parse_test.go

package wikiparse

import (
	"bytes"
	"encoding/xml"
	"strings"
	"testing"
)

const exemplar = `<mediawiki xmlns="http://www.mediawiki.org/xml/export-0.8/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.mediawiki.org/xml/export-0.8/ http://www.mediawiki.org/xml/export-0.8.xsd" version="0.8" xml:lang="en">
  <siteinfo>
    <sitename>Wikipedia</sitename>
    <base>http://en.wikipedia.org/wiki/Main_Page</base>
    <generator>MediaWiki 1.24wmf2</generator>
    <case>first-letter</case>
    <namespaces>
      <namespace key="-2" case="first-letter">Media</namespace>
      <namespace key="-1" case="first-letter">Special</namespace>
      <namespace key="0" case="first-letter" />
      <namespace key="1" case="first-letter">Talk</namespace>
      <namespace key="2" case="first-letter">User</namespace>
      <namespace key="3" case="first-letter">User talk</namespace>
      <namespace key="4" case="first-letter">Wikipedia</namespace>
      <namespace key="5" case="first-letter">Wikipedia talk</namespace>
      <namespace key="6" case="first-letter">File</namespace>
      <namespace key="7" case="first-letter">File talk</namespace>
      <namespace key="8" case="first-letter">MediaWiki</namespace>
      <namespace key="9" case="first-letter">MediaWiki talk</namespace>
      <namespace key="10" case="first-letter">Template</namespace>
      <namespace key="11" case="first-letter">Template talk</namespace>
      <namespace key="12" case="first-letter">Help</namespace>
      <namespace key="13" case="first-letter">Help talk</namespace>
      <namespace key="14" case="first-letter">Category</namespace>
      <namespace key="15" case="first-letter">Category talk</namespace>
      <namespace key="100" case="first-letter">Portal</namespace>
      <namespace key="101" case="first-letter">Portal talk</namespace>
      <namespace key="108" case="first-letter">Book</namespace>
      <namespace key="109" case="first-letter">Book talk</namespace>
      <namespace key="118" case="first-letter">Draft</namespace>
      <namespace key="119" case="first-letter">Draft talk</namespace>
      <namespace key="446" case="first-letter">Education Program</namespace>
      <namespace key="447" case="first-letter">Education Program talk</namespace>
      <namespace key="710" case="first-letter">TimedText</namespace>
      <namespace key="711" case="first-letter">TimedText talk</namespace>
      <namespace key="828" case="first-letter">Module</namespace>
      <namespace key="829" case="first-letter">Module talk</namespace>
    </namespaces>
  </siteinfo>
  <page>
    <title>AccessibleComputing</title>
    <ns>0</ns>
    <id>10</id>
    <redirect title="Computer accessibility" />
    <revision>
      <id>381202555</id>
      <parentid>381200179</parentid>
      <timestamp>2010-08-26T22:38:36Z</timestamp>
      <contributor>
        <username>OlEnglish</username>
        <id>7181920</id>
      </contributor>
      <minor />
      <comment>[[Help:Reverting|Reverted]] edits by [[Special:Contributions/76.28.186.133|76.28.186.133]] ([[User talk:76.28.186.133|talk]]) to last version by Gurch</comment>
      <text xml:space="preserve">#REDIRECT [[Computer accessibility]] {{R from CamelCase}}</text>
      <sha1>lo15ponaybcg2sf49sstw9gdjmdetnk</sha1>
      <model>wikitext</model>
      <format>text/x-wiki</format>
    </revision>
  </page>
</mediawiki>`

const smaller = `  <page>
    <title>AccessibleComputing</title>
    <id>10</id>
    <redirect />
    <revision>
      <id>381202555</id>
      <timestamp>2010-08-26T22:38:36Z</timestamp>
      <contributor>
        <username>OlEnglish</username>
        <id>7181920</id>
      </contributor>
      <minor />
      <comment>[[Help:Reverting|Reverted]] edits by [[Special:Contributions/76.28.186.133|76.28.186.133]] ([[User talk:76.28.186.133|talk]]) to last version by Gurch</comment>
      <text xml:space="preserve">#REDIRECT [[Computer accessibility]] {{R from CamelCase}}</text>
    </revision>
  </page>
`

