including 12 journals. Gherman is an outstanding contemporary figure.
Academician Gherman promoted home neurologya at the international level. Since 1989, he organized 12 scientific meetings of neurologists and neurosurgeons from the Republic of Moldova and România . Thanks to his contribution, Moldova became a member of the European Federation of Neurological Societies. Neurosurgeon Gherman saved life of hundreds of patients. For outstanding merit in activity, he was honored with the high titles of Emeritus Scholar of RM, the State Award, the Man of the Year and the Citizen of Honor of Falești town. He received several state distinctions. Gherman was a professor, a clinician and a well-known researcher, but a great patriot of the nation. The high school in his native village now bears his name. Gherman died on April 19, 2014.
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Diplacusis , also known as diplacusis binauralis , binauralis disharmonica or interaural pitch difference (IPD), is a hearing disorder whereby a single auditory stimulus is perceived as different pitches between ears. It is typically experienced as a secondary symptom of sensorineural hearing loss , although not all patients with sensorineural hearing loss experience diplacusis or tinnitus . [ 1 ] [ 2 ] The onset is usually spontaneous and can occur following an acoustic trauma , for example an explosive noise, or in the presence of an ear infection . [ 3 ] Sufferers may experience the effect permanently, or it may resolve on its own. Diplacusis can be particularly disruptive to individuals working within fields requiring acute audition, such as musicians, sound engineers or performing artists. [ 4 ] [ 5 ] [ 6 ] [ 7 ]
The term diplacusis has been used in cases which people with unilateral cochlear hearing losses or asymmetrical hearing losses, the same tone presented alternately to the two ears may be perceived as having different pitches in the two ears. [ 8 ] [ 9 ] The magnitude of the shift can be measured by getting the subject to adjust the frequency of a tone in one ear until its pitch matches that of the tone in the other ear. On presentation of a single tone alternating between ears (i.e. 1000 Hz left, 1000 Hz right, 1000 Hz left, ...), a given person will consistently mismatch these sinusoids the same amount between trials if doing a pitch-matching task. For example, a 1000 Hz tone in an unaffected ear may be heard as a slightly different pitch in the opposite ear, or have an imperfect tonal quality in the affected ear.
There are two theories on the cause of diplacusis: place theory and temporal theory. [ 10 ] Place theory posits that the cause is looking for the edge of the wave for the pitch and could explain diplacusis as a small differences between the two cochleas. [ 11 ]
Temporal theory posits that the cause is from looking at the phase locking to tell what the pitch is. This theory has a difficult time explaining diplacusis. There are some examples of pitch which do not have an "edge" on the basilar membrane, which this would account for—e.g., white noise, clicks, etc. [ 11 ] Both theories are under debate. [ 12 ] [ 13 ]
Normal human ears can discriminate between two frequencies that differ by as little as 0.2%. [ 14 ] If one ear has normal thresholds while the other has sensorineural hearing loss (SNHL), diplacusis may be present, as much as 15–20% (for example 200 Hz one ear => 240 Hz in the other). [ citation needed ] The pitch may be difficult to match because the SNHL ear hears the sound "fuzzy". Bilateral SNHL gives less diplacusis, but pitch distortions may persist. This may cause problems with music and speech understanding.
Treatment of diplacusis includes a full medical and audiological examination that may explain the nature of the problem. If needed, amplification may relieve the symptoms of diplacusis. Therapy in helping the patient understand the cause of the symptom and tinnitus retraining may provide some relief. In at least some cases, amplification makes no difference and there is no treatment other than waiting for natural resolution. Some individuals may find the provided amplification also increases the audibility of their pitch discrepancy. If onset is linked to an underlying medical cause, i.e. sudden sensorineural hearing loss, appropriate medical treatment is recommended.
Diplacusis is from the Greek words "diplous" (double) and "akousis" (hearing). [ 15 ]
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Diplegia , when used singularly, refers to paralysis affecting symmetrical parts of the body . This is different from hemiplegia which refers to spasticity restricted to one side of the body, paraplegia which refers to paralysis restricted to the legs and hip, and quadriplegia which requires the involvement of all four limbs but not necessarily symmetrical. [ 1 ] Diplegia is the most common cause of crippling in children, specifically in children with cerebral palsy . [ 2 ] Other causes may be due to injury of the spinal cord . There is no set course of progression for people with diplegia. Symptoms may get worse but the neurological part does not change. The primary parts of the brain that are affected by diplegia are the ventricles , fluid filled compartments in the brain, and the wiring from the center of the brain to the cerebral cortex . [ 3 ] There is also usually some degeneration of the cerebral neurons , [ 2 ] as well as problems in the upper motor neuron system. [ 1 ] The term diplegia can refer to any bodily area, such as the face , arms , or legs .
Facial diplegia refers to people with paralysis of both sides of their face. Bilateral occurs when the onset of the second side occurs within one month of the onset of the first side. [ 4 ] Facial diplegia occurs in 50% of patients with Guillain–Barré syndrome . Facioscapulohumeral muscular dystrophy (FSHD) is the second most common adult-onset muscular dystrophy with facial weakness being a distinct feature of FSHD in over 90% of cases. [ 5 ]
Facial paralysis is usually caused by traumatic , infectious , neurological , metabolic , toxic , vascular , and idiopathic conditions. [ 4 ] While over 50% of the cases of unilateral facial paralysis are caused by idiopathic conditions, less than 20% of bilateral cases are idiopathic. The most common infectious cause of facial diplegia is Lyme disease . [ 4 ]
The treatment for facial diplegia depends on the underlying cause. Some causes are usually treatable such as infectious, toxic, and vascular by treating the main problem first. After the underlying problem is cured, the facial paralysis usually will go away. [ citation needed ]
People with diplegia in their arms experience difficulties in reaching, pointing, grasping, releasing, manipulating objects and many other motor functions performed by the hands and arms. [ 6 ]
There are several ways of getting diplegia in the arms. It is very common for people with cerebral palsy to have diplegia of the arms. Although most people with cerebral palsy have diplegia in their legs, some people have diplegia in their arms. Other ways of getting paralysis of both arms is through a traumatic event or injury. [ citation needed ] Brachial amyotrophic diplegia , a regional variant of ALS , is a rare motor neuron disease characterized by diplegia in the arms. [ 7 ]
There are several different modes of treatment for people with paralysis in their upper limbs. For example, behavioral and environmental treatments may include physiotherapy , occupational therapy , motor learning, strength training, and neurodevelopment treatment. Another treatment may be through the use of splints and casts. Electrophysical agents may be used such as neuromuscular electrical stimulation (NMES). Sometimes pharmacological treatments are necessary such as Botulinum toxin type A. On more severe cases surgery of the upper limbs may be required. [ 6 ]
Diplegia of the legs consists of paralysis of both legs. There are 3 levels of severity. Mild diplegia means the person can usually walk but might walk a little differently, can usually play and run to a limited extent. Moderate diplegia means the person can usually walk but with a slight bend in the knees. They usually cannot run and have to use the handrails to go up and down steps. People with severe diplegia usually need crutches, a walker, or a wheelchair to be able to get around. [ 3 ]
Children with diplegia in the legs have a delayed growth in their leg muscles which causes the muscles to be short. This then causes the joints to become stiff and the range of motion to decrease as the child grows. “For the majority of children with diplegia, growth and development are not a problem. Children with diplegia are eventually able to walk, just normally later; they generally attend regular schools and become independently functioning adults.” [ 8 ]
The most common cause of diplegia in the legs is cerebral palsy . Paralysis of the legs may also be caused by trauma, injury, or genetics, but this is very rare. [ 3 ]
Usually occurs within 2 periods: [ 3 ]
Diplegia is usually not diagnosed before the age of 2 years yet the symptoms and signs of the earlier stages are typical and should enable the diagnosis to be made before the contractures have occurred. [ 9 ] Parents suspecting diplegia should take their child to the doctor to potentially get an earlier diagnosis. [ citation needed ]
This is broken up by age categories. Different ages require different forms of treatment which may include: therapy, bracing, walkers, wheelchairs, and surgery. Currently the treatments for children are concentrated primarily on independent walking but instead a more independence-oriented therapeutic approach would be more beneficial. [ 10 ] This way the child can still focus on walking but at the same time be taught to do things for themselves while using the best method of walking for them. This could include using a walker or wheelchair to get around and do things easier than focusing all the attention on walking so early.
For people requiring surgery, distal hamstring lengthening is the most common operation performed because it reduces knee flexion and improves knee motion. [ 11 ]
“This first year sees the development of many milestones, such as head control, reaching out for a toy, sitting, starting to vocalize sounds, and finger feeding.” [ 8 ] Most parents want their children to excel very fast, but there is a wide upper and lower range of development time for premature babies so it's very hard to diagnose cerebral palsy or diplegia this early. The most common symptom of a child with diplegia is stiff lower extremities. This should become apparent by the six month mark which means he or she does not have severe diplegia. During this age if a child is not moving his legs on his own then it is recommended to do some exercise, especially gentle stretching with the child. [ 8 ]
“This is the age at which the characteristics of diplegia become more noticeable, mainly because, unlike other children at this age, the child with diplegia is not walking.” [ 8 ] By the age of three, it is important for the child to be in a specialized school environment so the child can participate in physical therapy and learn social skills. Parents should not force the child to sit, crawl, or walk a certain way during this age period. Let the child do what's comfortable for them and allow the therapist to correct this problem. If you want to help your child walk more, then push toys are recommended for walking aids. Regular exams should be done to make sure the child's legs are growing normally and he or she is not having any problems with the hip. [ 8 ]
“This is the age range at which the child with diplegia makes the most significant physical improvement in motor function.” [ 8 ] During this time period the child makes major improvements in motor function. He or she should be in a regular school and focus on cognitive issues not therapy. A child using a walking aid for mobility to move around with the other children is not a bad thing. If a child is not walking yet, then this is usually caused by a problem in balance, muscle coordination, spasticity, or leg alignment. Each of these reasons should be looked into closely so the problem can be addressed and fixed. [ 8 ]
“By the time a child reaches this age the rate of physical improvement has leveled off in areas such as balance and coordination, and it's a good idea to refocus the child’s attention away from additional physical improvement and toward intellectual learning.” [ 8 ] During this time period a child should lean away from physical therapy and do more outdoor or social exercises such as sports and adaptive P.E. Usually by age 8-10 a child has reached maximum walking ability. This will usually decrease a little when a child hits puberty and gains height and weight because walking becomes harder during this changing period. Any significant problems in walking should be addressed with surgery at this stage. [ 8 ]
“During this time period of a child’s development, a major issue is separating from the family.” [ 8 ] Parents should learn how to cope with their child growing up and give them more freedom and independence. Teenagers need to make their own decisions and learn from them. One way to do this is for parents to compromise and let the child make smaller decisions so they feel important. Parents should also understand that their child may regress in walking some from increase in height and weight. Going back to therapy during puberty is recommended so the teenager can adjust to the increase in height and weight and not regress as much. [ 8 ]
In 1890 Sachs and Peterson first referenced to the term diplegia, along with the word paraplegia , for their cerebral palsy classification. In 1955 the word diplegia was used in the clinical field to describe a patient whose limbs were affected in a symmetrical way. This included limbs on the same side of the body thus including hemiplegia . Later in 1956 diplegia was presented as a form of bilateral cerebral palsy affecting like parts on either side of the body. In 1965 Milani Comparetti distinguished diplegia from tetraplegia by considering the patient's upper limb's ability to express a sufficient support reaction. Thus diplegia usually refers to just symmetry of one body part or limb, as the legs, or arms. While tetraplegia or quadriplegia refers to paralysis of all 4, both arms and legs. [ 12 ]
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Diplophonia, also known as diphthongia, is a phenomenon in which a voice is perceived as being produced with two concurrent pitches. [ 1 ] Diplophonia is a result of vocal fold vibrations that are quasi-periodic in nature. [ 2 ] It has been reported from old days, but there is no uniform interpretation of established mechanisms. [ 3 ] It has been established that diplophonia can be caused by various vocal fold pathologies, such as vocal folds polyp , vocal fold nodule , recurrent laryngeal nerve paralysis [ 3 ] or vestibular fold hypertrophy. [ 4 ]
The Voice Quality Symbol for diplophonia is V̬‼.
This medical article is a stub . You can help Wikipedia by expanding it .
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Directed attention fatigue ( DAF ) is a neuropsychological phenomenon that results from overuse of the brain’s inhibitory attention mechanisms, which handle incoming distractions while maintaining focus on a specific task. The greatest threat to a given focus of attention is competition from other stimuli that can cause a shift in focus. This is because one maintains focus on a particular thought by inhibiting all potential distractions and not by strengthening that central mental activity . [ 1 ] [ page needed ] Directed attention fatigue occurs when a particular part of the brain's global inhibitory system is overworked due to the suppression of increasing numbers of stimuli. This temporary condition is not a clinical illness or a personality disorder . It is rather a temporary fatigue of the inhibitory mechanisms in the brain . [ 2 ] [ unreliable medical source? ] According to inhibition theory , it is natural for one to alternate between periods of attention and distraction. Although one's efforts may involve very different tasks, each incoming stimulus calls upon the same directed attention mechanism. [ citation needed ]
Extreme levels of mental fatigue lead to an inability to perform regular tasks and irritability. Studies that require participants to carry out attention-demanding tasks under conditions of high distraction reveal how unpleasant a mentally fatigued person can be. After exposure to such an experience, individuals are less likely to help someone in need. They are also more aggressive, less tolerant, and less sensitive to socially important cues. Fatigue that is experienced by participants of these kinds of studies is induced by attention-intensive tasks, [ 3 ] and the observed effects of such fatigue are correlated with decline in inhibitory control. Signs of Directed Attention Fatigue include temporarily feeling unusually distractible, impatient, forgetful, or cranky when there is no associated illness. In more severe forms, it can lead to bad judgment, apathy, or accidents, and can contribute to increased stress levels. [ citation needed ]
There are 6 major areas of mental processing that are affected during onset of DAF, which are as follows: [ 4 ]
Overlap of symptoms from the six above categories is highly indicative of Directed Attention Fatigue.
Some symptoms of attention deficit hyperactivity disorder closely mirror the symptoms of directed attention fatigue. Like directed attention fatigue, ADHD involves the prefrontal cortex . Specifically, the right prefrontal cortex is less active among children with ADHD. Experimentation has shown that the severity of ADHD symptoms can be correlated to the degree of asymmetry between blood flow in the left and right prefrontal cortex. [ 5 ] [ non-primary source needed ] It is possible that DAF and ADHD involve disruption of the same underlying mechanism, and recent clinical evidence has found that the same treatments used for directed attention fatigue may reduce the symptoms of ADHD in children. [ 6 ] [ non-primary source needed ] However, it is important to note that unlike ADHD, DAF is a temporary condition rather than a clinical disorder. [ citation needed ]
The onset of directed attention fatigue can be triggered by a number of activities involving the use of the brain's inhibitory system. Activities that engage this system include multitasking, [ 7 ] working in an environment with disruptive background noise, [ citation needed ] a lack of sleep, [ 8 ] and rapidly changing focus during a prolonged period of attention. [ citation needed ] DAF can also be brought about by performing concentration-intensive tasks such as puzzle-solving or learning unfamiliar ideas. [ 7 ] [ 9 ] External factors such as stress resulting from emergencies, exams or work deadlines can also induce DAF. [ 8 ] Any illness or injury to the brain that interrupts the brain circuits involved in maintaining attention and inhibiting external stimuli (e.g., the posterior parietal cortex ) may also contribute to the development of directed attention fatigue. [ 10 ]
Directed attention, or voluntary attention, requires a great deal of concentration and focus, and is employed in tasks such as problem solving. This type of attention employs the inhibitory mechanisms of the brain, which help block incoming stimuli that are unrelated to the task at hand. [ 11 ] Several parts of the brain are involved in maintaining directed attention, primarily those located in the frontal lobe and the parietal lobe of the brain. Specifically, the mechanism of directed attention employs the prefrontal cortex (PFC), the anterior cingulate cortex (ACC) and the brain stem's basal ganglia . Some fMRI studies have shown that directed attention involves changes in the anterior cingulate cortex and the lateral prefrontal cortex, perhaps as a consequence of increased connectivity between these two areas. [ 12 ] Evidence also suggests that the right inferior frontal cortex (IFC) plays a specialized role in response inhibition. It seems that this region plays a key role in the integration of bottom-up response-related information and facilitates goal-directed behavior. [ 13 ] [ non-primary source needed ] While these areas of the brain are known to be involved in DAF, their specific molecular mechanisms in the perpetuation of DAF symptoms are not yet known. [ citation needed ]
The concept of stress is used in many situations that would be described as mental fatigue , but the two concepts are distinctly different. Stress involves preparation for an anticipated event that has been evaluated as being threatening or harmful. Though mental fatigue may well result from stressful circumstances, it also arises out of hard work on a project one enjoys. In such cases, there is no anticipation of threat or harm present but still the result is fatigue. Characteristic of mental fatigue is difficulty focusing. For a mentally fatigued person, paying attention to something uninteresting is burdensome, even though focusing on something of great interest poses no particular challenge. [ 14 ] [ page needed ] Hence, there are two types of attention, distinguished in terms of the effort involved in their use and their changes in attentional shift :
There are measures that can be taken in order to reduce the impact of DAF. These include reducing the number of distractions present in one's external environment, trying to clear one's mind of any internal distractions and taking short breaks during prolonged periods of focus. Directed attention fatigue can be reduced by getting a sufficient amount of sleep each night, because inhibitory attention chemicals are replenished during sleep. [ 16 ] [ unreliable medical source? ]
An aesthetic environment may also serve a restorative function in fostering recovery from mental fatigue. Research has shown that restorative experiences, such as clearing one's head and reflecting on one's life and priorities, may help combat Directed Attention Fatigue. As investigated by attention restoration theory , natural environments, such as forests, mountain landscapes or beaches, appear to be particularly effective for restoring attention, perhaps because they contain a vast amount of diverse, relatively weak stimuli, thus inciting the mind to wander freely while relaxing its strict focus. [ 17 ]
Ongoing research is examining ways in which the incidence of DAF can be decreased, and suggests that exposure to the natural environment may aid in the reduction of DAF symptoms. [ 18 ] Leading contributors include Rachel and Stephen Kaplan , environmental psychologists at the University of Michigan. Rachel and Stephen Kaplan were among the first to discover that extended periods of focused attention can lead to directed attention fatigue. [ 19 ] Their research suggests that directed attention fatigue can be alleviated with exposure to nature. Together, the Kaplans devised the attention restoration theory (ART), which states that a person is better able to maintain focused directed attention after spending time in the natural environment. [ 20 ] Core to the Kaplan's theory is their notion of "soft fascination" .
Similarly, it has been discovered that even brief amounts of time spent on a busy metropolitan street can affect one's ability to maintain focus on a given task. Experimental findings suggest that spending time in a natural environment or even looking at pictures of nature can improve maintenance of directed attention. [ 21 ] [ unreliable medical source? ]
The Landscape and Human Health Laboratory (LHHL) has completed studies examining the complex relationship between people and their environment. Researchers here discovered the correlation between Directed Attention Fatigue, irritability and aggression. Their findings suggest that people deprived of the restorative effects of nature display more aggressive qualities. Results also demonstrate that communities with several trees and other natural areas tend to be stronger, safer and house residents with a higher attention level. [ citation needed ] More recent experimentation done at the LHHL suggests that children possessing attention deficits increase their attention level after walking outdoors. [ 22 ] [ 23 ] [ non-primary source needed ]
A 2022 review by Sun et al. addressed whether directed attention fatigue is lessened after exposure to nature in mentally fatigued athletes. [ 24 ] Some of the reviewed studies used walks in nature, recorded video scenes of nature, pictures of nature scenes, or even nature sounds such as bird songs. [ 24 ] This review also compared alternative theories to attention restoration theory, including the strength model of self-regulation (SMSR), the attention-resource model, and the stress recovery theory.
A number of studies have been performed that specifically focus on directed attention fatigue experienced by cancer patients. Such studies suggests that the DAF experienced by cancer patients following surgery improves significantly through outdoor restorative activities for 20 minutes per day. [ 19 ] [ unreliable medical source? ]
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Disability studies is an academic discipline that examines the meaning, nature, and consequences of disability . Initially, the field focused on the division between "impairment" and "disability", where impairment was an impairment of an individual's mind or body, while disability was considered a social construct . [ 1 ] This premise gave rise to two distinct models of disability : the social and medical models of disability. In 1999 the social model was universally accepted as the model preferred by the field. [ 2 ]
However, in recent years, the division between the social and medical models has been challenged. [ 1 ] [ 3 ] Alternative models of disability have increased, allowing for greater complexity and specificity in how disability is theorized. [ 4 ] [ 5 ] Additionally, there has been an increased focus on interdisciplinary research. [ 6 ] For example, recent investigations suggest using "cross-sectional markers of stratification" [ 7 ] may help provide new insights on the non-random distribution of risk factors capable of worsening the disablement processes. Such risk factors can be acute or chronic stressors, which can increase cumulative risk factors (overeating, excessive drinking, etc.) The decline of immune function with age and decrease of inter-personal relationships which can impact cognitive function with age. [ 8 ]
Disability studies courses include work in disability history, theory, legislation, policy, ethics, and the arts. However, students are taught to focus on the lived experiences of individuals with disabilities in practical terms. The field is focused on increasing individuals with disabilities access to civil rights and improving their quality of life . [ 9 ]
Disability studies emerged in the 1980s primarily in the US, the UK, and Canada. In 1986, the Section for the Study of Chronic Illness, Impairment, and Disability of the Social Science Association (United States) was renamed the Society for Disability Studies . [ 10 ] The first US disabilities studies program emerged in 1994 at Syracuse University . [ 9 ] The first edition of the Disabilities Studies Reader (one of the first collections of academic papers related to disability studies) was published in 1997. [ 11 ] The field grew rapidly over the next ten years. In 2005, the Modern Language Association established disability studies as a "division of study". [ 9 ]
While disability studies primarily emerged in the US, the UK, and Canada, disability studies were also conducted in other countries through different lenses. For instance, Germany has been involved with queer disability studies since the beginning of the early 20th century. The disability studies in Germany are influenced by the written literary works of feminist sexologists who study how being disabled affects one's sexuality and ability to feel pleasure. In Norway, disability studies are focused on the literary context. [ 12 ]
A variation emerged in 2017 with the first accessibility studies program at Central Washington University with an interdisciplinary focus on social justice, universal design, and international Web Accessibility Guidelines (WAG3) as a general education knowledge base. [ 13 ]
Universities have long studied disabilities from a clinical perspective, [ 9 ] and discussions around the depathologization of disability began following the disability rights movement , which arose in the 1950s. In 1981, the United Nations ' International Year of Disabled Persons brought disability into the public sphere as a human rights issue. Five years later, the Social Science Association's Section for the Study of Chronic Illness, Impairment, and Disability was renamed the Society for Disability Studies , [ 10 ] and its journal Disability Studies Quarterly was the first journal in disability studies. The first US disabilities studies program emerged in 1994 at Syracuse University . [ 9 ] However, courses and programs were very few. In the 1997 first edition of the Disability Studies Reader , Lennard J. Davis wrote that "it had been virtually impossible to have someone teaching about disability within the humanities". [ 11 ] In the second edition, written ten years later, he writes that "all that has changed", but "just because disability studies is on the map, does not mean that is easy to find". [ 14 ]
Still the field continued to grow throughout the 2000s. In 2009 Disability Studies Quarterly published A Multinational Review of English-language Disability Studies Degrees and Courses . They found that from 2003 to 2008 the number of disability studies stand-alone studies programs in the US, UK, Australia, New Zealand, and Canada grew from 56 to 108 and the number of degree-granting programs grew from 212 to 420. A total of 17 degrees in disability studies were offered, with 11 programs in the US, 2 in the UK, 3 in Canada, and 1 in Australia. [ 15 ]
The 2014 article "Disability Studies: A New Normal" in The New York Times suggests that the expansion in disability studies programs is related to the 1990 passage of the Americans with Disabilities Act (ADA). Those raised after the passage of the ADA have entered colleges and the workforce, as Disability Studies has grown. In a 2014 article, Disability Studies Quarterly published an analysis on the relationships between student run groups and disability studies, from 2008 to 2012. Their article analyzes groups at four different universities and describes how professors have incorporated student activism into their curriculum and research. [ 16 ]
According to the transnational [ 17 ] Society for Disability Studies : [ 6 ]
Using an interdisciplinary, multidisciplinary approach. Disability sits at the intersection of many overlapping disciplines in the humanities, sciences, and social sciences. Programs in Disability Studies should encourage a curriculum that allows students, activists, teachers, artists, practitioners, and researchers to engage the subject matter from various disciplinary perspectives.
The social model of disability is expanded to chronic illness and to the broader work of the medical humanities . [ 18 ] Practitioners are working towards improving the healthcare for disabled people through disability studies. This multi-disciplinary field of inquiry draws on the experiences and perspectives of people with disabilities to address discrimination. Infinite Ability has done some preliminary work in India to introduce disability studies to medical students. [ 19 ] [ 20 ] [ 21 ] The medical humanities movement advocates use of literature in exploring illness, from practitioner and patient perspectives, with graphic medicine as an emerging strategy that combines comics-style medium and illness narrative.
