Asperger syndrome

Page semi-protected
From Wikipedia, the free encyclopedia

This is an old revision of this page, as edited by Jeremy68 (talk | contribs) at 20:12, 21 June 2012 (→‎Characteristics). The present address (URL) is a permanent link to this revision, which may differ significantly from the current revision.

Asperger syndrome
SpecialtyPsychiatry Edit this on Wikidata

Asperger syndrome (AS), also known as Asperger's syndrome or Asperger disorder, is an autism spectrum disorder (ASD) that is characterized by significant difficulties in social interaction, alongside restricted and repetitive patterns of behavior and interests. It differs from other autism spectrum disorders by its relative preservation of linguistic and cognitive development. Although not required for diagnosis, physical clumsiness and atypical use of language are frequently reported.[1][2]

The syndrome is named after the Austrian pediatrician Hans Asperger who, in 1944, studied and described children in his practice who lacked nonverbal communication skills, demonstrated limited empathy with their peers, and were physically clumsy.[3] The modern conception of Asperger syndrome came into existence in 1981[4] and went through a period of popularization,[5][6] becoming standardized as a diagnosis in the early 1990s. Many questions remain about aspects of the disorder.[7] For example, there is doubt about whether it is distinct from high-functioning autism (HFA);[8] partly because of this, its prevalence is not firmly established.[1] It has been proposed that the diagnosis of Asperger's be eliminated, to be replaced by a diagnosis of autism spectrum disorder on a severity scale.[9]

The exact cause is unknown. Although research suggests the likelihood of a genetic basis,[1] there is no known genetic etiology[10][11] and 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.[12] Most children improve as they mature to adulthood, but social and communication difficulties may persist.[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.[13][14]

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.[15] ASD, in turn, is a subset of the broader autism phenotype, which describes individuals who may not have ASD but do have autistic-like traits, such as social deficits.[16] 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.[17]

The extent of the overlap between AS and high-functioning autism (HFA—autism unaccompanied by mental retardation) is unclear.[8][18][19] The current ASD classification is to some extent an artifact of how autism was discovered,[20] and may not reflect the true nature of the spectrum;[21] methodological problems have beset Asperger syndrome as a valid diagnosis from the outset.[22][23] One of the proposed changes to the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5), to be published in May 2013,[24] would eliminate Asperger syndrome as a separate diagnosis, and fold it under autistic disorder (autism spectrum disorder), which would be rated on a severity scale.[9] Like the diagnosis of Asperger syndrome,[25] the proposed change is controversial,[26] and it has been argued that the syndrome's diagnostic criteria should be broadened.[25]

Asperger syndrome is also called Asperger's syndrome (AS),[1] Asperger (or Asperger's) disorder (AD),[18][27] or just Asperger's.[28] 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.[27] 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]

People with AS may not be as withdrawn around others as those with other, more debilitating, forms of autism; they approach others, even if awkwardly. For example, a person with AS may engage in a one-sided, long-winded speech about a favorite topic, while misunderstanding or not recognizing the listener's feelings or reactions, such as a 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] However, not all individuals with AS will approach others. Some of them may even display selective mutism, speaking not at all to most people and excessively to specific people. Some may choose to talk only to people they like.[29]

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 observations of social interaction into rigid behavioral guidelines, and apply these rules in awkward ways, such as forced eye contact, resulting in a demeanor that appears rigid or socially naive. Childhood desire for companionship can become numbed through a history of failed social encounters.[1]

The hypothesis that individuals with AS are predisposed to violent or criminal behavior has been investigated but is not supported by data.[1][30] More evidence suggests children with AS are victims rather than victimizers.[31] A 2008 review found that an overwhelming number of reported violent criminals with AS had coexisting psychiatric disorders such as schizoaffective disorder.[32]

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.[27]

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 weather data or star names, without necessarily having a 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.[33] They include hand movements such as flapping or twisting, and complex whole-body movements.[27] 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.[34]

According to the Adult Asperger Assessment (AAA) diagnostic test, a lack of interest in fiction and a positive preference towards non-fiction is common among adults with AS.[35]

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] Echolalia has also been observed in individuals with AS.[36]

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.[18] 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.[37]

Other

Individuals with Asperger syndrome may have signs or symptoms that are independent of the diagnosis, but can affect the individual or the family.[38] These include differences in perception and problems with motor skills, sleep, and emotions.

