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    <title>Autism</title>
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      <timestamp>2009-10-21T01:19:35Z</timestamp>
      <contributor>
        <username>Eubulides</username>
        <id>3573537</id>
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      <comment>
<p>Revert recent changes touting dextromethorphan. The cited source, Woodward <i>et al.</i> 2007 (PMID 17175572), said it didn't work.</p></comment>
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<p><b>Autism</b> is a <a href="Neurodevelopmental_disorder" title="Neurodevelopmental disorder">disorder of neural development</a> that is characterized by impaired <a href="Social_interaction" title="social interaction">social interaction</a> and <a href="Communication" title="communication">communication</a>, and by restricted and repetitive behavior. These signs all begin before a child is three years old.<sup id="_ref-DSM-IV-TR-299.00_a" class="reference"><a href="#_note-DSM-IV-TR-299.00" title="">[1]</a></sup> Autism involves many parts of the <a href="Human_brain" title="Human brain">brain</a>; how this occurs is not well understood.<sup id="_ref-Amaral_a" class="reference"><a href="#_note-Amaral" title="">[2]</a></sup> The two other <a href="Autism_spectrum_disorder" title="autism spectrum disorder">autism spectrum disorders</a> (ASD) are <a href="Asperger_syndrome" title="Asperger syndrome">Asperger syndrome</a>, which lacks delays in cognitive development and language, and <a href="PDD-NOS" title="PDD-NOS">PDD-NOS</a>, diagnosed when full criteria for the other two disorders are not met.<sup id="_ref-Johnson_a" class="reference"><a href="#_note-Johnson" title="">[3]</a></sup></p>
<p>Autism has a strong genetic basis, although the <a href="Heritability_of_autism" title="Heritability of autism">genetics of autism</a> are complex and it is unclear whether ASD is explained more by rare <a href="Mutation" title="mutation">mutations</a>, or by rare combinations of common genetic variants.<sup id="_ref-Abrahams_a" class="reference"><a href="#_note-Abrahams" title="">[4]</a></sup> In rare cases, autism is strongly associated with <a href="Teratology" title="Teratology">agents that cause birth defects</a>.<sup id="_ref-Arndt_a" class="reference"><a href="#_note-Arndt" title="">[5]</a></sup> <a href="Controversies_in_autism" title="Controversies in autism">Controversies</a> surround other proposed environmental <a href="Causes_of_autism" title="Causes of autism">causes</a>, such as <a href="Heavy_metal_(chemistry)" title="Heavy metal (chemistry)">heavy metals</a>, <a href="Pesticide" title="pesticide">pesticides</a> or childhood <a href="Vaccine" title="vaccine">vaccines</a>;<sup id="_ref-Rutter_a" class="reference"><a href="#_note-Rutter" title="">[6]</a></sup> the vaccine hypotheses are biologically implausible and lack convincing scientific evidence.<sup id="_ref-vaccines_a" class="reference"><a href="#_note-vaccines" title="">[7]</a></sup> The <a href="Prevalence" title="prevalence">prevalence</a> of autism is about 1–2 per 1,000 people; the prevalence of ASD is about 6 per 1,000, with about four times as many males as females. The number of people known to have autism has increased dramatically since the 1980s, partly due to changes in diagnostic practice; the question of whether actual prevalence has increased is unresolved.<sup id="_ref-Newschaffer_a" class="reference"><a href="#_note-Newschaffer" title="">[8]</a></sup></p>
<p>Parents usually notice signs in the first two years of their child's life.<sup id="_ref-CCD_a" class="reference"><a href="#_note-CCD" title="">[9]</a></sup> The signs usually develop gradually, but some autistic children first develop more normally and then <a href="Regressive_autism" title="Regressive autism">regress</a>.<sup id="_ref-Stefanatos_a" class="reference"><a href="#_note-Stefanatos" title="">[10]</a></sup> Although early behavioral or cognitive intervention can help autistic children gain self-care, social, and communication skills, there is no known cure.<sup id="_ref-CCD_b" class="reference"><a href="#_note-CCD" title="">[9]</a></sup> Not many children with autism live independently after reaching adulthood, though some become successful.<sup id="_ref-Howlin_a" class="reference"><a href="#_note-Howlin" title="">[11]</a></sup> An <a href="Sociological_and_cultural_aspects_of_autism" title="Sociological and cultural aspects of autism">autistic culture</a> has developed, with some individuals seeking a cure and others believing autism should be tolerated as a difference and not treated as a disorder.<sup id="_ref-Silverman_a" class="reference"><a href="#_note-Silverman" title="">[12]</a></sup></p>
<table id="toc" class="toc" summary="Contents">
<tr>
<td>
<div id="toctitle">
<h2>Contents</h2>
</div>
<ul>
<ul>
<li class="toclevel-1"><a href="#Characteristics">Characteristics</a>
</li>
<ul>
<li class="toclevel-2"><a href="#Social_development">Social development</a>
</li>
<li class="toclevel-2"><a href="#Communication">Communication</a>
</li>
<li class="toclevel-2"><a href="#Repetitive_behavior">Repetitive behavior</a>
</li>
<li class="toclevel-2"><a href="#Other_symptoms">Other symptoms</a>
</li>
</ul>
<li class="toclevel-1"><a href="#Classification">Classification</a>
</li>
<li class="toclevel-1"><a href="#Causes">Causes</a>
</li>
<li class="toclevel-1"><a href="#Mechanism">Mechanism</a>
</li>
<ul>
<li class="toclevel-2"><a href="#Pathophysiology">Pathophysiology</a>
</li>
<li class="toclevel-2"><a href="#Neuropsychology">Neuropsychology</a>
</li>
</ul>
<li class="toclevel-1"><a href="#Screening">Screening</a>
</li>
<li class="toclevel-1"><a href="#Diagnosis">Diagnosis</a>
</li>
<li class="toclevel-1"><a href="#Management">Management</a>
</li>
<li class="toclevel-1"><a href="#Prognosis">Prognosis</a>
</li>
<li class="toclevel-1"><a href="#Epidemiology">Epidemiology</a>
</li>
<li class="toclevel-1"><a href="#History">History</a>
</li>
<li class="toclevel-1"><a href="#References">References</a>
</li>
<li class="toclevel-1"><a href="#External_links">External links</a>
</li>
</ul>
</ul></td></tr></table><hr/>
<a id="Characteristics" name="Characteristics"/><h2>Characteristics</h2>
<p>Autism is a highly variable <a href="Neurodevelopmental_disorder" title="neurodevelopmental disorder">neurodevelopmental disorder</a><sup id="_ref-Geschwind_a" class="reference"><a href="#_note-Geschwind" title="">[13]</a></sup> that first appears during infancy or childhood, and generally follows a steady course without <a href="Remission_(medicine)" title="Remission (medicine)">remission</a>.<sup id="_ref-ICD-10-F84.0_a" class="reference"><a href="#_note-ICD-10-F84.0" title="">[14]</a></sup> Overt symptoms gradually begin after the age of six months, become established by age two or three years,<sup id="_ref-15" class="reference"><a href="#_note-15" title="">[15]</a></sup> and tend to continue through adulthood, although often in more muted form.<sup id="_ref-Rapin_a" class="reference"><a href="#_note-Rapin" title="">[16]</a></sup> It is distinguished not by a single symptom, but by a characteristic triad of symptoms: impairments in social interaction; impairments in communication; and restricted interests and repetitive behavior. Other aspects, such as atypical eating, are also common but are not essential for diagnosis.<sup id="_ref-Filipek_a" class="reference"><a href="#_note-Filipek" title="">[17]</a></sup> Autism's individual symptoms occur in the general population and appear not to associate highly, without a sharp line separating pathologically severe from common traits.<sup id="_ref-London_a" class="reference"><a href="#_note-London" title="">[18]</a></sup></p>
<a id="Social_development" name="Social_development"/><h3>Social development</h3>
<p>Social deficits distinguish autism and the related <a href="Autism_spectrum_disorder" title="autism spectrum disorder">autism spectrum disorders</a> (ASD; see <i><a href="#Classification" title="">Classification</a></i>) from other developmental disorders.<sup id="_ref-Rapin_b" class="reference"><a href="#_note-Rapin" title="">[16]</a></sup> People with autism have social impairments and often lack the intuition about others that many people take for granted. Noted autistic <a href="Temple_Grandin" title="Temple Grandin">Temple Grandin</a> described her inability to understand the <a href="Social_communication" title="social communication">social communication</a> of <a href="Neurotypical" title="neurotypical">neurotypicals</a>, or people with normal <a href="Neural_development" title="neural development">neural development</a>, as leaving her feeling "like an anthropologist on Mars".<sup id="_ref-19" class="reference"><a href="#_note-19" title="">[19]</a></sup></p>
<p>Unusual social development becomes apparent early in childhood. Autistic infants show less attention to social stimuli, smile and look at others less often, and respond less to their own name. Autistic toddlers differ more strikingly from <a href="Social_norms" title="social norms">social norms</a>; for example, they have less <a href="Eye_contact" title="eye contact">eye contact</a> and turn taking, and are more likely to communicate by manipulating another person's hand.<sup id="_ref-Volkmar_a" class="reference"><a href="#_note-Volkmar" title="">[20]</a></sup> Three- to five-year-old autistic children are less likely to exhibit social understanding, approach others spontaneously, imitate and respond to emotions, communicate nonverbally, and take turns with others. However, they do form <a href="Attachment_(psychology)" title="Attachment (psychology)">attachments</a> to their primary caregivers.<sup id="_ref-21" class="reference"><a href="#_note-21" title="">[21]</a></sup> Most autistic children display moderately less <a href="Attachment_in_children#Secure_attachment" title="Attachment in children">attachment security</a> than non-autistic children, although this difference disappears in children with higher mental development or less severe ASD.<sup id="_ref-22" class="reference"><a href="#_note-22" title="">[22]</a></sup> Older children and adults with ASD perform worse on tests of face and emotion recognition.<sup id="_ref-Sigman_a" class="reference"><a href="#_note-Sigman" title="">[23]</a></sup></p>
<p>Contrary to common beliefs, autistic children do not prefer being alone. Making and maintaining friendships often proves to be difficult for those with autism. For them, the quality of friendships, not the number of friends, predicts how lonely they feel. Functional friendships, such as those resulting in invitations to parties, may affect their quality of life more deeply.<sup id="_ref-Burgess_a" class="reference"><a href="#_note-Burgess" title="">[24]</a></sup></p>
<p>There are many anecdotal reports, but few systematic studies, of aggression and violence in individuals with ASD. The limited data suggest that, in children with mental retardation, autism is associated with aggression, destruction of property, and tantrums. A 2007 study interviewed parents of 67 children with ASD and reported that about two-thirds of the children had periods of severe tantrums and about one-third had a history of aggression, with tantrums significantly more common than in non-autistic children with language impairments.<sup id="_ref-Dominick_a" class="reference"><a href="#_note-Dominick" title="">[25]</a></sup> A 2008 Swedish study found that, of individuals aged 15 or older discharged from hospital with a diagnosis of ASD, those who committed violent crimes were significantly more likely to have other psychopathological conditions such as <a href="Psychosis" title="psychosis">psychosis</a>.<sup id="_ref-26" class="reference"><a href="#_note-26" title="">[26]</a></sup></p>