const larger = `  <page>
    <title>Autism</title>
    <id>25</id>
    <revision>
      <id>473043499</id>
      <timestamp>2012-01-24T21:00:41Z</timestamp>
      <contributor>
        <username>SandyGeorgia</username>
        <id>878749</id>
      </contributor>
      <comment>rv, wrong link, please read the cited source which is freely available</comment>
      <text xml:space="preserve">{{dablink|This article is about the classic autistic disorder; some writers use the word ''autism'' when referring to the range of disorders on the [[autism spectrum]] or to the various [[pervasive developmental disorder]]s.&lt;ref name=Caronna/&gt;}}
{{pp-semi-indef}}
{{pp-move-indef}}
&lt;!-- NOTES:
1) Please follow the Wikipedia style guidelines for editing medical articles [[WP:MEDMOS]], and medical referencing standards at [[WP:MEDRS]].
2) Use &lt;ref&gt; for explicitly cited references.
3) Reference anything you put here with notable references, as this subject tends to attract a lot of controversy.--&gt;
{{pp-move-indef}}
{{Infobox Disease
 | Name = Autism
 | Image = Autism-stacking-cans 2nd edit.jpg
 | Alt = Young red-haired boy facing away from camera, stacking a seventh can atop a column of six food cans on the kitchen floor. An open pantry contains many more cans.
 | Caption = Repetitively stacking or lining up objects is a behavior occasionally associated with individuals with autism.
 | DiseasesDB = 1142
 | ICD10 = {{ICD10|F|84|0|f|80}}
 | ICD9 =  299.00
 | ICDO =
 | OMIM =  209850
 | MedlinePlus = 001526
 | eMedicineSubj = med
 | eMedicineTopic = 3202
 | eMedicine_mult = {{eMedicine2|ped|180}}
 | MeshID = D001321
 | GeneReviewsID   = autism-overview
 | GeneReviewsName = Autism overview
}}
'''Autism''' is a [[Neurodevelopmental disorder|disorder of neural development]] characterized by impaired [[Interpersonal relationship|social interaction]] and [[communication]], and by restricted and repetitive behavior. These signs all begin before a child is three years old.&lt;ref name=DSM-IV-TR-299.00/&gt; Autism affects information processing in the [[Human brain|brain]] by altering how nerve cells and their [[synapse]]s connect and organize; how this occurs is not well understood.&lt;ref name=Levy/&gt; It is one of three recognized disorders in the [[autism spectrum]] (ASDs), the other two being [[Asperger syndrome]], which lacks delays in cognitive development and language, and [[PDD-NOS|Pervasive Developmental Disorder-Not Otherwise Specified]] (commonly abbreviated as PDD-NOS), which is diagnosed when the full set of criteria for autism or Asperger syndrome are not met.&lt;ref name=Johnson/&gt;

Autism has a strong genetic basis, although the [[Heritability of autism|genetics of autism]] are complex and it is unclear whether ASD is explained more by rare [[mutation]]s, or by rare combinations of common genetic variants.&lt;ref name=Abrahams/&gt; In rare cases, autism is strongly associated with [[Teratology|agents that cause birth defects]].&lt;ref name=Arndt/&gt; [[Controversies in autism|Controversies]] surround other proposed environmental [[Causes of autism|causes]], such as [[Heavy metal (chemistry)|heavy metals]], [[pesticide]]s or childhood [[vaccine]]s;&lt;ref name=Rutter/&gt; the vaccine hypotheses are biologically implausible and lack convincing scientific evidence.&lt;ref name=GerberOffit2009&gt;{{cite journal |author= Gerber JS, Offit PA |title= Vaccines and autism: a tale of shifting hypotheses |journal= Clin Infect Dis |volume=48 |issue=4 |pages=456–61 |year=2009 |pmid=19128068 |pmc= 2908388 |doi=10.1086/596476 |url=http://cid.oxfordjournals.org/content/48/4/456.full}}&lt;/ref&gt; The [[prevalence]] of autism is about 1–2 per 1,000 people worldwide; however, the [[Centers for Disease Control and Prevention]] (CDC) reports approximately 9 per 1,000 children in the United States are diagnosed with ASD.&lt;ref&gt;{{cite web|url=http://www.cdc.gov/ncbddd/autism/data.html CDC Data|title=Autism Spectrum Disorders - Data &amp; Statistics|work=[[Centers for Disease Control and Prevention]]|date=May 13, 2010|accessdate=December 25, 2010}}&lt;/ref&gt;&lt;ref name=vaccines/&gt; The number of people diagnosed with autism has increased dramatically since the 1980s, partly due to changes in diagnostic practice; the question of whether actual prevalence has increased is unresolved.&lt;ref name=Newschaffer/&gt;

