Asperger's Syndrome - Disorder

2009-08-10T02:07:00.000-07:00

Asperger syndrome
From Wikipedia, the free encyclopedia

Classification and external resources
ICD-10
F 84.5
ICD-9
299.80
OMIM
608638
DiseasesDB
31268
MedlinePlus
001549
eMedicine
ped/147
MeSH
F03.550.325.100

Asperger syndrome is an autism spectrum disorder, and people with it therefore show significant difficulties in social interaction, along with stereotypies and other restricted and repetitive patterns of behavior and interests. It differs from other autism spectrum disorders by its relative preservation of linguistic and cognitive development. Although not required for diagnosis, physical clumsiness and atypical use of language are frequently reported.[1][2]
Asperger syndrome is also called Asperger's syndrome,[1] Asperger (or Asperger's) disorder,[3][4] or just Asperger's.[5] It is named after the Austrian pediatrician Hans Asperger who, in 1944, described children in his practice who lacked nonverbal communication skills, demonstrated limited empathy with their peers, and were physically clumsy.[6] Fifty years later, it was standardized as a diagnosis, but questions about many aspects remain.[7] For example, there is lingering doubt about whether it is distinct from high-functioning autism (HFA);[8] partly because of this, its prevalence is not firmly established. The exact cause is unknown, although research supports the likelihood of a genetic basis; brain imaging techniques have not identified a clear common pathology.[1]

There is no single treatment, and the effectiveness of particular interventions is supported by only limited data.[1] Intervention is aimed at improving symptoms and function. The mainstay of management is behavioral therapy, focusing on specific deficits to address poor communication skills, obsessive or repetitive routines, and physical clumsiness.[9] Most individuals improve over time, but difficulties with communication, social adjustment and independent living continue into adulthood.[7] Some researchers and people with Asperger's have advocated a shift in attitudes toward the view that it is a difference, rather than a disability that must be treated or cured.[10]

Classification
Asperger syndrome (AS) is one of the autism spectrum disorders (ASD) or pervasive developmental disorders (PDD), which are a spectrum of psychological conditions that are characterized by abnormalities of social interaction and communication that pervade the individual's functioning, and by restricted and repetitive interests and behavior. Like other psychological development disorders, ASD begins in infancy or childhood, has a steady course without remission or relapse, and has impairments that result from maturation-related changes in various systems of the brain.[11] ASD, in turn, is a subset of the broader autism phenotype (BAP), which describes individuals who may not have ASD but do have autistic-like traits, such as social deficits.[12] Of the other four ASD forms, autism is the most similar to AS in signs and likely causes but its diagnosis requires impaired communication and allows delay in cognitive development; Rett syndrome and childhood disintegrative disorder share several signs with autism but may have unrelated causes; and pervasive developmental disorder not otherwise specified (PDD-NOS) is diagnosed when the criteria for a more specific disorder are unmet.[13]
The extent of the overlap between AS and high-functioning autism (HFA—autism unaccompanied by mental retardation) is unclear.[8][14][3] The current ASD classification is to some extent an artifact of how autism was discovered,[15] and may not reflect the true nature of the spectrum.[16] A panel session at a 2008 diagnosis-related autism research planning conference noted problems with the classification of AS as a distinct subgroup of ASD, and two of three breakout groups recommended eliminating AS as a separate diagnosis in future versions of the Diagnostic and Statistical Manual of Mental Disorders and of the International Statistical Classification of Diseases and Related Health Problems.[17]

Asperger syndrome is also called Asperger's syndrome (AS),[1] Asperger (or Asperger's) disorder (AD),[3][4] or just Asperger's.[5] There is little consensus among clinical researchers about whether the condition's name should end in "syndrome" or "disorder".[8]

Characteristics
A pervasive developmental disorder, Asperger syndrome is distinguished by a pattern of symptoms rather than a single symptom. It is characterized by qualitative impairment in social interaction, by stereotyped and restricted patterns of behavior, activities and interests, and by no clinically significant delay in cognitive development or general delay in language.[4] Intense preoccupation with a narrow subject, one-sided verbosity, restricted prosody, and physical clumsiness are typical of the condition, but are not required for diagnosis.[8]

Social interaction
Further information: Asperger syndrome and interpersonal relationships
The lack of demonstrated empathy is possibly the most dysfunctional aspect of Asperger syndrome.[2] Individuals with AS experience difficulties in basic elements of social interaction, which may include a failure to develop friendships or to seek shared enjoyments or achievements with others (for example, showing others objects of interest), a lack of social or emotional reciprocity, and impaired nonverbal behaviors in areas such as eye contact, facial expression, posture, and gesture.[1]

Unlike those with autism, people with AS are not usually withdrawn around others; they approach others, even if awkwardly. For example a person with AS may engage in a one-sided, long-winded speech about a favorite topic, while misunderstanding or not recognizing the listener's feelings or reactions, such as a need for privacy or haste to leave.[8] This social awkwardness has been called "active but odd".[1] This failure to react appropriately to social interaction may appear as disregard for other people's feelings, and may come across as insensitive.[8]

The cognitive ability of children with AS often allows them to articulate social norms in a laboratory context,[1] where they may be able to show a theoretical understanding of other people's emotions; however, they typically have difficulty acting on this knowledge in fluid, real-life situations.[8] People with AS may analyze and distill their observation of social interaction into rigid behavioral guidelines, and apply these rules in awkward ways, such as forced eye contact, resulting in a demeanor that appears rigid or socially naive. Childhood desire for companionship can become numbed through a history of failed social encounters.[1]

The hypothesis that individuals with AS are predisposed to violent or criminal behavior has been investigated but is not supported by data.[1][18] More evidence suggests children with AS are victims rather than victimizers.[19] A 2008 review found that an overwhelming number of reported violent criminals with AS had coexisting psychiatric disorders such as schizoaffective disorder.[20]

Restricted and repetitive interests and behavior
People with Asperger syndrome often display behavior, interests, and activities that are restricted and repetitive and are sometimes abnormally intense or focused. They may stick to inflexible routines, move in stereotyped and repetitive ways, or preoccupy themselves with parts of objects.[4]

Pursuit of specific and narrow areas of interest is one of the most striking features of AS.[1] Individuals with AS may collect volumes of detailed information on a relatively narrow topic such as dinosaurs or members of congress, without necessarily having genuine understanding of the broader topic.[1][8] For example, a child might memorize camera model numbers while caring little about photography.[1] This behavior is usually apparent by grade school, typically age 5 or 6 in the United States.[1] Although these special interests may change from time to time, they typically become more unusual and narrowly focused, and often dominate social interaction so much that the entire family may become immersed. Because narrow topics often capture the interest of children, this symptom may go unrecognized.[8]
Stereotyped and repetitive motor behaviors are a core part of the diagnosis of AS and other ASDs.[21] They include hand movements such as flapping or twisting, and complex whole-body movements.[4] These are typically repeated in longer bursts and look more voluntary or ritualistic than tics, which are usually faster, less rhythmical and less often symmetrical.[22]

Speech and language
Although individuals with Asperger syndrome acquire language skills without significant general delay and their speech typically lacks significant abnormalities, language acquisition and use is often atypical.[8] Abnormalities include verbosity, abrupt transitions, literal interpretations and miscomprehension of nuance, use of metaphor meaningful only to the speaker, auditory perception deficits, unusually pedantic, formal or idiosyncratic speech, and oddities in loudness, pitch, intonation, prosody, and rhythm.[1]

Three aspects of communication patterns are of clinical interest: poor prosody, tangential and circumstantial speech, and marked verbosity. Although inflection and intonation may be less rigid or monotonic than in autism, people with AS often have a limited range of intonation: speech may be unusually fast, jerky or loud. Speech may convey a sense of incoherence; the conversational style often includes monologues about topics that bore the listener, fails to provide context for comments, or fails to suppress internal thoughts. Individuals with AS may fail to monitor whether the listener is interested or engaged in the conversation. The speaker's conclusion or point may never be made, and attempts by the listener to elaborate on the speech's content or logic, or to shift to related topics, are often unsuccessful.[8]

Children with AS may have an unusually sophisticated vocabulary at a young age and have been colloquially called "little professors", but have difficulty understanding figurative language and tend to use language literally.[1] Children with AS appear to have particular weaknesses in areas of nonliteral language that include humor, irony, and teasing. Although individuals with AS usually understand the cognitive basis of humor they seem to lack understanding of the intent of humor to share enjoyment with others.[3] Despite strong evidence of impaired humor appreciation, anecdotal reports of humor in individuals with AS seem to challenge some psychological theories of AS and autism.[23]

Other
Individuals with Asperger syndrome may have signs or symptoms that are independent of the diagnosis, but can affect the individual or the family. These include differences in perception and problems with motor skills, sleep, and emotions.