<a id="Communication" name="Communication"/><h3>Communication</h3>
<p>About a third to a half of individuals with autism do not develop enough natural speech to meet their daily communication needs.<sup id="_ref-27" class="reference"><a href="#_note-27" title="">[27]</a></sup> Differences in communication may be present from the first year of life, and may include delayed onset of <a href="Babbling" title="babbling">babbling</a>, unusual gestures, diminished responsiveness, and vocal patterns that are not synchronized with the caregiver. In the second and third years, autistic children have less frequent and less diverse babbling, consonants, words, and word combinations; their gestures are less often integrated with words. Autistic children are less likely to make requests or share experiences, and are more likely to simply repeat others' words (<a href="Echolalia" title="echolalia">echolalia</a>)<sup id="_ref-Landa_a" class="reference"><a href="#_note-Landa" title="">[28]</a></sup><sup id="_ref-Tager-Flusberg_a" class="reference"><a href="#_note-Tager-Flusberg" title="">[29]</a></sup> or <a href="Pronoun_reversal" title="Pronoun reversal">reverse pronouns</a>.<sup id="_ref-Kanner1943_a" class="reference"><a href="#_note-Kanner1943" title="">[30]</a></sup> <a href="Joint_attention" title="Joint attention">Joint attention</a> seems to be necessary for functional speech, and deficits in joint attention seem to distinguish infants with ASD:<sup id="_ref-Johnson_b" class="reference"><a href="#_note-Johnson" title="">[3]</a></sup> for example, they may look at a pointing hand instead of the pointed-at object,<sup id="_ref-Volkmar_b" class="reference"><a href="#_note-Volkmar" title="">[20]</a></sup><sup id="_ref-Tager-Flusberg_b" class="reference"><a href="#_note-Tager-Flusberg" title="">[29]</a></sup> and they consistently fail to point at objects in order to comment on or share an experience.<sup id="_ref-Johnson_c" class="reference"><a href="#_note-Johnson" title="">[3]</a></sup> Autistic children may have difficulty with imaginative play and with developing symbols into language.<sup id="_ref-Landa_b" class="reference"><a href="#_note-Landa" title="">[28]</a></sup><sup id="_ref-Tager-Flusberg_c" class="reference"><a href="#_note-Tager-Flusberg" title="">[29]</a></sup></p>
<p>In a pair of studies, high-functioning autistic children aged 8–15 performed equally well, and adults better than individually matched controls at basic language tasks involving vocabulary and spelling. Both autistic groups performed worse than controls at complex language tasks such as figurative language, comprehension and inference. As people are often sized up initially from their basic language skills, these studies suggest that people speaking to autistic individuals are more likely to overestimate what their audience comprehends.<sup id="_ref-Williams_a" class="reference"><a href="#_note-Williams" title="">[31]</a></sup></p>
<a id="Repetitive_behavior" name="Repetitive_behavior"/><h3>Repetitive behavior</h3>

<p>Autistic individuals display many forms of repetitive or restricted behavior, which the Repetitive Behavior Scale-Revised (RBS-R)<sup id="_ref-Lam-Aman_a" class="reference"><a href="#_note-Lam-Aman" title="">[32]</a></sup> categorizes as follows.</p>
<p><a class="internal" href="File:Autistic-sweetiepie-boy-with-ducksinarow.jpg" title="Young boy asleep on a bed, facing the camera, with only the head visible and the body off-camera. On the bed behind the boy's head is a dozen or so toys carefully arranged in a line, ordered by size."><img src="Autistic-sweetiepie-boy-with-ducksinarow.jpg" alt="Young boy asleep on a bed, facing the camera, with only the head visible and the body off-camera. On the bed behind the boy's head is a dozen or so toys carefully arranged in a line, ordered by size." title="Young boy asleep on a bed, facing the camera, with only the head visible and the body off-camera. On the bed behind the boy's head is a dozen or so toys carefully arranged in a line, ordered by size." class="location-none type-thumb"/>
</a>
<div class="thumbcaption">A young boy with autism, and the precise line of toys he made</div></p>

<ul>
<li><b><a href="Stereotypy" title="Stereotypy">Stereotypy</a></b> is repetitive movement, such as hand flapping, making sounds, head rolling, or body rocking.</li>
<li><b><a href="Compulsive_behavior" title="Compulsive behavior">Compulsive behavior</a></b> is intended and appears to follow rules, such as arranging objects in stacks or lines.</li>
<li><b>Sameness</b> is resistance to change; for example, insisting that the furniture not be moved or refusing to be interrupted.</li>
<li><b><a href="Ritual#Psychology" title="Ritual">Ritualistic behavior</a></b> involves an unvarying pattern of daily activities, such as an unchanging menu or a dressing ritual. This is closely associated with sameness and an independent validation has suggested combining the two factors.<sup id="_ref-Lam-Aman_b" class="reference"><a href="#_note-Lam-Aman" title="">[32]</a></sup></li>
<li><b>Restricted behavior</b> is limited in focus, interest, or activity, such as preoccupation with a single television program, toy, or game.</li>
<li><b><a href="Self-injury" title="Self-injury">Self-injury</a></b> includes movements that injure or can injure the person, such as eye poking, <a href="Skin_picking" title="skin picking">skin picking</a>, hand biting, and head banging.<sup id="_ref-Johnson_d" class="reference"><a href="#_note-Johnson" title="">[3]</a></sup> A 2007 study reported that self-injury at some point affected about 30% of children with ASD.<sup id="_ref-Dominick_b" class="reference"><a href="#_note-Dominick" title="">[25]</a></sup></li></ul>
<p>No single repetitive behavior seems to be specific to autism, but only autism appears to have an elevated pattern of occurrence and severity of these behaviors.<sup id="_ref-33" class="reference"><a href="#_note-33" title="">[33]</a></sup></p>
<a id="Other_symptoms" name="Other_symptoms"/><h3>Other symptoms</h3>
<p>Autistic individuals may have symptoms that are independent of the diagnosis, but that can affect the individual or the family.<sup id="_ref-Filipek_b" class="reference"><a href="#_note-Filipek" title="">[17]</a></sup>
An estimated 0.5% to 10% of individuals with ASD show unusual abilities, ranging from splinter skills such as the memorization of trivia to the extraordinarily rare talents of prodigious <a href="Savant_syndrome" title="Savant syndrome">autistic savants</a>.<sup id="_ref-34" class="reference"><a href="#_note-34" title="">[34]</a></sup> Many individuals with ASD show superior skills in perception and attention, relative to the general population.<sup id="_ref-35" class="reference"><a href="#_note-35" title="">[35]</a></sup>
<a href="Sensory_system" title="Sensory system">Sensory</a> abnormalities are found in over 90% of those with autism, and are considered core features by some,<sup id="_ref-Geschwind-2009_a" class="reference"><a href="#_note-Geschwind-2009" title="">[36]</a></sup> although there is no good evidence that sensory symptoms differentiate autism from other developmental disorders.<sup id="_ref-37" class="reference"><a href="#_note-37" title="">[37]</a></sup> Differences are greater for under-responsivity (for example, walking into things) than for over-responsivity (for example, distress from loud noises) or for sensation seeking (for example, rhythmic movements).<sup id="_ref-38" class="reference"><a href="#_note-38" title="">[38]</a></sup>
An estimated 60%–80% of autistic people have motor signs that include <a href="Poor_muscle_tone" title="poor muscle tone">poor muscle tone</a>, <a href="Apraxia" title="Apraxia">poor motor planning</a>, and <a href="Toe_walking" title="toe walking">toe walking</a>;<sup id="_ref-Geschwind-2009_b" class="reference"><a href="#_note-Geschwind-2009" title="">[36]</a></sup> ASD is not associated with severe motor disturbances.<sup id="_ref-39" class="reference"><a href="#_note-39" title="">[39]</a></sup></p>
<p>Unusual eating behavior occurs in about three-quarters of children with ASD, to the extent that it was formerly a diagnostic indicator. Selectivity is the most common problem, although eating rituals and food refusal also occur;<sup id="_ref-Dominick_c" class="reference"><a href="#_note-Dominick" title="">[25]</a></sup> this does not appear to result in <a href="Malnutrition" title="malnutrition">malnutrition</a>. Although some children with autism also have <a href="Gastrointestinal" title="gastrointestinal">gastrointestinal</a> (GI) symptoms, there is a lack of published rigorous data to support the theory that autistic children have more or different GI symptoms than usual;<sup id="_ref-40" class="reference"><a href="#_note-40" title="">[40]</a></sup> studies report conflicting results, and the relationship between GI problems and ASD is unclear.<sup id="_ref-CCD_c" class="reference"><a href="#_note-CCD" title="">[9]</a></sup></p>
<p>At some point in childhood, about two-thirds of individuals with ASD are affected by <a href="Sleep" title="sleep">sleep</a> problems; these most commonly include symptoms of <a href="Insomnia" title="insomnia">insomnia</a> such as difficulty in falling asleep, frequent <a href="Middle-of-the-night_insomnia" title="middle-of-the-night insomnia">nocturnal awakenings</a>, and early morning awakenings. Sleep problems are associated with difficult behaviors and family stress, and are often a focus of clinical attention over and above the primary ASD diagnosis.<sup id="_ref-41" class="reference"><a href="#_note-41" title="">[41]</a></sup></p>
<p>Parents of children with ASD have higher levels of stress.<sup id="_ref-42" class="reference"><a href="#_note-42" title="">[42]</a></sup> Siblings of children with ASD report greater admiration of and less conflict with the affected sibling than siblings of unaffected children or those with Down syndrome; siblings of individuals with ASD have greater risk of negative well-being and poorer sibling relationships as adults.<sup id="_ref-43" class="reference"><a href="#_note-43" title="">[43]</a></sup></p>
<a id="Classification" name="Classification"/><h2>Classification</h2>
<p><a class="internal" href="File:Leo-Kanner.jpeg" title="Head and shoulders of a man in his early 60s in coat and tie, facing slightly to his right. He is balding and has a serious but slightly smiling expression."><img src="Leo-Kanner.jpeg" alt="Head and shoulders of a man in his early 60s in coat and tie, facing slightly to his right. He is balding and has a serious but slightly smiling expression." title="Head and shoulders of a man in his early 60s in coat and tie, facing slightly to his right. He is balding and has a serious but slightly smiling expression." class="location-none type-thumb"/>
</a>
<div class="thumbcaption"><a href="Leo_Kanner" title="Leo Kanner">Leo Kanner</a> introduced the label <i>early infantile autism</i> in 1943.</div></p>
<p>Autism is one of the five <a href="Pervasive_developmental_disorder" title="pervasive developmental disorder">pervasive developmental disorders</a> (PDD), which are characterized by widespread abnormalities of social interactions and communication, and severely restricted interests and highly repetitive behavior.<sup id="_ref-ICD-10-F84.0_b" class="reference"><a href="#_note-ICD-10-F84.0" title="">[14]</a></sup> These symptoms do not imply sickness, fragility, or emotional disturbance.<sup id="_ref-Rapin_c" class="reference"><a href="#_note-Rapin" title="">[16]</a></sup></p>