Feminism introduces the inclusion of intersectionality in disability studies. It focuses on race , gender , sexuality , class and other related systems of oppression that can also intersect with having a disability. [ 22 ] From a feminist standpoint, there is a large concern for grasping multiple positions and differences among social groups. [ 23 ] Some research on intersectionality and disability has focused on the aspect of being part of two or more stigmatized groups and how these are contributing factors to multiple forms of harassment, the paradox known as "Double Jeopardy". [ 24 ]
In academic settings and practices such as gender or women's studies the course work does not always highlight ideals of intersectionality and identity. But Sri Craven highlights the fact that in academia students and professors do not look at history in a culmination of the intersecting identities but rather focus in one perspective. [ 25 ] Craven and his colleagues include identities such as disability both mental and physical in an alternative course description to get students and faculty to think about identity, oppression and struggle in a new way. [ 25 ]
Recent scholarship has included studies that explore the intersection between disability and race. Christopher Bell 's work publicly challenged disability studies to engage with race, calling it "white disability studies". [ 26 ] His posthumous [ 27 ] volume on Blackness and Disability further developed his analysis. [ 28 ] These works engage with issues of neoliberal economic oppression. The 2009 publication of Fiona Kumari Campbell 's Contours of Ableism: The Production of Disability and Abledness signaled a new direction of research – studies in ableism, moving beyond preoccupations with disability to explore the maintenance of abledness in sexed, raced and modified bodies. [ 29 ] A. J. Withers' work critiques the social model of disability because, among other things, it erases the experiences of BIPOC people, women, trans and queer people and puts forward a more radical model of disability. [ 30 ] Other contemporary works, such as literary studies conducted by Sami Schalk explore the intersection of disability and race and the use of dis/ability as a metaphor within the genre of black women's speculative fiction . [ 31 ] Collectively, these works reflect an effort to deal with complex histories of marking racially "othered" bodies as physically, psychologically, or morally deficient, and traces this history of scientific racism to contemporary dynamics. Empirical studies show that minority students are disproportionately more likely to be removed from class or school for "behavioral" or academic reasons, and far more likely to be labeled with intellectual or learning disabilities. [ 32 ]
In addition to work by individual scholars, disability studies organizations have also begun to focus on disability and race and gender. The Society for Disability Studies created the Chris Bell Memorial Scholarship to honor Bell's commitment to diversity in disability studies. [ 33 ] Postsecondary disability studies programs increasingly engage with the intersectionality of oppression. The University of Manitoba offers a course on "Women with disabilities". [ 34 ] Several recent masters' student research papers at York University focus on issues related to women with disabilities and people of African descent with disabilities. [ 35 ]
Feminism integrates the social and political aspects that makes a body oppressed while allowing empowerment to be present in acknowledging its culture. Scholars of feminist disability studies include Rosemarie Garland-Thomson and Alison Kafer . [ 36 ] Garland-Thomson explains that these related systems of oppression pervades all aspects of culture by "its structuring institutions, social identities, cultural practices, political positions, historical communities, and the shared human experience of embodiment". Garland-Thomson further describes that "identity based critical enterprises have enriched and complicated our understandings of social justice, subject formation, subjugated knowledges and collective action". [ 37 ] Feminism works towards accessibility for everyone regardless of which societal oppressive behavior makes them a minority . Although physical adjustments are most commonly fought for in disability awareness, psychological exclusion also plays a major role oppressing people with disabilities. The intersection of disability and feminism is more common in American history than we [ who? ] think yet it does not show up in media, museums or archives that are dedicated to feminist work. Rachel Corbman, a professor of women's, gender and sexuality studies at Stony Brook University in New York highlights how the influence of lesbian feminist organizations like the Disabled Lesbian Alliance (DLA) are not represented in the archives of literature and documentation of events in the community. [ 38 ] The DLA work closely together to fight for visibility, accessibility and acceptance of individuals whether they are disabled, or lesbian or both. Corbman's article highlights the beginning of disability activism during the feminist movement of the 1970s and 1980s and how the intersecting identities enticed new members and activists from across the country to join the cause. Other disability-centered feminist organizations that are part of the feminist archives include the Lesbian Illness Support Group and Gay and Lesbian Blind (GLB). [ 38 ] Sara Ahmed elaborates the mental exclusiveness of privilege in "Atmospheric Walls": there is an atmosphere surrounding minority bodies, explaining why an intersectionally privileged person could be made uncomfortable simply by being in the same room as a person of color, or in this case someone with a disability. [ 39 ] Feminists and scholars also developed theories that put attention on the connection of gender and disability. Scholars like Thomas J. Gerschick argue that disability plays a big role in processing and experiencing gender, and people with disabilities often suffer stigmatization towards their gender, since their disabilities may make their body representation excluded by normative binary gender representation. [ 40 ] Gerschick also argues that this stigmatization can affect the gendering process and self-representation of people with disabilities. Ellen Samuels explores gender , queer sexualities, and disability. [ 41 ] [ 42 ] Feminists also look into how people with disabilities are politically oppressed and powerless. Abby L. Wilkerson argues that people with disabilities are politically powerless because they are often desexualized, and the lack of sexual agency leads to the lack of political agency. Wilkerson also indicates that the erotophobia towards minority groups like people with disabilities further oppresses them, since it prevents these groups from gaining political power through sexual agency and power. [ 43 ]
At the intersection of disability studies and critical theory is critical disability theory. [ 44 ] [ 45 ] [ 46 ] [ 47 ] The term crip theory originates in Carrie Sandahl's article "Queering the Crip or Crippling the Queer?: Intersections of Queer and Crip Identities in Solo Autobiographical Performance". It was published in 2003 as part of a journal issue titled "Desiring Disability: Queer Theory Meets Disability Studies". [ 48 ] Christopher Bell 's [ 27 ] Blackness and Disability ; [ 28 ] and the work of Robert McRuer both explore queerness and disability. Work includes the intersections of race and ethnicity with disability in the field of education studies and has attempted to bridge critical race theory with disability studies. [ 32 ]
Most of the literature above is written by individual authors in the United States but there is nothing on there from other countries that depicts disability and sexuality in the same context. Myren-Svelstad, a Norwegian scholar compares two deviant novels in Norway's society, Nini Roll Anker's Enken [the Widow] written in 1932 and Magnhild Haalke's Allis sønn [Alli's Son] written in 1935. [ 56 ] They both depict a queer man who is also disabled. The disability being depicted as someone whose mental capacity is significantly different than society's heteronormative view. The significance of the movements began to build momentum and most legal recognition in the 1980s. It was only in 1973 that the American Psychiatric Association removed homosexuality from their list of mental disorders. [ 57 ] In addition to this, it was about forty years later in 2013 that the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition ( DSM-5 ) changed the listing of transgender to "gender dysphoria". [ 58 ]
One of the most notable circumstances where the case of these two minority rights come together was the court case In re Guardianship of Kowalski , in which an accident that occurred in 1983 left 36-year-old Sharon Kowalski physically disabled with severe brain injuries. [ 59 ] The court granted guardianship of her to her homophobic parents who refused visitation rights to her long time partner, Karen Thompson. The court case lasted nearly ten years and was resolved by granting Thompson custody in 1991. [ 60 ] This was a major victory in the realm of gay rights but also called to attention the validity of rights for those who identified under the queer and disabled spectrum. Numerous support groups emerged from necessity to create safe spaces for those identifying in these specific minority groups such as the founding of the Rainbow Alliance of the Deaf in 1977, [ citation needed ] the Lesbian Disabled Veterans of America group in 1996 [ citation needed ] which then became the Gay, Lesbian, Bisexual and Transgender Disabled Veterans of America, and the San Francisco Gay Amputees group in 2006.
A 2012 study showed that disability was more common in LGBTQ individuals when compared to heterosexual peers. [ 61 ] It was also shown that the LGBTQ group with disabilities were noticeably younger in age than the heterosexual group. In a 2014 study of intersecting identities found that "disabled women whether gay, straight, bisexual or otherwise identifying have a harder time finding romantic relationships due to their socioeconomic status and ability. [ 62 ] Drummond and Brotman introduce the idea that the lesbian disabled community face many barriers because of discrimination in the form of ableism, homophobia, racism and more due to intersecting identities and interests. [ 62 ]
It is also a large topic of discussion to say that both groups have to undergo the same kind of "coming out" process in terms of their sexual identity, gender identity, and disability identity because of the lasting social stigma. [ 63 ] "Coming out" through sexual identity, gender identity, and disability identity is one example of "Double Jeopardy", as they are part of more than one stigmatized group.
Eli Clare writes at the intersection of disability and transgender studies, namely as to how these disciplines can learn from each other. Similarly to how there is a 'coming out' for both transgender people and people with disabilities, there is a lack of bodily privacy both groups are faced with, primarily due to an over-medicalization of the body. Clare also works to make the distinction between bodily and medical truths, where one's diagnosis and medical treatment as a transgender or disabled person does not dictate their embodiment and how they navigate the world. Eventually, Clare reaches the idea of a disability politics of transness, which "delves into the lived experiences of our bodies, that questions the idea of normal and the notion of cure, that values self-determination, that resists shame and the medicalization of identity". [ 64 ]
Queer studies , which emerged from women's studies , brings light towards the different kind of oppression queer and transgender people with disabilities have. Queer studies are commonly associated with people with disabilities who identify as "Crip" and is commonly believed that queer politics must incorporate crip politics. [ 65 ] Alison Kafer describes a first-person experience of identifying queer and crip both reappropriated terms in Kafer's Feminist Queer Crip . Kafer describes the politics of the crip future and "an insistence on thinking these imagined futures — and hence, these lived presents — differently". [ 52 ]
An aspect of disability studies that is not often talked about is that of the perception of seeing disabled individuals as invisible. [ 66 ] Also known as "queer/disabled invisibility". [ 66 ] In disability studies the individuals who are disabled who make it into academic course work are usually the ones who struggle not only with being disabled and facing ableist norms of society but they also have to contend with other identities such as being queer, a woman or a person of another race other than cis-gendered white male in America. Queer/disabled invisibility can also come up in forms of negative perceptions about the way a disabled individual is being raised. For instance, queer mothers raising a disabled child are often viewed as the cause of the child's disability. [ 67 ] Another example of queer and disabled negativity is highlighted in the life experiences of Josie, a young woman who does not identify as a particular gender, living with a lifelong illness and disability. [ 62 ] This young woman describes how she experienced sexism, ableism, homophobia and transphobia in a number of ways at her university, the queer community and medical providers because of her disability. The discrimination the women in these examples is part of the heteronormative, ableistic perspective in societies around the world today but are rarely discussed in the literature or during disability studies courses.
Within class comes multiple avenues for intersectionality through disability. Disability looks different from a middle class, upper class, and lower class perspective, as well as through race, gender, and ethnicity. One's social class can contribute to when a person becomes disabled, rather it be sooner or later. [ 52 ] For example, where there is poverty we will find disability. [ 68 ] This poverty can include social, economic, and cultural poverty. Having a disability can contribute to poverty just as poverty can contribute to having a disability. [ 69 ] People with disabilities are more likely to live in poverty and be unemployed than those who do not, resulting in lower socioeconomic status. [ 70 ] Some scholars have argued that disability, as it is understood today, is interlocked with class and capitalism. [ 71 ] [ 30 ] Intellectual disability, as it is understood today, is the product of the industrial revolution as workers unable to keep up with fast-paced factory work were pathologized. [ 72 ]
Robert McRuer challenges hegemonic, neoliberal capitalism as the agent that drives the dominant cultural and market priorities and further argues that capitalism drives compulsory able-bodiedness. [ 73 ] In Feminist, Queer, Crip , Alison Kafer states "My goal is to contextualize, historically and politically, the meanings typically attributed to disability, thereby positioning "disability" as a set of practices and associations that can be critiqued, contested, and transformed." [ 52 ]
The International Association of Accessibility Professionals [ 74 ] recognizes six different models for conceptualizing disability: social, medical, cultural affiliation, economic, charity, and functional solutions. Once universally accepted in the field, [ 2 ] there has been a developing counter-argument to the social model of disability since at least 2009. [ 3 ] In a 2014 Disability Studies Quarterly article, students involved in campus disability groups note that they actively seek cures for their chronic illnesses and "question the rejection of the medical model" of disability. [ 16 ] The cultural affiliation model accepts the person's disability completely and uses it a point of pride in being associated with other people in a similar condition. [ 75 ] The economic model recognizes the effect of bodily limitations on a person's ability to work, and there may be a need for economic support or accommodations for the person's disability [ 76 ] while the charity model regards people with disabilities as unfortunate and in need of assistance from the outside, with those providing charity viewed as benevolent contributors to a needy population. The functional solutions model of disability is a practical perspective that identifies the limitations (or "functional impairments") due to disability, with the intent to create and promote solutions to overcome those limitations. The primary task is to eliminate, or at least reduce, the impact of the functional limitations of the body through technological or methodological innovation. The pragmatism of the functional solution model deemphasizes the sociopolitical aspects of disability, and instead prioritizes inventiveness and entrepreneurship. This is the prevailing opinion behind compliance literature that promotes self-efficacy and self-advocacy skills for people with disabilities preparing for transition to independent living. [ 77 ]
The social model has also been challenged for creating a false separation between disability and impairment as impairment, not just disability, is socially constructed. [ 30 ] This critique draws on feminist arguments that the assertion that sex is biological but gender is social is a false dichotomy because sex is also socially constructed. [ 78 ] This is not a rejection of physical reality but draws attention to the social value put on some values, needs and accommodations and the denigration of others. [ 30 ]
There is discourse within disability studies to analyze the construction of mental illness. However, few post-structuralist disability scholars have focused their attention to impairments of the mind. [ 79 ] According to Carol Thomas, a reader in sociology at the Institute for Health Research, Lancaster University , this may be because disability scholars have in the past considered only the barriers confronted by people with physical disabilities. The experience of impairment, cognitive disability, and mental illness had been absent from the discussion.
It is unclear exactly which perspective of disability scholarship "psychological impairment" can fall under, and this has led to a hesitation on the part of scholars. [ 79 ] Scholars such as Peter Beresford (2002) suggest "the development of a 'social model of madness and distress ' " which would consider impairments of the mind. [ 79 ] Yet others may recommend the "embodied approach" to the study of mental illnesses. [ 79 ]
Although many activists with disabilities find empowerment in appropriating the term crip, not all people with disabilities feel comfortable using that identity. [ 80 ] There are many different terms used as an alternative to disability, for example Melwood, a nonprofit who uses the term "differing abilities", describes the label disability as "a limitation in the ability to pursue an occupation because of a physical or mental impairment; a disqualification, restriction or disadvantage and a lack of legal qualification to do something, was an inadequate or limiting 'label' for a cross section of people". [ 81 ] Because the term disability has a history of inferiority, it is believed by many that substituting the term will help eliminate the ableism that is embedded within it. Susan Wendell describes ableism in society "as a structure for people who have no weakness". [ 82 ] This also applies to anyone who has any intersectional disadvantages. Feminism identifies these disadvantages and strategizes how to deconstruct the system that supports marginalizing specific groups of people.
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In medical terminology , disarticulation is the separation of two bones at their joint , either traumatically by way of injury or by a surgeon during arthroplasty or amputation . [ 1 ]
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Disclosing tablets are chewable tablets that make dental plaque visible.
The tablets, sold over the counter in many countries, contain a dye (typically a vegetable dye, such as Phloxine B ) that stains the plaque a bright color (typically red or blue). After brushing , one chews a tablet and rinses. Colored stains on the teeth indicate areas where plaque remains after brushing, providing feedback to improve brushing technique. For self-examination, a dental mirror may be needed. [ 1 ]
More sophisticated varieties of plaque disclosing agents contain several dyes, which selectively stain plaque of different ages. With the most common variety, immature plaque stains red, mature purple, and pathological acidic plaque blue. This is owing to the blue dye washing off immature plaque, and acid degrading the red dye. In effect, red dye reveals new plaque, whilst blue dye reveals old plaque and a purple/pink colouring reveals built-up old and new plaque stuck together causing infections. Disclosing tablets are commonly used by those undergoing orthodontic treatments to prevent plaque build up in areas which are harder to brush. [ 2 ] [ 3 ]
An example of a dye with a patented use as a "Dental Plaque Disclosing Agent" is erythrosine . [ 4 ]
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Discoid meniscus is a rare human anatomic variant that usually affects the lateral meniscus of the knee . Usually a person with this anomaly has no complaints; however, it may present as pain, swelling, or a snapping sound heard from the affected knee. Strong suggestive findings on magnetic resonance imaging includes a thickened meniscal body seen on more than two contiguous sagittal slices.
The Watanabe classification of discoid lateral meniscus is: (A) Incomplete, (B) Complete, and (C) Wrisberg-ligament variant [ 1 ]
Normally, the meniscus is a thin crescent-shaped piece of cartilage that lies between the weight bearing joint surfaces of the femur and the tibia . It is attached to the lining of the knee joint along its periphery and serves to absorb about a third of the impact load that the joint cartilage surface sees and also provides some degree of stabilization for the knee. There are two menisci in the knee joint, with one on the outside (away from midline) being the lateral meniscus and the inner one (towards midline) the medial meniscus . A discoid meniscus is a congenital anomaly of the knee found in 3% of the population (up to 15% in Asia). It typically affects the lateral meniscus and may be found bilaterally (20%). Instead of the narrow crescent shape, as seen in a normal meniscus above, a discoid meniscus is thickened, and has a fuller crescent shape. In addition, a discoid meniscus does not taper as much towards the center of the joint and is shaped like a disc. The thickness of the meniscus, its diminished vascular blood supply, and in some instances, weak capsular attachment, makes it more prone to tears compared to a normal meniscus. The anomaly in itself is asymptomatic; however, a tear of the meniscus can result in pain, swelling, and snapping in the affected knee. The orthopedic classification of discoid menisci includes: complete, incomplete or Wrisberg-ligament types as depicted here. Coverage of the lateral tibial plateau determines the designation of complete or incomplete. The Wrisberg-ligament type has an abnormal posterior attachment by attaching to part of the posterior cruciate ligament .
Symptom is usually pain in the knee. And when the knee is bent or stretched it makes the sound of bouncing bones.
The transverse diameter of a normal meniscus is approximately 10 to 11 mm; therefore a normal meniscus body will be visible on only 2 slices of a MR with 4-5-mm sagittal slices. A discoid meniscus should be considered if more than two contiguous body segments are present. However, this method may lead to a false negative when evaluating people with the Wrisberg variant of discoid meniscus since it maintains a narrow crescent shape. Coronal and radial images of the meniscus are useful to demonstrate the extension of the aberrant meniscus into the joint as seen here. On coronal images, it is diagnosed when the horizontal measurement between the free margin and the periphery of the body is more than 1.4 cm. [ 2 ] Rarely, X-ray may show lateral joint space widening, squaring of the lateral condyle, cupping of the lateral tibial plateau and hypoplasia of the lateral tibial spine that suggest discoid meniscus.
In a patient complaining of acute onset knee pain, an X-ray study would be done to rule out any bony pathology such as a fracture . Since it is difficult to diagnose meniscal anomalies with X-ray , an MRI would be necessary to visualize the discoid meniscus. If the patient is asymptomatic and does not complain of significant locking sensation in the knee or pain, treatment is conservative and consists of stretching and strengthening exercises for the quadriceps and hamstring muscles. “In cases where there is significant disability, surgical excision may be needed. When the discoid meniscus is severely damaged, total excision of the meniscus may be necessary. In most cases where the meniscus is still generally intact, a partial excision to preserve the cushioning function may be sufficient.” [ 3 ] [ medical citation needed ]
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Discover Oncology , formerly Hormones and Cancer , is a bimonthly peer-reviewed medical journal covering research on all aspects of hormone action on cancer . It was established in 2010 and is published by Springer Science + Business Media on behalf of The Endocrine Society . The editor-in-chief is Carol A. Lange ( University of Minnesota ).
The journal is abstracted and indexed in:
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A disease-modifying treatment , disease-modifying drug , or disease-modifying therapy is a treatment that delays, slows or reverses the progression of a disease by targeting its underlying cause . [ 1 ] They are distinguished from symptomatic treatments that treat the symptoms of a disease but do not address its underlying cause. [ 2 ]
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Disease Models & Mechanisms (DMM) is a monthly peer-reviewed Open Access biomedical journal published by The Company of Biologists that launched in 2008. [ 1 ] DMM is partnered with Publons , is part of the Review Commons initiative and has two-way integration with bioRxiv . [ 2 ]
DMM publishes original research, resources and reviews that focus on the use of model systems to better understand, diagnose and treat human disease . [ 3 ]
Model systems of interest include: [ 4 ]
Disease areas of interest include: [ 5 ]
The journal operates on a continuous publication model. The final version of record is immediately released online as soon as it is ready. [ 1 ]
All papers are published as Open Access articles under the CC-BY licence . [ 6 ]
The journal is abstracted and/or indexed by: [ 7 ]
It is a member of OASPA (Open Access Scholarly Publishers Association) and is indexed in the DOAJ (Directory of Open Access Journals) . [ 8 ]
Disease Models & Mechanisms is a signatory of the San Francisco Declaration on Research Assessment (DORA) . [ 9 ]
The founding editor-in-chief was Vivian Siegel (2008-2013), followed by Ross Cagan (2013-2016) [ 10 ] and Monica J. Justice (2016-2020). [ 11 ]
Elizabeth Patton [ 12 ] was appointed Editor-in-Chief in December 2020, with Elaine Mardis as Deputy Editor-in-Chief.
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In agriculture , disease management is the practice of minimizing disease in crops to increase quantity or quality of harvest yield.
Organisms that cause infectious disease in crops include fungi , oomycetes , bacteria , viruses , viroids , virus-like organisms, phytoplasmas , protozoa , nematodes and parasitic plants . Crops can also suffer from ectoparasites including insects , mites , snails , slugs , and vertebrate animals, but these are not considered diseases.
Controlling diseases can be achieved by resistance genes , [ 1 ] fungicides , nematicides , quarantine , etc. Disease management can be a large part of farm operating costs. [ 2 ]
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Disease mongering is a pejorative term for the practice of widening the diagnostic boundaries of illnesses and aggressively promoting their public awareness in order to expand the markets for treatment.
Among the entities benefiting from selling and delivering treatments are pharmaceutical companies , physicians, alternative practitioners and other professional or consumer organizations . It is distinct from the promulgation of bogus or unrecognised diagnoses .
The term " monger " has ancient roots, providing the basis for many common compound forms such as cheesemonger, fishmonger , rumor monger and fleshmonger, for those who peddle such wares respectively. "Disease mongering" as a label for the "invention" or promotion of diseases in order to capitalize on their treatment was first used in 1992 by health writer Lynn Payer, who applied it to the Listerine mouthwash campaign against halitosis (bad breath).
Payer defined disease mongering as a set of practices which include the following: [ 1 ]
The incidence of conditions not previously defined as illness being medicalised as "diseases" is difficult to scientifically assess due to the inherent social and political nature of the definition of what constitutes a disease, and what aspects of the human condition should be managed according to a medical model. [ 2 ] For example, halitosis, the condition which prompted Payer to coin the phrase "disease mongering", isn't merely an imagined social stigma but can stem from any of a wide spectrum of conditions spanning from bacterial infection of the gums to kidney failure, and is recognized by the Scientific Council of the American Dental Association as "a recognizable condition which deserves professional attention". [ 3 ]
Australian journalist Ray Moynihan has argued that the pharmaceutical industry engages in disease mongering to enlarge its profits, and that it harms citizens. [ 4 ] His use of osteoporosis as an example of a "made up" disease in this article prompted an angry retort from the president of the British National Osteoporosis Society , stating that the article was insulting to people with osteoporosis and vastly understated the risk of disabling fractures associated with the disorder. [ 5 ] Moynihan published a satire of disease mongering in the 2006 April Fool's Day issue of BMJ titled "Scientists find new disease: motivational deficiency disorder ". [ 6 ]
Other conditions which have been cited as examples of disease mongering include: restless leg syndrome , [ 7 ] testosterone deficiency , [ 8 ] erectile dysfunction , [ 4 ] sluggish cognitive tempo , [ 9 ] Lyme disease , [ 1 ] and hypoactive sexual desire disorder . [ 10 ] Some of these conditions are recognized as medical disorders by professional medical societies [ 11 ] and the National Institute of Health and Clinical Excellence . [ 12 ] In 2014, an FDA advisory committee voted to limit the use of testosterone replacement therapy products due to potentially increased cardiovascular risk associated with their use. [ 13 ]
A 2006 Newcastle, New South Wales international conference, reported in PLoS Medicine , explored the phenomenon of disease mongering. [ 14 ]
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Disease or patient registries are collections of secondary data related to patients with a specific diagnosis, condition, or procedure, and they play an important role in post marketing surveillance of pharmaceuticals. [ 1 ] Registries are different from indexes in that they contain more extensive data.
In its simplest form, a disease registry could consist of a collection of paper cards kept inside "a shoe box" by an individual physician. Most frequently registries vary in sophistication from simple spreadsheets that only can be accessed by a small group of physicians to very complex databases that are accessed online across multiple institutions. [ 2 ]
They can provide health providers (or even patients) with reminders to check certain tests in order to reach certain quality goals.
Registries are less complex and simpler to set up than electronic medical records that according to a recent survey are only used by 9% of small offices where almost half of the US doctors work. [ 3 ]
An electronic medical record keeps track of all the patients a doctor follows but a registry only keeps track of a small sub population of patients with a specific condition.
More than 130 million Americans live with chronic diseases and chronic diseases account for 70% of all deaths in the US. "The medical care costs of people with chronic diseases account for more than 75% of the nation's $2 trillion medical care costs." [ 4 ]
Registries target certain conditions because medical expenses are unevenly distributed: most health care expenses are spent treating patients with a few chronic conditions. [ 5 ]
For example, the 2002 expenses with diabetes in the US was $132 billion, and this was around 12% of the US medical budget. Diabetes accounts for 25% of the Medicare budget. [ 6 ] Given this, diabetes is one of the conditions targeted by registries. Diabetes is also amenable to this because there is a target population that can be defined according to certain rules and there is evidence that certain tests like retina exams, LDL levels, HgbA1c levels can correlate with quality of care in diabetes. [ 7 ]
Because of the diabetes impact, New York City created a HbA1C Registry (NYCAR) to help health providers keep track of patients with diabetes. [ 8 ] Another example of disease registry is the New York State CABG Registry that tracks all cardiac bypass surgery performed in the state of New York. [ 9 ]
Cerebral palsy is an example of a chronic or lifelong medical condition. It is a major cause of childhood disability worldwide. The Australian cerebral palsy register represents an example of a recognized disease register. [ 10 ] The aim of the Australian CP register is to conduct surveillance or constant observation of cerebral palsy prevalence, clinical patterns and complications. It is also tasked with providing recommendations to public health policy makers and improving health service delivery to individuals with cerebral palsy. [ 11 ] More recently, several developing countries such as Bangladesh and Sri lanka have established cerebral palsy registers geared toward achieving the same above-noted aims. [ 12 ] [ 13 ] [ 14 ]
On a survey of 1040 US physician organizations published in Journal of the American Medical Association, [ 15 ] diabetes registries are used by 40.3%, asthma registries are used by 31.2% of physician organizations, CHF registries are used by 34.8% and depression registries are used by 15.7%.
Other tests like Pap smears are also useful to keep track in registries because there is evidence that when done annually in women of certain ages groups can detect and prevent cervical cancer. [ 16 ]
Many of measures tracked are based on evidence-based medicine and are defined and standardized by national organizations like the NCQA .
Patient registries are particularly useful for evaluating the safety of orphan drug products as well as the safety of drugs in specific populations. [ 17 ] However, it is getting more and more common to use data of different healthcare and disease registries innovatively for different purposes such as for generating evidence for healthcare efficiency, market access planning and pharmacovigilance [ 18 ]
Countries like Australia, Britain, Norway, Sweden, [ 19 ] and America [ 20 ] have a national joint replacement registry to track patients with artificial joints.
"The use of joint registries has proven beneficial abroad. In Australia, regulators use such data to force manufacturers to justify why poorly performing hips or knees should remain available, and products have been withdrawn as a result. In Sweden several years ago, surgeons alerted by their national registry stopped using a badly flawed hip long before their American counterparts did. A few medical organizations in the USA, like Kaiser Permanente, operate their own registries to good effect and the Hospital for Special Surgery in New York has recently set up a registry.
Experts say that the United States wastes billions of dollars annually on medical treatments which may not work. But the financial and human consequences are also large when evidence exists but is not collected." [ 21 ]
The cost-effectiveness of a disease registry is related with the cost-effectiveness of prevention of specific medical conditions. Increasing compliance through a registry with preventive measures like children vaccination or colonoscopy screening can actually be a cost-saving measure. [ 22 ] "A mammogram every 2 years for women aged 50–69 costs only about $9,000 per year of life saved. This cost compares favorably with other widely used clinical preventive services." [ 23 ]
Registries can be associated with pay-for-performance (P4P) quality based contracts for individual doctors, groups of doctors or even all doctors in a country. For example, the United Kingdom, rewards physicians according to 146 quality measures related with 10 chronic diseases that are tracked electronically. [ 24 ]
In the United States, Medicare also started a 1.5% P4P contract based on health measures that can be tracked by disease registries. [ 25 ]
The quality of a disease registry is contingent on the quality of its data and all the processes involved in updating it and keeping its integrity. In every registry there is always a risk of " garbage in, garbage out ". Issues that can affect a registry and its acceptance by a physician group:
Below is a growing list of patient registries.