Individuals with AS often have excellent auditory and visual perception.[24] Children with ASD often demonstrate enhanced perception of small changes in patterns such as arrangements of objects or well-known images; typically this is domain-specific and involves processing of fine-grained features.[25] Conversely, compared to individuals with high-functioning autism, individuals with AS have deficits in some tasks involving visual-spatial perception, auditory perception, or visual memory.[1] Many accounts of individuals with AS and ASD report other unusual sensory and perceptual skills and experiences. They may be unusually sensitive or insensitive to sound, light, touch, texture, taste, smell, pain, temperature, and other stimuli, and they may exhibit synesthesia;[26] these sensory responses are found in other developmental disorders and are not specific to AS or to ASD. There is little support for increased fight-or-flight response or failure of habituation in autism; there is more evidence of decreased responsiveness to sensory stimuli, although several studies show no differences.[27]

Hans Asperger's initial accounts[1] and other diagnostic schemes[28] include descriptions of physical clumsiness. Children with AS may be delayed in acquiring skills requiring motor dexterity, such as riding a bicycle or opening a jar, and may seem to move awkwardly or feel "uncomfortable in their own skin". They may be poorly coordinated, or have an odd or bouncy gait or posture, poor handwriting, or problems with visual-motor integration.[1][8] They may show problems with proprioception (sensation of body position) on measures of apraxia (motor planning disorder), balance, tandem gait, and finger-thumb apposition. There is no evidence that these motor skills problems differentiate AS from other high-functioning ASDs.[1]

Children with AS are more likely to have sleep problems, including difficulty in falling asleep, frequent nocturnal awakenings, and early morning awakenings.[29][30] AS is also associated with high levels of alexithymia, which is difficulty in identifying and describing one's emotions.[31] Although AS, lower sleep quality, and alexithymia are associated, their causative relationship is unclear.[30]

As with other forms of ASD, parents of children with AS have higher levels of stress.[32]

Causes
Further information: Causes of autism
Hans Asperger described common symptoms among his patients' family members, especially fathers, and research supports this observation and suggests a genetic contribution to Asperger syndrome. Although no specific gene has yet been identified, multiple factors are believed to play a role in the expression of autism, given the phenotypic variability seen in this group of children.[1][33] Evidence for a genetic link is the tendency for AS to run in families and an observed higher incidence of family members who have behavioral symptoms similar to AS but in a more limited form (for example, slight difficulties with social interaction, language, or reading).[9] Most research suggests that all autism spectrum disorders have shared genetic mechanisms, but AS may have a stronger genetic component than autism.[1] There is probably a common group of genes where particular alleles render an individual vulnerable to developing AS; if this is the case, the particular combination of alleles would determine the severity and symptoms for each individual with AS.[9]

A few ASD cases have been linked to exposure to teratogens (agents that cause birth defects) during the first eight weeks from conception. Although this does not exclude the possibility that ASD can be initiated or affected later, it is strong evidence that it arises very early in development.[34] Many environmental factors have been hypothesized to act after birth, but none has been confirmed by scientific investigation.[35]

Mechanism
Further information: Mechanism of autism
Asperger syndrome appears to result from developmental factors that affect many or all functional brain systems, as opposed to localized effects.[36] Although the specific underpinnings of AS or factors that distinguish it from other ASDs are unknown, and no clear pathology common to individuals with AS has emerged,[1] it is still possible that AS's mechanism is separate from other ASD.[37] Neuroanatomical studies and the associations with teratogens strongly suggest that the mechanism includes alteration of brain development soon after conception.[34] Abnormal migration of embryonic cells during fetal development may affect the final structure and connectivity of the brain, resulting in alterations in the neural circuits that control thought and behavior.[38] Several theories of mechanism are available; none is likely to provide a complete explanation.[39]

Functional magnetic resonance imaging provides some evidence for both underconnectivity and mirror neuron theories.[40][41]

The underconnectivity theory hypothesizes underfunctioning high-level neural connections and synchronization, along with an excess of low-level processes.[40] It maps well to general-processing theories such as weak central coherence theory, which hypothesizes that a limited ability to see the big picture underlies the central disturbance in ASD.[42] A related theory—enhanced perceptual functioning—focuses more on the superiority of locally oriented and perceptual operations in autistic individuals.[43]
The mirror neuron system (MNS) theory hypothesizes that alterations to the development of the MNS interfere with imitation and lead to Asperger's core feature of social impairment.[41][44] For example, one study found that activation is delayed in the core circuit for imitation in individuals with AS.[45] This theory maps well to social cognition theories like the theory of mind, which hypothesizes that autistic behavior arises from impairments in ascribing mental states to oneself and others,[46] or hyper-systemizing, which hypothesizes that autistic individuals can systematize internal operation to handle internal events but are less effective at empathizing by handling events generated by other agents.[47]

Other possible mechanisms include serotonin dysfunction[48] and cerebellar dysfunction.[49]

Screening
Parents of children with Asperger syndrome can typically trace differences in their children's development to as early as 30 months of age.[33] Developmental screening during a routine check-up by a general practitioner or pediatrician may identify signs that warrant further investigation.[1][9] The diagnosis of AS is complicated by the use of several different screening instruments,[9][28] including the Asperger Syndrome Diagnostic Scale (ASDS), Autism Spectrum Screening Questionnaire (ASSQ), Childhood Asperger Syndrome Test (CAST), Gilliam Asperger's Disorder Scale (GADS), Krug Asperger's Disorder Index (KADI),[50] and the Autism Spectrum Quotient (AQ; with versions for children,[51] adolescents[52] and adults[53]). None have been shown to reliably differentiate between AS and other ASDs.[1]

Diagnosis
Main article: Diagnosis of Asperger syndrome
Standard diagnostic criteria require impairment in social interaction, and repetitive and stereotyped patterns of behavior, activities and interests, without significant delay in language or cognitive development. Unlike the international standard,[11] U.S. criteria also require significant impairment in day-to-day functioning.[4] Other sets of diagnostic criteria have been proposed by Szatmari et al.[54] and by Gillberg and Gillberg.[55]

Diagnosis is most commonly made between the ages of four and eleven.[1] A comprehensive assessment involves a multidisciplinary team[2][9][56] that observes across multiple settings,[1] and includes neurological and genetic assessment as well as tests for cognition, psychomotor function, verbal and nonverbal strengths and weaknesses, style of learning, and skills for independent living.[9] The current "gold standard" in diagnosing ASDs combines clinical judgment with the Autism Diagnostic Interview-Revised (ADI-R)—a semistructured parent interview—and the Autism Diagnostic Observation Schedule (ADOS)—a conversation and play-based interview with the child.[7] Delayed or mistaken diagnosis can be traumatic for individuals and families; for example, misdiagnosis can lead to medications that worsen behavior.[56] Many children with AS are initially misdiagnosed with attention-deficit hyperactivity disorder (ADHD).[1] Diagnosing adults is more challenging, as standard diagnostic criteria are designed for children and the expression of AS changes with age;[57] adult diagnosis requires painstaking clinical examination and thorough medical history gained from both the individual and other people who know the person, focusing on childhood behavior.[58] Conditions that must be considered in a differential diagnosis include other ASDs, the schizophrenia spectrum, ADHD, obsessive compulsive disorder, major depressive disorder, semantic pragmatic disorder, nonverbal learning disorder,[56] Tourette syndrome,[22] stereotypic movement disorder and bipolar disorder.[33]

Underdiagnosis and overdiagnosis are problems in marginal cases. The cost of screening and diagnosis and the challenge of obtaining payment can inhibit or delay diagnosis. Conversely, the increasing popularity of drug treatment options and the expansion of benefits has motivated providers to overdiagnose ASD.[59] There are indications AS has been diagnosed more frequently in recent years, partly as a residual diagnosis for children of normal intelligence who do not have autism but have social difficulties.[60] In 2006, it was reported to be the fastest-growing psychiatric diagnosis in Silicon Valley children; also, there is a predilection for adults to self-diagnose it.[61] There are questions about the external validity of the AS diagnosis. That is, it is unclear whether there is a practical benefit in distinguishing AS from HFA and from PDD-NOS;[60] the same child can receive different diagnoses depending on the screening tool.[9] The debate about distinguishing AS from HFA is partly due to a tautological dilemma where disorders are defined based on severity of impairment, so that studies that appear to confirm differences based on severity are to be expected.[62]

Management
Further information: Autism therapies
Asperger syndrome treatment attempts to manage distressing symptoms and to teach age-appropriate social, communication and vocational skills that are not naturally acquired during development,[1] with intervention tailored to the needs of the individual child, based on multidisciplinary assessment.[63] Although progress has been made, data supporting the efficacy of particular interventions are limited.[1][64]