<p>Of the five PDD forms, <a href="Asperger_syndrome" title="Asperger syndrome">Asperger syndrome</a> is closest to autism in signs and likely causes; <a href="Rett_syndrome" title="Rett syndrome">Rett syndrome</a> and <a href="Childhood_disintegrative_disorder" title="childhood disintegrative disorder">childhood disintegrative disorder</a> share several signs with autism, but may have unrelated causes; <a href="PDD_not_otherwise_specified" title="PDD not otherwise specified">PDD not otherwise specified</a> (PDD-NOS; also called <i>atypical autism</i>) is diagnosed when the criteria are not met for a more specific disorder.<sup id="_ref-44" class="reference"><a href="#_note-44" title="">[44]</a></sup> Unlike with autism, people with Asperger syndrome have no substantial delay in <a href="Language_development" title="language development">language development</a>.<sup id="_ref-DSM-IV-TR-299.00_b" class="reference"><a href="#_note-DSM-IV-TR-299.00" title="">[1]</a></sup> The terminology of autism can be bewildering, with autism, Asperger syndrome and PDD-NOS often called the <i>autism spectrum disorders</i> (ASD)<sup id="_ref-CCD_d" class="reference"><a href="#_note-CCD" title="">[9]</a></sup> or sometimes the <i>autistic disorders</i>,<sup id="_ref-45" class="reference"><a href="#_note-45" title="">[45]</a></sup> whereas autism itself is often called <i>autistic disorder</i>, <i>childhood autism</i>, or <i>infantile autism</i>. In this article, <i>autism</i> refers to the classic autistic disorder; in clinical practice, though, <i>autism</i>, <i>ASD</i>, and <i>PDD</i> are often used interchangeably.<sup id="_ref-Caronna_a" class="reference"><a href="#_note-Caronna" title="">[46]</a></sup> ASD, in turn, is a subset of the broader autism <a href="Phenotype" title="phenotype">phenotype</a>, which describes individuals who may not have ASD but do have autistic-like <a href="Trait_(biology)" title="Trait (biology)">traits</a>, such as avoiding eye contact.<sup id="_ref-47" class="reference"><a href="#_note-47" title="">[47]</a></sup></p>
<p>The manifestations of autism cover a wide <a href="Spectrum_disorder" title="Spectrum disorder">spectrum</a>, ranging from individuals with severe impairments—who may be silent, <a href="Mentally_disabled" title="mentally disabled">mentally disabled</a>, and locked into hand flapping and rocking—to high functioning individuals who may have active but distinctly odd social approaches, narrowly focused interests, and verbose, <a href="Pedantic" title="pedantic">pedantic</a> communication.<sup id="_ref-48" class="reference"><a href="#_note-48" title="">[48]</a></sup> Because the behavior spectrum is continuous, boundaries between diagnostic categories are necessarily somewhat arbitrary.<sup id="_ref-Geschwind-2009_c" class="reference"><a href="#_note-Geschwind-2009" title="">[36]</a></sup> Sometimes the syndrome is divided into low-, medium- or <a href="High-functioning_autism" title="high-functioning autism">high-functioning autism</a> (LFA, MFA, and HFA), based on <a href="IQ" title="IQ">IQ</a> thresholds,<sup id="_ref-49" class="reference"><a href="#_note-49" title="">[49]</a></sup> or on how much support the individual requires in daily life; these subdivisions are not standardized and are controversial. Autism can also be divided into <a href="Syndrome" title="Syndrome">syndromal</a> and non-syndromal autism; the syndromal autism is associated with severe or profound <a href="Mental_retardation" title="mental retardation">mental retardation</a> or a congenital syndrome with physical symptoms, such as <a href="Tuberous_sclerosis" title="tuberous sclerosis">tuberous sclerosis</a>.<sup id="_ref-50" class="reference"><a href="#_note-50" title="">[50]</a></sup> Although individuals with Asperger syndrome tend to perform better cognitively than those with autism, the extent of the <a href="Diagnosis_of_Asperger_syndrome#Differences_from_high-functioning_autism" title="Diagnosis of Asperger syndrome">overlap between Asperger syndrome, HFA, and non-syndromal autism</a> is unclear.<sup id="_ref-51" class="reference"><a href="#_note-51" title="">[51]</a></sup></p>
<p>Some studies have reported diagnoses of autism in children due to a loss of language or social skills, as opposed to a failure to make progress, typically from 15 to 30 months of age. The validity of this distinction remains controversial; it is possible that <a href="Regressive_autism" title="regressive autism">regressive autism</a> is a specific subtype,<sup id="_ref-Stefanatos_b" class="reference"><a href="#_note-Stefanatos" title="">[10]</a></sup><sup id="_ref-Volkmar_c" class="reference"><a href="#_note-Volkmar" title="">[20]</a></sup><sup id="_ref-Landa_c" class="reference"><a href="#_note-Landa" title="">[28]</a></sup><sup id="_ref-Landa3_a" class="reference"><a href="#_note-Landa3" title="">[52]</a></sup> or that there is a continuum of behaviors between autism with and without regression.<sup id="_ref-53" class="reference"><a href="#_note-53" title="">[53]</a></sup></p>
<p>Research into causes has been hampered by the inability to identify biologically meaningful subpopulations<sup id="_ref-54" class="reference"><a href="#_note-54" title="">[54]</a></sup> and by the traditional boundaries between the disciplines of <a href="Psychiatry" title="psychiatry">psychiatry</a>, <a href="Psychology" title="psychology">psychology</a>, <a href="Neurology" title="neurology">neurology</a> and <a href="Pediatrics" title="pediatrics">pediatrics</a>.<sup id="_ref-55" class="reference"><a href="#_note-55" title="">[55]</a></sup> Newer technologies such as <a href="FMRI" title="fMRI">fMRI</a> can help identify biologically relevant <a href="Phenotype" title="phenotype">phenotypes</a> (observable traits) that can be viewed on <a href="Brain_scan" title="brain scan">brain scans</a>, to help further <a href="Neurogenetic" title="neurogenetic">neurogenetic</a> studies of autism.<sup id="_ref-56" class="reference"><a href="#_note-56" title="">[56]</a></sup> It has been proposed to classify autism using genetics as well as behavior, with the name <i>Type 1 autism</i> denoting rare autism cases that test positive for a mutation in the <a href="CNTNAP2" title="CNTNAP2">CNTNAP2</a> gene.<sup id="_ref-57" class="reference"><a href="#_note-57" title="">[57]</a></sup></p>
<a id="Causes" name="Causes"/><h2>Causes</h2>
<p>{{main}}</p>
<p>It has long been presumed that there is a common cause at the genetic, cognitive, and neural levels for autism's characteristic triad of symptoms.<sup id="_ref-Fractionable_a" class="reference"><a href="#_note-Fractionable" title="">[58]</a></sup> However, there is increasing suspicion that autism is instead a complex disorder whose core aspects have distinct causes that often co-occur.<sup id="_ref-Fractionable_b" class="reference"><a href="#_note-Fractionable" title="">[58]</a></sup><sup id="_ref-HappeTime_a" class="reference"><a href="#_note-HappeTime" title="">[59]</a></sup></p>
<p><a class="internal" href="File:Single_Chromosome_Mutations.png" title="Three diagrams of chromosome pairs A, B that are nearly identical. 1: B is missing a segment of A. 2: B has two adjacent copies of a segment of A. 3: B's copy of A's segment is in reverse order."><img src="Single_Chromosome_Mutations.png" alt="Three diagrams of chromosome pairs A, B that are nearly identical. 1: B is missing a segment of A. 2: B has two adjacent copies of a segment of A. 3: B's copy of A's segment is in reverse order." title="Three diagrams of chromosome pairs A, B that are nearly identical. 1: B is missing a segment of A. 2: B has two adjacent copies of a segment of A. 3: B's copy of A's segment is in reverse order." class="location-none type-thumb"/>
</a>
<div class="thumbcaption">Deletion (1), duplication (2) and inversion (3) are all <a href="Chromosome_abnormalities" title="chromosome abnormalities">chromosome abnormalities</a> that have been implicated in autism.<sup id="_ref-Beaudet_a" class="reference"><a href="#_note-Beaudet" title="">[60]</a></sup></div>
Autism has a strong genetic basis, although the <a href="Heritability_of_autism" title="Heritability of autism">genetics of autism</a> are complex and it is unclear whether ASD is explained more by rare <a href="Mutation" title="mutation">mutations</a> with major effects, or by rare multigene interactions of common genetic variants.<sup id="_ref-Abrahams_b" class="reference"><a href="#_note-Abrahams" title="">[4]</a></sup><sup id="_ref-61" class="reference"><a href="#_note-61" title="">[61]</a></sup> Complexity arises due to interactions among multiple genes, the environment, and <a href="Epigenetic" title="epigenetic">epigenetic</a> factors which do not change <a href="DNA" title="DNA">DNA</a> but are heritable and influence <a href="Gene_expression" title="gene expression">gene expression</a>.<sup id="_ref-Rapin_d" class="reference"><a href="#_note-Rapin" title="">[16]</a></sup> Studies of twins suggest that <a href="Heritability" title="heritability">heritability</a> is 0.7 for autism and 0.9 for the broader autism phenotype, and siblings of those with autism are about 25 times more likely to be autistic than the general population.<sup id="_ref-Geschwind-2009_d" class="reference"><a href="#_note-Geschwind-2009" title="">[36]</a></sup> However, most of the mutations that increase autism risk have not been identified. Typically, autism cannot be traced to a <a href="Mendelian" title="Mendelian">Mendelian</a> (single-gene) mutation or to a single <a href="Chromosome_abnormality" title="chromosome abnormality">chromosome abnormality</a> like <a href="Fragile_X_syndrome" title="fragile X syndrome">fragile X syndrome</a>, and none of the genetic syndromes associated with ASDs has been shown to selectively cause ASD.<sup id="_ref-Abrahams_c" class="reference"><a href="#_note-Abrahams" title="">[4]</a></sup> Numerous candidate genes have been located, with only small effects attributable to any particular gene.<sup id="_ref-Abrahams_d" class="reference"><a href="#_note-Abrahams" title="">[4]</a></sup> The large number of autistic individuals with unaffected family members may result from <a href="Copy_number_variation" title="copy number variation">copy number variations</a>—spontaneous <a href="Deletion_(genetics)" title="Deletion (genetics)">deletions</a> or <a href="Gene_duplication" title="Gene duplication">duplications</a> in genetic material during <a href="Meiosis" title="meiosis">meiosis</a>.<sup id="_ref-62" class="reference"><a href="#_note-62" title="">[62]</a></sup> Hence, a substantial fraction of autism cases may be traceable to genetic causes that are highly heritable but not inherited: that is, the mutation that causes the autism is not present in the parental genome.<sup id="_ref-Beaudet_b" class="reference"><a href="#_note-Beaudet" title="">[60]</a></sup></p>