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https://en.wikipedia.org/wiki/Disease_registry
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Disease suppressive soils function to prevent the establishment of pathogens in the rhizosphere of plants. These soils develop through the establishment of beneficial microbes, known as plant growth-promoting rhizobacteria (PGPR) in the rhizosphere of plant roots. [ 1 ] These mutualistic microbes function to increase plant health by fighting against harmful soil microbes either directly or indirectly. As beneficial bacteria occupy space around plant roots they outcompete harmful pathogens by releasing pathogenic suppressive metabolites. Recent research has demonstrated that disease-suppressive soils not only inhibit soilborne pathogens but also protect plants from insect pests. [ 2 ] In particular, these soils can enhance plant resistance to leaf-feeding insects by promoting beneficial rhizosphere bacteria and priming plant defense mechanisms.
Plant growth promoting rhizobacteria are bacteria that promote plant growth, through fixing nitrogen , producing growth hormones, or even suppressing pathogens. [ 3 ] A variety of PGPR genera provide a wide array of functions that directly improve plant health. Bacteria genera Rhizobium and Mesorhizobium work to fix nitrogen into a usable form. [ 4 ] Actinomyces and Azospirillum produce growth hormones that increase root growth and uptake of nutrients. [ 5 ]
While many of these genera increase plant health directly some PGPR promote plant health indirectly through pathogen suppression. [ 6 ] Pathogenic fungi create a complex of hyphae that migrate through the soil. When these fungi reach the rhizosphere they release enzymes that degrade the cell wall of plant root cells. This allows them to enter and infect the host plant and prevent the uptake of nutrients. Beneficial Pseudomonas and Bacillus produce fungal suppressing metabolites that break up this migrating fungal hyphae . [ 1 ] Over time, plants are able to create disease-suppressive soils in response to these pathogens through the increasing the abundance of these PGPR in their rhizosphere area.
Plants respond to pathogens by recruiting PGPR to their root rhizosphere from the bulk soil to fill in and prevent pathogen establishment. This ultimately leads to the development of disease-suppressive soils. PGPR are recruited through the natural release plant exudates from root cells as they push through the soil. [ 7 ] Different species of plants release different exudates and therefore recruit different microbial communities to their rhizosphere from the microbes already present in the surrounding bulk soil. [ 8 ]
If a beneficial microbe genera is not present in a soil plants are not able to recruit it as a defense. Therefore, suppressive soils are a function of the microbes already present in a soil and able to be recruited. The creation of these soils must be done by increasing PGPR in the overall bulk soil. Specific plants are able to recruit beneficial bacteria through the secretion of different root exudates. [ 9 ] A greater diversity of plants in a soil leads to a greater diversity of microbes in the rhizosphere and furthermore can lead to greater suppression of soil diseases. [ 10 ] Management, such as informed crop rotation and soil solarization , can create suppressive soils that naturally suppress pathogens. [ 11 ]
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The modern disease theory of alcoholism states that problem drinking is sometimes caused by a disease of the brain , characterized by altered brain structure and function. Today, alcohol use disorder (AUD) is used as a more scientific and suitable approach to alcohol dependence and alcohol -related problems. [ 1 ]
The largest association of physicians – the American Medical Association (AMA) – declared that alcoholism was an illness in 1956. [ 2 ] [ 3 ] In 1991, the AMA further endorsed the dual classification of alcoholism by the International Classification of Diseases under both psychiatric and medical sections.
Under the model of alcoholism , alcohol use disorder is viewed as chronic problem for which abstinence is required. [ 4 ] A brain disease model of addiction, based on the extent of neuroadaptation and impaired control, is main position advanced for proposing a disease model of alcohol use disorder. [ 5 ] However, if managed properly, damage to the brain can be stopped and to some extent reversed. [ 6 ] In addition to problem drinking, the disease is characterized by symptoms including an impaired control over alcohol, compulsive thoughts about alcohol, and distorted thinking . [ 7 ] Alcoholism can also lead indirectly, through excess consumption, to physical dependence on alcohol, and diseases such as cirrhosis of the liver.
The risk of developing alcoholism depends on many factors, such as environment. Those with a family history of alcoholism are more likely to develop it themselves (Enoch & Goldman, 2001); however, many individuals have developed alcoholism without a family history of the disease. Since the consumption of alcohol is necessary to develop alcoholism, the availability of and attitudes towards alcohol in an individual's environment affect their likelihood of developing the disease. Current evidence indicates that in both men and women, alcoholism is 50–60% genetically determined, leaving 40-50% for environmental influences. [ 8 ]
In a review in 2001, McLellan et al. compared the diagnoses, heritability, etiology (genetic and environmental factors), pathophysiology, and response to treatments (adherence and relapse) of drug dependence vs type 2 diabetes mellitus, hypertension, and asthma. They found that genetic heritability, personal choice, and environmental factors are comparably involved in the etiology and course of all of these disorders, providing evidence that drug (including alcohol) dependence is a chronic medical illness. [ 9 ]
According to the theory, genes play a strong role in the development of alcoholism.
Twin studies , adoption studies, and artificial selection studies have shown that a person's genes can predispose them to developing alcoholism. Evidence from twin studies show that concordance rates for alcoholism are higher for monozygotic twins than dizygotic twins —76% for monozygotic twins and 61% for dizygotic twins. [ 10 ] However, female twin studies demonstrate that females have much lower concordance rates than males. [ 10 ] Reasons for gender differences may include environmental factors, such as negative public attitudes towards female drinkers. [ 11 ]
Adoption studies also suggest a strong genetic tendency towards alcoholism. Studies on children separated from their biological parents demonstrates that sons of alcoholic biological fathers were more likely to become alcoholic, even though they have been separated and raised by non alcoholic parents. [ 10 ]
In artificial selection studies, specific strains of rats were bred to prefer alcohol. These rats preferred drinking alcohol over other liquids, resulting in a tolerance for alcohol and exhibited a physical dependency on alcohol. [ 10 ] Rats that were not bred for this preference did not have these traits. [ 12 ] [ 10 ] Upon analyzing the brains of these two strains of rats, it was discovered that there were differences in chemical composition of certain areas of the brain. This study suggests that certain brain mechanisms are more genetically prone to alcoholism. [ 13 ]
The convergent evidence from these studies present a strong case for the genetic basis of alcoholism. [ 14 ]
Historians debate who has primacy in arguing that habitual drinking carried the characteristics of a disease. Some note that Scottish physician Thomas Trotter was the first to characterize excessive drinking as a mental disease or medical defect. [ 15 ]
Others point to American physician Benjamin Rush (1745–1813), a signatory to the United States Declaration of Independence , who understood drunkenness to be what we would now call a "loss of control", as possibly the first to use the term addiction in this sort of meaning. [ 16 ]
My observations authorize me to say, that persons who have been addicted to them, should abstain from them suddenly and entirely. 'Taste not, handle not, touch not' should be inscribed upon every vessel that contains spirits in the house of a man, who wishes to be cured of habits of intemperance.
Rush argued that "habitual drunkenness should be regarded not as a bad habit but as a disease", describing it as "a palsy of the will". [ 17 ] Rush expounded his views in a book published in 1808. [ 18 ] His views are described by Valverde, [ 19 ] Levine [ 16 ] Spode, [ 20 ] and Perkins-McVey. [ 21 ] Already in 1802 the prominent German physician Christoph Wilhelm Hufeland had published a book on the “brandy plague” stating that the “infection” with spirits makes it “inevitably necessary to drink ever more.” [ 22 ] Later he wrote an enthusiastic preface to the book On the addiction to drink and a rational cure of it by German-Russian physician C. von Brühl-Cramer. [ 23 ] As Spode points out, this study marked the birth of a consistent "paradigm" of addiction as a mental illness, although it took many decades until this view was accepted. [ 24 ] Perkins-McVey argues that Rush, Trotter, and Brühl-Cramer each independently developed their own disease theories of alcoholism as a result of their shared interest in the Brunonian system of medicine , which classified alcohol as a stimulant of the vital force. [ 25 ] As Perkins-McVey argues, this "understanding of the disease of habitual drunkenness as a phenomena [ sic ] of stimulus dependence is arguably the primary vehicle driving the disease model in the works of Rush, Trotter, and Brühl-Cramer." [ 26 ] This shifts the discussion away from the question of historical priority, instead identifying a common conceptual influence on early disease theorists.
In 1849, Swedish physician Magnus Huss coined the term alcoholism in his book Alcoholismus chronicus . Some argue he was the first to systematically describe the physical characteristics of habitual drinking and claim that it was a mental disease. However, Huss regarded heavy drinking still as a vice (that causes a destruction of the nervous system). [ 27 ] Moreover, this came decades after Trotter, Rush, Hufeland and Brühl-Cramer wrote their works, and some historians argue that the idea that habitual drinking was a mental disease emerged even earlier. [ 28 ]
Given this controversy, the best one can say is that the idea that habitual alcohol drinking was a disease had become more acceptable by the second half of the nineteenth century, although many writers still argued it was a vice, a sin, and not the purview of medicine but of religion. [ 29 ]
Between 1980 and 1991, medical organizations, including the AMA, worked together to establish policies regarding their positions on the disease theory. These policies were developed in 1987 in part because third-party reimbursement for treatment was difficult or impossible unless alcoholism were categorized as a disease. The policies of the AMA, formed through consensus of the federation of state and specialty medical societies within their House of Delegates, state, in part:
"The AMA endorses the proposition that drug dependencies, including alcoholism, are diseases and that their treatment is a legitimate part of medical practice."
In 1991, the AMA further endorsed the dual classification of alcoholism by the International Classification of Diseases under both psychiatric and medical sections.
The disease theory is often interpreted as implying that problem drinkers are incapable of returning to 'normal' problem free drinking, and therefore that treatment should focus on total abstinence. Some critics have used evidence of controlled drinking in formerly dependent drinkers to dispute the disease theory of alcoholism. [ 30 ]
The first major empirical challenge to this interpretation of the disease theory followed a 1962 study by Dr. D. L. Davies. [ 31 ] Davies' follow-up of ninety-three problem drinkers found that seven of them were able to return to "controlled drinking" (less than seven drinks per day for at least seven years). Davies concluded that "the accepted view that no alcohol addict can ever again drink normally should be modified, although all patients should be advised to aim at total abstinence"; After the Davies study, several other researchers reported cases of problem drinkers returning to controlled drinking. [ 32 ] [ 33 ] [ 34 ] [ 35 ] [ 36 ] [ 37 ] [ 38 ] [ 39 ]
In 1976, a major study commonly referred to as the RAND report, published evidence of problem drinkers learning to consume alcohol in moderation. [ 40 ] The publication of the study renewed controversy over how people with a disease which reputedly leads to uncontrollable drinking could manage to drink controllably. Subsequent studies also reported evidence of return to controlled drinking. [ 41 ] [ 42 ] [ 43 ] [ 44 ] [ 45 ] Similarly, according to a 2002 National Institute on Alcohol Abuse and Alcoholism (NIAAA) study, [ 46 ] about one of every six (18%) of alcohol dependent adults in the U.S. whose dependence began over one year previously had become "low-risk drinkers" (less than fourteen drinks per week and five drinks per day for men, or less than seven per week and four per day for women). This modern longitudinal study surveyed more than 43,000 individuals representative of the U.S. adult population, rather than focusing solely on those seeking or receiving treatment for alcohol dependence. [ 47 ] "Twenty years after onset of alcohol dependence, about three-fourths of individuals are in full recovery; more than half of those who have fully recovered drink at low-risk levels without symptoms of alcohol dependence." [ 46 ] [ 48 ]
However, many researchers have debated the results of the smaller studies. A 1994 followup of the original seven cases studied by Davies suggested that he "had been substantially misled, and the paradox exists that a widely influential paper which did much to stimulate new thinking was based on faulty data." [ 49 ] The most recent study, a long-term (60 year) follow-up of two groups of alcoholic men by George Vaillant at Harvard Medical School concluded that "return to controlled drinking rarely persisted for much more than a decade without relapse or evolution into abstinence." [ 50 ] Vaillant also noted that "return-to-controlled drinking, as reported in short-term studies, is often a mirage."
The second RAND study, in 1980, found that alcohol dependence represents a factor of central importance in the process of relapse. [ 51 ] Among people with low dependence levels at admission, the risk of relapse appears relatively low for those who later drank without problems. But the greater the initial level of dependence, the higher the likelihood of relapse for nonproblem drinkers. [ 51 ] The second RAND study findings have been strengthened by subsequent research by Dawson et al. in 2005 which found that severity was associated positively with the likelihood of abstinent recovery and associated negatively with the likelihood of non-abstinent recovery or controlled drinking. [ 48 ] Other factors such as a significant period of abstinence or changes in life circumstances were also identified as strong influences for success in a book on Controlled Drinking published in 1981. [ 52 ]
As part of a harm reduction strategy, provision of small amounts of alcoholic beverages to homeless alcoholics at homeless shelters in Toronto and Ottawa reduced government costs and improved health outcomes. [ 53 ] [ 54 ]
In 1988, the US Supreme Court upheld a regulation whereby the Veterans' Administration was able to avoid paying benefits by presuming that primary alcoholism is always the result of the veteran's "own willful misconduct." The majority opinion written by Justice Byron R. White echoed the District of Columbia Circuit's finding that there exists "a substantial body of medical literature that even contests the proposition that alcoholism is a disease, much less that it is a disease for which the victim bears no responsibility". [ 55 ] He also wrote: "Indeed, even among many who consider alcoholism a 'disease' to which its victims are genetically predisposed, the consumption of alcohol is not regarded as wholly involuntary." However, the majority opinion stated in conclusion that "this litigation does not require the Court to decide whether alcoholism is a disease whose course its victims cannot control. It is not our role to resolve this medical issue on which the authorities remain sharply divided." The dissenting opinion noted that "despite much comment in the popular press, these cases are not concerned with whether alcoholism, simplistically, is or is not a 'disease.'" [ 56 ]
The American Bar Association "affirms the principle that dependence on alcohol or other drugs is a disease." [ 57 ]
Alcoholism is a disease with a known pathology and an established biomolecular signal transduction pathway [ 58 ] which culminates in ΔFosB overexpression within the D1-type medium spiny neurons of the nucleus accumbens ; [ 58 ] [ 59 ] [ 60 ] when this overexpression occurs, ΔFosB induces the addictive state. [ 58 ] [ 59 ] [ 60 ]
In 2004, the World Health Organization published a detailed report on alcohol and other psychoactive substances entitled "Neuroscience of psychoactive substance use and dependence". [ 61 ] It stated that this was the "first attempt by WHO to provide a comprehensive overview of the biological factors related to substance use and dependence by summarizing the vast amount of knowledge gained in the last 20-30 years. The report highlights the current state of knowledge of the mechanisms of action of different types of psychoactive substances, and explains how the use of these substances can lead to the development of dependence syndrome." The report states that "dependence has not previously been recognized as a disorder of the brain, in the same way that psychiatric and mental illnesses were not previously viewed as being a result of a disorder of the brain. However, with recent advances in neuroscience, it is clear that dependence is as much a disorder of the brain as any other neurological or psychiatric illness."
The American Society of Addiction Medicine and the American Medical Association both maintain extensive policy regarding alcoholism. The American Psychiatric Association recognizes the existence of alcoholism as the equivalent of alcohol dependence. The American Hospital Association , the American Public Health Association , the National Association of Social Workers , and the American College of Physicians classify alcoholism as a disease .
In the US, the National Institutes of Health has a specific institute, the National Institute on Alcohol Abuse and Alcoholism (NIAAA), concerned with the support and conduct of biomedical and behavioral research on the causes, consequences, treatment, and prevention of alcoholism and alcohol-related problems. It funds approximately 90 percent of all such research in the United States. The official NIAAA position is that "alcoholism is a disease. The craving that an alcoholic feels for alcohol can be as strong as the need for food or water. An alcoholic will continue to drink despite serious family, health, or legal problems. Like many other diseases, alcoholism is chronic, meaning that it lasts a person's lifetime; it usually follows a predictable course; and it has symptoms. The risk for developing alcoholism is influenced both by a person's genes and by his or her lifestyle." [ 62 ]
Certain medications including opioid antagonists such as naltrexone have been shown to be effective in the treatment of alcoholism. [ 63 ]
Some physicians, scientists and others have rejected the disease theory of alcoholism on logical, empirical and other grounds. [ 64 ] [ 65 ] [ 66 ] [ 67 ] [ 68 ] [ 69 ] Indeed, some addiction experts such as Stanton Peele are outspoken in their rejection of the disease model, and other prominent alcohol researchers such as Nick Heather have authored books intending to disprove the disease model. [ 70 ]
These critics hold that by removing some of the stigma and personal responsibility, the disease concept actually increases alcoholism and drug abuse and thus the need for treatment. [ 71 ] This is somewhat supported by a study which found that a greater belief in the disease theory of alcoholism and higher commitment to total abstinence to be factors correlated with increased likelihood that an alcoholic would have a full-blown relapse (substantial continued use) following an initial lapse (single use). [ 72 ] However, the authors noted that "the direction of causality cannot be determined from these data. It is possible that belief in alcoholism as a loss-of-control disease predisposes clients to relapse, or that repeated relapses reinforce clients' beliefs in the disease model."
One study published in 1996 found that only 25 percent of physicians believed that alcoholism is a disease. The majority believed alcoholism to be a social or psychological problem instead of a disease. [ 73 ]
Thomas R. Hobbs says that "Based on my experiences working in the addiction field for the past 10 years, I believe many, if not most, health care professionals still view alcohol addiction as a willpower or conduct problem and are resistant to look at it as a disease." [ 74 ]
The sociologist Lynn M. Appleton noted that "Despite all public pronouncements about alcoholism as a disease, medical practice rejects treating it as such. Not only does alcoholism not follow the model of a 'disease,' it is not amenable to standard medical treatment." She says that "Medical doctors' rejection of the disease theory of alcoholism has a strong basis in the biomedical model underpinning most of their training" and that "medical research on alcoholism does not support the disease model." [ 75 ] : 65 and 69
"Many doctors have been loath to prescribe drugs to treat alcoholism, sometimes because of the belief that alcoholism is a moral disorder rather than a disease," according to Dr. Bankole Johnson , Chairman of the Department of Psychiatry at the University of Virginia . [ 76 ] Dr Johnson's own pioneering work has made important contributions to the understanding of alcoholism as a disease. [ 77 ]
Frequency and quantity of alcohol use are not related to the presence of the condition; that is, people can drink a great deal without necessarily being alcoholic, and alcoholics may drink minimally or infrequently. [ 7 ] [ 78 ]
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Diseases of the Colon & Rectum is a monthly peer-reviewed medical journal covering colorectal surgery . It was established in 1958 and is published by Lippincott Williams and Wilkins on behalf of the American Society of Colon and Rectal Surgeons , of which it is the official journal. The editor-in-chief is Susan Galandiuk ( University of Louisville ). According to the Journal Citation Reports , the journal has a 2016 impact factor of 3.519. [ 1 ]
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Dismemberment is the act of completely disconnecting and/or removing the limbs , skin , and/or organs from a living or dead being. It has been practiced upon human beings as a form of capital punishment , especially in connection with regicide , but can occur as a result of a traumatic accident, or in connection with murder, suicide, or cannibalism . As opposed to surgical amputation of limbs, dismemberment is often fatal. In criminology , a distinction is made between offensive dismemberment, in which dismemberment is the primary objective of the dismemberer, and defensive dismemberment, in which the motivation is to destroy evidence. [ 1 ]
In 2019, American psychiatrists and medical professionals Michael H. Stone , Gary Brucato, and Ann Burgess proposed formal criteria by which "dismemberment" might be systematically distinguished from the act of mutilation , as these terms are commonly used interchangeably. They suggested that dismemberment involves "the entire removal, by any means, of a large section of the body of a living or dead person, specifically, the head (also termed decapitation ), arms, hands, torso, pelvic area, legs, or feet". Mutilation, by contrast, involves "the removal or irreparable disfigurement, by any means, of some smaller portion of one of those larger sections of a living or dead person. The latter would include castration (removal of the testes ), disembowelment (removal of internal organs ), and flaying (removal of the skin )." According to these parameters, removing a whole hand would constitute dismemberment, while removing or damaging a finger would be mutilation; decapitation of a full head would be dismemberment, while removing or damaging a part of the face would be mutilation; and removing a whole torso would be dismemberment, while removing or damaging a breast or the organs contained within the torso would be mutilation. [ 2 ]
Particularly in South Asia, execution by trained elephants was a form of capital punishment practiced for several centuries. The techniques by which the convicted person was executed varied widely but did, on occasion, include the elephant dismembering the victim by means of sharp blades attached to its feet. The Muslim traveler Ibn Battuta , visiting Delhi in the 1330s, has left the following eyewitness account of this particular type of execution by elephants: [ 3 ]
Upon a certain day, when I myself was present, some men were brought out who had been accused of having attempted the life of the Vizier. They were ordered, accordingly, to be thrown to the elephants, which had been taught to cut their victims to pieces. Their hoofs were cased with sharp iron instruments, and the extremities of these were like knives. On such occasions the elephant-driver rode upon them: and, when a man was thrown to them, they would wrap the trunk about him and toss him up, then take him with the teeth and throw him between their fore feet upon the breast, and do just as the driver should bid them, and according to the orders of the Emperor. If the order was to cut him to pieces, the elephant would do so with his irons, and then throw the pieces among the assembled multitude: but if the order was to leave him, he would be left lying before the Emperor, until the skin should be taken off, and stuffed with hay, and the flesh given to the dogs.
In the Holy Roman Empire emperor Charles V 's 1532 Constitutio Criminalis Carolina specifies how every dismemberment (quartering) should ideally occur: [ 4 ]
Concerning quartering: To cut and hack apart his entire body into four pieces, and thus be punished unto death, and such four parts are to be hanged on stakes publicly on four common thorough-fares.
Thus, the imperially approved way to dismember the convict within the Holy Roman Empire was by means of cutting , rather than dismemberment through ripping the individual apart. In paragraph 124 of the same code, beheading prior to quartering is mentioned as allowable when extenuating circumstances are present, whereas aggravating circumstances may allow pinching/ripping the criminal with glowing pincers, prior to quartering. [ 5 ]
The fate of Wilhelm von Grumbach in 1567, a maverick knight in the Holy Roman Empire who was fond of making his own private wars and was thus condemned for treason, is also worthy of note. Gout-ridden, he was carried to the execution site in a chair and bound fast to a table. The executioner then ripped out his heart, and stuck it in von Grumbach's face with the words: "von Grumbach! Behold your false heart!" Afterwards, the executioner quartered von Grumbach's body. His principal associate was given the same treatment, and an eyewitness stated that after his heart had been ripped out, Chancellor Brück screamed horribly for "quite some time". [ 6 ]
One example of a highly aggravated execution is illustrated by the fate of Bastian Karnhars on 16 July 1600. Karnhars was found guilty of 52 separate acts of murder, including the rape and murder of 8 women, and the murder of a child, whose heart he had allegedly eaten for rituals of black magic. To begin, Karnhars had three strips of flesh torn from his back, before being pinched 18 times with glowing pincers, having his fingers clipped off one by one, his arms and legs broken on the wheel , and finally, while still alive, quartered. [ 7 ]
In the seventeenth century, a number of travel reports speak of an exotic "Turkish" execution method, where first the waist of a man was constricted by ropes and cords, and then a swift bisection of the trunk was performed. William Lithgow presents a comparatively prosaic description of the method: [ 8 ]
If a Turke should happen to kill another Turke ... he is brought forth to the market place, and a blocke being brought hither of foure foote high; the malefactor is stripd naked; and then layd thereupon with his belly downeward, they drawe in his middle together so small with running cords, that they strike his body a two with one blow: his hinder parts they cast to be eaten by hungry dogges kept for the same purpose; and the forequarters and head they throw into a grievous fire, made there for the same end – and this is the punishment for man-slaughter.
George Sandys , however, during the same period, tells of a method as no longer in use, in a rather more mythologized way: [ 9 ]
... they twitch the offender about the waist with a towell, enforcing him to draw up his breath by often pricking him in the body, until they have drawn him within the compasse of a span; then tying it hard, they cut him off in the middle, and setting the body on a hot plate of copper, which seareth the veines, they so up-propping him during their cruell pleasure: who not only retaineth his sense, but the faculties of discourse, until he be taken downe; and then he departeth in an instant.
In 1850s Persia, a particular dismemberment technique called shekkeh is reported to have been used. Travelling as an official for the East India Company Robert Binning [ 10 ] describes it as follows: [ 11 ]
the criminal is hung up by the heels, head downwards, from a ladder or between two posts, and the executioner hacks away with a sword, until the body is bisected lengthways, terminating at the head. The two severed halves are then suspended on a camel, and paraded through the streets, for the edification of all beholders. When the shekkeh is to be inflicted in a merciful manner, the culprit's head is struck off, previous to bisecting the trunk.
Sikh martyr Bhai Mani Singh was dismembered on the orders of Zakaria Khan, the Mughal Subahdar of Lahore after failing to pay tribute. [ 12 ]
Veer Gokula Jat , was dismembered on the orders of Mughal emperor, Aurangzeb , in Agra . Gokula was executed for leading the “Jat Uprising of 1669”, one of the earliest organised revolt against Mughal Empire in India. [ 13 ]
Dismemberment was a form of capital punishment for convicts of high treason in the Korean kingdom of the Joseon Dynasty . This punishment was, for example, meted out to Hwang Sa-Yong in 1801. [ 14 ]
The Five Punishments is a Chinese variation invented during the Qin dynasty . During the Tang dynasty (AD 618–907), truncation of the body at the waist by means of a fodder knife was a death penalty reserved for those who were seen to have done something particularly treacherous or repugnant. [ 15 ] That practice of cutting in two did not originate in the Tang dynasty; in sources concerning the Han dynasty (206 BC – AD 220), no fewer than 33 cases of execution by cutting at the waist are mentioned, but occurs very rarely in earlier material. [ 16 ]
Lingchi was a form of torture and execution used from the 10th century until the early 20th century to punish heinous crimes such as treason. Often translated as "slow slicing" or "death by a thousand cuts", a knife was used to remove portions of the body until death. [ 17 ]
Dismemberment is no longer used by most modern governments as a form of execution or torture , though amputation is still carried out in countries that practice Sharia law . [ 18 ]
Dismemberment was carried out in the Medieval and Early Modern era and could be effected, for example, by tying a person's limbs to chains or other restraints, then attaching the restraints to separate movable entities (e.g. vehicles) and moving them in opposite directions. Depending on the forces supplied by the horses or other entities, joints of the hips and shoulders were quickly dislocated, but ultimate severing of the tendons and ligaments in order to fully dismember the limbs would sometimes require assistance with cuts from a blade.
Also referred to as "disruption", dismemberment could be brought about by chaining four horses to the condemned's arms and legs, thus making them pull him apart, as was the case with the executions of François Ravaillac in 1610, Michał Piekarski in 1620, and Robert-François Damiens in 1757. Ravaillac's extended torture and execution has been described like this: [ 19 ]
He was condemned to be tortured with red-hot pincers on four limbs and on each breast. His wounds were to be sprinkled with molten lead and boiling oil and his body was then to be torn in pieces by four horses, the remains being subsequently burnt.