Therapies
The ideal treatment for AS coordinates therapies that address core symptoms of the disorder, including poor communication skills and obsessive or repetitive routines. While most professionals agree that the earlier the intervention, the better, there is no single best treatment package.[9] AS treatment resembles that of other high-functioning ASDs, except that it takes into account the linguistic capabilities, verbal strengths, and nonverbal vulnerabilities of individuals with AS.[1] A typical program generally includes:[9]

the training of social skills for more effective interpersonal interactions,[65]
cognitive behavioral therapy to improve stress management relating to anxiety or explosive emotions,[66] and to cut back on obsessive interests and repetitive routines,
medication, for coexisting conditions such as major depressive disorder and anxiety disorder,[67]
occupational or physical therapy to assist with poor sensory integration and motor coordination,
social communication intervention, which is specialized speech therapy to help with the pragmatics of the give and take of normal conversation,[68]
the training and support of parents, particularly in behavioral techniques to use in the home.
Of the many studies on behavior-based early intervention programs, most are case studies of up to five participants, and typically examine a few problem behaviors such as self-injury, aggression, noncompliance, stereotypies, or spontaneous language; unintended side effects are largely ignored.[69] Despite the popularity of social skills training, its effectiveness is not firmly established.[70] A randomized controlled study of a model for training parents in problem behaviors in their children with AS showed that parents attending a one-day workshop or six individual lessons reported fewer behavioral problems, while parents receiving the individual lessons reported less intense behavioral problems in their AS children.[71]
Vocational training is important to teach job interview etiquette and workplace behavior to older children and adults with AS, and organization software and personal data assistants to improve the work and life management of people with AS are useful.[1]

Medications
No medications directly treat the core symptoms of AS.[67] Although research into the efficacy of pharmaceutical intervention for AS is limited,[1] it is essential to diagnose and treat comorbid conditions.[2] Deficits in self-identifying emotions or in observing effects of one's behavior on others can make it difficult for individuals with AS to see why medication may be appropriate.[67] Medication can be effective in combination with behavioral interventions and environmental accommodations in treating comorbid symptoms such as anxiety disorder, major depressive disorder, inattention and aggression.[1] The atypical neuroleptic medications risperidone and olanzapine have been shown to reduce the associated symptoms of AS;[1] risperidone can reduce repetitive and self-injurious behaviors, aggressive outbursts and impulsivity, and improve stereotypical patterns of behavior and social relatedness. The selective serotonin reuptake inhibitors (SSRIs) fluoxetine, fluvoxamine and sertraline have been effective in treating restricted and repetitive interests and behaviors.[1][2][33]

Care must be taken with medications; abnormalities in metabolism, cardiac conduction times, and an increased risk of type 2 diabetes have been raised as concerns with these medications,[72][73] along with serious long-term neurological side effects.[69] SSRIs can lead to manifestations of behavioral activation such as increased impulsivity, aggression and sleep disturbance.[33] Weight gain and fatigue are commonly reported side effects of risperidone, which may also lead to increased risk for extrapyramidal symptoms such as restlessness and dystonia [33] and increased serum prolactin levels.[74] Sedation and weight gain are more common with olanzapine,[73] which has also been linked with diabetes.[72] Sedative side-effects in school-age children[75] have ramifications for classroom learning. Individuals with AS may be unable to identify and communicate their internal moods and emotions or to tolerate side effects that for most people would not be problematic.[76]

Prognosis
There is some evidence that as many as 20% of children with AS "grow out" of it, and fail to meet the diagnostic criteria as adults.[7] As of 2006, no studies addressing the long-term outcome of individuals with Asperger syndrome are available and there are no systematic long-term follow-up studies of children with AS.[8] Individuals with AS appear to have normal life expectancy but have an increased prevalence of comorbid psychiatric conditions such as major depressive disorder and anxiety disorder that may significantly affect prognosis. Although social impairment is lifelong, outcome is generally more positive than with individuals with lower functioning autism spectrum disorders;[1] for example, ASD symptoms are more likely to diminish with time in children with AS or HFA.[77] Although most students with AS/HFA have average mathematical ability and test slightly worse in mathematics than in general intelligence, some are gifted in mathematics[78] and AS has not prevented some adults from major accomplishments such as winning the Nobel Prize.[79]

Children with AS may require special education services because of their social and behavioral difficulties although many attend regular education classes.[8] Adolescents with AS may exhibit ongoing difficulty with self care, organization and disturbances in social and romantic relationships; despite high cognitive potential, most young adults with AS remain at home, although some do marry and work independently.[1] The "different-ness" adolescents experience can be traumatic.[80] Anxiety may stem from preoccupation over possible violations of routines and rituals, from being placed in a situation without a clear schedule or expectations, or from concern with failing in social encounters;[1] the resulting stress may manifest as inattention, withdrawal, reliance on obsessions, hyperactivity, or aggressive or oppositional behavior.[66] Depression is often the result of chronic frustration from repeated failure to engage others socially, and mood disorders requiring treatment may develop.[1] Clinical experience suggests the rate of suicide may be higher among those with AS, but this has not been confirmed by systematic empirical studies.[81]

Education of families is critical in developing strategies for understanding strengths and weaknesses;[2] helping the family to cope improves outcomes in children.[19] Prognosis may be improved by diagnosis at a younger age that allows for early interventions, while interventions in adulthood are valuable but less beneficial.[2] There are legal implications for individuals with AS as they run the risk of exploitation by others and may be unable to comprehend the societal implications of their actions.[2]

Epidemiology
Further information: Conditions comorbid to autism spectrum disorders
Prevalence estimates vary enormously. A 2003 review of epidemiological studies of children found prevalence rates ranging from 0.03 to 4.84 per 1,000, with the ratio of autism to Asperger syndrome ranging from 1.5:1 to 16:1;[82] combining the average ratio of 5:1 with a conservative prevalence estimate for autism of 1.3 per 1,000 suggests indirectly that the prevalence of AS might be around 0.26 per 1,000.[83] Part of the variance in estimates arises from differences in diagnostic criteria. For example, a relatively small 2007 study of 5,484 eight-year-old children in Finland found 2.9 children per 1,000 met the ICD-10 criteria for an AS diagnosis, 2.7 per 1,000 for Gillberg and Gillberg criteria, 2.5 for DSM-IV, 1.6 for Szatmari et al., and 4.3 per 1,000 for the union of the four criteria. Boys seem to be more likely to have AS than girls; estimates of the sex ratio range from 1.6:1 to 4:1, using the Gillberg and Gillberg criteria.[84]
Anxiety disorder and major depressive disorder are the most common conditions seen at the same time; comorbidity of these in persons with AS is estimated at 65%.[1] Depression is common in adolescents and adults; children are likely to present with ADHD.[85] Reports have associated AS with medical conditions such as aminoaciduria and ligamentous laxity, but these have been case reports or small studies and no factors have been associated with AS across studies.[1] One study of males with AS found an increased rate of epilepsy and a high rate (51%) of nonverbal learning disorder.[86] AS is associated with tics, Tourette syndrome, and bipolar disorder, and the repetitive behaviors of AS have many similarities with the symptoms of obsessive-compulsive disorder and obsessive-compulsive personality disorder.[87] Although many of these studies are based on psychiatric clinic samples without using standardized measures, it seems reasonable to conclude that comorbid conditions are relatively common.[7]

History
Main article: History of Asperger syndrome
Named after the Austrian pediatrician Hans Asperger (1906–80), Asperger syndrome is a relatively new diagnosis in the field of autism.[88] In 1944, Asperger described four children in his practice[2] who had difficulty in integrating themselves socially. The children lacked nonverbal communication skills, failed to demonstrate empathy with their peers, and were physically clumsy. Asperger called the condition "autistic psychopathy" and described it as primarily marked by social isolation.[9] Unlike today's AS, autistic psychopathy could be found in people of all levels of intelligence, including those with mental retardation.[89] In the context of the Nazi eugenics policy of sterilizing and killing social deviants and the mentally handicapped, Asperger passionately defended the value of autistic individuals, writing "We are convinced, then, that autistic people have their place in the organism of the social community. They fulfil their role well, perhaps better than anyone else could, and we are talking of people who as children had the greatest difficulties and caused untold worries to their care-givers."[6]

Asperger also called his young patients "little professors",[6] and believed some would be capable of exceptional achievement and original thought later in life.[2] His paper was published during wartime and in German, so it was not widely read elsewhere.