<p>Some rare mutations may lead to autism by disrupting some <a href="Synapse" title="Synapse">synaptic</a> pathways, such as those involved with <a href="Cell_adhesion" title="cell adhesion">cell adhesion</a>.<sup id="_ref-Betancur_a" class="reference"><a href="#_note-Betancur" title="">[63]</a></sup> Gene replacement studies in mice suggest that autistic symptoms are closely related to later developmental steps that depend on activity in synapses and on activity-dependent changes.<sup id="_ref-Walsh_a" class="reference"><a href="#_note-Walsh" title="">[64]</a></sup> All known <a href="Teratogen" title="teratogen">teratogens</a> (agents that cause <a href="Birth_defect" title="birth defect">birth defects</a>) related to the risk of autism appear to act during the first eight weeks from <a href="Human_fertilization" title="Human fertilization">conception</a>, and though this does not exclude the possibility that autism can be initiated or affected later, it is strong evidence that autism arises very early in development.<sup id="_ref-Arndt_b" class="reference"><a href="#_note-Arndt" title="">[5]</a></sup> Although evidence for other environmental causes is anecdotal and has not been confirmed by reliable studies,<sup id="_ref-Rutter_b" class="reference"><a href="#_note-Rutter" title="">[6]</a></sup> extensive searches are underway.<sup id="_ref-Szpir_a" class="reference"><a href="#_note-Szpir" title="">[65]</a></sup> <a href="Environmental_factor" title="Environmental factor">Environmental factors</a> that have been claimed to contribute to or exacerbate autism, or may be important in future research, include certain foods, <a href="Infectious_disease" title="infectious disease">infectious disease</a>, <a href="Heavy_metals" title="heavy metals">heavy metals</a>, <a href="Solvent" title="solvent">solvents</a>, <a href="Diesel_exhaust" title="diesel exhaust">diesel exhaust</a>, <a href="PCBs" title="PCBs">PCBs</a>, <a href="Phthalates" title="phthalates">phthalates</a> and <a href="Phenol" title="phenol">phenols</a> used in <a href="Plastic" title="plastic">plastic</a> products, <a href="Pesticide" title="pesticide">pesticides</a>, <a href="Brominated_flame_retardant" title="brominated flame retardant">brominated flame retardants</a>, <a href="Ethanol" title="Ethanol">alcohol</a>, <a href="Smoking" title="smoking">smoking</a>, <a href="Illicit_drug" title="illicit drug">illicit drugs</a>, <a href="Vaccine" title="vaccine">vaccines</a>,<sup id="_ref-Newschaffer_b" class="reference"><a href="#_note-Newschaffer" title="">[8]</a></sup> and <a href="Prenatal_stress" title="prenatal stress">prenatal stress</a>.<sup id="_ref-66" class="reference"><a href="#_note-66" title="">[66]</a></sup> Parents may first become aware of autistic symptoms in their child around the time of a routine vaccination, and this has given rise to theories that vaccines or their preservatives cause autism. Although these theories lack convincing scientific evidence and are biologically implausible, parental concern about autism has led to lower rates of <a href="Childhood_immunizations" title="childhood immunizations">childhood immunizations</a> and higher likelihood of <a href="Measles#Public_health" title="Measles">measles outbreaks</a>.<sup id="_ref-vaccines_b" class="reference"><a href="#_note-vaccines" title="">[7]</a></sup></p>
<a id="Mechanism" name="Mechanism"/><h2>Mechanism</h2>
<p>Autism's symptoms result from maturation-related changes in various systems of the brain.<sup id="_ref-Penn_a" class="reference"><a href="#_note-Penn" title="">[67]</a></sup> How autism occurs is not well understood. Its mechanism can be divided into two areas: the <a href="Pathophysiology" title="pathophysiology">pathophysiology</a> of brain structures and processes associated with autism, and the <a href="Neuropsychological" title="neuropsychological">neuropsychological</a> linkages between brain structures and behaviors.<sup id="_ref-Penn_b" class="reference"><a href="#_note-Penn" title="">[67]</a></sup> The behaviors appear to have multiple pathophysiologies.<sup id="_ref-London_b" class="reference"><a href="#_note-London" title="">[18]</a></sup></p>
<a id="Pathophysiology" name="Pathophysiology"/><h3>Pathophysiology</h3>
<p><a class="internal" href="File:Autismbrain.jpg" title="Two diagrams of major brain structures implicated in autism. The upper diagram shows the cerebral cortex near the top and the basal ganglia in the center, just above the amygdala and hippocampus. The lower diagram shows the corpus callosum near the center, the cerebellum in the lower rear, and the brain stem in the lower center."><img src="Autismbrain.jpg" alt="Two diagrams of major brain structures implicated in autism. The upper diagram shows the cerebral cortex near the top and the basal ganglia in the center, just above the amygdala and hippocampus. The lower diagram shows the corpus callosum near the center, the cerebellum in the lower rear, and the brain stem in the lower center." title="Two diagrams of major brain structures implicated in autism. The upper diagram shows the cerebral cortex near the top and the basal ganglia in the center, just above the amygdala and hippocampus. The lower diagram shows the corpus callosum near the center, the cerebellum in the lower rear, and the brain stem in the lower center." class="location-none type-thumb"/>
</a>
<div class="thumbcaption">Autism affects the <a href="Amygdala" title="amygdala">amygdala</a>, <a href="Cerebellum" title="cerebellum">cerebellum</a>, and many other parts of the brain.<sup id="_ref-Amaral_b" class="reference"><a href="#_note-Amaral" title="">[2]</a></sup></div>
Unlike many other brain disorders such as <a href="Parkinson's" title="Parkinson's">Parkinson's</a>, autism does not have a clear unifying mechanism at either the molecular, cellular, or systems level; it is not known whether autism is a few disorders caused by mutations converging on a few common molecular pathways, or is (like intellectual disability) a large set of disorders with diverse mechanisms.<sup id="_ref-Geschwind_b" class="reference"><a href="#_note-Geschwind" title="">[13]</a></sup> Autism appears to result from developmental factors that affect many or all functional brain systems,<sup id="_ref-68" class="reference"><a href="#_note-68" title="">[68]</a></sup> and to disturb the timing of brain development more than the final product.<sup id="_ref-Amaral_c" class="reference"><a href="#_note-Amaral" title="">[2]</a></sup> <a href="Neuroanatomical" title="Neuroanatomical">Neuroanatomical</a> studies and the associations with teratogens strongly suggest that autism's mechanism includes alteration of brain development soon after conception.<sup id="_ref-Arndt_c" class="reference"><a href="#_note-Arndt" title="">[5]</a></sup> This anomaly appears to start a cascade of pathological events in the brain that are significantly influenced by environmental factors.<sup id="_ref-69" class="reference"><a href="#_note-69" title="">[69]</a></sup> Just after birth, the brain of an autistic child grows faster than usual, followed by normal or relatively slower growth in childhood. The early overgrowth seems to be most prominent in areas underlying the development of higher cognitive specialization.<sup id="_ref-Geschwind-2009_e" class="reference"><a href="#_note-Geschwind-2009" title="">[36]</a></sup> Hypotheses for the cellular and molecular bases of pathological early overgrowth include the following:
</p>
<ul>
<li>An excess of <a href="Neuron" title="neuron">neurons</a> that causes local overconnectivity in key brain regions.<sup id="_ref-70" class="reference"><a href="#_note-70" title="">[70]</a></sup></li>
<li>Disturbed <a href="Neuronal_migration" title="neuronal migration">neuronal migration</a> during early <a href="Gestation" title="gestation">gestation</a>.<sup id="_ref-Schmitz_a" class="reference"><a href="#_note-Schmitz" title="">[71]</a></sup><sup id="_ref-Persico_a" class="reference"><a href="#_note-Persico" title="">[72]</a></sup></li>
<li>Unbalanced excitatory–inhibitory networks.<sup id="_ref-Persico_b" class="reference"><a href="#_note-Persico" title="">[72]</a></sup></li>
<li>Abnormal formation of <a href="Synapse" title="synapse">synapses</a> and <a href="Dendritic_spine" title="dendritic spine">dendritic spines</a>,<sup id="_ref-Persico_c" class="reference"><a href="#_note-Persico" title="">[72]</a></sup> for example, by modulation of the <a href="Neurexin" title="neurexin">neurexin</a>–<a href="Neuroligin" title="neuroligin">neuroligin</a> <a href="Cell_adhesion" title="Cell adhesion">cell-adhesion</a> system,<sup id="_ref-73" class="reference"><a href="#_note-73" title="">[73]</a></sup> or by poorly regulated <a href="Protein_synthesis" title="Protein synthesis">synthesis of synaptic protein</a>.<sup id="_ref-74" class="reference"><a href="#_note-74" title="">[74]</a></sup> Disrupted synaptic development may also contribute to <a href="Epilepsy" title="epilepsy">epilepsy</a>, which may explain why the two conditions are associated.<sup id="_ref-75" class="reference"><a href="#_note-75" title="">[75]</a></sup></li></ul>

<p>Interactions between the <a href="Immune_system" title="immune system">immune system</a> and the <a href="Nervous_system" title="nervous system">nervous system</a> begin early during the <a href="Human_embryogenesis" title="Human embryogenesis">embryonic stage</a> of life, and successful neurodevelopment depends on a balanced immune response. It is possible that aberrant immune activity during critical periods of neurodevelopment is part of the mechanism of some forms of ASD.<sup id="_ref-76" class="reference"><a href="#_note-76" title="">[76]</a></sup> Although some abnormalities in the immune system have been found in specific subgroups of autistic individuals, it is not known whether these abnormalities are relevant to or secondary to autism's disease processes.<sup id="_ref-77" class="reference"><a href="#_note-77" title="">[77]</a></sup> As <a href="Autoantibodies" title="autoantibodies">autoantibodies</a> are found in conditions other than ASD, and are not always present in ASD,<sup id="_ref-78" class="reference"><a href="#_note-78" title="">[78]</a></sup> the relationship between immune disturbances and autism remains unclear and controversial.<sup id="_ref-Schmitz_b" class="reference"><a href="#_note-Schmitz" title="">[71]</a></sup></p>
<p>Several <a href="Neurotransmitter" title="neurotransmitter">neurotransmitter</a> abnormalities have been detected in autism, notably increased blood levels of <a href="Serotonin" title="serotonin">serotonin</a>. Whether these cause structural or behavioral abnormalities is unclear.<sup id="_ref-Penn_c" class="reference"><a href="#_note-Penn" title="">[67]</a></sup> Some data suggest an increase in several <a href="Growth_hormone" title="growth hormone">growth hormones</a>; other data argue for diminished <a href="Growth_factor" title="growth factor">growth factors</a>.<sup id="_ref-79" class="reference"><a href="#_note-79" title="">[79]</a></sup> Also, some <a href="Inborn_errors_of_metabolism" title="inborn errors of metabolism">inborn errors of metabolism</a> are associated with autism but probably account for less than 5% of cases.<sup id="_ref-Manzi_a" class="reference"><a href="#_note-Manzi" title="">[80]</a></sup></p>
<p>The <a href="Mirror_neuron_system" title="mirror neuron system">mirror neuron system</a> (MNS) theory of autism hypothesizes that distortion in the development of the MNS interferes with imitation and leads to autism's core features of social impairment and communication difficulties. The MNS operates when an animal performs an action or observes another animal perform the same action. The MNS may contribute to an individual's understanding of other people by enabling the modeling of their behavior via embodied simulation of their actions, intentions, and emotions.<sup id="_ref-81" class="reference"><a href="#_note-81" title="">[81]</a></sup> Several studies have tested this hypothesis by demonstrating structural abnormalities in MNS regions of individuals with ASD, delay in the activation in the core circuit for imitation in individuals with Asperger syndrome, and a correlation between reduced MNS activity and severity of the syndrome in children with ASD.<sup id="_ref-Iacoboni_a" class="reference"><a href="#_note-Iacoboni" title="">[82]</a></sup> However, individuals with autism also have abnormal brain activation in many circuits outside the MNS<sup id="_ref-83" class="reference"><a href="#_note-83" title="">[83]</a></sup> and the MNS theory does not explain the normal performance of autistic children on imitation tasks that involve a goal or object.<sup id="_ref-84" class="reference"><a href="#_note-84" title="">[84]</a></sup></p>