Individuals with AS often have excellent auditory and visual perception.[39] 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.[40] 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, and other stimuli;[41] 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.[42]

Hans Asperger's initial accounts[1] and other diagnostic schemes[43] 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.[44][45] AS is also associated with high levels of alexithymia, which is difficulty in identifying and describing one's emotions.[46] Although AS, lower sleep quality, and alexithymia are associated, their causal relationship is unclear.[45]

As with other forms of ASD, parents of children with AS have higher levels of stress.[47]

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 children with AS.[1][48] 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).[12] 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.[12]

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.[49] Many environmental factors have been hypothesized to act after birth, but none has been confirmed by scientific investigation.[50]

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.[51] 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 ASDs.[52] Neuroanatomical studies and the associations with teratogens strongly suggest that the mechanism includes alteration of brain development soon after conception.[49] 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.[53] Several theories of mechanism are available; none are likely to provide a complete explanation.[54]

Monochrome fMRI image of a horizontal cross-section of a human brain. A few regions, mostly to the rear, are highlighted in orange and yellow.
Functional magnetic resonance imaging provides some evidence for both underconnectivity and mirror neuron theories.[55][56]

The underconnectivity theory hypothesizes underfunctioning high-level neural connections and synchronization, along with an excess of low-level processes.[55] 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.[57] A related theory—enhanced perceptual functioning—focuses more on the superiority of locally oriented and perceptual operations in autistic individuals.[58]

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.[56][59] For example, one study found that activation is delayed in the core circuit for imitation in individuals with AS.[60] 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,[61] 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.[62]

Other possible mechanisms include serotonin dysfunction[63] and cerebellar dysfunction.[64]

Screening

Parents of children with Asperger syndrome can typically trace differences in their children's development to as early as 30 months of age.[48] Developmental screening during a routine check-up by a general practitioner or pediatrician may identify signs that warrant further investigation.[1][12] The diagnosis of AS is complicated by the use of several different screening instruments,[12][43] 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),[65] and the Autism Spectrum Quotient (AQ; with versions for children,[66] adolescents[67] and adults[68]). 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,[15] U.S. criteria also require significant impairment in day-to-day functioning.[27] Other sets of diagnostic criteria have been proposed by Szatmari et al.[69] and by Gillberg and Gillberg.[70]

Diagnosis is most commonly made between the ages of four and eleven.[1] A comprehensive assessment involves a multidisciplinary team[2][12][71] 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.[12] The "gold standard" in diagnosing ASDs combines clinical judgment with the Autism Diagnostic Interview-Revised (ADI-R)—a semistructured parent interview—and the Autism Diagnostic Observation Schedule (ADOS)—a conversation and play-based interview with the child.[7]

Delayed or mistaken diagnosis can be traumatic for individuals and families, and misdiagnosis can lead to the use of medications that worsen behavior.[71][72] For example, many children with AS are initially misdiagnosed with attention-deficit hyperactivity disorder (ADHD).[1]

Because the standard diagnostic criteria are designed for children and because the expression of AS changes with age, diagnosing adults is more challenging[73]. Because of these differences in presentation, adult diagnosis requires painstaking clinical examination and thorough medical history, gained from both the individual and other people who know the person, and focusing on childhood behavior.[35] 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,[71] Tourette syndrome,[34] stereotypic movement disorder, and bipolar disorder.[48]

Underdiagnosis and overdiagnosis are problems in marginal cases, and cost and difficulty of screening and assessment can delay diagnosis. Conversely, the increasing popularity of drug treatment options and the expansion of benefits has motivated providers to overdiagnose ASD.[74] 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 do have social difficulties.[75] In 2006, it was reported to be the fastest-growing psychiatric diagnosis in Silicon Valley children, and there may also be a predilection for adults to self-diagnose it.[76]

Questions have also been raised about the external validity of the AS diagnosis, and whether there is practical benefit in distinguishing AS from HFA or from PDD-NOS.[75] Thus, the same child may receive different diagnoses depending on the screening tool used.[12] 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.[77]