Lorna Wing popularized the term Asperger syndrome in the English-speaking medical community in her 1981 publication[90] of a series of case studies of children showing similar symptoms,[88] and Uta Frith translated Asperger's paper to English in 1991.[6] Sets of diagnostic criteria were outlined by Gillberg and Gillberg in 1989 and by Szatmari et al. in the same year.[84] AS became a standard diagnosis in 1992, when it was included in the tenth edition of the World Health Organization's diagnostic manual, International Classification of Diseases (ICD-10); in 1994, it was added to the fourth edition of the American Psychiatric Association's diagnostic reference, Diagnostic and Statistical Manual of Mental Disorders (DSM-IV).[9]

Hundreds of books, articles and websites now describe AS, and prevalence estimates have increased dramatically for ASD, with AS recognized as an important subgroup.[88] Whether it should be seen as distinct from high-functioning autism is a fundamental issue requiring further study,[2] and there are questions about the empirical validation of the DSM-IV and ICD-10 criteria.[8]

Cultural aspects
Further information: Sociological and cultural aspects of autism
People with Asperger syndrome may refer to themselves in casual conversation as aspies, coined by Liane Holliday Willey in 1999.[91] The word neurotypical (abbreviated NT) describes a person whose neurological development and state are typical, and is often used to refer to non-autistic people. The Internet has allowed individuals with AS to communicate and celebrate with each other in a way that was not previously possible because of their rarity and geographic dispersal. A subculture of aspies has formed. Internet sites like Wrong Planet have made it easier for individuals to connect.[10]

Autistic people have advocated a shift in perception of autism spectrum disorders as complex syndromes rather than diseases that must be cured. Proponents of this view reject the notion that there is an "ideal" brain configuration and that any deviation from the norm is pathological; they promote tolerance for what they call neurodiversity.[92] These views are the basis for the autistic rights and autistic pride movements.[93] There is a contrast between the attitude of adults with self-identified AS, who typically do not want to be cured and are proud of their identity, and parents of children with AS, who typically seek assistance and a cure for their children.[94]

Some researchers have argued that AS can be viewed as a different cognitive style, not a disorder or a disability.[10][95] In a 2002 paper, Simon Baron-Cohen wrote of those with AS, "In the social world there is no great benefit to a precise eye for detail, but in the worlds of math, computing, cataloguing, music, linguistics, engineering, and science, such an eye for detail can lead to success rather than failure." Baron-Cohen cited two reasons why it might still be useful to consider AS to be a disability: to ensure provision for legally required special support, and to recognize emotional difficulties from reduced empathy.[96] It has been argued that the genes for Asperger's combination of abilities have operated throughout recent human evolution and have made remarkable contributions to human history.[97]