Parents usually notice signs in the first two years of their child's life.&lt;ref name=CCD/&gt; The signs usually develop gradually, but some autistic children first develop more normally and then [[Regressive autism|regress]].&lt;ref name=Stefanatos/&gt; Early [[Lovaas technique|behavioral]] or cognitive intervention can help autistic children gain self-care, social, and communication skills.&lt;ref name=CCD/&gt; Although there is no known cure,&lt;ref name=CCD/&gt; there have been reported cases of children who recovered.&lt;ref name=Helt/&gt; Not many children with autism live independently after reaching adulthood, though some become successful.&lt;ref name=Howlin/&gt; An [[Sociological and cultural aspects of autism|autistic culture]] has developed, with some individuals seeking a cure and others believing autism should be accepted as a difference and not treated as a disorder.&lt;ref name=Silverman/&gt;

==Characteristics==
Autism is a highly variable [[neurodevelopmental disorder]]&lt;ref name=Geschwind/&gt; that first appears during infancy or childhood, and generally follows a steady course without [[Remission (medicine)|remission]].&lt;ref name=ICD-10-F84.0/&gt; Overt symptoms gradually begin after the age of six months, become established by age two or three years,&lt;ref&gt;{{vcite journal |author=Rogers SJ |title=What are infant siblings teaching us about autism in infancy? |title.= |journal=Autism Res |volume=2 |issue=3 |pages=125–37 |year=2009 |pmid=19582867 |doi=10.1002/aur.81 |pmc=2791538 }}&lt;/ref&gt; and tend to continue through adulthood, although often in more muted form.&lt;ref name=Rapin/&gt; 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.&lt;ref name=Filipek/&gt; 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.&lt;ref name=London/&gt;

===Social development===
Social deficits distinguish autism and the related [[autism spectrum disorder]]s (ASD; see ''[[#Classification|Classification]]'') from other developmental disorders.&lt;ref name=Rapin/&gt; People with autism have social impairments and often lack the intuition about others that many people take for granted. Noted autistic [[Temple Grandin]] described her inability to understand the [[social communication]] of [[neurotypical]]s, or people with normal [[neural development]], as leaving her feeling &quot;like an anthropologist on Mars&quot;.&lt;ref&gt;{{vcite book |title=[[An Anthropologist on Mars]]: Seven Paradoxical Tales |author=[[Oliver Sacks|Sacks O]] |publisher=Knopf |year=1995 |isbn=0-679-43785-1 }}&lt;/ref&gt;