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 based on multidisciplinary assessment.[78] Although progress has been made, data supporting the efficacy of particular interventions are limited.[1][79]

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.[12] 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:[12]

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.[84] Despite the popularity of social skills training, its effectiveness is not firmly established.[85] 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.[86] Vocational training is important to teach job interview etiquette and workplace behavior to older children and adults with AS, and organization software and personal data assistants can improve the work and life management of people with AS.[1]

Medications

No medications directly treat the core symptoms of AS.[82] 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.[82] 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 antipsychotic 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][48]

Care must be taken with medications, as side effects may be more common and harder to evaluate in individuals with AS, and tests of drugs' effectiveness against comorbid conditions routinely exclude individuals from the autism spectrum.[82] Abnormalities in metabolism, cardiac conduction times, and an increased risk of type 2 diabetes have been raised as concerns with these medications,[87][88] along with serious long-term neurological side effects.[84] SSRIs can lead to manifestations of behavioral activation such as increased impulsivity, aggression, and sleep disturbance.[48] 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[48] and increased serum prolactin levels.[89] Sedation and weight gain are more common with olanzapine,[88] which has also been linked with diabetes.[87] Sedative side-effects in school-age children[90] 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.[91]

Prognosis

There is some evidence that children with AS may see a lessening of symptoms; up to 20% of children may no longer meet the diagnostic criteria as adults, although social and communication difficulties may persist.[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.[1][7] Although social impairment is lifelong, the 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.[92] 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[93] and AS has not prevented some adults from major accomplishments such as winning the Nobel Prize.[94]

Although many attend regular education classes, some children with AS may utilize special education services because of their social and behavioral difficulties.[8] Adolescents with AS may exhibit ongoing difficulty with self care or organization, and disturbances in social and romantic relationships. Despite high cognitive potential, most young adults with AS remain at home, although some do marry and work independently.[1] The "different-ness" adolescents experience can be traumatic.[95] 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.[81] 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.[96]

Education of families is critical in developing strategies for understanding strengths and weaknesses;[2] helping the family to cope improves outcomes in children.[31] 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 autism prevalence rates ranging from 0.03 to 4.84 per 1,000, with the ratio of autism to Asperger syndrome ranging from 1.5:1 to 16:1;[97] combining the geometric mean ratio of 5:1 with a conservative prevalence estimate for autism of 1.3 per 1,000 suggests indirectly that the prevalence of AS might be around 0.26 per 1,000.[98] 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.[99]

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.[unreliable medical source?][25] 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.[100] 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.[101] However many of these studies are based on clinical samples or lack standardized measures; nonetheless, comorbid conditions are relatively common.[7]

History

Main article: History of Asperger syndrome

Named after the Austrian pediatrician Hans Asperger (1906–1980), Asperger syndrome is a relatively new diagnosis in the field of autism.[102] As a child, Asperger appears to have exhibited some features of the very condition named after him, such as remoteness and talent in language.[103][104] 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.[12] Fifty years later, several standardizations of AS as a diagnosis were tentatively proposed, many of which diverge significantly from Asperger's original work.[105]

Unlike today's AS, autistic psychopathy could be found in people of all levels of intelligence, including those with mental retardation.[106] In the context of the Nazi eugenics policy of sterilizing and killing social deviants and the mentally handicapped, Asperger passionately defended the value of autistic individuals, writing "We are convinced, then, that autistic people have their place in the organism of the social community. They fulfill their role well, perhaps better than anyone else could, and we are talking of people who as children had the greatest difficulties and caused untold worries to their care-givers."[3] Asperger also called his young patients "little professors",[3] 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[107] of a series of case studies of children showing similar symptoms,[102] and Uta Frith translated Asperger's paper to English in 1991.[3] Sets of diagnostic criteria were outlined by Gillberg and Gillberg in 1989 and by Szatmari et al. in the same year.[99] 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).[12]