In the case of Damiens, he was condemned to essentially the same fate as Ravaillac, but the execution did not quite work according to plan, as the eyewitness Giacomo Casanova could relate: [ 20 ]
Damiens' agony went on for hours as each torture was applied. When the horses failed to disconnect the sinews between his body and his limbs, his body, still alive, was quartered with a knife. His friend, the infamous Casanova, reports that he "watched the dreadful sight for four hours". "I was obliged to turn away my face and to stop my ears as I heard his piercing shrieks, half his body having been torn from him."
As late as in 1781, this gruesome punishment was meted out to the Peruvian rebel leader Túpac Amaru II by the Spanish colonial authorities. The following is an extract from the official judicial death sentence issued by the Spanish authorities which condemns Túpac Amaru II to torture and death. It was ordered in the sentence that Túpac Amaru II be condemned to have his tongue cut out, after watching the executions of his family, and to have his hands and feet tied
to four horses who will then be driven at once toward the four corners of the plaza, pulling the arms and legs from his body. The torso will then be taken to the hill overlooking the city ... where it will be burned in a bonfire ... Tupac Amaru's head will be sent to Tinta to be displayed for three days in the place of public execution and then placed upon a pike at the principal entrance to the city. One of his arms will be sent to Tungasuca, where he was the cacique, and the other arm to the capital province of Carabaya, to be similarly displayed in those locations. His legs will be sent to Livitica and Santa Rosas in the provinces of Chumbivilcas and Lampa, respectively. [ 21 ]
Chēliè ( simplified Chinese : 车裂 ; traditional Chinese : 車裂 ) was dismemberment by tying the limbs and head to five carts led by horses or oxen, which would pull the body apart. It was a form of torture and execution used in ancient China from the Warring States period until the Tang Dynasty . [ 22 ] [ 23 ]
Queen Brunhilda of Austrasia , executed in 613, is generally regarded to have suffered the same death, though one account has it that she was tied to the tail of a single horse and thus suffered more of a dragging death . The Liber Historiae Francorum , an eighth century chronicle, describes her death by dismemberment as follows: [ 24 ]
Then King Chlothar ordered that she be lifted onto a camel and led through the entire army. Then she was tied to the feet of wild horses and torn apart limb from limb. Finally, she died.
The story of Brunhilda being tied to the tail of a single horse (and then to die in some gruesome manner) is promoted, for example, by Ted Byfield (2003), in which he writes: "Then they tied her to the tail of a wild horse; whipped into frenzy, it kicked her to death". [ 25 ] The cited source for this claim, however, the seventh century Life of St. Columban by the monk Jonas, does not support this claim. In paragraph 58 in his work, Jonas just writes: "but Brunhilda he had placed first on a camel in mockery and so exhibited to all her enemies round about then she was bound to the tails of wild horses and thus perished wretchedly". [ 26 ]
The storyline of Brunhilda being tied to the tail of a single horse and being subsequently dragged to death has become a classical motif in artistic representations, as can be seen by the included image.
According to Olfert Dapper , a 17th-century Dutchman who meticulously collected reports from faraway countries from seamen and other travelers, a fairly frequent maritime death penalty among the Barbary corsairs was to affix the hands and feet to chains on four different ships. When the ships then sailed off in different directions, the chains grew taut, and the man in between was torn apart after a while. [ 27 ]
Roman military discipline could be extremely severe, and the emperor Aurelian (r. AD 270–275), who had a reputation for extreme strictness, instituted the rule that soldiers who seduced the wives of their hosts should have their legs fastened to two bent-down trees, which were then released, ripping the man in two. [ 28 ] Similarly, in an unsuccessful rebellion against the emperor Valens in AD 366, the usurper Procopius met the same fate. [ 29 ]
After the defeat of Darius III by Alexander the Great , the Persian empire was thrown into turmoil, and Darius was killed. One man, Bessus , claimed the throne as Artaxerxes V, but in 329 BC, Alexander had him executed. The manner of Bessus' death is disputed, and Waldemar Heckel writes: [ 30 ]
The exact details of Bessus' death are disputed. He may have been crucified, or torn apart by recoiling trees, or (what is most likely) mutilated before being sent to Ecbatana for execution.
The method of tying people to bent down trees, which are then allowed to recoil, ripping the individual to pieces in the process is, however, mentioned by several travelers to nineteenth century Persia. The British diplomat James Justinian Morier travelled as a special envoy to the Shah in 1808, and Morier writes the following concerning then-prevailing criminal justice: [ 31 ]
... for the King never pardons theft, and orders a convicted thief to be executed instantly. The mode is as follows: two young trees are by main strength brought together at their summits, and there fastened with cords together. The culprit is then brought out, and his legs are tied with ropes, which are again carried up and: fixed to the top of the trees. The cords that force the trees together are then cut; and, in the elasticity and power of this spring, the body of the thief is torn asunder, and left thus to hang divided on each separate tree. The inflexibility of the King in this point has given to the roads a security, which, in former times, was little known.
An obscure Christian martyr Severianus was, about the year AD 300, martyred in the following way, according to one tale: One stone was fastened to his head, another bound to his feet. His middle was then fastened by a rope to the top of a wall, and the stones released from the height. His body was ripped apart. [ 32 ]
During the reign of the Roman Emperor Diocletian a Christian named Shamuna withstood being torn apart in the following manner:
The governor immediately ordered that Shamuna should be made to kneel down on one side and that an iron chain should be fastened on his knee. This having been done, he hung him up head downwards by the foot with which he had made him kneel; the other he pulled downwards with a heavy piece of iron, which cannot be described in words: thus endeavouring to rend the champion in two. By this means the socket of the hip-bone was wrenched out of its place and Shamuna became lame.
Some time thereafter, Shamuna was taken down from his hanging position, and was beheaded instead. [ citation needed ]
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Disorders of consciousness are medical conditions that inhibit consciousness . [ 1 ] Some define disorders of consciousness as any change from complete self-awareness to inhibited or absent self-awareness and arousal. This category generally includes minimally conscious state and persistent vegetative state , but sometimes also includes the less severe locked-in syndrome and more severe but rare chronic coma . [ 1 ] [ 2 ] Differential diagnosis of these disorders is an active area of biomedical research . [ 3 ] [ 4 ] [ 5 ] Finally, brain death results in an irreversible disruption of consciousness. [ 1 ] While other conditions may cause a moderate deterioration (e.g., dementia and delirium ) or transient interruption (e.g., grand mal and petit mal seizures ) of consciousness, they are not included in this category. [ citation needed ]
Patients in such a dramatically altered state of consciousness present unique problems for diagnosis, prognosis and treatment. Assessment of cognitive functions remaining after a traumatic brain injury is difficult. Voluntary movements may be very small, inconsistent and easily exhausted. Quantification of brain activity differentiates patients who sometimes only differ by a brief and small movement of a finger. [ citation needed ]
Consciousness is a complex and multifaceted concept, divided into two main components: Arousal and Awareness .
Arousal is associated with functional brainstem neuron populations projecting to both thalamic and cortical neurons. [ 6 ] Therefore, the assessment of reflexes (Using the Glasgow Coma Scale) is important to investigate the functional integrity of the brainstem. Awareness is thought to be related with functional integrity of the cerebral cortex and its subcortical connections. The most important point regarding the classification of disorders of consciousness is, that consciousness cannot be measured objectively by any machine, although many scoring systems have been developed for the quantification of consciousness and neuroimaging techniques are important tools for clinical research, extending our understanding of underlying mechanisms involved. [ 7 ] [ 8 ] Disorders in consciousness represent immense social and ethical issues because the diagnosis is methodologically complex and needs careful interpretation. Also the ethical framework must be further developed to guide research in these patients. [ citation needed ]
In locked-in syndrome the patient has awareness, sleep-wake cycles, and meaningful behavior (viz., eye-movement), but is isolated due to quadriplegia and pseudobulbar palsy , resulting from the disruption of corticospinal and corticobulbar pathways. Locked-in syndrome is a condition in which a patient is aware and awake but cannot move or communicate verbally due to complete paralysis of nearly all voluntary muscles in the body except for the eyes. Eye or eyelid movements are the main method of communication. [ 9 ] Total locked-in syndrome is a version of locked-in syndrome where the eyes are paralyzed as well. [ 10 ]
In a minimally conscious state , the patient has intermittent periods of awareness and wakefulness. The criteria for minimally conscious state, that patients are not in a vegetative state but are not able to communicate consistently. This means, that patients have to show limited but reproducible signs of awareness of themself or their environment. This could be following of simple commands, intelligible speech or purposeful behavior (including movements or affective behavior in relation to external stimuli, but not reflexive activity). [ 11 ] Further improvement towards full conscious recovery is more likely in this state than in the vegetative state, but still some patients remain in the MCS constantly. [ 12 ]
In a persistent vegetative state , the patient has sleep-wake cycles, but lacks awareness, is not able to communicate and only displays reflexive and non-purposeful behavior. The term refers to an organic body that is able to grow and develop devoid of intellectual activity or social intercourse. [ 11 ] The diagnosis of the vegetative state should be questioned when there is any degree of sustained and reproducible visual pursuit or fixation or response to threatening gestures.
This state reflects an intact brainstem and allied structures but severely damaged white and gray matter in both cerebral hemispheres. The preservation of these structures maintains arousal and automatic functions. [ 13 ] The overall metabolism drops in average to 40-50% of the normal range. After four weeks in a vegetative state (VS), the patient is classified as in a persistent vegetative state. Here the metabolism drops to 30-40% of the normal range but seems to be a result of trans-synaptic neuronal degeneration. [ 14 ] Although the diagnosis is problematic, the formal absence of any sign of conscious perception or deliberate action is essential.
This diagnosis can be further classified as a permanent vegetative state (PVS) after approximately 1 year of being in a vegetative state after traumatic brain injury. [ 15 ]
Like coma, chronic coma results mostly from cortical or white-matter damage after neuronal or axonal injury, or from focal brainstem lesions. Usually the metabolism in the grey matter decreases to 50-70% of the normal range. The patient lacks awareness and arousal. The patient lies with eyes closed and is not aware of self or surroundings. Stimulation cannot produce spontaneous periods of wakefulness and eye-opening, unlike patients in vegetative state. In medicine, a coma (from the Greek κῶμα koma, meaning deep sleep) is a state of unconsciousness, lasting more than six hours in which a person cannot be awakened, fails to respond normally to painful stimuli, light, sound, lacks a normal sleep-wake cycle and does not initiate voluntary actions. Although, according to the Glasgow Coma Scale , a person with confusion is considered to be in the mildest coma. But cerebral metabolism has been shown to correlate poorly with the level of consciousness in patients with mild to severe injury within the first month after traumatic brain injury (TBI). [ 16 ] A person in a state of coma is described as comatose. In general patients surviving a coma recover gradually within 2–4 weeks. But recovery to full awareness and arousal is not always possible. Some patients do not progress further than vegetative state or minimally conscious state and sometimes this also results in prolonged stages before further recovery to complete consciousness. [ 17 ]
Although a coma patient may appear to be awake, they are unable to consciously feel, speak, hear, or move. For a patient to maintain consciousness, two important neurological components must function impeccably. The first is the cerebral cortex which is the gray matter covering the outer layer of the brain. The other is a structure located in the brainstem, called reticular activating system (RAS or ARAS). Injury to either or both of these components is sufficient to cause a patient to experience a coma. [ citation needed ]
Brain death is the irreversible end of all brain activity, and function (including involuntary activity necessary to sustain life). The main cause is total necrosis of the cerebral neurons following loss of brain oxygenation. After brain death the patient lacks any sense of awareness; sleep-wake cycles or behavior, and typically look as if they are dead or are in a deep sleep-state or coma. Although visually similar to a comatose state such as persistent vegetative state, the two should not be confused. Criteria for brain death differ from country to country. However, the clinical assessments are the same and require the loss of all brainstem reflexes and the demonstration of continuing apnea in a persistently comatose patient (< 4 weeks). [ 18 ] Functional imaging using PET or CT scans, typically show a hollow skull phenomenon. This confirms the absence of neuronal function in the whole brain.
Patients classified as brain dead are legally dead and can qualify as organ donors, in which their organs are surgically removed and prepared for a particular recipient. [ citation needed ]
Brain death is one of the deciding factors when pronouncing a trauma patient as dead. Determining function and presence of necrosis after trauma to the whole brain or brain-stem may be used to determine brain death, and is used in many states in the US. [ 19 ] [ 20 ]
Metabolic studies are useful, but they are not able to identify neural activity within a specific region to specific cognitive processes. Functionality can only be identified at the most general level: Metabolism in cortical and subcortical regions that may contribute to cognitive processes. [ citation needed ]
At present, there is no established relation between cerebral metabolic rates of glucose or oxygen as measured by PET and patient outcome. The decrease of cerebral metabolism occurs also when patients are treated with anesthetics to the point of unresponsiveness. Lowest value (28% of normal range) have been reported during propofol anesthesia. Also, deep sleep represents a phase of decreased metabolism (down to 40% of the normal range) [ 21 ] [ 22 ] In general, quantitative PET studies and the assessment of cerebral metabolic rates depends on many assumptions.
PET, for example, requires a correction factor, the lumped constant , which is stable in healthy brains. There are reports that a global decrease of this constant emerges after a traumatic brain injury. [ 23 ] But, not only the correction factors change due to TBI.
Another issue is the possibility of anaerobic glycolysis that could occur after TBI. In such a case, the glucose levels measured by the PET are not tightly connected to the oxygen consumption of the patient's brain. [ 24 ] Third point regarding PET scans is the overall measurement per unit volume of brain tissue. The imaging can be affected by the inclusion of metabolically inactive spaces e.g. cerebrospinal fluid in the case of gross hydrocephalus, which artificially lowers the calculated metabolism. [ 25 ] Also, the issue of radiation exposure must be considered in patients with already severely damaged brains and preclude longitudinal or follow-up studies. [ 26 ] [ 27 ]
Disorders of consciousness present a variety of ethical concerns. Most obvious is the lack of consent in any treatment decisions. Patients in PVS or MCS are not able to decide for the possibility of withdrawal of life-support. It is also a general question whether they should receive life-sustaining therapy and, if so, for what duration. The problems regarding a patient's consent also account for neuroimaging studies. Without patient's consent, such studies are perceived as unethical. [ 28 ] Additionally, only few patients have created advance directives before losing decision-making capacity. [ 29 ] Some studies demonstrated that some patients with disorders of consciousness may be aware despite clinical unresponsiveness. These findings could have a major impact on ethical and social issues. [ 30 ]
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Disorders of sex development ( DSDs ), also known as differences in sex development , variations in sex characteristics ( VSC ), [ 2 ] [ 3 ] sexual anomalies , or sexual abnormalities , are congenital conditions affecting the reproductive system , in which development of chromosomal , gonadal , or anatomical sex is atypical. [ 4 ] [ 5 ]
DSDs are subdivided into groups in which the labels generally emphasize the karyotype 's role in diagnosis: 46,XX; 46,XY; sex chromosome; XX, sex reversal; ovotesticular disorder; and XY, sex reversal. [ 6 ]
Infants born with atypical genitalia often cause confusion and distress for the family. Psychosexual development is influenced by numerous factors that include, but are not limited to, gender differences in brain structure, genes associated with sexual development, prenatal androgen exposure, interactions with family, and cultural and societal factors. [ 7 ] Because of the complex and multifaceted factors involved, communication and psychosexual support are all important.
A team of experts, or patient support groups, are usually recommended for cases related to sexual anomalies. This team of experts are usually derived from a variety of disciplines including pediatricians , neonatologists , pediatric urologists , pediatric general surgeons , endocrinologists , geneticists , radiologists , psychologists and social workers . [ 8 ] [ 9 ] [ 10 ] These professionals are capable of providing first line (prenatal) and second line diagnostic (postnatal) tests to examine and diagnose sexual anomalies.
DSDs are defined as "any problem noted at birth where the genitalia are atypical in relation to the chromosomes or gonads". [ 11 ] There are several types of DSDs, and their effect on the external and internal reproductive organs varies greatly.
A frequently used, casual social adjective for people with DSDs is " intersex ". Urologists were concerned that terms like intersex, hermaphrodite , and pseudohermaphrodite were confusing and pejorative with respect to humans. This led to the Chicago Consensus, recommending a new terminology based on the umbrella term disorders of sex development. [ 12 ] [ 13 ] Other than disorders of sex development, another term is congenital conditions of sex development (CCSD). Since 2006, people who were previously incorrectly categorized as hermaphrodites are now labelled as having ovotesticular syndrome .
DSDs are divided into the following categories, emphasizing the karyotype 's role in diagnosis: [ 14 ] [ 15 ]
The penis (males) and clitoris (females) have a common origin, both arising from an embryonic structure called the primordial phallus . In typical males, the urethra is located at the tip of the penis, while in typical females the urethra is located below the base of the clitoris. [ 16 ] It is also possible to have a urethral opening located along the shaft; this condition is known as hypospadias . [ 17 ]
Due to the significant and life-long impacts that DSDs can have on patients and their families, [ 18 ] it is widely accepted that children with DSDs should be managed by an experienced multidisciplinary team. [ 19 ] Health care providers generally agree that children with DSDs should be notified early. [ 20 ]
Appropriate and conservative medical intervention and age-appropriate child involvement in the treatment plan contribute greatly to successful outcomes for the entire range of DSDs. [ 21 ] [ 22 ]
In the normal prenatal stages of fetal development , the fetus is exposed to testosterone - albeit more in male fetuses than female ones. Upon the presence of the 5α-reductase enzyme , testosterone is converted to dihydrotestosterone (i.e. DHT). If DHT is present, the male external genitalia will develop.
Development of male external genitalia:
On the other hand, if maternal placenta estrogen is present without DHT, then the development of female external genitalia occurs. [ 26 ]
Development of female external genitalia (the vulva ):
However, in abnormal cases, sexual anomalies occur due to a variety of factors that lead to an excess of androgens in the fetus. The effects of excessive androgens differ in fetuses with XX chromosome (female) and XY chromosomes (male).
In XX chromosome fetuses, excess androgens result in ambiguous genitalia . This makes identification of external genitalia as male or female difficult. [ 28 ] Additionally, the individual may have clitoromegaly , a shallow vagina , early and rapid growth of pubic hair in childhood, delayed puberty , hirsutism , virilisation , irregular menstrual cycle in adolescence and infertility due to anovulation . [ 29 ]
In XY chromosome fetuses, excess androgens result in a functional and average-sized penis with extreme virilisation , but the inability for sperm production . [ 30 ] Additionally, the individual will also experience early and rapid growth of pubic hair during childhood and precocious puberty stages. [ 29 ]
Sexual anomalies often generate from genetic abnormalities caused by many factors, leading to different sexual development. These genetic abnormalities occur during the prenatal stage of an individual's fetal development. During this stage, genetic mutations can result from endocrine disrupters in the mother's diet or environmental factors. [ 31 ] The general causes of sexual anomalies can not be outlined due to the high variability of each individual's situations. Thus, the cause of each specific anomaly has to be studied independently.
Sexual differentiation occurs through various processes during the prenatal development period of the fetus. These processes are initiated and regulated by biological metabolites such as DNA , hormones and proteins . The initial steps of sexual differentiation begin with the development of the gonads and genitals. This process is consistent with both genders spanning over the course of the first 6 weeks following conception, during which the embryo remains pluripotent . [ 32 ] Differentiation of the gonads begins after the 6th week, which is determined by the sex-determining region Y (SRY) gene in the Y chromosome. [ 27 ]
The SRY gene plays an important role in developing the testes of a male individual. Following the development of the testes, hormones synthesized within the testes regulate the differentiation of both internal and external parts of the genitals. The absence of the testicles or the hormones synthesized may lead to irregular differentiation of the genitals. Genetic abnormalities or environmental factors that influence these procedures may lead to the incomplete development of the gonads and the genitals. These malformations can occur any time during the development or the birth of the embryo, manifesting as ambiguous genitals or dissonance within the genotypic and phenotypic sex of the individual, leading to a late onset of puberty, amenorrhea, a lack of or excess virilization, or later in life, infertility or early occurrence of menopause . [ 33 ]
DSDs caused by chromosomal variation generally do not present with genital ambiguity. This includes sex chromosome DSDs such as Klinefelter syndrome , Turner syndrome and 45,X or 46,XY gonadal dysgenesis . [ 34 ]
Males with Klinefelter syndrome usually have a karyotype of 47,XXY as a result of having two or more X chromosomes . [ 35 ] Affected patients generally have normal genital development, yet are infertile and have small, poor functioning testes , breast growth and delayed puberty. [ 35 ] The incidence for 47,XXY is 1 in 500 males, but severe and rare cases of Klinefelter syndrome presents as three or more X chromosomes. [ 35 ]
Turner syndrome is classified as aneuploidy or structural rearrangement of the X chromosome. Signs and symptoms of affected females vary among them, such as low birth weight, low-set ears, short stature, short neck and delayed puberty. [ 36 ] The incidence is 1 in 2500 live-born females, while most patients do not survive for more than one year after birth. [ 34 ]
Gonadal development disorders form a wide spectrum, classified by their cytogenetic and histopathological features. However, unsolved diagnosis and malignancy still represent difficulties in the sex determination of these patients. [ 37 ] Such disorders include partial or complete gonadal dysgenesis, ovotesticular DSD, testicular DSD and sex reversal . [ 8 ]
Genital abnormality can occur in the penis, scrotum or testes in males; and vagina and labia in females. [ 8 ] Sometimes, ambiguous genitalia could occur, where the clear distinction of external genitalia is absent in both male and female. Hence, examination (typically at birth) is carried out where the sex of the patient will be determined through imaging and blood tests . [ 8 ] Abnormal genital development includes disorders of fetal origin, disorders in androgen synthesis or action, disorders in anti-Müllerian hormone synthesis or action. [ 8 ]
In addition to the aforementioned sexual anomalies, there are other unclassified sexual anomalies. In males, this includes severe early-onset intrauterine growth restriction , isolated hypospadias , congenital hypogonadotropic hypogonadism , hypogonadism and cryptorchidism . In females, this includes Malformation syndromes , Müllerian agenesis / hypoplasia , uterine anomalies , vaginal atresia and labial adhesions . [ 8 ]
The treatment and/or management of DSDs with atypical genitalia will vary from person to person. This may include gender affirmation surgery , medical treatment and surgical treatment.
Gender affirmation plays a critical role in the management of sexual anomaly cases. Ultimately, the parents and a multidisciplinary team are responsible for assigning the sex that is affirmative the gender of the concerned person. The current guidelines of gender affirmation include the psychosocial effects in adults with etiological diagnosis, the potential for fertility, surgical opportunities and hormone replacement therapy in the course of puberty. [ 87 ] [ 10 ]
There are other factors considered during this process. This may include cultural and religious factors as well as the implications it has on the individual in later life. It is regulated by reference centers with groups specialised in managing cases of sexual anomalies. [ 10 ]
Hormonal treatment is an accepted and standardised approach to treat different congenital sexual anomalies. Patients that are deficient in hormones produced by the adrenal glands require immediate medical attention. They are given a hormone called hydrocortisone , a form of hormone replacement therapy, with the objective to induce puberty. [ 10 ]
Utilizing sex steroids as hormonal therapy is deemed controversial with concerns of its duration of initiation, dosage and regimen. [ 10 ] However, it is agreed amongst most clinicians that low doses of hormonal treatment should begin around the age of 11 to 12 years old and should be increased progressively. [ 10 ]
Surgical procedures are an alternative to hormonal treatment available for patients to address genital anomalies and improve the body's sexual functions. However, a common dilemma in these procedures is that they are often derived from the patient's expectation of 'normal' genitals from an aesthetic and functional standpoint. Oftentimes, this leads to extensive surgical interventions. [ 88 ]
In most cases, surgical procedures result in permanent changes to the appearance and function of the patient's body. Therefore, the decision to proceed with this arrangement must be a joint agreement between the family and the multidisciplinary team. The most ideal situation would be to include the patient as part of the decision-making process. However, cases where surgical treatments were performed at an early age are recognised as mutilation of the body. Subsequently, it has become increasingly common to defer surgical treatments until the patient is of appropriate age to be involved in the decision-making process. [ 10 ]
The Differences of Sex Development-Translational Research Network (DSD-TRN) is based in the United States and aims to improve DSD care across the United States. [ 89 ]
The International-Differences of Sex Development (I-DSD) is a research organization in Europe. This organization connects medical and research centers internationally in an effort to improve clinical practice, research, and general understanding of differences of sex development. [ 90 ] I-DSD regularly hosts a symposium to provide updates on current care in DSD internationally, facilitate networking for those in DSD Care, and promote high quality DSD research. [ 91 ]
Notable patient support and advocacy organizations include:
Even though the term disorder of sex development (DSD) is widely accepted by the medical community, its suitability and adequacy to represent these individuals are criticised by many support and advocacy groups . Firstly, the word 'disorder' carries negative connotations. Secondly, with current nomenclature , DSD is an overly generalised term for conditions that do not have differences in genital appearance or gender identity (e.g. Klinefelter syndrome and Turner syndrome ). Thirdly, the term 'DSD' lacks specificity and clarity; and therefore unhelpful in the diagnosis process. Hence, many support groups and advocates believe that the medical community should discontinue the use of 'DSD' as a designation tool. [ 93 ]
Furthermore, people who live with conditions regarding sexual abnormalities may encounter various mental and physical health problems. This may include traumatic experience with their own bodies, dissatisfaction with body image , low-self esteem, anxiety , depression , bipolar disorders , eating disorders , personality disorders , schizophrenia disorders, trauma and stress-related disorders, etc. [ 94 ]
Many intersex people are engaged in activism to stop hormonal treatments, citing the extreme and harmful nature of many of the treatments, further arguing that many of the treatments serve no medical purpose. [ 95 ]
The term disorders of sex development has generally been accepted by the medical community, as well as being a popular term in academic literature. [ 96 ] However, the term is not universal among patients or support groups. [ 97 ] One study stated that it can affect individuals covered by the description in a negative way, and that the terminology might impact choice and utilization of health care providers. [ 98 ] Another study found that most affected individuals did not find the term offensive. [ 99 ] The ICD-11 , which is the World Health Organization 's international guide to medical coding (effective as of January 1, 2022), references DSDs as intersex traits or conditions, as do some medical journals . [ 100 ] The Council of Europe [ 101 ] and Inter-American Commission on Human Rights [ 102 ] have called for a review of medical classifications that unnecessarily medicalize intersex traits. [ 101 ] [ 102 ] [ 103 ]
The DSD as a model was advocated for by intersex advocates to include all variation of atypical sexual development . Specifically the DSD exists as replacement for the " optimum gender rearing model ," which was the standard model for individuals with atypical sexual development. This model stated goal was to assign a gender binary , usually female via non-consensual medicalization , often via the falsification of medical records . After the publication of individuals who had undergone the OGR model and had gone through serious physiological distress , (such as David Reimer ), the model was discredited. The term "disorders of sexual development" was chosen to reflect the variation of sexual development over differences which effects all individuals, this however has been controversial, with many instead opting for "differentiation" or "variation." [ 104 ]
Sociological research in Australia on 272 "people born with atypical sex characteristics," published in 2016, found that 3% of respondents used the term "disorders of sex development" or "DSD" to define their sex characteristics, while 21% use the term when accessing medical services. In contrast, 60% used the term "intersex" in some form to self-describe their sex characteristics. [ 105 ] U.S. research by the Lurie Children's Hospital , Chicago, and the AIS-DSD Support Group (now InterConnect Support Group) published in 2017 found that "disorders of sex development" terminology may negatively affect care, give offense, and result in lower attendance at medical clinics. [ 106 ] [ 107 ]
A "dsd-LIFE" study in 2020 found that around 69% of 1,040 participants reported that DSD applied to their condition or that they felt neutral about the term, with most participants preferring terms that were specific to their somatic condition. [ 99 ]
The term DSD (and particularly its association with medical disorders ) has been controversial. The argument over terminology reflects a deeper disagreement over the extent to which intersex conditions require medical intervention, the appropriateness of certain interventions, and whether physicians and parents should make irreversible treatment decisions on behalf of young children if the condition is not life-threatening.