Notes
^ a b c d e f g h i j k l m n o p q r s t u v w x y z aa ab ac ad ae af ag ah ai aj ak al am an ao ap McPartland J, Klin A (2006). "Asperger's syndrome". Adolesc Med Clin 17 (3): 771–88. doi:10.1016/j.admecli.2006.06.010 (inactive 2008-06-25). PMID 17030291.
^ a b c d e f g h i j k Baskin JH, Sperber M, Price BH (2006). "Asperger syndrome revisited". Rev Neurol Dis 3 (1): 1–7. PMID 16596080.
^ a b c d Kasari C, Rotheram-Fuller E (2005). "Current trends in psychological research on children with high-functioning autism and Asperger disorder". Curr Opin Psychiatry 18 (5): 497–501. doi:10.1097/01.yco.0000179486.47144.61. PMID 16639107.
^ a b c d e f American Psychiatric Association (2000). "Diagnostic criteria for 299.80 Asperger's Disorder (AD)". Diagnostic and Statistical Manual of Mental Disorders (4th, text revision (DSM-IV-TR) ed.). ISBN 0-89042-025-4.
^ a b Rausch JL, Johnson ME (2008). "Diagnosis of Asperger's disorder". in Rausch JL, Johnson ME, Casanova MF (eds.). Asperger's Disorder. Informa Healthcare. pp. 19–62. ISBN 0-8493-8360-9.
^ a b c d Asperger H; tr. and annot. Frith U (1991) [1944]. "'Autistic psychopathy' in childhood". in Frith U. Autism and Asperger syndrome. Cambridge University Press. pp. 37–92. ISBN 0-521-38608-X.
^ a b c d e Woodbury-Smith MR, Volkmar FR (2008). "Asperger syndrome". Eur Child Adolesc Psychiatry 18: 2. doi:10.1007/s00787-008-0701-0. PMID 18563474.
^ a b c d e f g h i j k l m n o Klin A (2006). "Autism and Asperger syndrome: an overview". Rev Bras Psiquiatr 28 (suppl 1): S3–S11. doi:10.1590/S1516-44462006000500002. PMID 16791390. http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1516-44462006000500002&lng=en&nrm=iso&tlng=en.
^ a b c d e f g h i j k l National Institute of Neurological Disorders and Stroke (NINDS) (2007-07-31). "Asperger syndrome fact sheet". http://www.ninds.nih.gov/disorders/asperger/detail_asperger.htm. Retrieved on 2007-08-24. NIH Publication No. 05-5624.
^ a b c Clarke J, van Amerom G (2007). "'Surplus suffering': differences between organizational understandings of Asperger's syndrome and those people who claim the 'disorder'". Disabil Soc 22 (7): 761–76. doi:10.1080/09687590701659618.
^ a b World Health Organization (2006). "F84. Pervasive developmental disorders". International Statistical Classification of Diseases and Related Health Problems (10th (ICD-10) ed.).
^ Piven J, Palmer P, Jacobi D, Childress D, Arndt S (1997). "Broader autism phenotype: evidence from a family history study of multiple-incidence autism families" (PDF). Am J Psychiatry 154 (2): 185–90. PMID 9016266. http://ajp.psychiatryonline.org/cgi/reprint/154/2/185.pdf.
^ Lord C, Cook EH, Leventhal BL, Amaral DG (2000). "Autism spectrum disorders". Neuron 28 (2): 355–63. doi:10.1016/S0896-6273(00)00115-X. PMID 11144346.
^ Witwer AN, Lecavalier L (2008). "Examining the validity of autism spectrum disorder subtypes". J Autism Dev Disord 38 (9): 1611–24. doi:10.1007/s10803-008-0541-2. PMID 18327636.
^ Sanders JL (2009). "Qualitative or quantitative differences between Asperger's Disorder and autism? historical considerations". J Autism Dev Disord. doi:10.1007/s10803-009-0798-0. PMID 19548078.
^ Szatmari P (2000). "The classification of autism, Asperger's syndrome, and pervasive developmental disorder". Can J Psychiatry 45 (8): 731–38. PMID 11086556. http://ww1.cpa-apc.org:8080/Publications/Archives/CJP/2000/Oct/Classification.asp.
^ First MB (2008). "Autism and Other Pervasive Developmental Disorders Conference (February 3–5, 2008)". American Psychiatric Association. http://psych.org/MainMenu/Research/DSMIV/DSMV/DSMRevisionActivities/ConferenceSummaries/AutismConference.aspx. Retrieved on 2008-10-29.
^ Allen D, Evans C, Hider A, Hawkins S, Peckett H, Morgan H (2008). "Offending behaviour in adults with Asperger syndrome". J Autism Dev Disord 38 (4): 748–58. doi:10.1007/s10803-007-0442-9. PMID 17805955.
^ a b Tsatsanis KD (2003). "Outcome research in Asperger syndrome and autism". Child Adolesc Psychiatr Clin N Am 12 (1): 47–63. doi:10.1016/S1056-4993(02)00056-1. PMID 12512398. http://www.childpsych.theclinics.com/article/PIIS1056499302000561/fulltext.
^ Newman SS, Ghaziuddin M (2008). "Violent crime in Asperger syndrome: the role of psychiatric comorbidity". J Autism Dev Disord 38 (10): 1848–52. doi:10.1007/s10803-008-0580-8. PMID 18449633.
^ South M, Ozonoff S, McMahon WM (2005). "Repetitive behavior profiles in Asperger syndrome and high-functioning autism". J Autism Dev Disord 35 (2): 145–58. doi:10.1007/s10803-004-1992-8. PMID 15909401.
^ a b Rapin I (2001). "Autism spectrum disorders: relevance to Tourette syndrome". Adv Neurol 85: 89–101. PMID 11530449.
^ Lyons V, Fitzgerald M (2004). "Humor in autism and Asperger syndrome". J Autism Dev Disord 34 (5): 521–31. doi:10.1007/s10803-004-2547-8. PMID 15628606.
^ Frith U (2004). "Emanuel Miller lecture: confusions and controversies about Asperger syndrome". J Child Psychol Psychiatry 45 (4): 672–86. doi:10.1111/j.1469-7610.2004.00262.x. PMID 15056300.
^ Prior M, Ozonoff S (2007). "Psychological factors in autism". in Volkmar FR. Autism and Pervasive Developmental Disorders (2nd ed.). Cambridge University Press. pp. 69–128. ISBN 0-521-54957-4.
^ Bogdashina O (2003). Sensory Perceptional Issues in Autism and Asperger Syndrome: Different Sensory Experiences, Different Perceptual Worlds. Jessica Kingsley. ISBN 1-843101-66-1.
^ Rogers SJ, Ozonoff S (2005). "Annotation: what do we know about sensory dysfunction in autism? A critical review of the empirical evidence". J Child Psychol Psychiatry 46 (12): 1255–68. doi:10.1111/j.1469-7610.2005.01431.x. PMID 16313426.
^ a b Ehlers S, Gillberg C (1993). "The epidemiology of Asperger's syndrome. A total population study". J Child Psychol Psychiat 34 (8): 1327–50. doi:10.1111/j.1469-7610.1993.tb02094.x. PMID 8294522.
^ Polimeni MA, Richdale AL, Francis AJ (2005). "A survey of sleep problems in autism, Asperger's disorder and typically developing children". J Intellect Disabil Res 49 (4): 260–8. doi:10.1111/j.1365-2788.2005.00642.x. PMID 15816813.
^ a b Tani P, Lindberg N, Joukamaa M et al. (2004). "Asperger syndrome, alexithymia and perception of sleep". Neuropsychobiology 49 (2): 64–70. doi:10.1159/000076412. PMID 14981336.
^ Alexithymia and AS:
Fitzgerald M, Bellgrove MA (2006). "The overlap between alexithymia and Asperger's syndrome". J Autism Dev Disord 36 (4): 573–6. doi:10.1007/s10803-006-0096-z. PMID 16755385.
Hill E, Berthoz S (2006). "Response". J Autism Dev Disord 36 (8): 1143–5. doi:10.1007/s10803-006-0287-7. PMID 17080269.
Lombardo MV, Barnes JL, Wheelwright SJ, Baron-Cohen S (2007). "Self-referential cognition and empathy in autism". PLoS ONE 2 (9): e883. doi:10.1371/journal.pone.0000883. PMID 17849012. http://www.plosone.org/article/fetchArticle.action?articleURI=info:doi/10.1371/journal.pone.0000883.
^ Epstein T, Saltzman-Benaiah J, O'Hare A, Goll JC, Tuck S (2008). "Associated features of Asperger Syndrome and their relationship to parenting stress". Child Care Health Dev 34 (4): 503–11. doi:10.1111/j.1365-2214.2008.00834.x. PMID 19154552.
^ a b c d e f Foster B, King BH (2003). "Asperger syndrome: to be or not to be?". Curr Opin Pediatr 15 (5): 491–4. doi:10.1097/00008480-200310000-00008. PMID 14508298.
^ a b Arndt TL, Stodgell CJ, Rodier PM (2005). "The teratology of autism". Int J Dev Neurosci 23 (2–3): 189–99. doi:10.1016/j.ijdevneu.2004.11.001. PMID 15749245.
^ Rutter M (2005). "Incidence of autism spectrum disorders: changes over time and their meaning". Acta Paediatr 94 (1): 2–15. doi:10.1080/08035250410023124. PMID 15858952.
^ Müller RA (2007). "The study of autism as a distributed disorder". Ment Retard Dev Disabil Res Rev 13 (1): 85–95. doi:10.1002/mrdd.20141. PMID 17326118.
^ Rinehart NJ, Bradshaw JL, Brereton AV, Tonge BJ (2002). "A clinical and neurobehavioural review of high-functioning autism and Asperger's disorder". Aust N Z J Psychiatry 36 (6): 762–70. doi:10.1046/j.1440-1614.2002.01097.x. PMID 12406118.
^ Berthier ML, Starkstein SE, Leiguarda R (1990). "Developmental cortical anomalies in Asperger's syndrome: neuroradiological findings in two patients". J Neuropsychiatry Clin Neurosci 2 (2): 197–201. PMID 2136076.
^ Happé F, Ronald A, Plomin R (2006). "Time to give up on a single explanation for autism". Nat Neurosci 9 (10): 1218–20. doi:10.1038/nn1770. PMID 17001340.
^ a b Just MA, Cherkassky VL, Keller TA, Kana RK, Minshew NJ (2007). "Functional and anatomical cortical underconnectivity in autism: evidence from an FMRI study of an executive function task and corpus callosum morphometry". Cereb Cortex 17 (4): 951–61. doi:10.1093/cercor/bhl006. PMID 16772313. http://cercor.oxfordjournals.org/cgi/content/full/17/4/951.
^ a b Iacoboni M, Dapretto M (2006). "The mirror neuron system and the consequences of its dysfunction". Nat Rev Neurosci 7 (12): 942–51. doi:10.1038/nrn2024. PMID 17115076.
^ Happé F, Frith U (2006). "The weak coherence account: detail-focused cognitive style in autism spectrum disorders". J Autism Dev Disord 36 (1): 5–25. doi:10.1007/s10803-005-0039-0. PMID 16450045.
^ Mottron L, Dawson M, Soulières I, Hubert B, Burack J (2006). "Enhanced perceptual functioning in autism: an update, and eight principles of autistic perception". J Autism Dev Disord 36 (1): 27–43. doi:10.1007/s10803-005-0040-7. PMID 16453071.
^ Ramachandran VS, Oberman LM (2006). "Broken mirrors: a theory of autism" (PDF). Sci Am 295 (5): 62–9. PMID 17076085. http://cbc.ucsd.edu/pdf/brokenmirrors_asd.pdf. Retrieved on 2009-02-13.
^ Nishitani N, Avikainen S, Hari R (2004). "Abnormal imitation-related cortical activation sequences in Asperger's syndrome". Ann Neurol 55 (4): 558–62. doi:10.1002/ana.20031. PMID 15048895.
^ Baron-Cohen S, Leslie AM, Frith U (1985). "Does the autistic child have a 'theory of mind'?" (PDF). Cognition 21 (1): 37–46. doi:10.1016/0010-0277(85)90022-8. PMID 2934210. http://ruccs.rutgers.edu/~aleslie/Baron-Cohen%20Leslie%20&%20Frith%201985.pdf. Retrieved on 2007-06-28.
^ Baron-Cohen S (2006). "The hyper-systemizing, assortative mating theory of autism" (PDF). Prog Neuropsychopharmacol Biol Psychiatry 30 (5): 865–72. doi:10.1016/j.pnpbp.2006.01.010. PMID 16519981. http://autismresearchcentre.com/docs/papers/2006_BC_Neuropsychophamacology.pdf. Retrieved on 2009-06-08.
^ Murphy DG, Daly E, Schmitz N et al. (2006). "Cortical serotonin 5-HT2A receptor binding and social communication in adults with Asperger's syndrome: an in vivo SPECT study". Am J Psychiatry 163 (5): 934–6. doi:10.1176/appi.ajp.163.5.934. PMID 16648340.
^ Gowen E, Miall RC (2005). "Behavioural aspects of cerebellar function in adults with Asperger syndrome". Cerebellum 4 (4): 279–89. doi:10.1080/14734220500355332. PMID 16321884.