Hundreds of books, articles and websites now describe AS, and prevalence estimates have increased dramatically for ASD, with AS recognized as an important subgroup.[102] 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 identifying with Asperger syndrome may refer to themselves in casual conversation as aspies (a term first used in print by Liane Holliday Willey in 1999).[108] The word neurotypical (abbreviated NT) describes a person whose neurological development and state are typical, and is often used to refer to non-autistic people. The Internet has allowed individuals with AS to communicate and celebrate diversity with each other in a way that was not previously possible because of their rarity and geographic dispersal. A subculture of aspies has formed. Internet sites like Wrong Planet have made it easier for individuals to connect.[13]

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.[109] These views are the basis for the autistic rights and autistic pride movements.[110] 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.[111]

Some researchers have argued that AS can be viewed as a different cognitive style, not a disorder or a disability,[13] and that it should be removed from the standard Diagnostic and Statistical Manual, much as homosexuality was removed.[112] In a 2002 paper, Simon Baron-Cohen wrote of those with AS, "In the social world, there is no great benefit to a precise eye for detail, but in the worlds of maths, computing, 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.[14] 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.[113]

References

  1. ^ 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 aq ar McPartland J, Klin A (2006). "Asperger's syndrome". Adolesc Med Clin. 17 (3): 771–88. doi:10.1016/j.admecli.2006.06.010. PMID 17030291.
  2. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  3. ^ a b c d Asperger H; tr. and annot. Frith U (1991) [1944]. "'Autistic psychopathy' in childhood". In Frith U (ed.). Autism and Asperger syndrome. Cambridge University Press. pp. 37–92. ISBN 0-521-38608-X.{{cite book}}: CS1 maint: multiple names: authors list (link)
  4. ^ Klin A, Pauls D, Schultz R, Volkmar F (2005). "Three diagnostic approaches to Asperger syndrome: Implications for research". J of Autism and Dev Dis. 35 (2): 221–34. doi:10.1007/s10803-004-2001-y. PMID 15909408.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  5. ^ Wing L (1998). "The history of Asperger syndrome". Asperger syndrome or high-functioning autism?. New York: Plenum press. pp. 11–25. ISBN 0-306-45746-6. {{cite book}}: Unknown parameter |editors= ignored (|editor= suggested) (help)
  6. ^ Woodbury-Smith M, Klin A, Volkmar F (2005). "Asperger's Syndrome: A Comparison of Clinical Diagnoses and Those Made According to the ICD-10 and DSM-IV". J of Autism and Dev Disord. 35 (2): 235–240. doi:10.1007/s10803-004-2002-x. PMID 15909409.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  7. ^ a b c d e f Woodbury-Smith MR, Volkmar FR (2009). "Asperger syndrome". Eur Child Adolesc Psychiatry. 18 (1): 2–11. doi:10.1007/s00787-008-0701-0. PMID 18563474. {{cite journal}}: Unknown parameter |month= ignored (help)
  8. ^ 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.
  9. ^ a b "299.80 Asperger's Disorder". DSM-5 Development. American Psychiatric Association. Archived from the original on 25 December 2010. Retrieved 2010-12-21. {{cite web}}: Unknown parameter |deadurl= ignored (|url-status= suggested) (help)
  10. ^ Matson JL, Minshawi NF (2006). "Etiology and prevalence". Early intervention for autism spectrum disorders: a critical analysis. Amsterdam: Elsevier Science. p. 33. ISBN 0-08-044675-2.
  11. ^ Klauck SM (2006). "Genetics of autism spectrum disorder" (PDF). Eur J of Hum Genet. 14 (6): 714–720. doi:10.1038/sj.ejhg.5201610.
  12. ^ 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". Archived from the original on 21 August 2007. Retrieved 2007-08-24. {{cite web}}: Unknown parameter |deadurl= ignored (|url-status= suggested) (help) NIH Publication No. 05-5624.
  13. ^ 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.
  14. ^ a b 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, with slightly different wording in the quoted text, is in: Baron-Cohen S (2002). "Is Asperger's syndrome necessarily a disability?" (PDF). Cambridge: Autism Research Centre. Archived from the original (PDF) on 17 December 2008. Retrieved 2008-12-02. {{cite web}}: Unknown parameter |deadurl= ignored (|url-status= suggested) (help)