Unusual social development becomes apparent early in childhood.&lt;!-- ref name=Volkmar/ --&gt; 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 [[social norms]]; for example, they have less [[eye contact]] and turn taking, and do not have the ability to use simple movements to express themselves, such as the deficiency to point at things.&lt;ref name=Volkmar/&gt; 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 [[Attachment (psychology)|attachments]] to their primary caregivers.&lt;ref&gt;{{vcite journal |journal=Ment Retard Dev Disabil Res Rev |year=2004 |volume=10 |issue=4 |pages=221–33 |title=Early detection of core deficits in autism |author=Sigman M, Dijamco A, Gratier M, Rozga A |doi=10.1002/mrdd.20046 |pmid=15666338 }}&lt;/ref&gt; Most autistic children display moderately less [[Attachment in children#Secure attachment|attachment security]] than non-autistic children, although this difference disappears in children with higher mental development or less severe ASD.&lt;ref&gt;{{vcite journal |journal=J Child Psychol Psychiatry |year=2004 |volume=45 |issue=6 |pages=1123–34 |title=Autism and attachment: a meta-analytic review |author=Rutgers AH, Bakermans-Kranenburg MJ, van IJzendoorn MH, van Berckelaer-Onnes IA |doi=10.1111/j.1469-7610.2004.t01-1-00305.x |pmid=15257669 }}&lt;/ref&gt; Older children and adults with ASD perform worse on tests of face and emotion recognition.&lt;ref name=Sigman&gt;{{vcite journal |journal=Annu Rev Clin Psychol |year=2006 |volume=2 |pages=327–55 |title=Autism from developmental and neuropsychological perspectives |author=Sigman M, Spence SJ, Wang AT |doi=10.1146/annurev.clinpsy.2.022305.095210 |pmid=17716073 }}&lt;/ref&gt;

Children with high-functioning autism suffer from more intense and frequent loneliness compared to non-autistic peers, despite the common belief that children with autism prefer to be 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 the quality of life more deeply.&lt;ref name=Burgess/&gt;

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 [[tantrum]]s. 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.&lt;ref name=Dominick/&gt; 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 [[psychosis]].&lt;ref&gt;{{vcite journal |journal=J Interpers Violence |year=2008 |title=Risk factors for violent offending in autism spectrum disorder: a national study of hospitalized individuals |author=Långström N, Grann M, Ruchkin V, Sjöstedt G, Fazel S |volume=24 |issue=8 |pages=1358–70 |doi=10.1177/0886260508322195 |pmid=18701743 }}&lt;/ref&gt;

===Communication===
About a third to a half of individuals with autism do not develop enough natural speech to meet their daily communication needs.&lt;ref&gt;{{vcite journal |journal=J Intellect Disabil Res |year=2006 |volume=50 |issue=9 |pages=621–32 |title=The ComFor: an instrument for the indication of augmentative communication in people with autism and intellectual disability |author=Noens I, van Berckelaer-Onnes I, Verpoorten R, van Duijn G |doi=10.1111/j.1365-2788.2006.00807.x |pmid=16901289 }}&lt;/ref&gt; Differences in communication may be present from the first year of life, and may include delayed onset of [[babbling]], 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 ([[echolalia]])&lt;ref name=Landa/&gt;&lt;ref name=Tager-Flusberg/&gt; or [[Pronoun reversal|reverse pronouns]].&lt;ref name=Kanner1943/&gt; [[Joint attention]] seems to be necessary for functional speech, and deficits in joint attention seem to distinguish infants with ASD:&lt;ref name=Johnson&gt;{{vcite journal |journal=Pediatrics |year=2007 |volume=120 |issue=5 |pages=1183–215 |title=Identification and evaluation of children with autism spectrum disorders |author=Johnson CP, Myers SM, Council on Children with Disabilities |doi=10.1542/peds.2007-2361 |pmid=17967920 |url=http://pediatrics.aappublications.org/cgi/content/full/120/5/1183 |laysummary=http://aap.org/advocacy/releases/oct07autism.htm |laysource=AAP |laydate=2007-10-29 }}&lt;/ref&gt; for example, they may look at a pointing hand instead of the pointed-at object,&lt;ref name=Volkmar/&gt;&lt;ref name=Tager-Flusberg/&gt; and they consistently fail to point at objects in order to comment on or share an experience.&lt;ref name=Johnson/&gt; Autistic children may have difficulty with imaginative play and with developing symbols into language.&lt;ref name=Landa&gt;{{vcite journal |journal=Ment Retard Dev Disabil Res Rev |year=2007 |volume=13 |issue=1 |pages=16–25 |title=Early communication development and intervention for children with autism |author=Landa R |doi=10.1002/mrdd.20134 |pmid=17326115 }}&lt;/ref&gt;&lt;ref name=Tager-Flusberg&gt;{{vcite journal |journal=Pediatr Clin North Am |year=2007 |volume=54 |issue=3 |pages=469–81 |title=Language disorders: autism and other pervasive developmental disorders |author=Tager-Flusberg H, Caronna E |doi=10.1016/j.pcl.2007.02.011 |pmid=17543905 }}&lt;/ref&gt;

In a pair of studies, high-functioning autistic children aged 8–15 performed equally well as, 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.&lt;ref name=Williams/&gt;

===Repetitive behavior===

Autistic individuals display many forms of repetitive or restricted behavior, which the Repetitive Behavior Scale-Revised (RBS-R)&lt;ref name=Lam-Aman/&gt; categorizes as follows.