^ Campbell JM (2005). "Diagnostic assessment of Asperger's disorder: a review of five third-party rating scales". J Autism Dev Disord 35 (1): 25–35. doi:10.1007/s10803-004-1028-4. PMID 15796119.
^ Auyeung B, Baron-Cohen S, Wheelwright S, Allison C (2008). "The Autism Spectrum Quotient: Children's Version (AQ-Child)" (PDF). J Autism Dev Disord 38 (7): 1230–40. doi:10.1007/s10803-007-0504-z. PMID 18064550. http://autismresearchcenter.com/docs/papers/2008_Auyeung_etal_ChildAQ.pdf. Retrieved on 2009-01-02.
^ Baron-Cohen S, Hoekstra RA, Knickmeyer R, Wheelwright S (2006). "The Autism-Spectrum Quotient (AQ)—adolescent version" (PDF). J Autism Dev Disord 36 (3): 343–50. doi:10.1007/s10803-006-0073-6. PMID 16552625. http://autismresearchcenter.com/docs/papers/2006_BC_Hoekstra_etal_AQ-adol.pdf. Retrieved on 2009-01-02.
^ Woodbury-Smith MR, Robinson J, Wheelwright S, Baron-Cohen S (2005). "Screening adults for Asperger Syndrome using the AQ: a preliminary study of its diagnostic validity in clinical practice" (PDF). J Autism Dev Disord 35 (3): 331–5. doi:10.1007/s10803-005-3300-7. PMID 16119474. http://autismresearchcentre.com/docs/papers/2005_Woodbury-Smith_etal_ScreeningAdultsForAS.pdf. Retrieved on 2009-01-02.
^ Szatmari P, Bremner R, Nagy J (1989). "Asperger's syndrome: a review of clinical features". Can J Psychiatry 34 (6): 554–60. PMID 2766209.
^ Gillberg IC, Gillberg C (1989). "Asperger syndrome—some epidemiological considerations: a research note". J Child Psychol Psychiatry 30 (4): 631–8. doi:10.1111/j.1469-7610.1989.tb00275.x. PMID 2670981.
^ a b c Fitzgerald M, Corvin A (2001). "Diagnosis and differential diagnosis of Asperger syndrome". Adv Psychiatric Treat 7 (4): 310–8. doi:10.1192/apt.7.4.310. http://apt.rcpsych.org/cgi/content/full/7/4/310.
^ Tantam D (2003). "The challenge of adolescents and adults with Asperger syndrome". Child Adolesc Psychiatr Clin N Am 12 (1): 143–63. doi:10.1016/S1056-4993(02)00053-6. PMID 12512403. http://www.childpsych.theclinics.com/article/PIIS1056499302000536/fulltext.
^ Roy M, Dillo W, Emrich HM, Ohlmeier MD (2009). "Asperger's syndrome in adulthood". Dtsch Arztebl Int 106 (5): 59–64. doi:10.3238/arztebl.2009.0059. PMID 19562011.
^ Shattuck PT, Grosse SD (2007). "Issues related to the diagnosis and treatment of autism spectrum disorders". Ment Retard Dev Disabil Res Rev 13 (2): 129–35. doi:10.1002/mrdd.20143. PMID 17563895.
^ a b Klin A, Volkmar FR (2003). "Asperger syndrome: diagnosis and external validity". Child Adolesc Psychiatr Clin N Am 12 (1): 1–13. doi:10.1016/S1056-4993(02)00052-4. PMID 12512395. http://www.childpsych.theclinics.com/article/PIIS1056499302000524/fulltext.
^ Markel H (2006-04-13). "The trouble with Asperger's syndrome". Medscape Today (WebMD).
^ Toth K, King BH (2008). "Asperger's syndrome: diagnosis and treatment". Am J Psychiatry 165 (8): 958–63. doi:10.1176/appi.ajp.2008.08020272. PMID 18676600.
^ Khouzam HR, El-Gabalawi F, Pirwani N, Priest F (2004). "Asperger's disorder: a review of its diagnosis and treatment". Compr Psychiatry 45 (3): 184–91. doi:10.1016/j.comppsych.2004.02.004. PMID 15124148.
^ Attwood T (2003). "Frameworks for behavioral interventions". Child Adolesc Psychiatr Clin N Am 12 (1): 65–86. doi:10.1016/S1056-4993(02)00054-8. PMID 12512399. http://www.childpsych.theclinics.com/article/PIIS1056499302000548/fulltext.
^ Krasny L, Williams BJ, Provencal S, Ozonoff S (2003). "Social skills interventions for the autism spectrum: essential ingredients and a model curriculum". Child Adolesc Psychiatr Clin N Am 12 (1): 107–22. doi:10.1016/S1056-4993(02)00051-2. PMID 12512401. http://www.childpsych.theclinics.com/article/PIIS1056499302000512/fulltext.
^ a b Myles BS (2003). "Behavioral forms of stress management for individuals with Asperger syndrome". Child Adolesc Psychiatr Clin N Am 12 (1): 123–41. doi:10.1016/S1056-4993(02)00048-2. PMID 12512402. http://www.childpsych.theclinics.com/article/PIIS1056499302000482/fulltext.
^ a b c Towbin KE (2003). "Strategies for pharmacologic treatment of high functioning autism and Asperger syndrome". Child Adolesc Psychiatr Clin N Am 12 (1): 23–45. doi:10.1016/S1056-4993(02)00049-4. PMID 12512397. http://www.childpsych.theclinics.com/article/PIIS1056499302000494/fulltext.
^ Paul R (2003). "Promoting social communication in high functioning individuals with autistic spectrum disorders". Child Adolesc Psychiatr Clin N Am 12 (1): 87–106. doi:10.1016/S1056-4993(02)00047-0. PMID 12512400. http://www.childpsych.theclinics.com/article/PIIS1056499302000470/fulltext.
^ a b Matson JL (2007). "Determining treatment outcome in early intervention programs for autism spectrum disorders: a critical analysis of measurement issues in learning based interventions". Res Dev Disabil 28 (2): 207–18. doi:10.1016/j.ridd.2005.07.006. PMID 16682171.
^ Rao PA, Beidel DC, Murray MJ (2008). "Social skills interventions for children with Asperger's syndrome or high-functioning autism: a review and recommendations". J Autism Dev Disord 38 (2): 353–61. doi:10.1007/s10803-007-0402-4. PMID 17641962.
^ Sofronoff K, Leslie A, Brown W (2004). "Parent management training and Asperger syndrome: a randomized controlled trial to evaluate a parent based intervention". Autism 8 (3): 301–17. doi:10.1177/1362361304045215. PMID 15358872.
^ a b Newcomer JW (2007). "Antipsychotic medications: metabolic and cardiovascular risk". J Clin Psychiatry 68 (suppl 4): 8–13. PMID 17539694.
^ a b Chavez B, Chavez-Brown M, Sopko MA, Rey JA (2007). "Atypical antipsychotics in children with pervasive developmental disorders". Pediatr Drugs 9 (4): 249–66. doi:10.2165/00148581-200709040-00006. PMID 17705564.
^ Staller J (2006). "The effect of long-term antipsychotic treatment on prolactin". J Child Adolesc Psychopharmacol 16 (3): 317–26. doi:10.1089/cap.2006.16.317. PMID 16768639.
^ Stachnik JM, Nunn-Thompson C (2007). "Use of atypical antipsychotics in the treatment of autistic disorder". Ann Pharmacother 41 (4): 626–34. doi:10.1345/aph.1H527. PMID 17389666.
^ Blacher J, Kraemer B, Schalow M (2003). "Asperger syndrome and high functioning autism: research concerns and emerging foci". Curr Opin Psychiatry 16 (5): 535–542. doi:10.1097/00001504-200309000-00008.
^ Coplan J, Jawad AF (2005). "Modeling clinical outcome of children with autistic spectrum disorders". Pediatrics 116 (1): 117–22. doi:10.1542/peds.2004-1118. PMID 15995041. http://pediatrics.aappublications.org/cgi/content/full/116/1/117. Lay summary – press release (2005-07-05).
^ Chiang HM, Lin YH (2007). "Mathematical ability of students with Asperger syndrome and high-functioning autism" (PDF). Autism 11 (6): 547–56. doi:10.1177/1362361307083259. PMID 17947290. http://aut.sagepub.com/cgi/reprint/11/6/547. Retrieved on 2009-03-06.
^ Herera S (2005-02-25). "Mild autism has 'selective advantages'". CNBC. http://www.msnbc.msn.com/id/7030731/. Retrieved on 2007-11-14.
^ Moran M (06 Oct 2006). "Asperger's may be answer to diagnostic mysteries". Psychiatr News 41 (19): 21. http://pn.psychiatryonline.org/cgi/content/full/41/19/21.
^ Gillberg C (2008). "Asperger syndrome—mortality and morbidity". in Rausch JL, Johnson ME, Casanova MF (eds.). Asperger's Disorder. Informa Healthcare. pp. 63–80. ISBN 0-8493-8360-9.
^ Fombonne E, Tidmarsh L (2003). "Epidemiologic data on Asperger disorder". Child Adolesc Psychiatr Clin N Am 12 (1): 15–21. doi:10.1016/S1056-4993(02)00050-0. PMID 12512396. http://www.childpsych.theclinics.com/article/PIIS1056499302000500/fulltext.
^ Fombonne E (2007). "Epidemiological surveys of pervasive developmental disorders". in Volkmar FR. Autism and Pervasive Developmental Disorders (2nd ed.). Cambridge University Press. pp. 33–68. ISBN 0-521-54957-4.
^ a b Mattila ML, Kielinen M, Jussila K et al. (2007). "An epidemiological and diagnostic study of Asperger syndrome according to four sets of diagnostic criteria". J Am Acad Child Adolesc Psychiatry 46 (5): 636–46. doi:10.1097/chi.0b013e318033ff42. PMID 17450055.
^ Ghaziuddin M, Weidmer-Mikhail E, Ghaziuddin N (1998). "Comorbidity of Asperger syndrome: a preliminary report". J Intellect Disabil Res 42 (4): 279–83. PMID 9786442.
^ Cederlund M, Gillberg C (2004). "One hundred males with Asperger syndrome: a clinical study of background and associated factors". Dev Med Child Neurol 46 (10): 652–60. doi:10.1017/S0012162204001100. PMID 15473168.
^ Gillberg C, Billstedt E (2000). "Autism and Asperger syndrome: coexistence with other clinical disorders". Acta Psychiatr Scand 102 (5): 321–30. doi:10.1034/j.1600-0447.2000.102005321.x. PMID 11098802.
^ a b c Baron-Cohen S, Klin A (2006). "What's so special about Asperger Syndrome?" (PDF). Brain Cogn 61 (1): 1–4. doi:10.1016/j.bandc.2006.02.002. PMID 16563588. http://www.elsevier.com/authored_subject_sections/S05/S05_360/pdf/klin.pdf.
^ Wing L (1991). "The relationship between Asperger's syndrome and Kanner's autism". in Frith U. Autism and Asperger syndrome. Cambridge University Press. pp. 93–121. ISBN 0-521-38608-X.
^ Wing L (1981). "Asperger's syndrome: a clinical account". Psychol Med 11 (1): 115–29. doi:10.1017/S0033291700053332. PMID 7208735. http://www.mugsy.org/wing2.htm. Retrieved on 2007-08-15.
^ Willey LH (1999). Pretending to be Normal: Living with Asperger's Syndrome. Jessica Kingsley. ISBN 1-85302-749-9.
^ Williams CC (2005). "In search of an Asperger". in Stoddart KP. Children, Youth and Adults with Asperger Syndrome: Integrating Multiple Perspectives. Jessica Kingsley. pp. 242–52. ISBN 1-84310-319-2. "The life prospects of people with AS would change if we shifted from viewing AS as a set of dysfunctions, to viewing it as a set of differences that have merit."
^ Dakin CJ (2005). "Life on the outside: A personal perspective of Asperger syndrome". in Stoddart KP. Children, Youth and Adults with Asperger Syndrome: Integrating Multiple Perspectives. Jessica Kingsley. pp. 352–61. ISBN 1-84310-319-2.
^ Clarke J, van Amerom G (2008). "Asperger's syndrome: differences between parents' understanding and those diagnosed". Soc Work Health Care 46 (3): 85–106. doi:10.1300/J010v46n03_05. PMID 18551831.
^ Molloy H, Vasil L (2002). "The social construction of Asperger Syndrome: the pathologising of difference?". Disabil Soc 17 (6): 659–69. doi:10.1080/0968759022000010434.
^ Baron-Cohen S (2002). "Is Asperger syndrome necessarily viewed as a disability?". Focus Autism Other Dev Disabl 17 (3): 186–91. doi:10.1177/10883576020170030801. A preliminary, freely readable draft is in: Baron-Cohen S (2002). "Is Asperger's syndrome necessarily a disability?" (PDF). Cambridge: Autism Research Centre. http://autismresearchcentre.com/docs/papers/2002_BC_ASDisability.pdf. Retrieved on 2008-12-02.
^ Baron-Cohen S (2008). "The evolution of brain mechanisms for social behavior". in Crawford C, Krebs D (eds.). Foundations of Evolutionary Psychology. Lawrence Erlbaum. pp. 415–32. ISBN 0-8058-5957-8.