National and international medical classifications which pathologise variations in sex characteristics should be reviewed with a view to eliminating obstacles to the effective enjoyment, by intersex persons, of human rights, including the right to the highest attainable standard of health. [ 101 ]
While the 2006 clinical consensus statement that introduced the term, [ 4 ] its 2016 update, [ 67 ] included some sex chromosome anomalies within the term DSD, the inclusion of those conditions is opposed by some clinicians. [ citation needed ] Medical historian David Griffiths has identified continued controversy about the relationship between sex chromosome variations and intersex/DSD classifications. [ 126 ]
Similarly, some clinicians have proposed that congenital adrenal hyperplasia be excluded. [ 127 ] Human rights advocate Morgan Carpenter has remarked that this proposal appears motivated by support for contentious medical interventions . [ 128 ]
A member of the legal committee for the World Professional Association for Transgender Health and co-founder of the Australian and New Zealand Professional Association for Transgender Health has described "transsexualism" as "an intersex condition and a disorder of sexual development therapeutically medically treated by hormonal therapy and Genital Reassignment Surgery". [ 129 ] Such views are contested. [ 130 ]
There is particular contention around female-presenting athletes with DSDs (which can cause an elevated level of testosterone) competing in female-only sports events. [ 131 ]
World Athletics claimed that while 46 XY DSD occurs in roughly 1 in 20,000 people in the general population, it is found in about 7 in 1,000 elite female athletes (with a prevalence 140 times higher) arguing that this offers significant performance advantage. Within the scientific community there is ongoing debate over whether any physiological advantage, in fact, exists. [ 132 ]
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Disseminated disease can refer to disseminated cancer which is the movement of cancerous cells from the original tumor to other areas of the body, [ 1 ] or disseminated infection which is the pathogen's entry into the host, growth, and dissemination, which results in illness. [ 2 ]
After exiting the main tumor , cancer cells circulate throughout the body. They are known as circulating tumor cells once they are in the blood. Few circulating tumor cells can disseminate to distant locations and remain tumor cells. The amount of disseminated tumor cells that can develop into metastases is even lower. [ 3 ]
This article about a disease , disorder, or medical condition is a stub . You can help Wikipedia by expanding it .
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Disseminated intravascular coagulation ( DIC ) is a condition in which blood clots form throughout the body, blocking small blood vessels . [ 1 ] Symptoms may include chest pain , shortness of breath , leg pain, problems speaking, or problems moving parts of the body. [ 1 ] As clotting factors and platelets are used up, bleeding may occur. [ 1 ] This may include blood in the urine , blood in the stool , or bleeding into the skin. [ 1 ] Complications may include organ failure . [ 2 ]
Relatively common causes include sepsis , surgery , major trauma , cancer , and complications of pregnancy . [ 1 ] Less common causes include snake bites , frostbite , and burns . [ 1 ] There are two main types: acute (rapid onset) and chronic (slow onset). [ 1 ] Diagnosis is typically based on blood tests . [ 2 ] Findings may include low platelets , low fibrinogen , high INR , or high D-dimer . [ 2 ]
Treatment is mainly directed towards the underlying condition. [ 2 ] [ 3 ] Other measures may include giving platelets , cryoprecipitate , or fresh frozen plasma . [ 2 ] Evidence to support these treatments, however, is poor. [ 2 ] Heparin may be useful in the slowly developing form. [ 2 ] About 1% of people admitted to hospital are affected by the condition. [ 4 ] In those with sepsis, rates are between 20% and 50%. [ 4 ] The risk of death among those affected varies from 20% to 50%. [ 4 ]
In DIC, the underlying cause usually leads to symptoms and signs, and DIC is discovered on laboratory testing. The onset of DIC can be sudden, as in endotoxic shock or amniotic fluid embolism , or it may be insidious and chronic, as in cancer. DIC can lead to multiorgan failure and widespread bleeding. [ 5 ]
DIC can occur in the following conditions: [ 5 ] [ 6 ] [ 7 ] [ 8 ]
Liver disease , HELLP syndrome , thrombotic thrombocytopenic purpura , hemolytic uremic syndrome , and malignant hypertension may mimic DIC but originate via other pathways. [ 9 ] It is not the same as conditions where the blood vessels leak, such as capillary leak syndrome . [ 10 ]
Under homeostatic conditions, the body is maintained in a finely tuned balance of coagulation and fibrinolysis . The activation of the coagulation cascade yields thrombin that converts fibrinogen to fibrin ; the stable fibrin clot being the final product of hemostasis . The fibrinolytic system then functions to break down fibrinogen and fibrin. Activation of the fibrinolytic system generates plasmin (in the presence of thrombin), which is responsible for the lysis of fibrin clots. The breakdown of fibrinogen and fibrin results in polypeptides called fibrin degradation products (FDPs) or fibrin split products (FSPs). In a state of homeostasis between clot formation and clot dissolution, the presence of plasmin is critical, as it is the central proteolytic enzyme of coagulation and is necessary for the breakdown of fibrin clots, or fibrinolysis. [ 11 ]
In DIC, the processes of coagulation and fibrinolysis are dysregulated, and the result is widespread clotting with resultant bleeding. Regardless of the triggering event of DIC, once initiated, the pathophysiology of DIC is similar in all conditions. One critical mediator of DIC is the release of a transmembrane glycoprotein called tissue factor (TF). TF is present on the surface of many cell types (including endothelial cells, macrophages, and monocytes) and is not normally in contact with the general circulation, but is exposed to the circulation after vascular damage. For example, TF is released in response to exposure to cytokines (particularly interleukin 1 ), tumor necrosis factor , and endotoxin . [ 12 ] This plays a major role in the development of DIC in septic conditions. TF is also abundant in tissues of the lungs, brain, and placenta. This helps to explain why DIC readily develops in patients with extensive trauma. Upon exposure to blood and platelets, TF binds with activated factor VIIa (normally present in trace amounts in the blood), forming the extrinsic tenase complex. This complex further activates factor IX and X to IXa and Xa, respectively, leading to the common coagulation pathway and the subsequent formation of thrombin and fibrin. [ 7 ]
The release of endotoxin is the mechanism by which Gram-negative sepsis provokes DIC. In acute promyelocytic leukemia , treatment causes the destruction of leukemic granulocyte precursors, resulting in the release of large amounts of proteolytic enzymes from their storage granules, causing microvascular damage. Other malignancies may enhance the expression of various oncogenes that result in the release of TF and plasminogen activator inhibitor-1 (PAI-1), which prevents fibrinolysis. [ 13 ]
Excess circulating thrombin results from the excess activation of the coagulation cascade. The excess thrombin cleaves fibrinogen, which ultimately leaves behind multiple fibrin clots in the circulation. These excess clots trap platelets to become larger clots, which leads to microvascular and macrovascular thrombosis. This lodging of clots in the microcirculation, in the large vessels, and in the organs is what leads to the ischemia, impaired organ perfusion, and end-organ damage that occurs with DIC. [ 14 ] [ 15 ]
Coagulation inhibitors are also consumed in this process. Decreased inhibitor levels will permit more clotting so that a positive feedback loop develops in which increased clotting leads to more clotting. At the same time, thrombocytopenia occurs and this has been attributed to the entrapment and consumption of platelets. Clotting factors are consumed in the development of multiple clots, which contributes to the bleeding seen with DIC. [ 14 ] [ 15 ]
Simultaneously, excess circulating thrombin assists in the conversion of plasminogen to plasmin, resulting in fibrinolysis. The breakdown of clots results in an excess of FDPs, which have powerful anticoagulant properties, contributing to hemorrhage. The excess plasmin also activates the complement and kinin systems. Activation of these systems leads to many of the clinical symptoms that patients experiencing DIC exhibits, such as shock, hypotension, and increased vascular permeability. The acute form of DIC is considered an extreme expression of the intravascular coagulation process with a complete breakdown of the normal homeostatic boundaries. DIC is associated with a poor prognosis and a high mortality rate. [ 14 ] [ 15 ]
There has been a recent challenge however to the basic assumptions and interpretations of the pathophysiology of DIC. A study of sepsis and DIC in animal models has shown that a highly expressed receptor on the surface of hepatocytes, termed the Ashwell-Morell receptor , is responsible for thrombocytopenia in bacteremia and sepsis due to Streptococcus pneumoniae (SPN) and possibly other pathogens. The thrombocytopenia observed in SPN sepsis was not due to increased consumption of coagulation factors such as platelets, but instead was the result of this receptor's activity, enabling hepatocytes to ingest and rapidly clear platelets from circulation. [ 16 ] By removing prothrombotic components before they participate in the coagulopathy of DIC, the Ashwell-Morell receptor lessens the severity of DIC, reducing thrombosis and tissue necrosis, and promoting survival. The hemorrhage observed in DIC and among some tissues lacking this receptor may therefore be secondary to increased thrombosis with loss of the mechanical vascular barrier. [ 14 ] [ 15 ]
Activation of the intrinsic and extrinsic coagulation pathways causes excess thrombus formation in the blood vessels. Consumption of coagulation factors due to extensive coagulation in turn causes bleeding. [ 14 ] [ 15 ]
The diagnosis of DIC is not made on a single laboratory value, but rather the constellation of laboratory markers and a consistent history of an illness known to cause DIC. Laboratory markers consistent with DIC include: [ 3 ] [ 7 ] [ 17 ]
A diagnostic algorithm has been proposed by the International Society of Thrombosis and Haemostasis. This algorithm appears to be 91% sensitive and 97% specific for the diagnosis of overt DIC. A score of 5 or higher is compatible with DIC and it is recommended that the score is repeated daily, while a score below 5 is suggestive but not affirmative for DIC and it is recommended that it is repeated only occasionally: [ 17 ] [ 18 ] It has been recommended that a scoring system be used in the diagnosis and management of DIC in terms of improving outcome. [ 19 ]
Treatment of DIC is centered on treating the underlying condition. Transfusions of platelets or fresh frozen plasma can be considered in cases of significant bleeding, or those with a planned invasive procedure. The target goal of such transfusion depends on the clinical situation. Cryoprecipitate can be considered in those with a low fibrinogen level. Treatment of thrombosis with anticoagulants such as heparin is rarely used due to the risk of bleeding. [ citation needed ]
Recombinant human activated protein C was previously recommended in those with severe sepsis and DIC, but drotrecogin alfa has been shown to confer no benefit and was withdrawn from the market in 2011. [ 21 ]
Recombinant factor VII has been proposed as a "last resort" in those with severe hemorrhage due to obstetric or other causes, but conclusions about its use are still insufficient. [ 22 ]
Prognosis varies depending on the underlying disorder, and the extent of the intravascular thrombosis (clotting). The prognosis for those with DIC, regardless of cause, is often grim: between 20% and 50% of patients will die. [ 23 ] DIC with sepsis (infection) has a significantly higher rate of death than DIC associated with trauma. [ 23 ]
DIC is observed in approximately 1% of academic hospital admissions. [ 24 ] DIC occurs at higher rates in people with bacterial sepsis (83%), [ 25 ] severe trauma (31%), [ 26 ] and cancer (6.8%). [ 27 ]
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Dissociated sensory loss is a pattern of neurological damage caused by a lesion to a single tract in the spinal cord which involves preservation of fine touch and proprioception with selective loss of pain and temperature .
Understanding the mechanisms behind these selective lesions requires a brief discussion of the anatomy involved.
Loss of pain and temperature are due to damage to the lateral spinothalamic tracts , which cross the central part of the cord close to the level where they enter it and travel up the spinal column on the opposite side to the one they innervate (i.e. they ascend contralaterally ). Note that a lesion of the lateral spinothalamic tract at a given level will not result in sensory loss for the dermatome of the same level; this is due to the fibers of the tract of Lissauer which transmit the neuron one or two levels above the affected segment (thus bypassing the segmental lesion on the contralateral side).
Loss of fine touch and proprioception are due to damage to the dorsal columns , which do not cross the cord until the brainstem , and so travel up the column on the same side to the one they innervate (i.e. they ascend ipsilaterally ).
This means that a lesion of the dorsal columns will cause loss of touch and proprioception below the lesion and on the same side as it, while a lesion of the spinothalamic tracts will cause loss of pain and temperature below the lesion and on the opposite side to it. [ 1 ]
Dissociated sensory loss always suggests a focal lesion within the spinal cord or brainstem. [ citation needed ]
The location of cord lesions affects presentation—for instance, a central lesion (such as that of syringomyelia ) will knock out second order neurons of the spinothalamic tract as they cross the centre of the cord, and will cause loss of pain and temperature without loss of fine touch or proprioception.
Other causes of dissociated sensory loss include:
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Distal Revascularization and Interval Ligation (DRIL) is a surgical method of treating vascular access steal syndrome .
DRIL was first proposed by Harry Schanzer and colleagues in 1988. [ 1 ]
A short distal bypass is created and the artery just distal to the AV anastomosis is ligated.
This surgery article is a stub . You can help Wikipedia by expanding it .
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https://en.wikipedia.org/wiki/Distal_Revascularization_and_Interval_Ligation
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In medicine, distress is an aversive state in which a person is unable to completely adapt to difficult situations and their resulting effects and shows maladaptive behaviors. [ 1 ] It can be evident in the presence of various phenomena, such as inappropriate social interaction (e.g., aggression, passivity, or withdrawal).
Distress is the opposite of eustress , a positive emotion that motivates people.
Stress can be created by influences such as work , school, peers or co-workers, family and death. Other influences vary by age.
People under constant distress are more likely to become sick, mentally or physically. There is a clear response association between psychological distress and major causes of mortality across the full range of distress. [ 2 ]
Higher education has been linked to a reduction in psychological distress in both men and women, and these effects persist throughout the aging process, not just immediately after receiving education. However, this link does lessen with age. The major mechanism by which higher education plays a role on reducing stress in men is more so related to labor-market resources rather than social resources as in women. [ 3 ]
In the clinic, distress is a patient reported outcome that has a huge impact on patient's quality of life. To assess patient distress, a Hospital Anxiety and Depression Scale (HADS) questionnaire is most commonly used. The score from the HADS questionnaire guides a clinician to recommend lifestyle modifications or further assessment for mental disorders like depression . [ 4 ]
People often find ways of dealing with distress, in both negative and positive ways. Examples of positive ways are listening to music, calming exercises, coloring, sports and similar healthy distractions. [ 5 ] Negative ways can include but are not limited to use of drugs including alcohol, and expression of anger, which are likely to lead to complicated social interactions, thus causing increased distress. [ 6 ]
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An informal or primary caregiver is an individual in a cancer patient's life that provides unpaid assistance and cancer-related care. [ 1 ] Caregiving is defined as the processing of assisting someone who cannot care for themselves, which includes physical, mental, emotional, social, and spiritual needs. [ 2 ] Due to the typically late onset of cancer, caregivers are often the spouses or children of patients, but may also be parents, other family members, or close friends. [ 3 ] Taking care of family members at home is a complicated experience. [ 2 ] The relationships involved constantly shift and change, in expected and unexpected ways. [ 2 ] The expected or expected changes can negatively affect physical health, emotions, social life, and spiritual well-being of the caregiver. [ 2 ] Informal caregivers are a major form of support for the cancer patient because they provide most care outside of the hospital environment. This support includes:
With medical advances in cancer screening and treatment, cancer has become a chronic rather than an acute disease with the result that patients survive longer with cancer. [ 6 ] As a result, there has been a push towards outpatient care in recent years. [ 6 ] [ 8 ] [ 9 ] Consequently, informal caregivers are now taking on the responsibility of caring for a loved one with cancer. Informal caregivers have become so essential that they are estimated to provide an average of 55% of the care needed. [ 6 ] For years, research has been reporting the physical, psychological, financial, social, and spiritual repercussions of cancer on the patient. With the discovery of the distress, particularly psychological, that cancer could cause in patients, researchers also began to investigate whether caring for someone with cancer could have similar effects on informal caregivers. Over the years, many stressors have been identified and the effects of caring for a loved one with cancer are becoming well documented. Research in this area is continuing not only to better understand the caregiver's experience, but also to learn how their adjustment to the caregiver role impacts their ability to provide care to the cancer patient.
Cancer patients and caregivers are psychologically affected by cancer, however the way it affects them differs in many respects. Both patients and caregivers report significant unmet needs in the areas of managing daily life, emotions, and social identity. [ 10 ] Studies Indicate that patients are less concerned with these daily life issues than their caregivers. [ 10 ] Caregivers may be more concerned with these daily life issues because they are neglecting their own needs in order to improve the care of the patient. [ 1 ] Men and women may have different perceptions of the cancer and its effects depending on their role as either the patient or the caregiver. [ 11 ]
Many researchers and clinicians have divided the cancer trajectory in order to explain the changes that occur to the patient and caregiver at various points throughout the cancer trajectory. [ 12 ]
The initial or acute phase encompasses the time of diagnosis. [ 9 ] A number of stressors can lead to caregiver psychological distress with the diagnosis of treatment. At this point in the trajectory, the most salient psychological outcomes revolve around fear, [ 1 ] [ 13 ] uncertainty, [ 5 ] [ 13 ] sadness [ 13 ] and feelings of powerlessness or helplessness. [ 1 ] [ 13 ] Additionally, in studies where cancer recurrence was not evaluated, caregivers report the highest levels of anxiety and post-traumatic stress symptoms during this phase. [ 14 ] Caregivers are often frightened and upset by the diagnosis of their loved one, but they have an additional responsibility of trying to support the patient as they go through this difficult time. In the process of providing support, caregivers are often overlooked and have no one to turn to with their own concerns. [ 4 ] This period is full of uncertainty, with both the patient and the caregiver not knowing what to expect in terms of treatment, recovery, and overall outcome. [ 13 ] This can lead to significant psychological distress for some caregivers.
The chronic phase encompasses the treatment for cancer. [ 9 ] Along with the psychological repercussions typical of the initial phase, many other psychological outcomes become relevant as the patient undergoes cancer treatment due to a number of additional stressors that the caregiver must deal with. These additional stressors may cause "intrapsychic strain, such as guilt or changes in the caregiver's self-concept" (Haley, 2003, p. 153). [ 4 ] For a minority of caregivers, they may meet the criteria for a psychiatric diagnosis, typically of depression or an anxiety disorder. [ 15 ] But for the majority, any distress they experience does not reach clinically diagnosable levels, although they may exhibit depressive symptoms. [ 5 ] Currently, it remains uncertain how levels of psychological distress change with time. Some studies report that psychological distress decreases over time, but others report that it increases. [ 15 ] This increase may be a result of caregivers neglecting their own needs while caring for the patient. For some, this emotional repression may lead to feelings of resentment towards the patient. [ 9 ] At this point of the trajectory (and ongoing), caregivers may also begin to exhibit symptoms of burnout due to the increased work-burden of caring for someone with cancer. [ 9 ] There are many physical and emotional components to burnout. Amongst the emotional components, caregivers may experience frustration, anger, depression, resentment and insecurity. [ 9 ]
The resolution phase encompasses the completion of treatment, but there are a number of directions that the cancer trajectory can go from this point. [ 9 ] For some families, resolution may consist of the movement into palliative care and bereavement. For others, this may involve a transition into survivorship, where the patient may go into remission or may experience cancer recurrence. Caregivers may experience the same fears, uncertainties, burnout and feelings of guilt or sadness as caregivers in the previous stages. However, depending on the path that the family experiences after treatment, there are additional psychological repercussions for caregivers.
Palliative care is an especially demanding task for cancer caregivers than less progressive cancer because the care required for those with terminal cancer tends to be more demanding. [ 15 ] Caregivers in this situation often report high caregiver burden lasting the entire period. [ 5 ] Caregiver distress also tends to increase as patients progress through this phase, causing a lower caregiver quality of life . [ 15 ] [ 16 ] In some instances, caregivers even report higher levels of distress than the patient during this phase. [ 17 ] Having a difficult time with caregiving increases distress caregivers face as they enter the bereavement period after the death of their loved one, [ 18 ] whereas finding meaning in caring for their loved one may relate to better long term adjustment for caregivers. [ 19 ] Before bereavement, loved ones often face anticipatory grief , where they mourn and prepare for the loss of their loved one. [ 19 ] Families often react with fears of abandonment, anxiety, hopelessness and helplessness, and an intensified attachment to their loved one. Upon the death of their loved one, caregivers typically experience grief , which in a minority of cases may be complicated by a diagnosis of Major Depressive Disorder later in the grief process. [ 19 ] Some caregivers experience unresolved grief, which can lead to Prolonged Grief Disorder (PGD), which is included in the eleventh edition of the International Classification of Diseases and the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders . [ 20 ] In a 2022 meta-analysis, the prevalence rate of Prolonged Grief Disorder in families experiencing bereavement due to a member with cancer was estimated at 14.2%. [ 20 ] Differences in the prevalence of grief disorders among bereaved familial cancer caregivers shows evidence for higher rates of PGD in females, those with a religious affiliation, spousal caregiving, and coping with death from neurological cancer. [ 20 ] Females and spouses commonly experience higher burdens from caregiving, as evidence has pointed to them providing more direct care in cancer caregiving. [ 20 ] Psychological predictors of poor adjustment to grief include anxiety, depression, psychological distress, demoralization and anticipatory grief symptoms. [ 21 ] Pre-loss grief in cancer caregivers, which refers to feeling grief prior to the death of the patient, has been linked to higher prolonged grief rates. [ 22 ] Feeling prepared for the death of the patient has also been linked to grief disorders, as unpreparedness has been shown to be associated with prolonged grief and major depressive disorder. [ 22 ] A 2024 systematic review, which analyzed bereaved Taiwanese family members involved in cancer care, found that preparedness for death could be related to higher rates of complicated grief. [ 23 ] Conversations between the caregiver and healthcare staff on how to better prepare for the impending loss have been shown to be predictors of better adjustment in grief disorders. [ 21 ] The caregiver's relationship with the patient pre and post cancer diagnosis has been shown to impact bereavement adjustment. Factors such as, communication problems with the patient and family, ambivalent or dependent relationships with the deceased loved one, family tensions, and difficult decision making, have been shown to impact grief adjustment. [ 24 ] Depression and PTSD can be a greater concern for caregivers with unresolved tensions with their loved one, whereas stronger bonds during the palliative phase seems to be related to a healthier transition into bereavement for the caregiver. [ 17 ]
As patients and caregivers enter the survivorship period after the completion of primary treatment, they often feel uncertain and overwhelmed by what lies before them. [ 25 ] Patients often leave their last treatment session without much direction as to what they should expect next. [ 26 ] This is distressing for the caregiver as well because caregiving continues into this phase of the cancer trajectory because of the long-term and late effects of treatment, the psychological distress patients face, and any other related factors. A common concern faced by survivors and their caregivers is how to return to their "normal" life without cancer. [ 27 ] As well, survivors and caregivers are often uncertain and fearful about death and cancer recurrence, [ 5 ] even in the absence of cancer-related symptoms.
Cancer recurrence has been called "one of the most stressful events in the course of illness for both patients and their families". [ 5 ] Research on the effect that recurrence has on caregivers is mixed. Some caregivers may report even poorer quality of life than the recurrent survivors themselves, as well as depressive moods, fears about recurrence and hopelessness. [ 5 ] In contrast, some caregivers report lower levels of strain in recurrence than with the initial cancer, presumably because they had adapted to the stress of chronic illness. [ 28 ]
Along with psychological repercussions of cancer, some caregivers also experience physical effects due to caregiving. This is particularly true of highly burdensome caregiving, [ 5 ] as is typically the case with older or palliative patients . Commonly, caregivers report sleep disturbances, such as fatigue or insomnia. [ 1 ] [ 6 ] [ 13 ] [ 16 ] [ 29 ] In caregivers of advanced stage patients, these disturbed sleep patterns are associated with symptoms of depression. [ 5 ] [ 29 ] Sometimes, caregivers may also experience a loss of appetite or may meet the criteria for an eating disorder. [ 6 ] [ 13 ] For caregivers experiencing burnout, there are also often physical effects. These include: headaches, insomnia, backaches, lethargy, lingering colds, gastrointestinal upset, and cardiovascular problems. [ 9 ] Other reported physical repercussions of caregiving include: impaired immunity, [ 1 ] [ 9 ] high blood pressure, [ 1 ] and arthritis. [ 5 ] As is the case with psychological distress, research suggests that the physical repercussions that caregivers experience may be due to them neglecting their own needs and physical health in order to improve the care of the patient. [ 1 ]
A number of factors regarding relationships with the patient, spouse, family or others can increase caregiver distress. One major factor is the social role changes they often face [ 4 ] [ 5 ] [ 15 ] – for example, being a caregiver and a parent. Caregiving can also cause a decrease in the social activities that the caregiver usually engages in because they are required to take on extra tasks to help their loved one. [ 4 ] For some caregivers, this role strain can cause depression, resentment, or a loss of intimacy with the patient. In some families, the stress of caregiving can also lead to increased family conflict. [ 4 ] For most ill patients and their spousal caregivers, scores of marital satisfaction tend to be very similar to the normal population. [ 30 ] [ 31 ] But for a minority, cancer and caregiving can cause relationship strain and can impact the couple's intimacy. [ 5 ] Depending on the type of cancer, caregivers have also reported changes in their sexual relationships (usually decreases in sexual activity). [ 5 ] [ 13 ] This may be because of the physical changes and body image issues certain cancer patients can face from treatment or from the cancer itself. [ 32 ] [ 33 ]
There are often issues cited with the dissemination of practical knowledge for caregivers of cancer patients. [ 1 ] [ 8 ] [ 13 ] [ 34 ] Caregivers often feel underprepared when taking on a caregiver role because they are misinformed, or do not have full information, on the progression the disease may take or the treatment needed for it. [ 1 ] [ 34 ] There is also a lack of information or communication between the caregiver and medical staff regarding how they should provide care. [ 1 ] [ 34 ] Often, caregivers have little knowledge of the resources available to them to assist in their roles, or to help them cope with the psychological difficulties they themselves are having. [ 1 ] Educating the caregiver has been shown to decrease stress levels. [ 35 ]
Caregivers with low income tend to have a more negative caregiver experience. [ 6 ] Some spousal caregivers may feel required to quit their job in order to fulfill care requirements. [ 36 ] Other partners may choose to work more in order to try to offset some of the financial pressures. [ 1 ] [ 9 ] [ 13 ] The fiscal pressures of losing an income source, increasing expenditures to pay for treatment, and having a lower household income to pay for daily expenditures [ 4 ] [ 36 ] have been linked with causing significant distress in caregivers. [ 1 ] [ 5 ]
The physical and mental impairments that are caused by cancer may also cause significant problems for the caregiver. [ 1 ] [ 6 ] [ 14 ] [ 35 ] The patients' ability to function on their own and to independently take care of themselves, termed functional status , has a strong effect on caregivers. [ 1 ] [ 6 ] Caregivers of patients with low functionality, or who almost entirely rely on the caregiver for their needs, may cause particular distress for the caregiver. [ 35 ] Strongly linked to this, the type of help that caregivers are required to provide may be a stronger predictor of their caregiver burden than the time they must commit to helping. [ 6 ] This is a function of the patient's functional status: having to help with personal tasks because the patient is unable to take care of himself or herself tends to cause greater caregiver burden than having to engage in non-personal tasks. [ 37 ] Survivors who suffer from a decreased mental capacity, much like low functioning survivors, also put increased strain on their caregivers. [ 37 ] The duration of care, and the patient's ability to cope with the symptoms of cancer and cancer treatment have also been linked to the levels of distress reported by caregivers. [ 37 ] In addition, patients who show more distress, concern or hopelessness, or who appraise the illness or caregiving more negatively tend to have caregivers with a lower quality of life . [ 6 ]
Results about the differential effects of gender on patient and caregiver distress are mixed, but a recent meta-analysis has indicated that regardless of role (i.e. patient or caregiver), women are more distressed by cancer than men. [ 38 ] It is widely known that women play significant roles in health by being primary caregivers, for their families and working in healthcare, both formally and informally. [ 2 ] There are patterns in society that reinforce and continue differences and inequalities between men and women when caring for someone with cancer. [ 2 ] Women who care for their spouses often feel overly responsible and may sacrifice their own needs more than men in similar roles. [ 2 ] These caregiving roles for women often lack support, recognition, and pay. [ 2 ] Women often have a double burden, in terms of working a job and being a care provider for the family. [ 39 ] Women who care for both of their parents have reported negative effects on their marriage, more than effects reported by husbands in spousal caregiving. [ 39 ] Daughter caregivers, who care for a loved one with cancer, report greater levels of anxiety and depression in comparison to husbands providing care to a spouse. [ 39 ] Husband caregivers may deny feelings of depression, due to traditional gender roles, which can create adverse effects on the family unit. [ 39 ] Research has shown that wives providing care for their husbands reported emotional distress due to the lack of communication husband's elicited in regards to their emotions. [ 39 ]
The age of the patient and caregiver can affect the psychological effect that cancer has on them. However, which age group of caregivers (young adult, middle age or elderly) are more distressed by caregiving is still unconfirmed. Some suggest that younger caregivers suffer from more psychological distress, [ 5 ] but others suggest that elderly caregivers are more at risk for distress. [ 40 ] This may be a function of the phase of the cancer trajectory that caregivers are undergoing: studies tend to find high distress amongst younger caregivers in the acute and chronic phases, and high distress amongst elderly caregivers in the resolution (specifically, bereavement) phase of caregiving. [ 5 ] Elderly caregivers are also at greater risk for negative effects on their physical health than are younger caregivers. [ 1 ] Older caregivers are more likely to have comorbid health conditions and decreased physical ability. In relation to their psychological health, older caregivers may be at higher risk because of a higher likelihood of social isolation than younger caregivers. However, older caregivers are usually more satisfied with their role than are younger caregivers. [ 41 ] Among women, this may be explained by the finding that younger female caregivers tend to perceive demands on their time due to role strain more negatively. [ 42 ] Role strain tends to be more severe for later middle age caregivers due to their many responsibilities with family and work. [ 43 ] Caregivers in this age group may also be more prone to emotional distress, and ultimately, a decreased quality of life. [ 40 ] This is because the caregivers are at higher risk of experiencing social isolation, career interruption, and a lack of time for themselves, their families and their friends. [ 44 ] The age of the cancer patient can also affect the physical and psychological burden on caregivers. Given that the highest percentage of individuals with cancer are older adults, caregiving for older cancer patients can be complicated by other comorbid diseases such as dementia. [ 4 ] The spouses of elderly cancer patients are likely to be elderly themselves, which may cause the caregiving to take an even more significant toll on their well being.