<p><a class="internal" href="File:Powell2004Fig1A.jpeg" title="A human brain viewed from above. About 10% is highlighted in yellow and 10% in blue. There is only a tiny (perhaps 0.5%) green region where they overlap."><img src="Powell2004Fig1A.jpeg" alt="A human brain viewed from above. About 10% is highlighted in yellow and 10% in blue. There is only a tiny (perhaps 0.5%) green region where they overlap." title="A human brain viewed from above. About 10% is highlighted in yellow and 10% in blue. There is only a tiny (perhaps 0.5%) green region where they overlap." class="location-none type-thumb"/>
</a>
<div class="thumbcaption">Autistic individuals tend to use different areas of the brain (yellow) for a movement task compared to a control group (blue).<sup id="_ref-Powell_a" class="reference"><a href="#_note-Powell" title="">[85]</a></sup></div>
ASD-related patterns of low function and aberrant activation in the brain differ depending on whether the brain is doing social or nonsocial tasks.<sup id="_ref-86" class="reference"><a href="#_note-86" title="">[86]</a></sup>
In autism there is evidence for reduced functional connectivity of the <a href="Default_network" title="default network">default network</a>, a large-scale brain network involved in social and emotional processing, with intact connectivity of the <a href="Task-positive_network" title="task-positive network">task-positive network</a>, used in sustained attention and goal-directed thinking. In people with autism the two networks are not negatively correlated in time, suggesting an imbalance in toggling between the two networks, possibly reflecting a disturbance of <a href="Self-referential" title="self-referential">self-referential</a> thought.<sup id="_ref-87" class="reference"><a href="#_note-87" title="">[87]</a></sup> A 2008 brain-imaging study found a specific pattern of signals in the <a href="Cingulate_cortex" title="cingulate cortex">cingulate cortex</a> which differs in individuals with ASD.<sup id="_ref-88" class="reference"><a href="#_note-88" title="">[88]</a></sup></p>
<p>The underconnectivity theory of autism hypothesizes that autism is marked by underfunctioning high-level neural connections and synchronization, along with an excess of low-level processes.<sup id="_ref-89" class="reference"><a href="#_note-89" title="">[89]</a></sup> Evidence for this theory has been found in <a href="Functional_neuroimaging" title="functional neuroimaging">functional neuroimaging</a> studies on autistic individuals<sup id="_ref-Williams_b" class="reference"><a href="#_note-Williams" title="">[31]</a></sup> and by a <a href="Brain_wave" title="brain wave">brain wave</a> study that suggested that adults with ASD have local overconnectivity in the <a href="Cerebral_cortex" title="Cerebral cortex">cortex</a> and weak functional connections between the <a href="Frontal_lobe" title="frontal lobe">frontal lobe</a> and the rest of the cortex.<sup id="_ref-90" class="reference"><a href="#_note-90" title="">[90]</a></sup> Other evidence suggests the underconnectivity is mainly within each <a href="Cerebral_hemisphere" title="Cerebral hemisphere">hemisphere</a> of the cortex and that autism is a disorder of the <a href="Cerebral_cortex#Association_areas" title="Cerebral cortex">association cortex</a>.<sup id="_ref-91" class="reference"><a href="#_note-91" title="">[91]</a></sup></p>
<p>From studies based on <a href="Event-related_potential" title="event-related potential">event-related potentials</a>, transient changes to the brain's electrical activity in response to stimuli, there is considerable evidence for differences in autistic individuals with respect to attention, orientiation to auditory and visual stimuli, novelty detection, language and face processing, and information storage; several studies have found a preference for non-social stimuli.<sup id="_ref-92" class="reference"><a href="#_note-92" title="">[92]</a></sup> For example, <a href="Magnetoencephalography" title="magnetoencephalography">magnetoencephalography</a> studies have found evidence in autistic children of delayed responses in the brain's processing of auditory signals.<sup id="_ref-93" class="reference"><a href="#_note-93" title="">[93]</a></sup></p>
<a id="Neuropsychology" name="Neuropsychology"/><h3>Neuropsychology</h3>
<p>Two major categories of <a href="Cognitive" title="cognitive">cognitive</a> theories have been proposed about the links between autistic brains and behavior.</p>
<p>The first category focuses on deficits in <a href="Social_cognition" title="social cognition">social cognition</a>. The <a href="Empathizing%E2%80%93systemizing_theory" title="empathizing–systemizing theory">empathizing–systemizing theory</a> postulates that autistic individuals can systemize—that is, they can develop internal rules of operation to handle events inside the brain—but are less effective at empathizing by handling events generated by other agents. An extension, the extreme male brain theory, hypothesizes that autism is an extreme case of the male brain, defined psychometrically as individuals in whom systemizing is better than empathizing;<sup id="_ref-E-S-theory_a" class="reference"><a href="#_note-E-S-theory" title="">[94]</a></sup> this extension is controversial, as many studies contradict the idea that baby boys and girls respond differently to people and objects.<sup id="_ref-95" class="reference"><a href="#_note-95" title="">[95]</a></sup>  </p>
<p>These theories are somewhat related to the earlier <a href="Theory_of_mind" title="theory of mind">theory of mind</a> approach, which hypothesizes that autistic behavior arises from an inability to ascribe mental states to oneself and others. The theory of mind hypothesis is supported by autistic children's atypical responses to the <a href="Sally%E2%80%93Anne_test" title="Sally–Anne test">Sally–Anne test</a> for reasoning about others' motivations,<sup id="_ref-E-S-theory_b" class="reference"><a href="#_note-E-S-theory" title="">[94]</a></sup> and the mirror neuron system theory of autism described in <i><a href="#Pathophysiology" title="">Pathophysiology</a></i> maps well to the hypothesis.<sup id="_ref-Iacoboni_b" class="reference"><a href="#_note-Iacoboni" title="">[82]</a></sup> However, most studies have found no evidence of impairment in autistic individuals' ability to understand other people's basic emotions or goals; instead, data suggests that impairments are found in understanding more complex social emotions or in considering others' viewpoints.<sup id="_ref-96" class="reference"><a href="#_note-96" title="">[96]</a></sup></p>
<p>The second category focuses on nonsocial or general processing. <a href="Executive_dysfunction" title="Executive dysfunction">Executive dysfunction</a> hypothesizes that autistic behavior results in part from deficits in <a href="Working_memory" title="working memory">working memory</a>, planning, <a href="Inhibition_Theory" title="Inhibition Theory">inhibition</a>, and other forms of executive function.<sup id="_ref-Kenworthy_a" class="reference"><a href="#_note-Kenworthy" title="">[97]</a></sup> Tests of core executive processes such as eye movement tasks indicate improvement from late childhood to adolescence, but performance never reaches typical adult levels.<sup id="_ref-98" class="reference"><a href="#_note-98" title="">[98]</a></sup> A strength of the theory is predicting stereotyped behavior and narrow interests;<sup id="_ref-99" class="reference"><a href="#_note-99" title="">[99]</a></sup> two weaknesses are that executive function is hard to measure<sup id="_ref-Kenworthy_b" class="reference"><a href="#_note-Kenworthy" title="">[97]</a></sup> and that executive function deficits have not been found in young autistic children.<sup id="_ref-Sigman_b" class="reference"><a href="#_note-Sigman" title="">[23]</a></sup> </p>
<p><a href="Weak_central_coherence_theory" title="Weak central coherence theory">Weak central coherence theory</a> hypothesizes that a limited ability to see the big picture underlies the central disturbance in autism. One strength of this theory is predicting special talents and peaks in performance in autistic people.<sup id="_ref-100" class="reference"><a href="#_note-100" title="">[100]</a></sup> A related theory—enhanced perceptual functioning—focuses more on the superiority of locally oriented and <a href="Perceptual" title="perceptual">perceptual</a> operations in autistic individuals.<sup id="_ref-101" class="reference"><a href="#_note-101" title="">[101]</a></sup> These theories map well from the underconnectivity theory of autism.</p>
<p>Neither category is satisfactory on its own; social cognition theories poorly address autism's rigid and repetitive behaviors, while the nonsocial theories have difficulty explaining social impairment and communication difficulties.<sup id="_ref-HappeTime_b" class="reference"><a href="#_note-HappeTime" title="">[59]</a></sup> A combined theory based on multiple deficits may prove to be more useful.<sup id="_ref-102" class="reference"><a href="#_note-102" title="">[102]</a></sup></p>
<a id="Screening" name="Screening"/><h2>Screening</h2>
<p>About half of parents of children with ASD notice their child's unusual behaviors by age 18 months, and about four-fifths notice by age 24 months.<sup id="_ref-Landa3_b" class="reference"><a href="#_note-Landa3" title="">[52]</a></sup> As postponing treatment may affect long-term outcome, any of the following signs is reason to have a child evaluated by a specialist without delay:
</p>
<ul>
<li>No <a href="Babbling" title="babbling">babbling</a> by 12 months.</li>
<li>No <a href="Gesture" title="Gesture">gesturing</a> (pointing, waving goodbye, etc.) by 12 months.</li>
<li>No single words by 16 months.</li>
<li>No two-word spontaneous phrases (other than instances of <a href="Echolalia" title="echolalia">echolalia</a>) by 24 months.</li>
<li>Any loss of any language or social skills, at any age.<sup id="_ref-Filipek_c" class="reference"><a href="#_note-Filipek" title="">[17]</a></sup></li></ul>
<p>The <a href="American_Academy_of_Pediatrics" title="American Academy of Pediatrics">American Academy of Pediatrics</a> recommends that all children be <a href="Screening_(medicine)" title="Screening (medicine)">screened</a> for ASD at the 18- and 24-month well-child doctor visits, using autism-specific formal screening tests.<sup id="_ref-Johnson_e" class="reference"><a href="#_note-Johnson" title="">[3]</a></sup> In contrast, the UK National Screening Committee recommends against screening for ASD in the general population, because screening tools have not been fully validated and interventions lack sufficient evidence for effectiveness.<sup id="_ref-103" class="reference"><a href="#_note-103" title="">[103]</a></sup> Screening tools include the Modified Checklist for Autism in Toddlers (M-CHAT), the Early Screening of Autistic Traits Questionnaire, and the First Year Inventory; initial data on M-CHAT and its predecessor CHAT on children aged 18–30 months suggests that it is best used in a clinical setting and that it has low <a href="Sensitivity_(tests)" title="Sensitivity (tests)">sensitivity</a> (many false-negatives) but good <a href="Specificity_(tests)" title="Specificity (tests)">specificity</a> (few false-positives).<sup id="_ref-Landa3_c" class="reference"><a href="#_note-Landa3" title="">[52]</a></sup> It may be more accurate to precede these tests with a broadband screener that does not distinguish ASD from other developmental disorders.<sup id="_ref-104" class="reference"><a href="#_note-104" title="">[104]</a></sup> Screening tools designed for one culture's norms for behaviors like eye contact may be inappropriate for a different culture.<sup id="_ref-105" class="reference"><a href="#_note-105" title="">[105]</a></sup> <a href="Genetic_screening" title="Genetic screening">Genetic screening</a> for autism is generally still impractical.<sup id="_ref-McMahon_a" class="reference"><a href="#_note-McMahon" title="">[106]</a></sup></p>