[[File:Autistic-sweetiepie-boy-with-ducksinarow.jpg|thumb|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.|A young boy with autism, and the precise line of toys he made]]

*'''[[Stereotypy]]''' is repetitive movement, such as hand flapping, making sounds, head rolling, or body rocking.
*'''[[Compulsive behavior]]''' is intended and appears to follow rules, such as arranging objects in stacks or lines.
*'''Sameness''' is resistance to change; for example, insisting that the furniture not be moved or refusing to be interrupted.
*'''[[Ritual#Psychology|Ritualistic behavior]]''' 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.&lt;ref name=Lam-Aman&gt;{{vcite journal |journal=J Autism Dev Disord |year=2007 |volume=37 |issue=5 |pages=855–66 |title=The Repetitive Behavior Scale-Revised: independent validation in individuals with autism spectrum disorders |author=Lam KSL, Aman MG |doi=10.1007/s10803-006-0213-z |pmid=17048092 }}&lt;/ref&gt;
*'''Restricted behavior''' is limited in focus, interest, or activity, such as preoccupation with a single television program, toy, or game.
*'''[[Self-injury]]''' includes movements that injure or can injure the person, such as eye poking, [[skin picking]], hand biting, and head banging.&lt;ref name=Johnson/&gt; A 2007 study reported that self-injury at some point affected about 30% of children with ASD.&lt;ref name=Dominick/&gt;
No single repetitive or self-injurious behavior seems to be specific to autism, but only autism appears to have an elevated pattern of occurrence and severity of these behaviors.&lt;ref&gt;{{vcite journal |journal=J Autism Dev Disord |year=2000 |volume=30 |issue=3 |pages=237–43 |title=Varieties of repetitive behavior in autism: comparisons to mental retardation |author=Bodfish JW, Symons FJ, Parker DE, Lewis MH |doi=10.1023/A:1005596502855 |pmid=11055459 }}&lt;/ref&gt;