External links
Pervasive Developmental Disorders portal
Asperger's Syndrome at the Open Directory Project

To view information on another disease, click on Digestive Diseases Library

Depression Medications

2007-08-12T17:14:00.000-07:00

Selective Serotonin Reuptake Inhibitors
Selective serotonin reuptake inhibitor (SSRI) medications affect the levels of serotonin in the brain. For many people, these medications are the first choice to treat depression. Examples of these medications are fluoxetine (Prozac, Prozac Weekly, Sarafem), sertraline (Zoloft), paroxetine (Paxil, Paxil CR), escitalopram (Lexapro), fluvoxamine, and citalopram (Celexa).

How do SSRIs work?
The antidepressant action of SSRIs is not thoroughly understood but is possibly due to the ability of SSRIs to block the uptake of serotonin, thereby providing higher levels of serotonin at the brain receptor site.

Who should not use these medications?
Individuals who are allergic to SSRIs
Individuals who are currently taking, or have taken within the past 2 weeks, thioridazine (Mellaril), pimozide (Orap), or monoamine oxidase inhibitors (MAOIs) such as phenelzine (Nardil) and tranylcypromine (Parnate)
Individuals must not take MAOIs or thioridazine for at least 5 weeks after stopping SSRIs.Use
SSRIs may be administered as oral tablets, capsules, or liquid once or twice a day.

Prozac Weekly is administered once each week.
Do not discontinue these medications abruptly, but gradually taper use to avoid withdrawal-like symptoms such as agitation, anxiety, confusion, dizziness, headache, and insomnia.

Elderly individuals typically require lower doses of SSRIs.Children: Fluoxetine (Prozac) is the only SSRI approved by the FDA for treatment of depression in children aged 8-18 years.
Drug or food interactions: Tell the doctor what medications are currently being taken because many medicines interact with SSRIs. Do not take any nonprescription or herbal medications without first consulting the doctor or pharmacist. The following are examples of interactions, but they do not represent a complete list.

When an SSRI is administered with 5-HT1 agonists, such as sumatriptan or zolmitriptan, weakness and incoordination, although rare, have been reported.

SSRIs may increase the blood levels and risk of toxicity of certain medications, including the following:

Highly protein-bound medicines such as warfarin (Coumadin) and digoxin
Antiarrhythmic medicines such as propafenone (Rythmol) or flecainide (Tambocor)
Beta blockers such as propranolol (Inderal) or metoprolol (Lopressor, Toprol XL)
Tricyclic antidepressants such as amitriptyline (Elavil)
Benzodiazepines such as alprazolam (Xanax), diazepam (Valium), midazolam (Versed), or
triazolam (Halcion)
Carbamazepine (Tegretol)
Cisapride (Propulsid)
Clozapine (Clozaril)
Cyclosporine (Neoral, Sandimmune)
Haloperidol (Haldol)
Thioridazine (Mellaril)
Phenytoin (Dilantin)
Pimozide (Orap)
Theophylline (Theo-Dur, TheoBid)

The following substances may increase toxicity of SSRIs:

Alcohol or other drugs that depress the central nervous system
Diuretics (water pills)
MAOIs (may cause serious, and sometimes fatal, reactions)
St. John’s wort
Decongestants such as pseudoephedrine (Sudafed)
Lithium
Sibutramine (Meridia)
Zolpidem (Ambien) or other medications used for insomnia

Side Effects: This is NOT a complete list of side effects reported with SSRIs. A doctor, health care provider, or pharmacist can discuss a more complete list of side effects.

Photosensitivity (increased risk of sunburn) (Use protective clothing, such as long sleeves and hats, and sunscreen to decrease the risk of sunburn.)
Rash
Nausea
Dry mouth
Constipation
Low blood sodium levels (in people who are dehydrated or taking diuretics)
Low blood sugar levels
Drowsiness (Caution is advised when operating machinery, driving, or performing other tasks that require alertness.)
Sexual dysfunction such as delayed ejaculation, erectile difficulties, and impotence (in men) and difficulty reaching climax or orgasm (in women)
Withdrawal-like symptoms in newborns (Women who take SSRIs in late pregnancy [third trimester] may have newborns who require prolonged hospitalization due to withdrawal-like symptoms such as shortness of breath, constant crying, feeding difficulty, or low blood sugar levels.)
Manic episodes in persons with bipolar disorder (If not combined with a mood-stabilizing medication, SSRIs may induce manic episodes in individuals with bipolar disorder [manic depression].)
Kidney or liver impairment precautions (The doctor may draw blood samples to check for kidney or liver impairment before prescribing SSRIs.)

Tricyclic Antidepressants
Tricyclic antidepressants (TCAs) are often prescribed in severe cases of depression or when SSRI medications do not work. Tricyclic antidepressants include:

amitriptyline (Elavil),
amoxapine (Asendin),
desipramine (Norpramin),
doxepin (Adapin, Sinequan, Zonalon),
imipramine (Tofranil),
nortriptyline (Aventyl, Pamelor),
protriptyline (Vivactil), and
trimipramine (Surmontil).

How do TCAs work? TCAs block the uptake of serotonin and norepinephrine, thereby providing higher levels of these neurotransmitters at the brain receptor site. Besides increasing norepinephrine and serotonin, amoxapine also increases the neurotransmitter dopamine.

Who should not use these medications?
Individuals who have allergic reactions to TCAs
Individuals in the acute recovery phase following a heart attack
Individuals with glaucoma
Individuals with urine retention
Individuals who are currently taking or have taken MAOIs within the past 2 weeks (Phenelzine [Nardil], and tranylcypromine [Parnate], are examples of MAOIs.) (Do not start taking MAOIs for at least 2 weeks after stopping TCAs. This is a general warning; see drug and food interactions for low-dose use together.)
Individuals taking some medications that alter heart rhythm such as thioridazine (Mellaril) or cisapride (Propulsid)Use

Tricyclic antidepressants are taken orally by tablet, capsule, or oral solution.
Elderly individuals and adolescents often require lower doses.Elderly: Elderly individuals require lower doses. Elderly individuals are more susceptible to sedative effects and may feel faint when standing up, therefore increasing the risk of falls and injuries.