<a id="Diagnosis" name="Diagnosis"/><h2>Diagnosis</h2>
<p><a href="Medical_diagnosis" title="Medical diagnosis">Diagnosis</a> is based on behavior, not cause or mechanism.<sup id="_ref-London_c" class="reference"><a href="#_note-London" title="">[18]</a></sup><sup id="_ref-107" class="reference"><a href="#_note-107" title="">[107]</a></sup> Autism is defined in the <a href="DSM-IV-TR" title="DSM-IV-TR">DSM-IV-TR</a> as exhibiting at least six symptoms total, including at least two symptoms of qualitative impairment in social interaction, at least one symptom of qualitative impairment in communication, and at least one symptom of restricted and repetitive behavior. Sample symptoms include lack of social or emotional reciprocity, stereotyped and repetitive use of language or idiosyncratic language, and persistent preoccupation with parts of objects. Onset must be prior to age three years, with delays or abnormal functioning in either social interaction, language as used in social communication, or symbolic or imaginative play. The disturbance must not be better accounted for by <a href="Rett_syndrome" title="Rett syndrome">Rett syndrome</a> or <a href="Childhood_disintegrative_disorder" title="childhood disintegrative disorder">childhood disintegrative disorder</a>.<sup id="_ref-DSM-IV-TR-299.00_c" class="reference"><a href="#_note-DSM-IV-TR-299.00" title="">[1]</a></sup> <a href="ICD-10" title="ICD-10">ICD-10</a> uses essentially the same definition.<sup id="_ref-ICD-10-F84.0_c" class="reference"><a href="#_note-ICD-10-F84.0" title="">[14]</a></sup></p>
<p>Several diagnostic instruments are available. Two are commonly used in autism research: the <a href="Autism_Diagnostic_Interview-Revised" title="Autism Diagnostic Interview-Revised">Autism Diagnostic Interview-Revised</a> (ADI-R) is a semistructured parent interview, and the <a href="Autism_Diagnostic_Observation_Schedule" title="Autism Diagnostic Observation Schedule">Autism Diagnostic Observation Schedule</a> (ADOS) uses observation and interaction with the child. The <a href="Childhood_Autism_Rating_Scale" title="Childhood Autism Rating Scale">Childhood Autism Rating Scale</a> (CARS) is used widely in clinical environments to assess severity of autism based on observation of children.<sup id="_ref-Volkmar_d" class="reference"><a href="#_note-Volkmar" title="">[20]</a></sup></p>
<p>A <a href="Pediatrician" title="pediatrician">pediatrician</a> commonly performs a preliminary investigation by taking developmental history and physically examining the child. If warranted, diagnosis and evaluations are conducted with help from ASD specialists, observing and assessing cognitive, communication, family, and other factors using standardized tools, and taking into account any associated <a href="Medical_conditions" title="medical conditions">medical conditions</a>.<sup id="_ref-Dover_a" class="reference"><a href="#_note-Dover" title="">[108]</a></sup> A pediatric <a href="Neuropsychologist" title="neuropsychologist">neuropsychologist</a> is often asked to assess behavior and cognitive skills, both to aid diagnosis and to help recommend educational interventions.<sup id="_ref-Kanne_a" class="reference"><a href="#_note-Kanne" title="">[109]</a></sup> A <a href="Differential_diagnosis" title="differential diagnosis">differential diagnosis</a> for ASD at this stage might also consider <a href="Mental_retardation" title="mental retardation">mental retardation</a>, <a href="Hearing_impairment" title="hearing impairment">hearing impairment</a>, and a <a href="Specific_language_impairment" title="specific language impairment">specific language impairment</a><sup id="_ref-Dover_b" class="reference"><a href="#_note-Dover" title="">[108]</a></sup> such as <a href="Landau%E2%80%93Kleffner_syndrome" title="Landau–Kleffner syndrome">Landau–Kleffner syndrome</a>.<sup id="_ref-110" class="reference"><a href="#_note-110" title="">[110]</a></sup> The presence of autism can make it harder to diagnose coexisting psychiatric disorders such as <a href="Types_of_psychological_depression" title="Types of psychological depression">depression</a>.<sup id="_ref-111" class="reference"><a href="#_note-111" title="">[111]</a></sup></p>
<p><a href="Clinical_genetics" title="Clinical genetics">Clinical genetics</a> evaluations are often done once ASD is diagnosed, particularly when other symptoms already suggest a genetic cause.<sup id="_ref-Caronna_b" class="reference"><a href="#_note-Caronna" title="">[46]</a></sup> Although genetic technology allows clinical geneticists to link an estimated 40% of cases to genetic causes,<sup id="_ref-112" class="reference"><a href="#_note-112" title="">[112]</a></sup> consensus guidelines in the U.S. and UK are limited to high-resolution chromosome and <a href="Fragile_X" title="fragile X">fragile X</a> testing.<sup id="_ref-Caronna_c" class="reference"><a href="#_note-Caronna" title="">[46]</a></sup> A <a href="Genotype" title="genotype">genotype</a>-first model of diagnosis has been proposed, which would routinely assess the genome's copy number variations.<sup id="_ref-113" class="reference"><a href="#_note-113" title="">[113]</a></sup> As new genetic tests are developed several ethical, legal, and social issues will emerge. Commercial availability of tests may precede adequate understanding of how to use test results, given the complexity of autism's genetics.<sup id="_ref-McMahon_b" class="reference"><a href="#_note-McMahon" title="">[106]</a></sup> <a href="Metabolic" title="Metabolic">Metabolic</a> and <a href="Neuroimaging" title="neuroimaging">neuroimaging</a> tests are sometimes helpful, but are not routine.<sup id="_ref-Caronna_d" class="reference"><a href="#_note-Caronna" title="">[46]</a></sup></p>
<p>ASD can sometimes be diagnosed by age 14 months, although diagnosis becomes increasingly stable over the first three years of life: for example, a one-year-old who meets diagnostic criteria for ASD is less likely than a three-year-old to continue to do so a few years later.<sup id="_ref-Landa3_d" class="reference"><a href="#_note-Landa3" title="">[52]</a></sup> In the UK the National Autism Plan for Children recommends at most 30 weeks from first concern to completed diagnosis and assessment, though few cases are handled that quickly in practice.<sup id="_ref-Dover_c" class="reference"><a href="#_note-Dover" title="">[108]</a></sup> A 2009 U.S. study found the average age of formal ASD diagnosis was 5.7 years, far above recommendations, and that 27% of children remained undiagnosed at age 8 years.<sup id="_ref-114" class="reference"><a href="#_note-114" title="">[114]</a></sup> Although the symptoms of autism and ASD begin early in childhood, they are sometimes missed; years later, adults may seek diagnoses to help them or their friends and family understand themselves, to help their employers make adjustments, or in some locations to claim disability living allowances or other benefits.<sup id="_ref-115" class="reference"><a href="#_note-115" title="">[115]</a></sup></p>
<p>Underdiagnosis and overdiagnosis are problems in marginal cases, and much of the recent increase in the number of reported ASD cases is likely due to changes in diagnostic practices. The increasing popularity of drug treatment options and the expansion of benefits has given providers incentives to diagnose ASD, resulting in some overdiagnosis of children with uncertain symptoms. Conversely, the cost of screening and diagnosis and the challenge of obtaining payment can inhibit or delay diagnosis.<sup id="_ref-116" class="reference"><a href="#_note-116" title="">[116]</a></sup> It is particularly hard to diagnose autism among the <a href="Visually_impaired" title="visually impaired">visually impaired</a>, partly because some of its diagnostic criteria depend on vision, and partly because autistic symptoms overlap with those of common blindness syndromes.<sup id="_ref-117" class="reference"><a href="#_note-117" title="">[117]</a></sup></p>
<a id="Management" name="Management"/><h2>Management</h2>
<p>{{main}}
<a class="internal" href="File:Opening_a_window_to_the_autistic_brain.jpg" title="A young child points, in front of a woman who smiles and points in the same direction."><img src="Opening_a_window_to_the_autistic_brain.jpg" alt="A young child points, in front of a woman who smiles and points in the same direction." title="A young child points, in front of a woman who smiles and points in the same direction." class="location-none type-thumb"/>
</a>
<div class="thumbcaption">A three-year-old with autism points to fish in an aquarium, as part of an experiment on the effect of intensive shared-attention training on language development.<sup id="_ref-Powell_b" class="reference"><a href="#_note-Powell" title="">[85]</a></sup></div>
The main goals of treatment are to lessen associated deficits and family distress, and to increase quality of life and functional independence. No single treatment is best and treatment is typically tailored to the child's needs.<sup id="_ref-CCD_e" class="reference"><a href="#_note-CCD" title="">[9]</a></sup> Studies of interventions have methodological problems that prevent definitive conclusions about <a href="Efficacy" title="efficacy">efficacy</a>.<sup id="_ref-118" class="reference"><a href="#_note-118" title="">[118]</a></sup> Although many <a href="Psychosocial" title="psychosocial">psychosocial</a> interventions have some positive evidence, suggesting that some form of treatment is preferable to no treatment, the methodological quality of <a href="Systematic_review" title="systematic review">systematic reviews</a> of these studies has generally been poor, their clinical results are mostly tentative, and there is little evidence for the relative effectiveness of treatment options.<sup id="_ref-119" class="reference"><a href="#_note-119" title="">[119]</a></sup> Intensive, sustained <a href="Special_education" title="special education">special education</a> programs and <a href="Behavior_therapy" title="behavior therapy">behavior therapy</a> early in life can help children acquire self-care, social, and job skills,<sup id="_ref-CCD_f" class="reference"><a href="#_note-CCD" title="">[9]</a></sup> and often improve functioning and decrease symptom severity and maladaptive behaviors;<sup id="_ref-Rogers_a" class="reference"><a href="#_note-Rogers" title="">[120]</a></sup> claims that intervention by around age three years is crucial are not substantiated.<sup id="_ref-121" class="reference"><a href="#_note-121" title="">[121]</a></sup> Available approaches include <a href="Applied_behavior_analysis" title="applied behavior analysis">applied behavior analysis</a> (ABA), developmental models, <a href="TEACCH" title="TEACCH">structured teaching</a>, <a href="Speech_and_language_therapy" title="speech and language therapy">speech and language therapy</a>, <a href="Social_skills" title="social skills">social skills</a> therapy, and <a href="Occupational_therapy" title="occupational therapy">occupational therapy</a>.<sup id="_ref-CCD_g" class="reference"><a href="#_note-CCD" title="">[9]</a></sup> Educational interventions have some effectiveness in children: intensive ABA treatment has demonstrated effectiveness in enhancing global functioning in preschool children<sup id="_ref-122" class="reference"><a href="#_note-122" title="">[122]</a></sup> and is well-established for improving intellectual performance of young children.<sup id="_ref-Rogers_b" class="reference"><a href="#_note-Rogers" title="">[120]</a></sup> Neuropsychological reports are often poorly communicated to educators, resulting in a gap between what a report recommends and what education is provided.<sup id="_ref-Kanne_b" class="reference"><a href="#_note-Kanne" title="">[109]</a></sup> It is not known whether treatment programs for children lead to significant improvements after the children grow up,<sup id="_ref-Rogers_c" class="reference"><a href="#_note-Rogers" title="">[120]</a></sup> and the limited research on the effectiveness of adult residential programs shows mixed results.<sup id="_ref-123" class="reference"><a href="#_note-123" title="">[123]</a></sup></p>