Individuals of lower socio-economic status may experience the increased burden of financial strain due to the expenses involved in cancer care. [ 5 ] [ 6 ] Research has shown that many family caregivers suffer from financial difficulties, such as cutting down time at work or having to quit their job due to the burden of caregiving. [ 45 ] Several studies have highlighted many more adverse outcomes in caregiving related to finances including lost hours, lower retirement benefits, and depending on others for financial aid. [ 45 ] This may cause them to experience more psychological distress from cancer caregiving than other caregivers. Caregivers with lower levels of education have been shown to report more satisfaction from caregiving. [ 6 ]
Caregivers can sustain their quality of life by deriving self-esteem from caregiving. [ 6 ] Caregivers' beliefs and perceptions can also strongly impact their adjustment to caregiving. For instance, caregivers who believe their coping strategies are effective, or caregivers who perceive sufficient help from their support networks, are less likely to be depressed. [ 28 ] In fact, these factors relate more strongly to their levels of depression than stress does.
Personality factors may play a role in caregiver adjustment to cancer. For instance, caregivers that are high on neuroticism are more likely to suffer from depression. [ 15 ] On the other hand, caregivers that are more optimistic [ 4 ] or who acquire a sense of mastery from caregiving [ 1 ] tend to adjust better to the experience. Caregivers who remain emotionally resilient and maintain a realistic attitude and approach to care have been shown to cope well with adverse health outcomes. [ 46 ] Along these lines, caregivers who use problem-solving coping strategies or who seek social support are less distressed than those that use avoidant or impulsive strategies. [ 33 ] Some caregivers also report that spirituality helps them cope with the difficulties of caregiving and watching a loved one endure their cancer. [ 13 ] A 2020 literature review, found that caregivers who are affiliated with religion have lower rates of major depression. [ 47 ] Religious beliefs may aid in coping, as faith may motivate individuals to endure the difficulties of caregiving. [ 47 ] Religious practices such as, meditation, pastoral care, and bible readings, have been shown to be effective coping skills. [ 47 ]
The caregiver's relationship to the patient can be an important factor in their adjustment to caregiving. Spouses, followed by adult daughters, are the most likely family members to provide care. [ 4 ] Spouses generally tend to have the most difficulty adjusting to this experience, [ 4 ] [ 6 ] especially the female spouse. [ 2 ] Wives who care for their husbands often feel more negative effects from caregiving. [ 2 ] Adult daughters also tend to express difficulty, which may be a factor of age more-so than the relationship with the patient in that spouses tend to be older caregivers than adult children. [ 2 ]
Many studies have suggested that intervention may curb stress levels of caregivers. [ 1 ] [ 4 ] [ 5 ] [ 34 ] There are many types of interventions available for cancer caregivers including: educational, [ 4 ] problem-solving skills training [ 1 ] [ 4 ] and grief therapy . [ 1 ] [ 4 ] Family-focused grief therapy has been shown to significantly improve overall distress levels and depression in those affected by cancer. [ 19 ] Interventions designed to identify vulnerable caregivers before the patient's death can help prevent caregivers from experiencing abnormal grief up to 12 months post-loss. [ 48 ] To identify vulnerable familial caregivers, interventions need to focus on specific demographic characteristics that predict grief disorders (older age, women, spousal caregivers, lack of religion, lack of social support, caregiver burden, closeness to the patient, and unpreparedness for death) and the presence of a dysfunctional family unit. [ 48 ] Interventions that show effectiveness for grief disorders in bereaved cancer caregivers include cognitive-behavioral models, which include web-based therapies and interventions that identify dysfunction in a family unit. [ 49 ] Both, early hospice referrals and hospital bereavement support programs, have been shown to help bereaved family caregivers and reduce barriers in accessibility. [ 49 ] Depression in caregivers may be pronounced if the cancer patient is enrolled in hospice nearing death as opposed to earlier in the palliative care journey. [ 49 ] Early hospice enrollment and preventing the patient from dying in a hospital have been associated to better grief outcomes in cancer caregivers. [ 49 ] Additionally, interventions that increased patients general knowledge about their specific disease have been reported to reduce anxiety, distress and help them take a more active part in the decision making process. [ 34 ] Interventions by members of the healthcare system designed to teach caregivers proficiency in both the physical and psychological care of patients have been shown to benefit both partners. [ 50 ] Interventions that focus on both the patient and the caregiver as a couple have proven more effective in helping adaptation to cancer than those that try to help the patient or caregiver individually, largely due to the inclusion of training in supportive communication, sexual counselling and partner support. [ 51 ] Furthermore, interventions that target young adults or adolescents (15-25 years) are especially needed, as in comparison with younger children, they are more likely to avoid coping or talking about their feelings related to the death of a sibling from cancer. [ 52 ] This age group, who has experienced the death of a parent or sibling to cancer, has been shown to have an increased likelihood for several adverse psychosocial impacts including separation anxiety disorder , self-harm , substance abuse disorder , and conduct disorder . [ 52 ] Interventions that target unmet needs reported by young adults and adolescents, such as social support and help with coping skills, could prevent grief and distress post-loss. [ 52 ] Support groups for young adults and adolescents who have lost a parent to cancer have been shown to improve life satisfaction and global wellbeing. [ 52 ] Finally, spirituality has been demonstrated to be related to quality of life for caregivers. [ 53 ] [ 7 ] [ 54 ] Religion has been shown to be a protective factor on bereavement outcomes in bereaved family cancer caregivers. [ 55 ] In a 2024 systematic review, bereaved Taiwanese caregivers felt comforted by continuing a relationship with the deceased patient by performing rituals and ancestor worship, serving as a protective factor in the grieving process. [ 55 ] In a 2005 study of bereaved adults, who experienced a recent loss, religious coping was linked to less outpatient physical healthcare visits at baseline assessment. [ 56 ]
Not every caregiver experiences only negative consequences from cancer caregiving. For some caregivers, there are personal benefits that stem from caring for their loved one, and the benefits found might help to buffer the negative experiences that caregivers frequently face. [ 1 ] The concept of post-traumatic growth is of particular note when discussing the benefits of cancer caregiving, and cancer in general. Post-traumatic growth is a positive psychological growth that occurs as a result of a traumatic incident. Studies have found that within the cancer caregiver population, strong predictors of post-traumatic growth are: less education, being employed, or displaying high avoidance tendencies pre-surgery, and framing coping strategies in a positive style. [ 57 ] Furthermore, individuals who engage in religious coping or have high perceived social support are more likely to report post-traumatic growth. Other benefits of caregiving include: an improved sense of self-worth, [ 4 ] [ 5 ] [ 6 ] increased self-satisfaction, [ 1 ] [ 4 ] [ 5 ] [ 6 ] a sense of mastery, [ 4 ] [ 6 ] increased intimacy with their ill loved one, [ 4 ] and a sense of meaning. [ 1 ] [ 4 ] Experiencing a loved one's cancer may also cause significant lifestyle changes for caregivers. For instance, caregivers may become more proactive by engaging in health behaviours such as increased exercise, better diets and increased screening. [ 5 ] [ 9 ] However, this finding is not conclusive; some studies report that certain behaviours such as screening tend to decrease amongst caregivers. [ 5 ]
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Divaricate means branching, or having separation or a degree of separation. The angle between branches is wide. [ 1 ]
In botany, the term is often used to describe the branching pattern of plants . Plants are said to be divaricating when their growth form is such that each internode diverges widely from the previous internode, producing an often tightly interlaced shrub or small tree. [ 3 ] Of the 72 small leaved shrubs found on the Banks Peninsula , for example, some 38 are divaricating. [ 4 ]
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In medicine or biology , a diverticulum is an outpouching of a hollow (or a fluid-filled) structure in the body. [ 1 ] Depending upon which layers of the structure are involved, diverticula are described as being either true or false. [ 2 ]
In medicine, the term usually implies the structure is not normally present, but in embryology , the term is used for some normal structures arising from others, as for instance the thyroid diverticulum , which arises from the tongue . [ 3 ]
The word comes from Latin dīverticulum , "bypath" or "byway".
Diverticula are described as being true or false depending upon the layers involved:
Most of these pathological types of diverticula are capable of harboring an enterolith . If the enterolith stays in place, it may cause no problems, but a large enterolith expelled from a diverticulum into the lumen can cause obstruction. [ 13 ]
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The Division of Select Agents and Toxins (DSAT) of the Centers for Disease Control and Prevention is responsible for the Select Agent Program and the Etiologic Agent Import Permit Program. They inspect the laboratories of more than 300 organizations approved to use and transfer select agents , and put regulations in place to minimize risk in the use of these bacterial agents and toxins. [ 1 ]
DSAT investigates incidents related to the laboratory use of select agents and toxins and refers cases to the FBI and HHS Office of Inspector General when necessary. [ 2 ]
They also review experiments that are deemed "restricted experiments" because of their increased risk. [ 3 ]
Samuel S. Edwin became the director of the division in 2016. [ 4 ] The office's 2016 budget was approximately $21.5 million.
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Dizziness is an imprecise term that can refer to a sense of disorientation in space, vertigo , or lightheadedness . [ 1 ] It can also refer to disequilibrium [ 2 ] or a non-specific feeling, such as giddiness or foolishness . [ 3 ]
Dizziness is a common medical complaint, affecting 20–30% of persons. [ 4 ] Dizziness is broken down into four main subtypes: vertigo (~25–50%), disequilibrium (less than ~15%), presyncope (less than ~15%), and nonspecific dizziness (~10%). [ 5 ]
Many conditions cause dizziness because multiple parts of the body are required for maintaining balance including the inner ear , eyes , muscles , skeleton , and the nervous system . [ 7 ] Thus dizziness can be caused by a variety of problems and may reflect a focal process (such as one affecting balance or coordination ) or a diffuse one (such as a toxic exposure or low perfusion state). [ 8 ]
Common causes of dizziness include:
Dizziness may occur from an abnormality involving the brain (in particular the brainstem or cerebellum ), inner ear , eyes, heart, vascular system, fluid or blood volume, spinal cord, peripheral nerves , or body electrolytes . Dizziness can accompany certain serious events, such as a concussion or brain bleed, epilepsy and seizures (convulsions), stroke , and cases of meningitis and encephalitis . However, the most common subcategories can be broken down as follows: 40% peripheral vestibular dysfunction, 10% central nervous system lesion, 15% psychiatric disorder, 25% presyncope/disequilibrium, and 10% nonspecific dizziness. [ 14 ] Some vestibular pathologies have symptoms that are comorbid with mental disorders. [ 15 ]
While traditional medical teaching has focused on determining the cause of dizziness based on the category (such as vertigo vs. presyncope), research published in 2017 suggests that this analysis is of limited clinical utility. [ 16 ] [ 17 ]
Medical conditions that often have dizziness as a symptom include: [ 14 ] [ 18 ] [ 7 ] [ 19 ]
In medicine, disequilibrium refers to impaired equilibrioception that can be characterised as a sensation of impending fall or of the need to obtain external assistance for proper locomotion. It is sometimes described as a feeling of improper tilt of the floor, or as a sense of floating. This sensation can originate in the inner ear or other motion sensors, or in the central nervous system. Neurologic disorders tend to cause constant vertigo or disequilibrium and usually have other symptoms of neurologic dysfunction associated with the vertigo. Many medications used to treat seizures, depression, anxiety, and pain affect the vestibular system and the central nervous system which can cause the symptom of disequilibrium. [ 21 ]
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Doceree is a pharmaceutical advertising and healthcare marketing company headquartered in Short Hills, New Jersey . [ 1 ] [ 2 ] [ 3 ] It operates in 25 countries, including the United States, India, Australia, and nations in Europe and Southeast Asia . [ 4 ] The company provides platforms for pharmaceutical and life sciences organizations to communicate with healthcare professionals. Doceree maintains additional offices in Noida, India , and London, UK . [ 1 ]
Doceree was founded in 2020 by Harshit Jain, an alumnus of Northwestern University and a former physician in the United States. [ 5 ] [ 6 ] Harshit's career began in 2007 with Altruista Health, a startup using insurance data for health risk assessment and wellness promotion. In 2015, he sold Altruista Health to Capricorn Health Advisors. He later divested another venture, established in 2009 in India, to A.D.A.M. Ebix in 2016. Before founding Doceree, Dr. Jain worked with McCann Health as Vice President and Country Manager, taking on roles such as Innovation Lead across Asia , Europe , and the Americas . [ 7 ]
In 2019, Harshit left his position and founded Doceree. [ 8 ] The company’s name, Doceree, is derived from the Latin word docere , meaning “to teach,” which is also the root of the word “doctor” in English. Doceree launched operations in 2020, [ 9 ] initially in India and the U.S., [ 1 ] before expanding into the UK, Europe, Asia-Pacific , and the GCC countries . [ 10 ] In June 2023, the company announced the launch of Doceree Enterprise, a demand-side platform focused on healthcare professionals. [ 4 ]
Since its inception, Doceree has raised over $60 million in funding. In 2020, it closed a seed funding round of $1 million. [ 11 ] This was followed by an $11 million Series A round in 2022, led by Eight Roads Ventures. [ 12 ] In 2023, the company raised $35 million in a Series B round, led by Creaegis with participation from F-Prime Capital and Eight Roads Ventures. [ 13 ] [ 4 ] [ 14 ] In 2024, it reportedly received additional investment from Creaegis amounting to ₹113.5 crore (approximately $13.6 million). [ 15 ]
Doceree has collaborated with healthcare data providers and analytics firms, including Pulse by HIMSS, WebMD, and Phunware, to integrate first-party data into its advertising ecosystem. The company is also a member of industry organizations such as the Association of National Advertisers (ANA) and the Network Advertising Initiative (NAI).
In May 2023, Doceree entered a partnership with Hello Health Group, a health and wellness content company, [ 16 ] to expand into eight Southeast Asian countries , including Vietnam , Indonesia , Malaysia , Cambodia , Myanmar , Singapore , the Philippines , and Taiwan . [ 13 ] [ 2 ] [ 17 ] [ 18 ]
Doceree also launched a YouTube-based interview series titled, The Next Marketing with HJ , hosted by founder Harshit Jain. The show features discussions with professionals in the healthcare marketing and pharmaceutical advertising sectors such as Harjot Singh , Ritesh Patel, Nancy Phelan , George C.D. Griffith, Jeffrey Erb , Karima Sharif-Ali, and Richard Springham. [ 19 ]
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A doctor's visit , also known as a physician office visit or a consultation , or a ward round in an inpatient care context, is a meeting between a patient with a physician to get health advice or treatment plan for a symptom or condition , most often at a professional health facility such as a doctor's office , clinic or hospital . According to a survey in the United States , a physician typically sees between 50 and 100 patients per week, but it may vary with medical specialty , but differs only little by community size such as metropolitan versus rural areas. [ 1 ]
The four great cornerstones of diagnostic medicine are anatomy (structure: what is there), physiology (how the structure/s work), pathology (what goes wrong with the anatomy and physiology), and psychology (mind and behavior). In addition, the physician should consider the patient in their 'well' context rather than simply as a walking medical condition. This means the socio-political context of the patient (family, work, stress, beliefs) should be assessed as it often offers vital clues to the patient's condition and further management.
A patient typically presents a set of complaints (the symptoms ) to the physician, who then performs a diagnostic procedure , which generally includes obtaining further information about the patient's symptoms, previous state of health, living conditions, and so forth. The physician then makes a review of systems (ROS) or systems inquiry , which is a set of ordered questions about each major body system in order: general (such as weight loss), endocrine, cardio-respiratory, etc. Next comes the actual physical examination and other medical tests ; the findings are recorded, leading to a list of possible diagnoses . These will be investigated in order of probability.
The next task is to enlist the patient's agreement to a management plan, which will include treatment as well as plans for follow-up. Importantly, during this process the healthcare provider educates the patient about the causes, progression, outcomes, and possible treatments of his ailments, as well as often providing advice for maintaining health.
The physician's expertise comes from his knowledge of what is healthy and normal contrasted with knowledge and experience of other people who have had similar symptoms (unhealthy and abnormal), and the proven ability to relieve it with medicines ( pharmacology ) or other therapies about which the patient may initially have little knowledge.
A survey in the United States came to the result that, overall, a physician sees each patient for 13 to 16 minutes. [ 1 ] Anesthesiologists , neurologists , and radiologists spend more time with each patient, with 25 minutes or more. [ 1 ] On the other hand, primary care physicians spend a median of 13 to 16 minutes per patient, whereas dermatologists and ophthalmologists spend the least time, with a median of 9 to 12 minutes per patient. [ 1 ] Overall, female physicians spend more time with each patient than do male physicians. [ 1 ]
For the patient, the time spent at the hospital can be substantially longer due to various waiting times, administrative steps or additional care from other health personnel. Regarding wait time, patients that are well informed of the necessary procedures in a clinical encounter, and the time it is expected to take, are generally more satisfied even if there is a longer waiting time. [ 3 ]
With increasing access to computers and published online medical articles, the internet has increased the ability to perform self-diagnosis instead of going to a professional health care provider. Doctors may be fearful of misleading information and being inundated by emails from patients which take time to read and respond to (time for which they are not paid). [ 4 ] About three-quarters of the U.S. population reports having a primary care physician , but the Primary Care Assessment Survey found "a significant erosion" in the quality of primary care from 1996 to 2000, most notably in the interpersonal treatment and thoroughness of physical examinations. [ 5 ]
A study systematically assessed advice given by professional general practitioners , typically in the form of verbal-only consultation, for weight-loss to obese patients. They found it rarely included effective methods, was mostly generic, and was rarely tailored to patients' existing knowledge and behaviours. [ 6 ] [ 7 ]
The National Institute on Aging has produced a list of "Tips for Talking With Your Doctor" that includes asking "if your doctor has any brochures , fact sheets , DVDs, CDs, cassettes, or videotapes about your health conditions or treatments" – for example if a patient's blood pressure was found to be high, the patient could get "brochures explaining what causes high blood pressure and what [the person] can do about it". [ 8 ]
Telehealth is the distribution of health-related services and information via electronic information and telecommunication technologies . [ 9 ] It allows long-distance patient and clinician contact, care, advice, reminders, education, intervention, monitoring, and remote admissions. [ 10 ] [ 11 ]
A scientific review indicates that, in general, outcomes of telemedicine are or can be as good as in-person care with health care use staying similar. [ 15 ]
Electronic medical records could also be studied to quantify disease burdens – such as the number of deaths from antimicrobial resistance [ 23 ] – or help identify causes of, factors of, links between , [ 24 ] [ 25 ] and contributors to diseases, [ 26 ] [ 27 ] [ 28 ] especially when combined with genome-wide association studies . [ 29 ] [ 30 ]
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Doctory or daktari is a referral term for practising modern medicine arising in the Indian subcontinent during colonialism . The concept, has been framed by historical sociologist Neshat Quaiser and is now part of the social history of South Asian medicine & health and colonial studies.
In the Indian subcontinent, modern medicine—which became closely associated with colonialism—was referred to as " doctory " or daktari ilaj . The doctor and doctory ilaaj emerged as powerful symbols of colonialism and the colonial state. The doctor was one of the most visible representatives of European knowledge. He looked, dressed and spoke differently. He was certainly not equivalent to the Hakim . The doctor with his stethoscope created an aura and mystery around himself. He symbolised ' modern medicine '. In fact, being visited by a doctor became a symbol of high status and modernity. [ 1 ]
It is a label for the practice of indigenous medicine in South Asia. In social history of South-Asian medicine, this concept has been in discussion. [ 2 ]
According to Nandani Bhattacharya, the term 'doctory' has a deep political resonance. [ 3 ]
During the period British rule in India(1700s to 1900s), western medicine had begun to take over and was spreading with time. The administration hired many Indians as "native doctors" in the inferior medical service, which had been primarily made up of Europeans, after they had training in Western medicine. Most of the colonial government's support for indigenous medical systems was progressively withdrawn. The assertions made by Western medicine was that it is a more logical and “superior” medical system caused the practitioners of these systems, the 'vaidyas' and 'hakims', to lose a great deal of their status. While some of them turned into purists and defended and promoted their systems, others incorporated Western medical concepts and practices into their training and clinical work.
Initially, the loose adoption of this Western medical practice, looks and behaviour came out as a 'doctory'. Later, it changed into a bigger spectrum and was given symbolic meaning. [ 4 ]
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The doctor–patient relationship is a central part of health care and the practice of medicine . A doctor–patient relationship is formed when a doctor attends to a patient's medical needs and is usually through consent. [ 1 ] This relationship is built on trust, respect, communication, and a common understanding of both the doctor and patients' sides. The trust aspect of this relationship goes is mutual: the doctor trusts the patient to reveal any information that may be relevant to the case, and in turn, the patient trusts the doctor to respect their privacy and not disclose this information to outside parties.
A ceremonial dynamic of the doctor–patient relationship is that the doctor is encouraged by the Hippocratic Oath to follow certain ethical guidelines. [ 2 ] [ 3 ] Additionally, the healthiness of a doctor–patient relationship is essential to keep the quality of the patient's healthcare high as well as to ensure that the doctor is functioning at their optimum. In more recent times, healthcare has become more patient-centered and this has brought a new dynamic to this ancient relationship. [ citation needed ]
A patient must have confidence in the competence of their physician and must feel that they can confide in them. For most physicians, the establishment of good rapport with a patient is important. Some medical specialties, such as psychiatry and family medicine , emphasize the physician–patient relationship more than others, such as pathology or radiology , which have very little contact with patients.
The quality of the patient–physician relationship is important to both parties. The doctor and patient's values and perspectives about disease, life, and time available play a role in building up this relationship. A strong relationship between the doctor and patient may lead to frequent, freely-offered quality information about the patient's disease and as a result, better healthcare for the patient and their family. Enhancing both the accuracy of the diagnosis and the patient's knowledge about the disease contributes to a good relationship between the doctor and the patient. [ 4 ] In a poor doctor–patient relationship, the physician's ability to make a full assessment may be compromised and the patient may be more likely to distrust the diagnosis and proposed treatment. The downstream effects of this mistrust may include decreased patient adherence to the physician's medical advice , which could result in poorer health outcomes for the patient. In these circumstances, and also in cases where there is genuine divergence of medical opinions, a second opinion from another physician may be sought, or the patient may choose to go to another physician that they trust more. Additionally, the benefits of any placebo effect are also based upon the patient's subjective assessment (conscious or unconscious) of the physician's credibility and skills. [ 5 ]
Michael and Enid Balint together pioneered the study of the physician patient relationship in the UK. Michael Balint's "The Doctor, His Patient and the Illness" (1957) outlined several case histories in detail and became a seminal text. [ 6 ] Their work is continued by the Balint Society , The International Balint Federation [ 7 ] and other national Balint societies in other countries. It is one of the most influential works on the topic of doctor–patient relationships. In addition, a Canadian physician known as Sir William Osler was known as one of the "Big Four" professors at the time that the Johns Hopkins Hospital was first founded. [ 8 ] At the Johns Hopkins Hospital, Osler had invented the world's first medical residency system. [ 9 ] In terms of efficacy (i.e. the outcome of treatment), the doctor–patient relationship seems to have a "small, but statistically significant impact on healthcare outcomes". [ 10 ] However, due to a relatively small sample size and a minimally effective test, researchers concluded additional research on this topic is necessary. [ 10 ] Recognizing that patients receive the best care when they work in partnership with doctors, the UK General Medical Council issued guidance for both of doctors named "Ethical guidance for doctors", [ 11 ] as well as for patients "What to expect from your doctor" in April 2013. [ 12 ]
The default medical practice for showing respect to patients and their families is for the doctor to be truthful in informing the patient of their health and to be direct in asking for the patient's consent before giving treatment. Historically in many cultures there has been a shift from paternalism , the view that the "doctor always knows best", to the idea that patients must have a choice in the provision of their care and be given the right to provide informed consent to medical procedures. [ 13 ] There can be issues with how to handle informed consent in a doctor–patient relationship; [ 14 ] for instance, with patients who do not want to know the truth about their condition. Furthermore, there are ethical concerns regarding the use of placebo . Does giving a sugar pill lead to an undermining of trust between doctor and patient? Is deceiving a patient for his or her own good compatible with a respectful and consent-based doctor–patient relationship? [ 15 ] These types of questions come up frequently in the healthcare system and the answers to all of these questions are usually far from clear but should be informed by medical ethics .