  15. ^ a b World Health Organization (2006). "F84. Pervasive developmental disorders". International Statistical Classification of Diseases and Related Health Problems (10th (ICD-10) ed.). ISBN 92-4-154419-8. {{cite book}}: |access-date= requires |url= (help); External link in |chapterurl= (help); Unknown parameter |chapterurl= ignored (|chapter-url= suggested) (help)
  16. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  17. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  18. ^ a b c 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.
  19. ^ 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.
  20. ^ Sanders JL (2009). "Qualitative or quantitative differences between Asperger's Disorder and autism? historical considerations". J Autism Dev Disord. 39 (11): 1560–7. doi:10.1007/s10803-009-0798-0. PMID 19548078.
  21. ^ Szatmari P (2000). "The classification of autism, Asperger's syndrome, and pervasive developmental disorder". Can J Psychiatry. 45 (8): 731–38. PMID 11086556.
  22. ^ Matson JL, Minshawi NF (2006). "History and development of autism spectrum disorders". Early intervention for autism spectrum disorders: a critical analysis. Amsterdam: Elsevier Science. p. 21. ISBN 0-08-044675-2.
  23. ^ Schopler E (1998). "Premature popularization of Asperger syndrome". Asperger syndrome or high-functioning autism?. New York: Plenum press. pp. 388–90. ISBN 0-306-45746-6. {{cite book}}: Unknown parameter |editors= ignored (|editor= suggested) (help)
  24. ^ "DSM-5 development". American Psychiatric Association. 2010. Archived from the original on 13 February 2010. Retrieved 2010-02-20. {{cite web}}: Unknown parameter |deadurl= ignored (|url-status= suggested) (help)
  25. ^ a b c Ghaziuddin M (2010). "Should the DSM V drop Asperger syndrome?". J Autism Dev Disord. 40 (9): 1146–8. doi:10.1007/s10803-010-0969-z. PMID 20151184. Cite error: The named reference "Ghaziuddin" was defined multiple times with different content (see the help page).
  26. ^ Faras H, Al Ateeqi N, Tidmarsh L (2010). "Autism spectrum disorders". Ann Saudi Med. 30 (4): 295–300. doi:10.4103/0256-4947.65261. PMC 2931781. PMID 20622347.{{cite journal}}: CS1 maint: multiple names: authors list (link) CS1 maint: unflagged free DOI (link)
  27. ^ a b c d e 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. {{cite book}}: |access-date= requires |url= (help); External link in |chapterurl= (help); Unknown parameter |chapterurl= ignored (|chapter-url= suggested) (help)
  28. ^ Rausch JL, Johnson ME (2008). "Diagnosis of Asperger's disorder". In Rausch JL, Johnson ME, Casanova MF (eds.) (ed.). Asperger's Disorder. Informa Healthcare. pp. 19–62. ISBN 0-8493-8360-9. {{cite book}}: |editor= has generic name (help)CS1 maint: multiple names: editors list (link)
  29. ^ Brasic JR (2010-07-07). "Asperger's Syndrome". Medscape eMedicine. Retrieved 2010-11-25.
  30. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  31. ^ 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.
  32. ^ 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.
  33. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  34. ^ a b Rapin I (2001). "Autism spectrum disorders: relevance to Tourette syndrome". Adv Neurol. 85: 89–101. PMID 11530449.
  35. ^ a b 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. PMC 2695286. PMID 19562011.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  36. ^ Frith U (1996). "Social communication and its disorder in autism and Asperger syndrome". J. Psychopharmacol. (Oxford). 10 (1): 48–53. doi:10.1177/026988119601000108. PMID 22302727. {{cite journal}}: Unknown parameter |month= ignored (help)
  37. ^ 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.
  38. ^ Filipek PA; Accardo PJ; Baranek GT; et al. (1999). "The screening and diagnosis of autistic spectrum disorders". J Autism Dev Disord. 29 (6): 439–84. doi:10.1023/A:1021943802493. PMID 10638459. {{cite journal}}: Unknown parameter |author-separator= ignored (help)
  39. ^ 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.
  40. ^ Prior M, Ozonoff S (2007). "Psychological factors in autism". In Volkmar FR (ed.). Autism and Pervasive Developmental Disorders (2nd ed.). Cambridge University Press. pp. 69–128. ISBN 0-521-54957-4.
  41. ^ Bogdashina O (2003). Sensory Perceptional Issues in Autism and Asperger Syndrome: Different Sensory Experiences, Different Perceptual Worlds. Jessica Kingsley. ISBN 1-84310-166-1.
  42. ^ 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.
  43. ^ 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.