<p>Many medications are used to treat ASD symptoms that interfere with integrating a child into home or school when behavioral treatment fails.<sup id="_ref-Rapin_e" class="reference"><a href="#_note-Rapin" title="">[16]</a></sup><sup id="_ref-124" class="reference"><a href="#_note-124" title="">[124]</a></sup> More than half of U.S. children diagnosed with ASD are prescribed <a href="Psychoactive_drug" title="psychoactive drug">psychoactive drugs</a> or <a href="Anticonvulsant" title="anticonvulsant">anticonvulsants</a>, with the most common drug classes being <a href="Antidepressant" title="antidepressant">antidepressants</a>, <a href="Stimulant" title="stimulant">stimulants</a>, and <a href="Antipsychotic" title="antipsychotic">antipsychotics</a>.<sup id="_ref-125" class="reference"><a href="#_note-125" title="">[125]</a></sup> Aside from antipsychotics,<sup id="_ref-126" class="reference"><a href="#_note-126" title="">[126]</a></sup> there is scant reliable research about the effectiveness or safety of drug treatments for adolescents and adults with ASD.<sup id="_ref-127" class="reference"><a href="#_note-127" title="">[127]</a></sup> A person with ASD may respond atypically to medications, the medications can have <a href="Adverse_effect_(medicine)" title="Adverse effect (medicine)">adverse effects</a>,<sup id="_ref-CCD_h" class="reference"><a href="#_note-CCD" title="">[9]</a></sup> and no known medication relieves autism's core symptoms of social and communication impairments.<sup id="_ref-128" class="reference"><a href="#_note-128" title="">[128]</a></sup> Experiments in mice have reversed or reduced some symptoms related to autism by replacing or modulating gene function after birth,<sup id="_ref-Walsh_b" class="reference"><a href="#_note-Walsh" title="">[64]</a></sup> suggesting the possibility of targeting therapies to specific rare mutations known to cause autism.<sup id="_ref-Betancur_b" class="reference"><a href="#_note-Betancur" title="">[63]</a></sup></p>
<p>Although many <a href="Alternative_therapies_for_developmental_and_learning_disabilities" title="Alternative therapies for developmental and learning disabilities">alternative therapies and interventions</a> are available, few are supported by scientific studies.<sup id="_ref-Sigman_c" class="reference"><a href="#_note-Sigman" title="">[23]</a></sup><sup id="_ref-129" class="reference"><a href="#_note-129" title="">[129]</a></sup><sup id="_ref-Aman_a" class="reference"><a href="#_note-Aman" title="">[130]</a></sup> Treatment approaches have little empirical support in <a href="Quality_of_life" title="Quality of life">quality-of-life</a> contexts, and many programs focus on success measures that lack predictive validity and real-world relevance.<sup id="_ref-Burgess_b" class="reference"><a href="#_note-Burgess" title="">[24]</a></sup> Scientific evidence appears to matter less to service providers than program marketing, training availability, and parent requests.<sup id="_ref-131" class="reference"><a href="#_note-131" title="">[131]</a></sup> Though most alternative treatments, such as <a href="Melatonin" title="melatonin">melatonin</a>, have only mild adverse effects<sup id="_ref-132" class="reference"><a href="#_note-132" title="">[132]</a></sup> some may place the child at risk. A 2008 study found that compared to their peers, autistic boys have significantly thinner bones if on <a href="Casein#Casein-free_diet" title="Casein">casein-free diets</a>;<sup id="_ref-133" class="reference"><a href="#_note-133" title="">[133]</a></sup> in 2005, botched <a href="Chelation_therapy" title="chelation therapy">chelation therapy</a> killed a five-year-old child with autism.<sup id="_ref-134" class="reference"><a href="#_note-134" title="">[134]</a></sup></p>
<p>Treatment is expensive; indirect costs are more so. For someone born in 2000, a U.S. study estimated an average lifetime cost of ${{formatprice}} (<a href="Net_present_value" title="net present value">net present value</a> in 2011 dollars, inflation-adjusted from 2003 estimate{{inflation-fn}}), with about 10% <a href="Medical_care" title="medical care">medical care</a>, 30% extra education and other care, and 60% lost economic productivity.<sup id="_ref-135" class="reference"><a href="#_note-135" title="">[135]</a></sup> Publicly supported programs are often inadequate or inappropriate for a given child, and unreimbursed out-of-pocket medical or therapy expenses are associated with likelihood of family financial problems;<sup id="_ref-136" class="reference"><a href="#_note-136" title="">[136]</a></sup> one 2008 U.S. study found a 14% average loss of annual income in families of children with ASD,<sup id="_ref-137" class="reference"><a href="#_note-137" title="">[137]</a></sup> and a related study found that ASD is associated with higher probability that <a href="Child_care" title="child care">child care</a> problems will greatly affect parental employment.<sup id="_ref-138" class="reference"><a href="#_note-138" title="">[138]</a></sup> U.S. states increasingly require private health insurance to cover autism services, shifting costs from publicly funded education programs to privately funded health insurance.<sup id="_ref-139" class="reference"><a href="#_note-139" title="">[139]</a></sup> After childhood, key treatment issues include residential care, job training and placement, sexuality, social skills, and <a href="Estate_planning" title="estate planning">estate planning</a>.<sup id="_ref-Aman_b" class="reference"><a href="#_note-Aman" title="">[130]</a></sup></p>
<a id="Prognosis" name="Prognosis"/><h2>Prognosis</h2>
<p>There is no known cure.<sup id="_ref-CCD_i" class="reference"><a href="#_note-CCD" title="">[9]</a></sup> Children recover occasionally, so that they lose their diagnosis of ASD;<sup id="_ref-Helt_a" class="reference"><a href="#_note-Helt" title="">[140]</a></sup> this occurs sometimes after intensive treatment and sometimes not. It is not known how often recovery happens;<sup id="_ref-Rogers_d" class="reference"><a href="#_note-Rogers" title="">[120]</a></sup> reported rates in unselected samples of children with ASD have ranged from 3% to 25%.<sup id="_ref-Helt_b" class="reference"><a href="#_note-Helt" title="">[140]</a></sup> A few autistic children have acquired speech at age 5 or older.<sup id="_ref-141" class="reference"><a href="#_note-141" title="">[141]</a></sup> Most children with autism lack <a href="Social_support" title="social support">social support</a>, meaningful relationships, future employment opportunities or <a href="Self-determination_theory" title="Self-determination theory">self-determination</a>.<sup id="_ref-Burgess_c" class="reference"><a href="#_note-Burgess" title="">[24]</a></sup> Although core difficulties tend to persist, symptoms often become less severe with age.<sup id="_ref-Rapin_f" class="reference"><a href="#_note-Rapin" title="">[16]</a></sup> Few high-quality studies address long-term <a href="Prognosis" title="prognosis">prognosis</a>. Some adults show modest improvement in communication skills, but a few decline; no study has focused on autism after midlife.<sup id="_ref-142" class="reference"><a href="#_note-142" title="">[142]</a></sup> Acquiring language before age six, having an <a href="IQ" title="IQ">IQ</a> above 50, and having a marketable skill all predict better outcomes; <a href="Independent_living" title="independent living">independent living</a> is unlikely with severe autism.<sup id="_ref-143" class="reference"><a href="#_note-143" title="">[143]</a></sup> A 2004 British study of 68 adults who were diagnosed before 1980 as autistic children with IQ above 50 found that 12% achieved a high level of independence as adults, 10% had some friends and were generally in work but required some support, 19% had some independence but were generally living at home and needed considerable support and supervision in daily living, 46% needed specialist residential provision from facilities specializing in ASD with a high level of support and very limited autonomy, and 12% needed high-level hospital care.<sup id="_ref-Howlin_b" class="reference"><a href="#_note-Howlin" title="">[11]</a></sup> A 2005 Swedish study of 78 adults that did not exclude low IQ found worse prognosis; for example, only 4% achieved independence.<sup id="_ref-144" class="reference"><a href="#_note-144" title="">[144]</a></sup> A 2008 Canadian study of 48 young adults diagnosed with ASD as preschoolers found outcomes ranging through poor (46%), fair (32%), good (17%), and very good (4%); 56% of these young adults had been employed at some point during their lives, mostly in volunteer, sheltered or <a href="Part-time" title="part-time">part-time</a> work.<sup id="_ref-145" class="reference"><a href="#_note-145" title="">[145]</a></sup> Changes in diagnostic practice and increased availability of effective early intervention make it unclear whether these findings can be generalized to recently diagnosed children.<sup id="_ref-Newschaffer_c" class="reference"><a href="#_note-Newschaffer" title="">[8]</a></sup></p>
<a id="Epidemiology" name="Epidemiology"/><h2>Epidemiology</h2>
<p>{{Main}}
<a class="internal" href="File:US-autism-6-17-1996-2007.png" title="Bar chart versus time. The graph rises steadily from 1996 to 2007, from about 0.7 to about 5.3. The trend curves slightly upward."><img src="US-autism-6-17-1996-2007.png" alt="Bar chart versus time. The graph rises steadily from 1996 to 2007, from about 0.7 to about 5.3. The trend curves slightly upward." title="Bar chart versus time. The graph rises steadily from 1996 to 2007, from about 0.7 to about 5.3. The trend curves slightly upward." class="location-left type-thumb"/>
</a>
<div class="thumbcaption">Reports of autism cases per 1,000 children grew dramatically in the U.S. from 1996 to 2007. It is unknown how much, if any, growth came from changes in autism's <a href="Prevalence" title="prevalence">prevalence</a>.</div>
Most recent <a href="Review" title="review">reviews</a> tend to estimate a prevalence of 1–2 per 1,000 for autism and close to 6 per 1,000 for ASD;<sup id="_ref-Newschaffer_d" class="reference"><a href="#_note-Newschaffer" title="">[8]</a></sup> because of inadequate data, these numbers may underestimate ASD's true prevalence.<sup id="_ref-Caronna_e" class="reference"><a href="#_note-Caronna" title="">[46]</a></sup> <a href="PDD-NOS" title="PDD-NOS">PDD-NOS</a>'s prevalence has been estimated at 3.7 per 1,000, Asperger syndrome at roughly 0.6 per 1,000, and <a href="Childhood_disintegrative_disorder" title="childhood disintegrative disorder">childhood disintegrative disorder</a> at 0.02 per 1,000.<sup id="_ref-Fombonne-2009_a" class="reference"><a href="#_note-Fombonne-2009" title="">[146]</a></sup> The number of reported cases of autism increased dramatically in the 1990s and early 2000s. This increase is largely attributable to changes in diagnostic practices, referral patterns, availability of services, age at diagnosis, and public awareness,<sup id="_ref-Fombonne-2009_b" class="reference"><a href="#_note-Fombonne-2009" title="">[146]</a></sup><sup id="_ref-147" class="reference"><a href="#_note-147" title="">[147]</a></sup> though unidentified environmental risk factors cannot be ruled out.<sup id="_ref-Rutter_c" class="reference"><a href="#_note-Rutter" title="">[6]</a></sup> The available evidence does not rule out the possibility that autism's true prevalence has increased;<sup id="_ref-Fombonne-2009_c" class="reference"><a href="#_note-Fombonne-2009" title="">[146]</a></sup> a real increase would suggest directing more attention and funding toward changing environmental factors instead of continuing to focus on genetics.<sup id="_ref-Szpir_b" class="reference"><a href="#_note-Szpir" title="">[65]</a></sup></p>