Shared decision-making involves both the doctor and patient being involved in decisions about treatment. There are varied perspective on what shared decision making involves, but the most commonly used definition involves the sharing of information by both parties, both parties taking steps to build consensus, and reaching an agreement about treatment. [ 16 ] : 4
The doctor does not recommend what the patient should do, rather the patient's autonomy is respected and they choose what medical treatment they want to have done. An alternative practice, for the doctor to make a person's health decisions without considering that person's treatment goals or having that person's input into the decision-making process, is considered grossly unethical and against the idea of personal autonomy and freedom.
The spectrum of a physician's inclusion of a patient into treatment decisions is well represented in Ulrich Beck 's World at Risk . At one end of this spectrum is Beck's Negotiated Approach to risk communication , in which the communicator maintains an open dialogue with the patient and settles on a compromise on which both patient and physician agree. A majority of physicians employ a variation of this communication model to some degree, as it is only with this technique that a doctor can maintain the open cooperation of his or her patient. At the opposite end of this spectrum is the Technocratic Approach to risk communication, in which the physician exerts authoritarian control over the patient's treatment and pushes the patient to accept the treatment plan with which they are presented in a paternalistic manner. This communication model places the physician in a position of omniscience and omnipotence over the patient and leaves little room for patient contribution to a treatment plan. [ 17 ]
Physician communication style is crucial to the quality and strength of the doctor–patient relationship. Patient-centered communication, which involves asking open-ended questions, having a warm disposition, encouraging emotional expression , and demonstrating interest in the patient's life, has been shown to positively affect the doctor–patient relationship. Additionally, this type of communication has been shown to decrease other negative attitudes or assumptions the patient might have about doctors or healthcare as a whole, and has even been shown to improve treatment compliance. [ 18 ] Another form of communication beneficial to the patient-provider relationship is self-disclosure by the physician in particular. Historically, medical teaching institutions have discouraged physicians from disclosing personal or emotional information to patients, as neutrality and professionalism were prioritized. However, self-disclosure by physicians has been shown to increase rapport, the patient's trust, their intention to disclose information, and the patient's desire to continue with the physician. These effects were shown to be associated with empathy , which is another important dimension which is often under-emphasized in physician training. [ 19 ] A physician's response to emotional expression by their patient can also determine the quality of the relationship, and influence how comfortable patients are in discussing sensitive issues, feelings, or information that may be critical for their diagnosis or care. More passive, neutral response styles which allow for patients to elaborate on their feelings have been shown to be more beneficial for patients, and make them feel more comfortable. Physician avoidance or dismissal of a patient's emotional expression may discourage the patient from opening up, and may be harmful to their relationship with their provider. [ 20 ] [ 21 ]
Historically, in the paternalistic model, a physician tended to be viewed as dominant or superior to the patient due to the inherent power dynamic of physician's control over the patient's health, treatment course, and access to knowledge about their condition. In this model, physicians tended to convey only the information necessary to convince the patient of their proposed treatment course. The physician–patient relationship is also complicated by the patient's suffering ( patient derives from the Latin patior , "suffer") and limited ability to relieve it without the physician's intervention, potentially resulting in a state of desperation and dependency on the physician. A physician should be aware of these disparities in order to establish a comfortable, trust-based environment and optimize communication with the patient. Additionally, it may be beneficial for the doctor–patient relationship to create a practice of shared care with increased emphasis on patient empowerment in taking a greater degree of responsibility for their care. [ 22 ] [ 23 ]
Patients who seek a doctor's help typically do not know or understand the medical science behind their condition, which is why they go to a doctor in the first place. A patient with no medical or scientific background may not be able to understand what is going on with their body without their doctor explaining it to them. As a result, this can be a frightening and frustrating experience, filled with a sense of powerlessness and uncertainty for the patient, [ 22 ] [ 23 ] though in rare conditions, this pattern tends not to be followed, and due to lack of expertise patients are forced to learn about their conditions. [ 24 ] : 155
An in-depth discussion of diagnosis, lab results, and treatment options and outcomes in layman's terms that the patient can understand can be reassuring and give the patient a sense of agency over their condition. Concurrently, this type of strong communication between a doctor and their patient can strengthen the physician–patient relationship as well as promote better treatment adherence and health outcomes. [ 22 ] [ 23 ]
Under certain conditions healthcare workers are able to treat patients involuntarily , imprison them , or involuntarily administer drugs to alter the patients' ability to think. They may also engage in forms of "informal coercion" where information or access to social services can be used to control a patient.
Lying in the doctor–patient relationship is common. [ 25 ] : 164 Doctors provide minimal information to patients after medical errors. Doctors may lie to patients to displace culpability for poor outcomes and say they avoid giving patients information because it may confuse patients, cause pain, or undermine hope. They may lie to avoid uncomfortable conversation about disability or death, or to encourage patients to accept a particular treatment option. [ 25 ] : 165 The experience of being lied to may undermine an individual's trust in others or themselves and reduce faith in one's church, community or society and result in avoidant behaviour to avoid being wounded. Patients may seek financial and legal retribution. [ 25 ] : 166
Patients may lie to doctors for financial reasons such as to receive disability payments , for access to medication, or to avoid incarceration. Patients may lie out of embarrassment or shame. [ 25 ] : 165 Palmeira and Sterne suggest that healthcare workers acknowledging the motivations of patients to lie to appear in a positive light to reduce deception by patients. [ 25 ] : 167
Palmeira and Sterne offer different psychological framings and motivations for lying. From the perspective of attachment theory , lying may be used to avoid revealing information about an individual, to avoid intimacy and therefore the risk of rejection or shame, or to exaggerate to obtain protection or care. They also discuss the idea of protecting or maintaining an ego ideal . [ 25 ] : 165 Generally, Palmeira and Sterne suggestion discussions about the amount of information and detail parties wish to discuss, viewing obtaining truth as an ongoing process to increase truthfulness in doctor–patient interactions. Palmeira and Sterne suggest that physicians acknowledge their lack of knowledge, and discuss the amount of detail they wish to discuss to avoid deception. [ 25 ] : 167
Physicians have a tendency of overestimating their communication skills, [ 26 ] as well as the amount of information they provide their patients. [ 27 ] Extensive research conducted on 700 orthopedic surgeons and 807 patients, for instance, found that 75% of the surgeons perceived they satisfactorily communicated with their patients, whereas only 21% of the patients were actually satisfied with their communication. [ 28 ] Physicians also show a high likelihood of underestimating their patients' information needs and desires, especially for patients who were not college educated or from economically disadvantaged backgrounds. [ 29 ] [ 30 ] There is pervasive evidence that patients' personal attributes such as age, sex, and socioeconomic status may influence how informative physicians are with their patients. [ 29 ] [ 30 ] Patients who are better educated and from upper or upper middle-class positions generally receive higher quality and quantity of information from physicians than do those toward the other end of the social spectrum, although both sides have an equal desire for information. [ 30 ]
Race, ethnicity and language has consistently proven to have a significant impact on how physicians perceive and interact with patients. [ 31 ] According to a study of 618 medical encounters between mainly Caucasian physicians and Caucasian and African American patients, physicians perceived African Americans to be less intelligent and educated, less likely to be interested in an active lifestyle, and more likely to have substance abuse problems than Caucasians. [ 32 ] A study of patients of color showed that having a white physician led to increased experience of microaggressions . [ 33 ] Studies in Los Angeles emergency departments have found that Hispanic males and African Americans were less than half as likely to receive pain medication than Caucasians, despite physicians' estimates that patients were experiencing an equivalent level of pain. [ 31 ] Another study showed that ethnic-minority groups of varying races reported lower-quality healthcare experiences than non-Hispanic Whites, specifically in treatment decision involvement and information received regarding medications. [ 34 ] Other studies show that physicians exhibited substantially less rapport building and empathetic behavior with both Black and Hispanic patients than Caucasians, despite the absence of language barriers. [ 31 ] [ 18 ] [ 21 ]
Mistrust of physicians or the healthcare system in general falls under the umbrella of medical mistrust. Medical mistrust negatively impacts the doctor–patient relationship, as a patient who has little faith in their physician is less likey to listen to their advice, follow their treatment plans, and feel comfortable disclosing information about themselves. Some forms of communication by the physician, such as self-disclosure and patient-centered communication, have been shown to decrease medical mistrust in patients. [ 35 ] [ 36 ]
Medical mistrust has been shown to be greater for minority group patients, and is associated with decreased compliance, which can contribute to poorer health outcomes. Research of breast cancer patients showed that African American women who received concerning mammogram results were less likely to discuss this with their doctor if they had greater medical mistrust. [ 37 ] Another study showed that women with higher physician mistrust waited longer to report symptoms to a doctor and receive a diagnosis of ovarian cancer . [ 38 ] Two studies showed that African American patients had more medical mistrust than white patients, and were less likely to undergo a recommended surgery as a result. [ 35 ] [ 36 ]
Medical mistrust can also develop if physicians appear to be profit seeking. Physicians might alter how they communicate with patients about the price of care to avoid the appearance of pecuniary interest in order to secure their trust. [ 39 ]
A dilemma may arise in situations where determining the most efficient treatment, or encountering avoidance of treatment, creates a disagreement between the physician and the patient, for any number of reasons. In such cases, the physician needs strategies for presenting unfavorable treatment options or unwelcome information in a way that minimizes strain on the doctor–patient relationship while benefiting the patient's overall physical health and best interests. When the patient either can not or will not do what the physician knows is the correct course of treatment, the patient becomes non-adherent. Adherence management coaching becomes necessary to provide positive reinforcement of unpleasant options.
For example, according to a Scottish study, [ 40 ] patients want to be addressed by their first name more often than is currently the case. In this study, most of the patients either liked (223) or did not mind (175) being called by their first names. Only 77 individuals disliked being called by their first name, most of whom were aged over 65. [ 40 ] On the other hand, most patients do not want to call the doctor by his or her first name. [ 40 ]
Some familiarity with the doctor generally makes it easier for patients to talk about intimate issues such as sexual subjects, but for some patients, a very high degree of familiarity may make the patient reluctant to reveal such intimate issues. [ 41 ]
Transitions of patients between health care practitioners may decrease the quality of care in the time it takes to reestablish proper doctor–patient relationships. Generally, the doctor–patient relationship is facilitated by continuity of care in regard to attending personnel. Special strategies of integrated care may be required where multiple health care providers are involved, including horizontal integration (linking similar levels of care, e.g. multiprofessional teams) and vertical integration (linking different levels of care, e.g. primary, secondary and tertiary care). [ 42 ]
Researchers have studied the doctor–patient relationship using the theory of conversation analysis . [ 43 ] One of the key concepts in conversation analysis is turn-taking . The process of turn-taking between health care professionals and the patients has a profound impact on the relationship between them. In most scenarios, a doctor will walk into the room in which the patient is being held and will ask a variety of questions involving the patient's history, examination, and diagnosis . [ 44 ] These are often the foundation of the relationship between the doctor and the patient as this interaction tends to be the first they have together. This can go a long way into impacting the future of the relationship throughout the patient's care. All speech acts between individuals seek to accomplish the same goal, sharing and exchanging information and meeting each participants conversational goals. [ 44 ]
Research carried out in medical scenarios analyzed 188 situations in which an interruption occurred between a physician and a patient. Of these 188 analyzed situations, research found that the doctor is much more likely (67% of the time, 126 occasions) as compared to the patient (33% of the time, 62 occasions). [ 44 ] This shows that physicians are practicing a form of conversational dominance in which they see themselves as far superior to the patient in terms of importance and knowledge and therefore dominate all aspects of the conversation. A question that comes to mind considering this is if interruptions hinder or improve the condition of the patient. Constant interruptions from the patient whilst the doctor is discussing treatment options and diagnoses can be detrimental or lead to less effective efforts in patient treatment. This is extremely important to take note of as it is something that can be addressed in quite a simple manner. This research conducted on doctor–patient interruptions also indicates that males are much more likely to interject out of turn in a conversation than women. [ 44 ] Men's social predisposition to interject becomes problematic when it negatively impacts a woman physician's messages to her patients who are men: she may not be able to finish her statements and the patient will not benefit from what she was about to say, and the physician herself may fall prey to the socially conventional man's interjection by letting it cut short her professional commentary. Conversely, men physicians need to encourage women patients to articulate their reactions and questions, since women interrupt in conversations statistically less often than men do. [ 44 ]
A hurdle can arise from how the thinking process goes: a patient typically relates their story in chronological order, where symptoms, test results, consulting opinions, diagnoses and treatment are intertwined. A provider tends to design their approach in a step-by-step analytical manner, extracting as much details out of symptomatology, then past medical and social history then tests then coming to a suggested diagnosis and management plan. Addressing this upfront and at the onset of the visit and carving enough time for both can help avoid unnecessary interruptions on either part, improve provider-patient relation and constructively facilitate care.
An example of where other people present in a doctor–patient encounter may influence their communication is one or more parents present at a minor 's visit to a doctor. These may provide psychological support for the patient, but in some cases it may compromise the doctor–patient confidentiality and inhibit the patient from disclosing uncomfortable or intimate subjects.
When visiting a health provider about sexual issues, having both partners of a couple present is often necessary, and is typically a good thing, but may also prevent the disclosure of certain subjects, and, according to one report, increases the stress level. [ 41 ]
Having family around when dealing with difficult medical circumstances or treatments can also lead to complications. Family members, in addition to the patient needing treatment may disagree on the treatment needing to be done. This can lead to tension and discomfort for the patient and the doctor, putting further strain on the relationship.
With the extensive use of technology in healthcare, a new dynamic has risen in this relationship. Telehealth is the use of telecommunications and/or electronic information to support a patient. [ 45 ] This applies to clinical care, health-related education, and health administration. [ 46 ] An important fact about telehealth is that it increases the quality of the doctor–patient relationship by making health resources more easily available, affordable, and more convenient for both parties. Challenges with using telehealth are that it is harder to get reimbursements, to acquire cross-state licensure, to have common standards, maintain privacy, and have proper guiding principles. [ 45 ] The types of care that can be provided via telehealth include general health care (wellness visits), prescriptions for medicine, dermatology, eye exams, nutrition counseling, and mental health counseling. Just like with an in-person visit, it is important to prepare for a telehealth consultation beforehand and have good communication with the healthcare provider. [ 47 ]
An interesting outcome of telehealth is that doctors have started to play a different role in the relationship. With patients having more access to information, medical knowledge, and their health data; doctors play the role of a translator between technical data and the patients. This has caused a shift in the way that the doctors see themselves concerning the doctor–patient relationship. Doctors who are engaged in telehealth see themselves as a guide to the patient and undertake the role of a guardian and information manager in the description, collection, and sharing of their patient's data. This is the new dynamic that has risen in this ancient relationship and one which will continue to evolve. [ 48 ]
Dr. Rita Charon launched the narrative medicine movement in 2001 with an article in the Journal of the American Medical Association . In the article she claimed that better understanding the patient's narrative could lead to better medical care. [ 49 ]
Researchers and Ph.D.s in a BMC Medical Education journal conducted a recent study that resulted in five key conclusions about the needs of patients from their health care providers. First, patients want their providers to provide reassurance. Second, patients feel anxious asking their providers questions; they want their providers to tell them it is okay to ask questions. Third, patients want to see their lab results and for the doctor to explain what they mean. Fourth, patients simply do not want to feel judged by their providers. And fifth, patients want to be participants in medical decision-making; they want providers to ask them what they want. [ 50 ]
An example of how body language affects patient perception of care is that the time spent with the patient in the emergency department is perceived as longer if the doctor sits down during the encounter. [ 51 ]
Rude behaviour by patients can have a negative effect on medical outcomes. A study showed that staff who received or witnessed rude behaviour by patients relatives had reduced ability to effectively carry out some of their simpler and more procedural tasks. This is important because if the medical staff are not performing sufficiently in what should be simple tasks, their ability to work effectively in critical conditions will also be impaired. This is consistent with research showing that rudeness by medical staff to one another decreases effectiveness. [ 52 ] [ 53 ]
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Doege–Potter syndrome ( DPS ) is a paraneoplastic syndrome [ 1 ] in which hypoglycemia is associated with solitary fibrous tumors . The hypoglycemia is the result of the tumors producing insulin-like growth factor 2 . [ 2 ] The syndrome was first described in 1930, by Karl Walter Doege (1867–1932), a German-American physician [ 3 ] and by Roy Pilling Potter (1879–1968), an American radiologist, working independently; [ 4 ] the full term Doege–Potter syndrome was infrequently used until the publication of a 2000 article [ 5 ] using the eponym . [ 6 ]
DPS is rare (as of 1976, less than one hundred cases were described [ 7 ] ), with a malignancy rate of 12–15%. Actual rates of hypoglycemia associated with a fibrous tumor are quite rare (a 1981 study of 360 solitary fibrous tumors of the lungs found that only 4% caused hypoglycemia [ 8 ] ), and are linked to large tumors with high rates of mitosis . [ 9 ] Removal of the tumor will normally resolve the symptoms. [ 1 ] [ 9 ]
Tumors causing DPS tend to be quite large; [ 10 ] in one case a 3 kg (6.6 lb), 23×21×12 cm (9.1×8.3×4.7 in) mass was removed, sufficiently large to cause a collapsed lung . [ 5 ] In X-rays , they appear as a single mass with visible, defined borders, appearing at the edges of the lungs or a fissure dividing the lobes of the lungs. [ 10 ] Similar hypoglycemic effects have been related to mesenchymal tumors. [ 6 ]
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Dogliotti's principle is a principle in epidural anaesthesia first described by Professor Achille Mario Dogliotti in 1933. [ 1 ] It is a method for the identification of the epidural space , a potential space . As a needle is advanced through the ligamentum flavum , to the epidural space , with constant pressure applied to the piston of a syringe, loss of resistance occurs once the needle enters the epidural space due to the change in pressure. [ 2 ] [ 3 ] The identification of this space, allows subsequent administration of epidural anaesthesia, a technique used primarily for analgesia during childbirth . [ citation needed ]
This technique remains in use at present [update] , and is commonly referred to the loss of resistance to saline technique (LORS) or its variation, the loss of resistance to air technique (LORA). These use, respectively, saline or air to identify the epidural space. The LORS technique is generally favoured due to the increased complication risk with the LORA technique such as pneumocephalus or air embolism . [ 3 ] [ 4 ] [ 5 ]
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Don't Make Me Angry [ 1 ] is a British documentary series for the Channel Four by John Walsh of Walsh Bros Ltd. Each episode featured a story of anger and how its triggers and results were stopping the teenagers and their families from having a normal life. Shot in an observational documentary style, the psychologist Rachel Andrew provided the on screen advice. [ 2 ] [ clarification needed ]
There have been 5 screenings of this series on Channel Four from 2005 to 2009 below are the details for the first UK transmissions.
There have been 10 screenings of this series on Channel 4 from 2006 to 2009 below are the details for the first UK transmissions.
In 2006 the series was nominated for a BAFTA . [ 3 ]
Series two won the World Medal Young Adult Special at the New York Television Festival Awards. [ 4 ]
One episode was listed by the Children and Young People Now website. [ 5 ]
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Brussels Donald Lewis Leake (November 6, 1931 – December 31, 1997) [ 1 ] was an oral surgeon, and inventor of the alloplastic tray, a method for reconstruction of jaws without the need for bone grafts. [ 2 ] He gained his D.M.D. from Harvard University in 1962, and an M.D. from Stanford University in 1969. In 1970, Leake was employed at Harvard Medical School as an oral surgeon, and since 1971, Leake had been a Professor of Oral and Maxillofacial Surgery at UCLA .
Leake is also a noted oboist, having studied with Henri de Busscher , and in 1956 gained Premier Prix avec Distinction in Oboe, and Premier Prix avec la Plus Grande Distinction in Chamber Music from the Conservatoire Royal de Musique in Brussels. He received an M.A. in music history in 1957, and continued his musical career in parallel with his dental one.
This biographical article related to a physician in the United States is a stub . You can help Wikipedia by expanding it .
This dentistry article is a stub . You can help Wikipedia by expanding it .
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The Donald Reid Medal is awarded triennially by the London School of Hygiene and Tropical Medicine in recognition of distinguished contributions to epidemiology .
The medal was instituted in 1979 in memory of Professor Donald Reid (1914–1977), who was director of the Department of Medical Statistics and Epidemiology at the London School of Hygiene and Tropical Medicine from 1961 until his sudden death in 1977. [ 1 ] The medal was created by the distinguished medal sculptor Louis Osman . [ 2 ] The School Council of the London School of Hygiene and Tropical Medicine and the Royal College of Physicians of London propose names for the medal and the eventual recipient of the medal is then nominated by a Committee composed of the Dean of the London School of Hygiene and Tropical Medicine , two members nominated by the School Council, two members nominated by the president of the Royal College of Physicians (not being members of the staff of the London School of Hygiene and Tropical Medicine) and one member nominated by the Faculty of Public Health Medicine. [ 3 ]
Although the award is officially given every three years, there has been a period in which this regularity was not observed. After Jeremiah Stamler received the medal in 1988, it was not then awarded for five years until 1993 (to Richard Peto ), and then not for a further four years until 1997 (Brian MacMahon). Thus, in this 9-year period when three awards should have been made, only two were. In 1991, when the award was not made at all, the London School of Hygiene and Tropical Medicine was undergoing a period of restructuring following the appointment of Professor Richard Feachem as the Dean (the former Dean, Professor Gordon Smith having retired in 1989). The award made in 1993 was either two years late, or one year early because no 1994 award was made either. However, the 1997 award was made in accordance with the three-year cycle and re-established the regularity of the award.
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Door-to-balloon is a time measurement in emergency cardiac care (ECC), specifically in the treatment of ST segment elevation myocardial infarction (or STEMI). The interval starts with the patient's arrival in the emergency department , and ends when a catheter guidewire crosses the culprit lesion in the cardiac cath lab . Because of the adage that "time is muscle", meaning that delays in treating a myocardial infarction increase the likelihood and amount of cardiac muscle damage due to localised hypoxia , [ 1 ] [ 2 ] [ 3 ] [ 4 ] ACC / AHA guidelines recommend a door-to-balloon interval of no more than 90 minutes. [ 5 ] As of 2006 in the United States, fewer than half of STEMI patients received reperfusion with primary percutaneous coronary intervention (PCI) within the guideline-recommended timeframe. [ 6 ] It has become a core quality measure for the Joint Commission on Accreditation of Healthcare Organizations (TJC). [ 7 ] [ 8 ] [ 9 ]
The benefit of prompt, expertly performed primary percutaneous coronary intervention over thrombolytic therapy for acute ST elevation myocardial infarction is now well established. [ 10 ] Few hospitals can provide PCI within the 90 minute interval, [ 11 ] which prompted the American College of Cardiology (ACC) to launch a national Door to Balloon (D2B) Initiative in November 2006. The D2B Alliance seeks to "take the extraordinary performance of a few hospitals and make it the ordinary performance of every hospital." [ 12 ] Over 800 hospitals have joined the D2B Alliance as of March 16, 2007. [ 13 ]
The D2B Alliance advocates six key evidence-based strategies and one optional strategy to help reduce door-to-balloon times: [ 12 ] [ 14 ]
On May 30, 2007, the American Heart Association launched 'Mission: Lifeline', a "community-based initiative aimed at quickly activating the appropriate chain of events critical to opening a blocked artery to the heart that is causing a heart attack." [ 15 ] It is seen as complementary to the ACC's D2B Initiative. [ 16 ] The program will concentrate on patient education to make the public more aware of the signs of a heart attack and the importance of calling 9-1-1 for emergency medical services (EMS) for transport to the hospital. [ 15 ] In addition, the program will attempt to improve the diagnosis of STEMI patients by EMS personnel. [ 15 ] According to Alice Jacobs, MD, who led the work group that addressed STEMI systems, [ 17 ] when patients arrive at non-PCI hospitals they will stay on the EMS stretcher with paramedics in attendance while a determination is made as to whether or not the patient will be transferred. [ 17 ] For walk-in STEMI patients at non-PCI hospitals, EMS calls to transfer the patient to a PCI hospital should be handled with the same urgency as a 9-1-1 call. [ 17 ]
Although incorporating a prehospital 12 lead ECG into critical pathways for STEMI patients is listed as an optional strategy by the D2B Alliance, the fastest median door-to-balloon times have been achieved by hospitals with paramedics who perform 12 lead ECGs in the field. [ 18 ] EMS can play a key role in reducing the first-medical-contact-to-balloon time, sometimes referred to as EMS-to-balloon (E2B) time, [ 19 ] by performing a 12 lead ECG in the field and using this information to triage the patient to the most appropriate medical facility. [ 20 ] [ 21 ] [ 22 ] [ 23 ]
Depending on how the prehospital 12 lead ECG program is structured, the 12 lead ECG can be transmitted to the receiving hospital for physician interpretation, interpreted on-site by appropriately trained paramedics, or interpreted on-site by paramedics with the help of computerized interpretive algorithms. [ 24 ] Some EMS systems utilize a combination of all three methods. [ 19 ] Prior notification of an inbound STEMI patient enables time saving decisions to be made prior to the patient's arrival. This may include a "cardiac alert" or "STEMI alert" that calls in off duty personnel in areas where the cardiac cath lab is not staffed 24 hours a day. [ 19 ] The 30-30-30 rule takes the goal of achieving a 90-minute door-to-balloon time and divides it into three equal time segments. Each STEMI care provider (EMS, the emergency department, and the cardiac cath lab) has 30 minutes to complete its assigned tasks and seamlessly "hand off" the STEMI patient to the next provider. [ 19 ] In some locations, the emergency department may be bypassed altogether. [ 25 ]
Bradley et al. (Circulation 2006) performed a qualitative analysis of 11 hospitals in the National Registry of Myocardial Infarction that had median door-to-balloon times = or < 90 minutes. They identified 8 themes that were present in all 11 hospitals: [ 6 ]
Granger et al. (Circulation 2007) identified the following criteria of an ideal primary PCI center. [ 24 ]
Granger et al. (Circulation 2007) identified the following barriers to timely access to primary PCI. [ 24 ]
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Dopamine dysregulation syndrome ( DDS ) is a dysfunction of the reward system observed in some individuals taking dopaminergic medications for an extended length of time. It is characterized by severely disinhibited patterns of behavior, [ 1 ] [ 2 ] leading to problems such as addiction to the offending medication, gambling addiction , or compulsive sexual behavior , [ 3 ] along with a general orientation towards immediate gratification. It typically occurs in people with Parkinson's disease (PD) or restless legs syndrome (RLS) who have taken dopamine agonist medications for an extended period of time. [ 3 ]
The most common symptom is craving for the dopaminergic medication. However, other behavioral symptoms can appear independently of cravings or co-occur with it. [ 4 ] Cravings are an intense impulse of the subject to obtain medication even in the absence of symptoms that indicate its intake. [ 4 ] To fulfill this need, the person will self-administer extra doses. When self-administration is not possible, aggressive outbursts or the use of strategies such as symptom simulation or bribery to access additional medication can also appear. [ 4 ]
Hypomania , manifesting with feelings of euphoria , omnipotence , or grandiosity are prone to appear in those moments when medication effects are at their maximum; dysphoria , characterized by sadness , psychomotor slowing , fatigue or apathy are typical with dopamine replacement therapy (DRT) withdrawal. [ 4 ] Different impulse-control disorders have been described including compulsive gambling , compulsive shopping , eating disorders , and hypersexuality . [ 4 ] Behavioral disturbances, most commonly aggressive tendencies, are the norm. Psychosis is also common. [ 4 ]
Parkinson's disease is a common neurodegenerative disease characterized by a degeneration of dopamine neurons in the substantia nigra and a loss of dopamine in the putamen . It is described as a motor disease, but it also produces cognitive and behavioral symptoms. The most common treatment is dopamine replacement therapy , which consists in the administration of levodopa ( L -DOPA) or dopamine agonists (e.g., pramipexole or ropinirole ) to patients. Dopamine replacement therapy is well known to improve motor symptoms but its effects in cognitive and behavioral symptoms are more complex. [ 5 ] Dopamine has been related to the normal learning of stimuli with behavioral and motivational significance, attention , and most importantly the reward system . [ 6 ] In accordance with the role of dopamine in reward processing, addictive drugs stimulate dopamine release. [ 6 ] Although the exact mechanism has yet to be elucidated, the role of dopamine in the reward system and addiction has been proposed as the origin of DDS. [ 6 ] Models of addiction have been used to explain how dopamine replacement therapy produces DDS. [ 4 ] One of these models of addiction proposes that over the usage course of a drug there is a habituation to the rewarding effects that it produces at the initial stages. This habituation is thought to be dopamine mediated. With long-term administration of levodopa, the reward system gets used to it and needs higher quantities. As the user increases drug intake there is a loss of dopaminergic receptors in the striatum which acts in addition to an impairment in goal-direction mental functions to produce an enhancement of sensitization to dopamine therapy. The behavioral and mood symptoms of the syndrome are produced by the dopamine overdose . [ 6 ]
Diagnosis of the syndrome is clinical since there are no laboratory tests to confirm it. For diagnosis a person with documented responsiveness to medication has to increase medication intake beyond dosage needed to relieve their parkinsonian symptoms in a pathological addiction-like pattern. A current mood disorder (e.g., depression , anxiety , or hypomania ), behavioral disorder (e.g., excessive gambling, shopping, or sexual tendency, aggression, or social isolation) or an altered perception about the effect of medication also have to be present. [ 7 ] A questionnaire on the typical symptoms of DDS has also been developed and can help in the diagnosis process. [ 8 ]
The main prevention measure proposed is the prescription of the lowest possible dose of dopamine replacement therapy to individuals at risk. [ 6 ] The minimization of the use of dopamine agonists, and of short duration formulations of L -DOPA can also decrease risk of the syndrome. [ 6 ]
First choice management measure consists in the enforcement of a dopaminergic drug dosage reduction. If this decrease is maintained, dysregulation syndrome features soon decrease. [ 6 ] Cessation of dopamine agonists therapy may also be of use. [ 9 ] Some behavioral characteristics may respond to psychotherapy ; and social support is important to control risk factors . In some cases antipsychotic drugs may also be of use in the presence of psychosis, aggression, gambling, or hypersexuality. [ 6 ]
Based upon five case reports, [ 10 ] [ 11 ] valproate may have efficacy in controlling the symptoms of levodopa-induced DDS that arise from the use of levodopa for the treatment of Parkinson's disease . [ 12 ] [ 13 ] [ 14 ]
DDS is not common among PD patients. Prevalence may be around 4%. [ 3 ] [ 7 ] Its prevalence is higher among males with an early onset of the disease. [ 4 ] Previous substance abuse such as heavy drinking or drug intake seems to be the main risk factor along with a history of affective disorder . [ 4 ]
PD was first formally described in 1817; [ 15 ] however, L-dopa did not enter clinical practice until almost 1970. [ 16 ] [ 17 ] In these initial works there were already reports of neuropsychiatric complications. [ 17 ] During the following decades cases featuring DDS symptoms in relation to dopamine therapy such as hypersexuality, gambling or punding , appeared. [ 18 ] [ 19 ] [ 20 ] DDS was first described as a syndrome in the year 2000. [ 21 ] Three years later the first review articles on the syndrome were written, showing an increasing awareness of the DDS importance. [ 3 ] [ 6 ] [ 4 ] Diagnostic criteria were proposed in 2005. [ 7 ]
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Dopamine transporter deficiency syndrome ( DTDS ), also known as infantile parkinsonism-dystonia, is a rare movement disorder that causes progressively worsening dystonia and parkinsonism . It is the first known inherited dopamine 'transportophathy.' [ 1 ]
DTDS is an extremely rare disease; only about 20 affected individuals have been described in the medical literature. Researchers believe this condition is likely underdiagnosed because its signs and symptoms overlap with other movement disorders , including cerebral palsy . [ 2 ]
The onset of DTDS is a continuum that ranges from early-onset DTDS (in the first 6 months) to atypical later-onset DTDS (in childhood, adolescence, or adulthood).