  44. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  45. ^ 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. {{cite journal}}: Unknown parameter |author-separator= ignored (help)
  46. ^ Alexithymia and AS:
  47. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  48. ^ 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.
  49. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  50. ^ Rutter M (2005). "Incidence of autism spectrum disorders: changes over time and their meaning". Acta Paediatr. 94 (1): 2–15. doi:10.1111/j.1651-2227.2005.tb01779.x. PMID 15858952.
  51. ^ 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. PMC 3315379. PMID 17326118.
  52. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  53. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  54. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  55. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  56. ^ 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.
  57. ^ 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.
  58. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  59. ^ Ramachandran VS, Oberman LM (2006). "Broken mirrors: a theory of autism" (PDF). Sci Am. 295 (5): 62–9. doi:10.1038/scientificamerican1106-62. PMID 17076085. Archived from the original (PDF) on 5 February 2009. Retrieved 2009-02-13. {{cite journal}}: Unknown parameter |deadurl= ignored (|url-status= suggested) (help)
  60. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  61. ^ 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. Archived from the original (PDF) on 28 June 2007. Retrieved 2007-06-28. {{cite journal}}: Unknown parameter |deadurl= ignored (|url-status= suggested) (help)CS1 maint: multiple names: authors list (link)
  62. ^ 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. Retrieved 2009-06-08.
  63. ^ 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. {{cite journal}}: Unknown parameter |author-separator= ignored (help)
  64. ^ 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.
  65. ^ 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.
  66. ^ 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. Archived from the original (PDF) on 5 February 2009. Retrieved 2009-01-02. {{cite journal}}: Unknown parameter |deadurl= ignored (|url-status= suggested) (help)CS1 maint: multiple names: authors list (link)
  67. ^ 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. Archived from the original (PDF) on 5 February 2009. Retrieved 2009-01-02. {{cite journal}}: Unknown parameter |deadurl= ignored (|url-status= suggested) (help)CS1 maint: multiple names: authors list (link)
  68. ^ 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. Archived from the original (PDF) on 17 December 2008. Retrieved 2009-01-02. {{cite journal}}: Unknown parameter |deadurl= ignored (|url-status= suggested) (help)CS1 maint: multiple names: authors list (link)
  69. ^ Szatmari P, Bremner R, Nagy J (1989). "Asperger's syndrome: a review of clinical features". Can J Psychiatry. 34 (6): 554–60. PMID 2766209.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  70. ^ 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.
  71. ^ 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.
  72. ^ Leskovec TJ, Rowles BM, Findling RL (2008). "Pharmacological treatment options for autism spectrum disorders in children and adolescents". Harv Rev Psychiatry. 16 (2): 97–112. doi:10.1080/10673220802075852. PMID 18415882.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  73. ^ 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.
  74. ^ 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.
  75. ^ 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.
  76. ^ Markel H (2006-04-13). "The trouble with Asperger's syndrome". Medscape Today. WebMD.
  77. ^ 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.
  78. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  79. ^ 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.
  80. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  81. ^ 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.
  82. ^ a b c d 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.
  83. ^ 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.
  84. ^ 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.
  85. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  86. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  87. ^ a b Newcomer JW (2007). "Antipsychotic medications: metabolic and cardiovascular risk". J Clin Psychiatry. 68 (suppl 4): 8–13. PMID 17539694.