<p>Boys are at higher risk for ASD than girls. The sex ratio averages 4.3:1 and is greatly modified by cognitive impairment: it may be close to 2:1 with mental retardation and more than 5.5:1 without.<sup id="_ref-Newschaffer_e" class="reference"><a href="#_note-Newschaffer" title="">[8]</a></sup> Although the evidence does not implicate any single pregnancy-related risk factor as a cause of autism, the risk of autism is associated with advanced age in either parent, and with diabetes, bleeding, and use of psychiatric drugs in the mother during pregnancy.<sup id="_ref-148" class="reference"><a href="#_note-148" title="">[148]</a></sup> The risk is greater with older fathers than with older mothers; two potential explanations are the known increase in mutation burden in older sperm, and the hypothesis that men marry later if they carry genetic liability and show some signs of autism.<sup id="_ref-Geschwind-2009_f" class="reference"><a href="#_note-Geschwind-2009" title="">[36]</a></sup> Most professionals believe that race, ethnicity, and socioeconomic background do not affect the occurrence of autism.<sup id="_ref-149" class="reference"><a href="#_note-149" title="">[149]</a></sup></p>
<p>Autism is associated with several other conditions:
</p>
<ul>
<li><b><a href="Genetic_disorder" title="Genetic disorder">Genetic disorders</a></b>. About 10–15% of autism cases have an identifiable <a href="Mendelian" title="Mendelian">Mendelian</a> (single-gene) condition, <a href="Chromosome_abnormality" title="chromosome abnormality">chromosome abnormality</a>, or other genetic syndrome,<sup id="_ref-150" class="reference"><a href="#_note-150" title="">[150]</a></sup> and ASD is associated with several genetic disorders.<sup id="_ref-151" class="reference"><a href="#_note-151" title="">[151]</a></sup></li>
<li><b><a href="Mental_retardation" title="Mental retardation">Mental retardation</a></b>. The fraction of autistic individuals who also meet criteria for mental retardation has been reported as anywhere from 25% to 70%, a wide variation illustrating the difficulty of assessing autistic intelligence.<sup id="_ref-152" class="reference"><a href="#_note-152" title="">[152]</a></sup> For ASD other than autism, the association with mental retardation is much weaker.<sup id="_ref-153" class="reference"><a href="#_note-153" title="">[153]</a></sup></li>
<li><b><a href="Anxiety_disorder" title="Anxiety disorder">Anxiety disorders</a></b> are common among children with ASD; there are no firm data, but studies have reported prevalences ranging from 11% to 84%. Many anxiety disorders have symptoms that are better explained by ASD itself, or are hard to distinguish from ASD's symptoms.<sup id="_ref-154" class="reference"><a href="#_note-154" title="">[154]</a></sup></li>
<li><b><a href="Epilepsy" title="Epilepsy">Epilepsy</a></b>, with variations in risk of epilepsy due to age, cognitive level, and type of <a href="Language_disorder" title="language disorder">language disorder</a>.<sup id="_ref-155" class="reference"><a href="#_note-155" title="">[155]</a></sup></li>
<li>Several <b><a href="Metabolic_defect" title="metabolic defect">metabolic defects</a></b>, such as <a href="Phenylketonuria" title="phenylketonuria">phenylketonuria</a>, are associated with autistic symptoms.<sup id="_ref-Manzi_b" class="reference"><a href="#_note-Manzi" title="">[80]</a></sup></li>
<li><b><a href="Minor_physical_anomalies" title="Minor physical anomalies">Minor physical anomalies</a></b> are significantly increased in the autistic population.<sup id="_ref-156" class="reference"><a href="#_note-156" title="">[156]</a></sup></li>
<li><b>Preempted diagnoses</b>. Although the DSM-IV rules out concurrent diagnosis of many other conditions along with autism, the full criteria for <a href="ADHD" title="ADHD">ADHD</a>, <a href="Tourette_syndrome" title="Tourette syndrome">Tourette syndrome</a>, and other of these conditions are often present and these comorbid diagnoses are increasingly accepted.<sup id="_ref-157" class="reference"><a href="#_note-157" title="">[157]</a></sup></li></ul>

<a id="History" name="History"/><h2>History</h2>
<p>{{see}}</p>
<p>A few examples of autistic symptoms and treatments were described long before autism was named. The <i><a href="Table_talk_(literature)" title="Table talk (literature)">Table Talk</a></i> of <a href="Martin_Luther" title="Martin Luther">Martin Luther</a> contains the story of a 12-year-old boy who may have been severely autistic.<sup id="_ref-158" class="reference"><a href="#_note-158" title="">[158]</a></sup> According to Luther's notetaker <a href="Johannes_Mathesius" title="Johannes Mathesius">Mathesius</a>, Luther thought the boy was a soulless mass of flesh <a href="Demonic_possession" title="Demonic possession">possessed by the devil</a>, and suggested that he be suffocated.<sup id="_ref-159" class="reference"><a href="#_note-159" title="">[159]</a></sup> The earliest well-documented case of autism is that of Hugh Blair of Borgue, as detailed in a 1747 court case in which his brother successfully petitioned to annul Blair's marriage to gain Blair's inheritance.<sup id="_ref-160" class="reference"><a href="#_note-160" title="">[160]</a></sup> The <a href="Wild_Boy_of_Aveyron" title="Wild Boy of Aveyron">Wild Boy of Aveyron</a>, a <a href="Feral_child" title="feral child">feral child</a> caught in 1798, showed several signs of autism; the medical student <a href="Jean_Marc_Gaspard_Itard" title="Jean Marc Gaspard Itard">Jean Itard</a> treated him with a behavioral program designed to help him form social attachments and to induce speech via imitation.<sup id="_ref-Wolff_a" class="reference"><a href="#_note-Wolff" title="">[161]</a></sup></p>
<p>The <a href="New_Latin" title="New Latin">New Latin</a> word <i>autismus</i> (English translation <i>autism</i>) was coined by the <a href="Swiss" title="Swiss">Swiss</a> psychiatrist <a href="Eugen_Bleuler" title="Eugen Bleuler">Eugen Bleuler</a> in 1910 as he was defining symptoms of <a href="Schizophrenia" title="schizophrenia">schizophrenia</a>. He derived it from the Greek word <i>autós</i> (αὐτός, meaning <i>self</i>), and used it to mean morbid self-admiration, referring to "autistic withdrawal of the patient to his fantasies, against which any influence from outside becomes an intolerable disturbance".<sup id="_ref-162" class="reference"><a href="#_note-162" title="">[162]</a></sup></p>
<p>The word <i>autism</i> first took its modern sense in 1938 when <a href="Hans_Asperger" title="Hans Asperger">Hans Asperger</a> of the <a href="Vienna_General_Hospital" title="Vienna General Hospital">Vienna University Hospital</a> adopted Bleuler's terminology <i>autistic psychopaths</i> in a lecture in German about <a href="Child_psychology" title="child psychology">child psychology</a>.<sup id="_ref-163" class="reference"><a href="#_note-163" title="">[163]</a></sup> Asperger was investigating an ASD now known as <a href="Asperger_syndrome" title="Asperger syndrome">Asperger syndrome</a>, though for various reasons it was not widely recognized as a separate diagnosis until 1981.<sup id="_ref-Wolff_b" class="reference"><a href="#_note-Wolff" title="">[161]</a></sup> <a href="Leo_Kanner" title="Leo Kanner">Leo Kanner</a> of the <a href="Johns_Hopkins_Hospital" title="Johns Hopkins Hospital">Johns Hopkins Hospital</a> first used <i>autism</i> in its modern sense in English when he introduced the label <i>early infantile autism</i> in a 1943 report of 11 children with striking behavioral similarities.<sup id="_ref-Kanner1943_b" class="reference"><a href="#_note-Kanner1943" title="">[30]</a></sup> Almost all the characteristics described in Kanner's first paper on the subject, notably "autistic aloneness" and "insistence on sameness", are still regarded as typical of the autistic spectrum of disorders.<sup id="_ref-HappeTime_c" class="reference"><a href="#_note-HappeTime" title="">[59]</a></sup> It is not known whether Kanner derived the term independently of Asperger.<sup id="_ref-Lyons_a" class="reference"><a href="#_note-Lyons" title="">[164]</a></sup></p>
<p>Kanner's reuse of <i>autism</i> led to decades of confused terminology like <i>infantile schizophrenia</i>, and child psychiatry's focus on maternal deprivation led to misconceptions of autism as an infant's response to "<a href="Refrigerator_mother" title="refrigerator mother">refrigerator mothers</a>". Starting in the late 1960s autism was established as a separate syndrome by demonstrating that it is lifelong, distinguishing it from mental retardation and schizophrenia and from other developmental disorders, and demonstrating the benefits of involving parents in active programs of therapy.<sup id="_ref-165" class="reference"><a href="#_note-165" title="">[165]</a></sup> As late as the mid-1970s there was little evidence of a genetic role in autism; now it is thought to be one of the most heritable of all psychiatric conditions.<sup id="_ref-166" class="reference"><a href="#_note-166" title="">[166]</a></sup> Although the rise of parent organizations and the destigmatization of childhood ASD have deeply affected how we view ASD,<sup id="_ref-Wolff_c" class="reference"><a href="#_note-Wolff" title="">[161]</a></sup> parents continue to feel <a href="Social_stigma" title="social stigma">social stigma</a> in situations where their autistic children's behaviors are perceived negatively by others,<sup id="_ref-167" class="reference"><a href="#_note-167" title="">[167]</a></sup> and many <a href="Primary_care_physician" title="primary care physician">primary care physicians</a> and <a href="Medical_specialist" title="medical specialist">medical specialists</a> still express some beliefs consistent with outdated autism research.<sup id="_ref-168" class="reference"><a href="#_note-168" title="">[168]</a></sup> The <a href="Internet" title="Internet">Internet</a> has helped autistic individuals bypass nonverbal cues and emotional sharing that they find so hard to deal with, and has given them a way to form online communities and work remotely.<sup id="_ref-169" class="reference"><a href="#_note-169" title="">[169]</a></sup> <a href="Sociological_and_cultural_aspects_of_autism" title="Sociological and cultural aspects of autism">Sociological and cultural aspects of autism</a> have developed: some in the community seek a cure, while others believe that autism is simply another way of being.<sup id="_ref-Silverman_b" class="reference"><a href="#_note-Silverman" title="">[12]</a></sup><sup id="_ref-170" class="reference"><a href="#_note-170" title="">[170]</a></sup></p>
<a id="References" name="References"/><h2>References</h2>
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<a id="External_links" name="External_links"/><h2>External links</h2>
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