Children: The following TCAs are approved in the United States for treating adolescents with depression who are older than 12 years:

Amitriptyline
Desipramine
Doxepin
Nortriptyline
Protriptyline
Trimipramine
Amoxapine (approved for persons older than 16 years)

Drug or food interactions: Tell the doctor what medications are currently being taken because many medicines interact with TCAs. Do not take any nonprescription or herbal medications without first consulting the doctor or pharmacist. The following are examples of interactions, but they do not represent a complete list.

TCAs may increase the blood levels and/or risk of toxicity of the following medications:

MAOIs (These may cause serious and sometimes fatal reactions; some TCAs have been used safely with MAOIs, but the dose of TCAs must be increased very slowly and the person must strictly adhere to MAOI dietary restrictions.)
Sympathomimetics such as pseudoephedrine (Sudafed)
The following substances may increase the toxicity of TCAs:
Alcohol or other drugs that depress the central nervous system such as medications taken for insomnia
Medications, such as antihistamines (Benadryl), that may produce similar side effects
Antifungal medications such as ketoconazole (Nizoral) or fluconazole (Diflucan)
SSRIs, venlafaxine, and nefazodone (may increase risk for serotonin syndrome—symptoms include hypertension, fever, muscle tremor, or confusion)
Tramadol (Ultram) (may increase risk of seizures)
Medications such as cisapride, thioridazine, quinidine, antihistamines, erythromycin, dofetilide, and pimozide that also increase the risk for abnormal heart rhythm
Valproic acid
Other interactions include the following:

TCAs may decrease the ability for clonidine to lower blood pressure levels.
Carbamazepine may decrease TCA effectiveness.
St. John’s wort may decrease TCA effectiveness and increase the risk of serotonin syndrome.

Side Effects: This is NOT a complete list of possible side effects reported with TCAs. A doctor, health care provider, or pharmacist can discuss a more complete list of side effects.

Confusion, agitation, or hallucinations (Contact a doctor immediately if these occur.)
Severe diarrhea, fever, sweating, muscle stiffness, or tremors (These may be symptoms of neuroleptic malignant syndrome. Contact a doctor immediately.)
Rapid or abnormal heartbeat or fainting (Contact a doctor immediately if these occur.)
Changes in sexual interest or ability
Manic episodes in persons with bipolar disorder (If not combined with a mood-stabilizing medication, SSRIs may induce manic episodes in individuals with bipolar disorder [manic depression].)
Drowsiness (Caution is advised when operating machinery, driving, or performing other tasks that require alertness.)
Photosensitivity (increased risk of sunburn) (Use protective clothing, such as long sleeves and hats, and sunscreen to decrease the risk of sunburn.)
Rash
Nausea
Dry mouth
Urine retention
Blurred vision
Constipation
Lightheadedness when standing up from a sitting or lying position (Stand up gradually from lying down or sitting positions.)
Seizures (TCAs lower the threshold for seizures, that is, seizures may occur more easily in the person taking TCAs. Caution is advised for individuals prone to seizures or those who have a history of seizures.)

Monoamine Oxidase Inhibitors
Monoamine oxidase inhibitors (MAOIs) include:

isocarboxazid (Marplan),
phenelzine (Nardil), and
tranylcypromine (Parnate).

These medications are rarely used because of strict dietary requirements and life-threatening drug and food interactions. Because of these drug and food interactions, MAOIs may not be taken with many other types of medicines, and some foods that are high in tyramine, dopamine, or tryptophan must be avoided as well.

How do MAOIs work? These drugs inhibit monoamine oxidase. Monoamine oxidase is an enzyme in the body that is responsible for metabolizing (breaking down) neurotransmitters such as norepinephrine, epinephrine, dopamine, and serotonin. The result of MAOIs is an increase in the concentration of neurotransmitters. Some of these neurotransmitters increase blood pressure.

Who should not use these medications? In many circumstances, the use of MAOIs is dangerous.

Individuals who are allergic to MAOIs
Individuals with diseases, such as pheochromocytoma or hypertension, that cause increased blood pressure
Individuals with diseases, such as heart failure or other heart disease, severe impaired renal function, and stroke or other cerebrovascular disease, in which increased blood pressure is likely to aggravate the condition
Individuals with a history of headache
Individuals with liver disease
Individuals using other drugs that may elevate blood pressure or cause additive effects (see drug interactions)
Individuals consuming foods with high tyramine content—MAOIs may lead to dangerously elevated blood pressure (see food interactions)

Use

MAOIs are administered orally.
MAOIs are rarely the first antidepressant drug prescribed, but they are an option when initial treatments do not work or are not tolerated.
MAOIs are not a good choice for elderly or debilitated individuals.
Children: Phenelzine is not approved for children younger than 16 years. Tranylcypromine is not approved for children or adolescents.

Drug or food interactions: Tell the doctor what medications are currently being taken because many drugs interact with MAOIs. Do not take any nonprescription or herbal medications without first consulting the doctor or pharmacist. The following are examples of interactions, but they do not represent a complete list.

The risk for serotonin syndrome may be increased by SSRIs, TCAs, atomoxetine (Strattera), duloxetine, dextromethorphan (in many cough syrups), dexfenfluramine, 5-HT1 agonists (such as sumatriptan or zolmitriptan), venlafaxine (Effexor), St. John’s wort, or ginkgo. Serotonin syndrome is a serious side effect and may be fatal. Symptoms include fever, muscle stiffness, and changes in mental status such as confusion or hallucinations.
The risk of neuroleptic malignant syndrome (restlessness, sweating, fever, confusion, and muscle stiffness) may increase with lithium and tramadol (Ultram).
Morphine, meperidine (Demerol), and other narcotic pain relievers may cause hypotension and depress the central nervous system and respirations.
The following drugs may increase the risk of hypertensive crisis when taken with MAOIs or within 2 weeks of stopping MAOIs:

Decongestants such as pseudoephedrine (Sudafed)
Stimulants such as
amphetamine, cocaine, methamphetamine, or ephedrine (ma huang, ephedra)
Cyclobenzaprine (Flexeril)
Dopamine, methyldopa (Aldomet), or levodopa (Sinemet)
Epinephrine (EpiPen)
Methylphenidate (Ritalin) or Adderall
Buspirone

MAOIs may increase side effects of the following drugs:

Bupropion
- Increases risk of seizures, agitation, and psychotic changes
Antidiabetic agents - Increases risk for low blood sugar levels, depression, and seizures
Mirtazapine - May increase risk for seizures
Carbamazepine - May result in high blood pressure, fever, and seizures

Do not eat foods high in tyramine, dopamine, or tryptophan while taking MAOIs or for 2 weeks after discontinuing MAOIs. Tyramine, dopamine, and tryptophan are chemicals that can interact with MAOIs and cause hypertensive crisis, which is an extremely dangerous side effect. Foods high in these chemicals should be avoided. They include the following:

Dairy products Cheese, particularly Blue, Camembert, Cheddar, Emmenthaler,
Stilton, and Swiss, which contain very high amounts of tyramine, Yogurt
Meat and fish products

o Anchovies
o Beef or chicken liver
o Other meats or fish that have not been refrigerated, are fermented, or are spoiled
o Caviar
o Fermented
o sausages such as bologna, pepperoni, salami, and summer sausage
o Game meat
o Meats prepared with tenderizer
o Herring
o Shrimp paste

Alcoholic beverages

Beer
Red wine, especially Chianti
Sherry
Distilled spirits and
liqueurs
Fruits and vegetables
Fruits such as bananas, raspberries, dried fruits, and overripe fruits (especially avocados and figs)
Bean cure, miso soup, sauerkraut, soy sauce, and yeast extracts (such as Marmite)
Foods containing other chemicals that increase blood pressure
Broad beans (fava beans)
Caffeine containing beverages such as coffee, tea, and cola
Chocolate
Ginseng

Side Effects: This is NOT a complete list of side effects reported with MAOIs. A doctor, health care provider, or pharmacist can discuss a more complete list of side effects.

Hypertensive crisis (Hypertensive crisis is the most serious reaction and involves dramatic increases in blood pressure and requires immediate care from the doctor. The hypertensive crisis usually occurs within several hours after ingestion of a drug or food that interacts with MAOIs. Hypertensive crisis can be fatal. Symptoms include severe headache, rapid heart rate, chest pain, neck stiffness, nausea, vomiting, sweating [may include a fever or cold, clammy skin], dilated pupils, and eye sensitivity to light.)
Manic episodes in persons with bipolar disorder (If not combined with a mood-stabilizing drug, MAOIs may induce manic episodes in individuals with bipolar disorder [manic depression].)
Increased heart rate or blood pressure in people with hyperthyroid conditions

For information on another disease, click on Digestive Diseases Library

Digestive Diseases Library