The main symptom of DTDS, presenting in 80-99% of DTDS patients, is Parkinsonism . [ 3 ] This is a neurological anomaly resulting from degeneration of dopamine-generating cells in the substantia nigra , and is characterized by shaking and tremors , rigidity , slowness of movement, and difficulty with walking and gait . [ 4 ]
Various other symptoms present less commonly (30-79%), including bradykinesia (slowness of movement), acid reflux , muscular hypertonia , and chorea . [ 3 ]
DTDS is caused by mutations in the SLC6A3 gene, which codes for the dopamine transporter protein DAT . In contrast to various mutations that up-regulate DAT activity, which is implicated in clinical depression , this mutation results in DAT down-regulation and, consequently, DTDS. [ 5 ] Known DTDS-related SLC6A3 mutations include:
In vitro replication of SLC6A3 mutations like those present in DTDS demonstrate multifaceted loss of dopamine transporter functions. Dopamine intake is universally impaired. These mutants also demonstrated diminished dopamine binding affinity , reduced cell surface transporter, loss of post-translational dopamine transporter glycosylation , and failure of amphetamine -mediated dopamine efflux . [ 1 ]
The age at which signs and symptoms appear seems to be related to the severity of DAT dysfunction. Early-onset DTDS movement problems in infancy most often have transporter activity that is less than 5 percent of normal. Those whose movement problems appear in childhood or later tend to have somewhat higher levels of transporter activity, although they are still lower than normal. Researchers speculate that higher levels of transporter activity may delay the onset of the disease in these individuals.
DTDS is inherited in an autosomal recessive pattern, which means, for affected individuals, both copies of the gene in each cell have SLC6A3 mutations. As such, each sibling of an affected individual has a 25% chance of being affected, a 50% chance of being an asymptomatic carrier , and 25% chance of being unaffected and not a carrier. Once a SLC6A3 pathogenic variant is identified within an affected family member, carrier testing for at-risk relatives and prenatal testing or preimplantation genetic diagnosis for pregnancies can be options considered for genetic counseling .
Diagnosis of SLC6A3-negative DTDS is established in a proband via molecular genetic testing , looking for biallelic (i.e. homozygous or compound heterozygous ) pathogenic SLC6A3 variants . DTDS-positive patients are further identified by matching their genetic testing results with known characteristic clinical, laboratory, and imaging findings. [ 5 ]
To date, another potential diagnostic tool is neurotransmitter analysis of patient cerebrospinal fluid . All individuals tested with classical early-onset, SLC6A3-related DTDS display raised homovanillic acid (HVA) levels with normal 5-hydroxyindoleacetic acid (5-HIAA, a serotonin metabolite ) levels. DTDS patients demonstrate a HVA:5-HIAA ratio of 5.0-13.0, above the normal range of 1.0-4.0. In addition, the patients have normal pterin profiles. [ 5 ]
Mutant constructs of human dopamine transporter can be used for in vitro functional analysis of any particular mutant's dopamine uptake and cocaine-analogue binding. [ 6 ]
A multidisciplinary approach to long-term management of this progressive disorder is optimal. [ 1 ] Treatment can be split into three categories: treatment of DTDS manifestations, prevention of secondary complications , and monitoring of overall disease progression. [ 5 ]
Treatment to control the chorea and dyskinesia in the early stages of DTDS is done with tetrabenazine and benzodiazepines . The dystonia is more difficult to control and the first-line agents include pramipexole and ropinirole ; adjuncts include trihexyphenidyl , baclofen , gabapentin , and clonidine for severe dystonia, and chloral hydrate and benzodiazepines for exacerbations of dystonia or status dystonicus . [ 5 ]
Regular physiotherapy is recommended to reduce the risk of contractures , shortening and hardening of the muscles. Feeding may become difficult and alternative feeding strategies including nasogastric tubes or percutaneous endoscopic gastrostomies may become necessary due to progressive bulbar dysfunction. The influenza vaccine is used in combination with prophylactic antibiotics to prevent chest infections . [ 5 ]
Patients are evaluated every six to 12 months for early evidence of hip dislocation and spinal deformities . Risk of pulmonary aspiration is evaluated with regular swallowing assessments. Nutritional assessments are performed regularly to ensure adequate caloric intake .
Preliminary experiments have examined the potential of drugs to act as pharmacological chaperones of DAT to rescue DTDS mutations. Bupropion and ibogaine appear to promote DAT maturation and functional activity by acting as pharmacological chaperones in the endoplasmic reticulum . These two drugs rescue DAT maturation and functional activity of two DTDS-associated mutations (A314V and R445C). [ 7 ] Preclinical experiments in mice have demonstrated efficacy and safety of a potential treatment using stereotactic injection of AAV vector to deliver working copies of the DAT gene. [ 8 ]
A variety of support and advocacy groups exist to connect with other patients and families or provide valuable services.
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Dora Elisabeth Jacobsohn (1908–1983) was a German-Swedish physiologist and endocrinologist . Considered one of the early pioneers of the field of neuroendocrinology , [ 1 ] she is best known for her work with Geoffrey Harris showing that the anterior pituitary gland is controlled by the hypothalamus via the hypophyseal portal system .
Jacobsohn was born in Berlin in 1908. [ 1 ] She earned her M.D. in Germany in 1933, but she was not allowed to practice medicine in Germany because she was Jewish . [ 2 ] Fleeing Nazi Germany , Jacobsohn moved to Sweden in 1934, where she had family. [ 2 ] There, she met Axel Westman at the Uppsala University Hospital , who permitted her to observe and assist in his endocrinological research on ovulation and reproduction in hypophysectomized (pituitary removed) animals. [ 3 ] [ 2 ] Although Jacobsohn was not permitted to do research as she was a foreigner without a Swedish degree, she worked with Westman at Lund University and ran clinical hormone assays for the hospital. Nonetheless, she published over 22 research papers during this 10 year collaboration. [ 2 ] [ 3 ] In 1944, she gained Swedish citizenship and in 1948, a Swedish medical degree, with a thesis on mammary gland development. [ 2 ] This allowed her to finally become a professor at Lund University. [ 3 ] In 1952, the Royal Physiographic Society in Lund changed their rules to accept women, and she was elected a society Fellow. [ 2 ] [ 3 ] In 1964, she was promoted to Director of Experimental Endocrinology at Lund University. [ 3 ]
Jacobsohn never married, and died in 1983 after a nearly year-long coma due to a traffic accident. [ 3 ]
In collaboration with Geoffrey Harris at Cambridge , Jacobsohn performed a series of elegant transplantation experiments, showing that pituitary grafts could only stimulate ovulation when in connection with the hypothalamus / mid brain, not the temporal lobe or other parts of the body. [ 4 ] [ 5 ] This first showed that the anterior pituitary must be controlled by, and in contact with, the brain via the hypothalamus. Further, they showed that the blood vessels (via the hypophyseal portal system), rather than nervous stimulation, was necessary for stimulating the anterior pituitary. [ 4 ] This work founded the brain's role in hormonal regulation, helping to establish the field of neuroendocrinology .
She also did work showing that the posterior pituitary is required for milk ejection , later discovered to be mediated by the hormone oxytocin . [ 5 ] Later in her career, she studied the effects of androgens and sex steroids on sexual development in rodents. [ 6 ]
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The Dorn method is a form of manual, holistic alternative therapy used to correct misalignments in the spinal column and other joints .
During a treatment, the practitioner palpates the patient's spine. If any 'unbalanced' areas are found, possible underlying misalignments are palpated with gentle pressure using the thumb or hand against the spinous processes , while the patient enacts guided movements such as swinging the leg or arms to distract the muscles' inertia; this is similar to the principle of mechanics known as 'counter pressure'. [ 1 ] In case of pain, the patient is advised to stop the procedure in order to avoid any damage to the body.
This article about alternative medicine is a stub . You can help Wikipedia by expanding it .
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https://en.wikipedia.org/wiki/Dorn_method
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On 1 July 1940, in the town of Dorohoi in Romania , Romanian military units carried out a pogrom against the local Jews , during which, according to an official Romanian report, 53 Jews were murdered, and dozens injured. According to the town's Jews, the number of fatalities was between 165 and 200. These acts were committed before Romania entered World War II , before it became Germany 's ally, and before the German military entered the country. [ 1 ] [ 2 ]
Although the Romanian government had taken steps against Jews, including antisemitic laws, and seizure of Jewish property, these military actions against the Jews were not endorsed by the government; when the conspiracy against the Jews was discovered by the military command, troops were sent to put an end to the abuse. The perpetrators, however, were not punished. [ 1 ] [ 2 ]
The Molotov–Ribbentrop Pact (August 1939) gave the Soviet Union a green light to take back Bessarabia in June 1940 (see June 1940 Soviet Ultimatum , and Soviet occupation of Bessarabia and Northern Bukovina ).
During the Romanian Army's withdrawal from Bessarabia, some of the local residents demonstrated their joy. Attacks on the soldiers by locals are also documented. Various reports speak of attacks on the retreating soldiers by Jews, though their veracity is disputed, and some have been proven to be fabrications. [ 1 ] Additionally, although the reports defined all of them as "Jews", among the celebrators and attackers were Ukrainians , Russians , pro- Communists , newly released criminals, and ethnic Romanians. These reports, regardless of veracity, did much to incite many Romanians against Jews, strengthening existing Anti-Semitic sentiment. [ 1 ] [ 2 ]
The Romanian people were traumatized and frustrated by giving up these areas without a war, and the regime's position weakened significantly. The government scapegoated the Jews, with the press' support:
Confronted with an extremely serious crisis and doubting their regime could survive, Romanian government officials turned the Jews into a political "lightning rod," channeling popular discontent toward the minority. Notable in this report is the reaction of the Romanian press, whose rage was directed more toward Jews than the Soviets, the real aggressors. Given that the Romanian press was censored in 1940, the government must have played a role in this bias. A typical form of anticipatory scapegoating was to let Jewish leaders know that the Romanian authorities might launch acts of repression against the Jews. [ 1 ]
The incited Romanians, and especially the Romanian soldiers, looked for ways to take revenge on the Jews. In 1930, the population of Dorohoi was 15,866, of which 5,788 were Jews. Although local Jews had long suffered from Antisemitism , it was greatly increased by the passing of Romanian refugees, who were spreading tales of Jews' scheming against the Romanians. [ 1 ] [ 2 ]
On 30 June 1940, soldiers from the two brigades stationed in the area went from door to door warning the Romanian residents of the "revenge" about to take place against the Jews. The Christians placed religious icons in their windows, drew crosses on their homes, or raised Romanian national flags , to let the rioters know not to harm them. In the town, the rumor spread that harming the Jews would be allowed for 24 hours. [ 1 ] [ 2 ]
In an incident between Romanian and Soviet military men in Herţa , neighboring Dorohoi, the Soviets killed a Romanian officer, and a Jewish-Romanian soldier, Iancu Solomon, who was trying to defend the officer. The two were laid to rest in separate funerals. A firing squad was sent to Solomon's funeral, made up of 10 Jewish soldiers from the battalions stationed nearby. Some local Jews also participated in the funeral. Right after the coffin was lowered into the grave, many shots were heard, and the local Jews ran and hid in the local cleansing room. The Jewish soldiers, turning to the cemetery gates, were surrounded by soldiers from the 3rd Border Patrol battalion , commanded by a Colonel . The Jews, peering from the cleansing room, saw the Jewish soldiers disarmed and stripped of their uniforms. They were put up against the cemetery's back wall and shot by the Romanian soldiers. Seven were killed instantly, and three injured. The Romanians placed a submachine gun in the hands of the already dead Emil Bercovici, the senior Jewish soldier, to stage the notion that he had started firing on the Romanians. An especially strong downpour begun, stopping the killing for a while, and allowing some of the Jewish crowd to slip away. Many Romanian soldiers, commanded by a Lieutenant, removed the Jews from the cleansing room using violence and threats. They were led to a ditch outside the cemetery. Two old men and one child managed to escape before the shooting began. The soldiers continued hunting the Jews hiding in the cemetery with the help of the place's Romanian keeper. [ 1 ] [ 2 ]
Concurrently, soldiers led by officers and sergeant majors burst into the town shouting "the Bolsheviks are coming". The soldiers raped, robbed, tortured and murdered Jews for 24 hours. The lives of many were saved due to the great attention the soldiers gave to the robberies. Many acts of cruelty were committed, among them: [ 1 ] [ 2 ]
The life of the head of the local Jewish community, Dr. Isac Axler, was saved after he managed to prove to the soldiers stopping his carriage that he had been discharged from the Romanian military with the rank of Colonel, and was awarded two medals of valor. [ 1 ] [ 2 ]
Jews walking in the streets were stopped by officers, had their papers checked, and when their Jewish identity was confirmed, murdered. [ 1 ] [ 2 ]
At this point, the local 29th infantry brigade , who were not privy to the murder plot, stepped in. The brigade sent a company to patrol the town and restore order. After local Romanians shouted at the soldiers and told them that Jews were firing at soldiers, Lieutenant Vasile Isăceanu took "precautionary measures" - he ordered ten Jewish soldiers, disarmed of their weapons, to march in front of the unit. Soon the unit's soldiers joined the persecution of the Jews, arresting them under false charges of firing at soldiers. The battalion's vice commander, Stino, prevented the soldiers from executing the detained Jews, and saved from certain death 20 Jewish soldiers, who were already stripped bare, waiting to be executed. [ 1 ] [ 2 ]
A downpour stopped the killings, but not the looting. Some local Roma (Gypsies) joined this activity, stole as much as they could from Jewish homes and thanked the soldiers with song and dance. [ 1 ] [ 2 ]
The pogrom was stopped by order of General Constantin Sănătescu , who discovered the events by accident, seeing injured Jews. He ordered Colonel Ilasievici to investigate the matter. [ 1 ] [ 2 ]
On 2 July, the day after the pogrom, the Romanian military's Chief of Staff reported that the 3rd brigade "took revenge" on the Jews because of the difficulties they had had with the Jews of Bessarabia. According to his report, the soldiers killed four Jews, injured 15, and plundered several shops. [ 1 ] [ 2 ]
The military prosecutor of the 8th Corps headed a committee to investigate the events, with the participation of doctors and the town's representatives. On 3 July, the military prosecutor found 50 unidentified corpses, among them 11 women, five children and six non-local Jewish soldiers. The prosecutor did not determine the identity of the murderers, and only determined that the deaths were the results of gunshot wounds. The bodies were buried quickly by a company of troops, due to the advanced stage of decomposition they were in. Officially, it was determined that 53 Jews were murdered, but the Jews claimed, according to the community's records, that the number of victims was between 165 and 200. The bodies in the ditch outside the cemetery were not exhumed from their mass grave, and were not counted. [ 1 ] [ 2 ]
The local head of police, Gheorghe Pamfil, composed a report about a "skirmish event", resulting in the death of a few Jews. [ 1 ] [ 2 ]
The officers of the 3rd brigade were transferred to other positions, and the brigade left the town with its carriages filled with loot. Among the pillaged goods were cans of paint , which were not properly sealed, and the convoy's trail was marked with paint stolen from the Jews. [ 1 ] [ 2 ]
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https://en.wikipedia.org/wiki/Dorohoi_pogrom
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Dorothy Ann Malcolm Geddes OBE FRCS (8 May 1936 – 14 March 1998) was the first woman to be appointed to a professorship of dentistry in the United Kingdom.
Dorothy Ann Malcolm Geddes was born in Alloa , Scotland on 8 May 1936. She attended Brechin High School , going on to study dentistry at the University of Edinburgh , graduating in 1959. She worked for most of her career at University of Glasgow where she was Dean of the Faculty of Dental Surgery. Geddes' specialism was oral surgery. She was the first woman to be awarded Fellowship in Dental Surgery (FRCS) of the Royal College of Surgeons of Edinburgh , in 1963. [ 1 ] [ 2 ] [ 3 ] She was a distinguished teacher and researcher and gained a personal chair. She was President of the Royal Odonto-Chirugical Society of Scotland , President of the West of Scotland Branch of the British Dental Association , and Convener of the Dental Council .
Geddes died 14 March 1998. The University of Glasgow established the Dorothy Geddes Multimedia Laboratory to promote the application of new, cutting-edge technology to the teaching of oral biology. [ 4 ] The university also awards the Geddes Research Fellowship and medal.
She is remembered as a "modest, quiet woman with a wicked sense of humour, who is remembered with universal affection and more than a little awe". [ 5 ]
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https://en.wikipedia.org/wiki/Dorothy_Geddes
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Dose-dense chemotherapy is a chemotherapy treatment plan in which drugs are given with less time between treatments than in a standard chemotherapy treatment plan. [ 1 ]
The Gompertzian model of tumor cell growth shows tumor cells growing fastest when the tumor is small. When a large (slow growing) tumor is surgically removed, microtumors or individual neoplastic cells that remain will be able to grow at their fastest rate. Standard treatment may include chemotherapy once every three weeks. This would allow bone marrow and gastrointestinal tract recovery before the next treatment and would inhibit the tumor for a short time, but allow rapid growth for a short time before the next treatment. [ 2 ]
By decreasing the dose and increasing the frequency, the fast growth can be prevented, allowing for faster and more effective cure rate. Although the dose is reduced in each treatment, the total quantity of chemotherapy may or may not be increased over the duration of the typical treatment time. For example, in standard treatment of ovarian cancer , paclitaxel is given at 175 mg/m 2 body surface every three weeks. In dose dense therapy paclitaxel is given at 50–80 mg/m 2 every week (150–240 mg/m 2 in 3-weeks). [ 2 ]
This article incorporates public domain material from Dictionary of Cancer Terms . U.S. National Cancer Institute .
This oncology article is a stub . You can help Wikipedia by expanding it .
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https://en.wikipedia.org/wiki/Dose-dense_chemotherapy
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Dose area product (DAP) is a quantity used in assessing the radiation risk from diagnostic X-ray radiography examinations and interventional procedures, like angiography . It is defined as the absorbed dose multiplied by the area irradiated, expressed in gray - centimetres squared (Gy·cm 2 [ 1 ] – sometimes the prefixed units dGy·cm 2 , mGy·cm 2 or cGy·cm 2 are also used). [ 2 ] Gray (Gy) is the SI unit of absorbed dose of ionizing radiation , while the milligray (mGy) is its subunit, numerically equivalent to the millisievert (mSv) as used to quantify equivalent and effective doses for gamma (γ) and X-rays. [ 3 ]
Manufacturers of DAP meters usually calibrate them in terms of absorbed dose to air. DAP reflects not only the dose within the radiation field but also the area of tissue irradiated. Therefore, it may be a better indicator of the overall risk of inducing cancer than the dose within the field. It also has the advantage of being easily measured, with the permanent installation of a DAP meter on the X-ray set.
Due to the divergence of a beam emitted from a "point source", the area irradiated (A) increases with the square of distance from the source (A ∝ d 2 ), while radiation intensity (I) decreases according to the inverse square of distance (I ∝ 1/d 2 ). Consequently, the product of intensity and area, and therefore DAP, is independent of distance from the source.
DICOM "X-Ray Acquisition Dose Module" metadata within each medical imaging study often includes various DAP and dose length product (DLP) parameters. [ 4 ]
An ionization chamber is placed beyond the X-ray collimators and must intercept the entire X-ray field for an accurate reading. Different parameters of the X-ray set, such as peak voltage (kVp), X-ray tube current (mA), exposure time, or the area of the field, can also be changed. For example, a 5 cm × 5 cm X-ray field with an entrance dose of 1 mGy will yield a 25 mGy·cm 2 DAP value. When the field is increased to 10 cm × 10 cm with the same entrance dose, the DAP increases to 100 mGy·cm 2 , which is four times the previous value.
Kerma area product (KAP) [ 1 ] is a related quantity, which for all practical radiation protection purposes is equal to dose area product. However, strictly speaking D A P = K A P × ( 1 − g ) {\displaystyle \mathrm {DAP} =\mathrm {KAP} \times (1-g)} , where g is the fraction of energy of liberated charged particles that is lost in radiative processes in the material [ 5 ] and the dose is expressed in absorbed dose to air. The value of g for diagnostic X-rays is only a fraction of a percent.
Adult coronary angiography and PCI procedures expose patients to an average DAP in the range of 20 to 106 Gy·cm 2 and 44 to 143 Gy·cm 2 respectively. [ 6 ]
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https://en.wikipedia.org/wiki/Dose_area_product
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In external beam Radiotherapy , transverse and longitudinal dose measurements are taken by a radiation detector in order to characterise the radiation beams from medical linear accelerators . [ 1 ] Typically, an ionisation chamber and water phantom are used to create these radiation dose profiles. Water is used due to its tissue equivalence.
Transverse dose measurements are performed in the x (crossplane) or y (inplane) directions perpendicular to the radiation beam, and at a given depth (z) in the phantom. These are known as dose profiles .
Dose measurements taken along the z direction create radiation dose distribution known as a depth-dose curve.
This oncology article is a stub . You can help Wikipedia by expanding it .
This nuclear medicine article is a stub . You can help Wikipedia by expanding it .
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https://en.wikipedia.org/wiki/Dose_profile
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DVS (Dose Verification System) , developed by Sicel Technologies, was an implantable telemetric, radiation sensor. [ 1 ] The device was used to measure the amount of radiation that was delivered to tumor and/or healthy tissue. The DVS sensor contained a dosimeter and wireless transmitter inside a sealed, biocompatible glass capsule measuring 0.8 inches (20mm) long and 0.08 inches (2.1mm) across. The sensor was implantable transluminally or transdermally. The device had limited adoption by the radiation oncology community, sales were thus inadequate for profitability.
The company (Sicel) eventually ceased to exist circa 2011. [ 2 ]
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https://en.wikipedia.org/wiki/Dose_verification_system
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A double-contrast barium enema is a form of contrast radiography in which x-rays of the colon and rectum are taken using two forms of contrast to make the structures easier to see. [ 1 ] A liquid containing barium (that is, a radiocontrast agent ) is put into the rectum. Barium (usually as a sulfate) outlines the colon and rectum on an x-ray and helps show abnormalities. Air is also put into the rectum and colon to further enhance the x-ray.
Double-contrast barium enemas are less invasive than a colonoscopy and have comparatively fewer issues in a viable large bowel. [ 2 ]
This article incorporates public domain material from Dictionary of Cancer Terms . U.S. National Cancer Institute .
This oncology article is a stub . You can help Wikipedia by expanding it .
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https://en.wikipedia.org/wiki/Double-contrast_barium_enema
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