  88. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  89. ^ 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.
  90. ^ 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.
  91. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  92. ^ 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. {{cite journal}}: Unknown parameter |laydate= ignored (help); Unknown parameter |laysource= ignored (help); Unknown parameter |laysummary= ignored (help)
  93. ^ Chiang HM, Lin YH (2007). "Mathematical ability of students with Asperger syndrome and high-functioning autism". Autism. 11 (6): 547–56. doi:10.1177/1362361307083259. PMID 17947290. Archived from the original (PDF) on 7 April 2009. Retrieved 2009-03-06. {{cite journal}}: Unknown parameter |deadurl= ignored (|url-status= suggested) (help)
  94. ^ Herera S (2005-02-25). "Mild autism has 'selective advantages'". CNBC. Archived from the original on 1 November 2007. Retrieved 2007-11-14. {{cite news}}: Unknown parameter |deadurl= ignored (|url-status= suggested) (help)
  95. ^ Moran M (2006). "Asperger's may be answer to diagnostic mysteries". Psychiatr News. 41 (19): 21.
  96. ^ Gillberg C (2008). "Asperger syndrome—mortality and morbidity". In Rausch JL, Johnson ME, Casanova MF (eds.) (ed.). Asperger's Disorder. Informa Healthcare. pp. 63–80. ISBN 0-8493-8360-9. {{cite book}}: |editor= has generic name (help)CS1 maint: multiple names: editors list (link)
  97. ^ 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.
  98. ^ Fombonne E (2007). "Epidemiological surveys of pervasive developmental disorders". In Volkmar FR (ed.). Autism and Pervasive Developmental Disorders (2nd ed.). Cambridge University Press. pp. 33–68. ISBN 0-521-54957-4.
  99. ^ 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. {{cite journal}}: Unknown parameter |author-separator= ignored (help)
  100. ^ 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:10.1111/j.1469-8749.2004.tb00977.x. PMID 15473168.
  101. ^ 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.
  102. ^ 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.
  103. ^ Lyons V, Fitzgerald M (2007). "Did Hans Asperger (1906–1980) have Asperger Syndrome?". J Autism Dev Disord. 37 (10): 2020–1. doi:10.1007/s10803-007-0382-4. PMID 17917805.
  104. ^ Osborne L (2002). American Normal: The Hidden World of Asperger Syndrome. Copernicus. p. 19. ISBN 0-387-95307-8.
  105. ^ Hippler K, Klicpera C (2003). "A retrospective analysis of the clinical case records of 'autistic psychopaths' diagnosed by Hans Asperger and his team at the University Children's Hospital, Vienna". Philos. Trans. R. Soc. Lond., B, Biol. Sci. 358 (1430): 291–301. doi:10.1098/rstb.2002.1197. PMC 1693115. PMID 12639327. {{cite journal}}: Unknown parameter |month= ignored (help)
  106. ^ Wing L (1991). "The relationship between Asperger's syndrome and Kanner's autism". In Frith U (ed.). Autism and Asperger syndrome. Cambridge University Press. pp. 93–121. ISBN 0-521-38608-X.
  107. ^ Wing L (1981). "Asperger's syndrome: a clinical account". Psychol Med. 11 (1): 115–29. doi:10.1017/S0033291700053332. PMID 7208735. Archived from the original on 17 August 2007. Retrieved 2007-08-15. {{cite journal}}: Unknown parameter |deadurl= ignored (|url-status= suggested) (help)
  108. ^ Willey LH (1999). Pretending to be Normal: Living with Asperger's Syndrome. Jessica Kingsley. pp. 71, 104. ISBN 1-85302-749-9.
  109. ^ Williams CC (2005). "In search of an Asperger". In Stoddart KP (ed.). 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.
  110. ^ Dakin CJ (2005). "Life on the outside: A personal perspective of Asperger syndrome". In Stoddart KP (ed.). Children, Youth and Adults with Asperger Syndrome: Integrating Multiple Perspectives. Jessica Kingsley. pp. 352–61. ISBN 1-84310-319-2.
  111. ^ 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.
  112. ^ Allred S (2009). "Reframing Asperger syndrome: lessons from other challenges to the Diagnostic and Statistical Manual and ICIDH approaches". Disabil Soc. 24 (3): 343–55. doi:10.1080/09687590902789511.
  113. ^ Baron-Cohen S (2008). "The evolution of brain mechanisms for social behavior". In Crawford C, Krebs D (eds.) (ed.). Foundations of Evolutionary Psychology. Lawrence Erlbaum. pp. 415–32. ISBN 0-8058-5957-8. {{cite book}}: |editor= has generic name (help)

External links

Template:Link FA Template:Link FA Template:Link GA Template:Link GA

Retrieved from "https://en.wikipedia.org/w/index.php?title=Asperger_syndrome&oldid=498719912"