===Other symptoms===
Autistic individuals may have symptoms that are independent of the diagnosis, but that can affect the individual or the family.&lt;ref name=Filipek&gt;{{vcite journal |author=Filipek PA, Accardo PJ, Baranek GT ''et al.'' |author.= |title=The screening and diagnosis of autistic spectrum disorders |journal=J Autism Dev Disord |year=1999 |volume=29 |issue=6 |pages=439–84 |doi=10.1023/A:1021943802493 |pmid=10638459 }} This paper represents a consensus of representatives from nine professional and four parent organizations in the US.&lt;/ref&gt;
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 [[Savant syndrome|autistic savant]]s.&lt;ref&gt;{{vcite journal |author=Treffert DA |title=The savant syndrome: an extraordinary condition. A synopsis: past, present, future |journal=Philos Trans R Soc Lond B Biol Sci |volume=364 |issue=1522 |pages=1351–7 |year=2009 |pmid=19528017 |doi=10.1098/rstb.2008.0326 |url=http://rstb.royalsocietypublishing.org/content/364/1522/1351.full |laysummary=http://www.wisconsinmedicalsociety.org/savant_syndrome/overview_of_savant_syndrome |laysource=Wisconsin Medical Society |pmc=2677584 }}&lt;/ref&gt; Many individuals with ASD show superior skills in perception and attention, relative to the general population.&lt;ref&gt;{{vcite journal |author=Plaisted Grant K, Davis G |title=Perception and apperception in autism: rejecting the inverse assumption |journal=Philos Trans R Soc Lond B Biol Sci |volume=364 |issue=1522 |pages=1393–8 |year=2009 |pmid=19528022 |doi=10.1098/rstb.2009.0001 |pmc=2677593 |url=http://rstb.royalsocietypublishing.org/content/364/1522/1393.full }}&lt;/ref&gt;
[[Sensory system|Sensory]] abnormalities are found in over 90% of those with autism, and are considered core features by some,&lt;ref name=Geschwind-2009&gt;{{vcite journal |author=Geschwind DH |title=Advances in autism |journal=Annu Rev Med |volume=60 |pages=367–80 |year=2009 |pmid=19630577 |doi=10.1146/annurev.med.60.053107.121225 }}&lt;/ref&gt; although there is no good evidence that sensory symptoms differentiate autism from other developmental disorders.&lt;ref&gt;{{vcite journal |journal=J Child Psychol Psychiatry |year=2005 |volume=46 |issue=12 |pages=1255–68 |title=Annotation: what do we know about sensory dysfunction in autism? A critical review of the empirical evidence |author=Rogers SJ, Ozonoff S |doi=10.1111/j.1469-7610.2005.01431.x |pmid=16313426 }}&lt;/ref&gt; 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).&lt;ref&gt;{{vcite journal |journal=J Autism Dev Disord |year=2009 |title=A meta-analysis of sensory modulation symptoms in individuals with autism spectrum disorders |author=Ben-Sasson A, Hen L, Fluss R, Cermak SA, Engel-Yeger B, Gal E |doi=10.1007/s10803-008-0593-3 |pmid=18512135 |volume=39 |issue=1 |pages=1–11 }}&lt;/ref&gt;
An estimated 60%–80% of autistic people have motor signs that include [[poor muscle tone]], [[Apraxia|poor motor planning]], and [[toe walking]];&lt;ref name=Geschwind-2009/&gt; deficits in motor coordination are pervasive across ASD and are greater in autism proper.&lt;ref&gt;{{vcite journal |author=Fournier KA, Hass CJ, Naik SK, Lodha N, Cauraugh JH |title=Motor coordination in autism spectrum disorders: a synthesis and meta-analysis |journal=J Autism Dev Disord |volume= |issue= |pages= |year=2010 |pmid=20195737 |doi=10.1007/s10803-010-0981-3 }}&lt;/ref&gt;

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;&lt;ref name=Dominick&gt;{{vcite journal |journal=Res Dev Disabil |year=2007 |volume=28 |issue=2 |pages=145–62 |title=Atypical behaviors in children with autism and children with a history of language impairment |author=Dominick KC, Davis NO, Lainhart J, Tager-Flusberg H, Folstein S |doi=10.1016/j.ridd.2006.02.003 |pmid=16581226 }}&lt;/ref&gt; this does not appear to result in [[malnutrition]]. Although some children with autism also have [[gastrointestinal]] (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;&lt;ref&gt;{{vcite journal |journal=J Autism Dev Disord |year=2005 |volume=35 |issue=6 |pages=713–27 |title=Gastrointestinal factors in autistic disorder: a critical review |author=Erickson CA, Stigler KA, Corkins MR, Posey DJ, Fitzgerald JF, McDougle CJ |doi=10.1007/s10803-005-0019-4 |pmid=16267642 }}&lt;/ref&gt; studies report conflicting results, and the relationship between GI problems and ASD is unclear.&lt;ref&gt;{{vcite journal |author=Buie T, Campbell DB, Fuchs GJ 3rd ''et al.'' |author.= |title=Evaluation, diagnosis, and treatment of gastrointestinal disorders in individuals with ASDs: a consensus report |journal=Pediatrics |volume=125 |issue=Suppl 1 |pages=S1–18 |year=2010 |pmid=20048083 |doi=10.1542/peds.2009-1878C |url=http://pediatrics.aappublications.org/cgi/content/full/125/Supplement_1/S1 }}&lt;/ref&gt;

Parents of children with ASD have higher levels of [[stress (biological)|stress]].&lt;ref&gt;{{vcite journal |journal=Pediatrics |year=2007 |volume=119 |issue=5 |pages=e1040–6 |title=Psychological functioning and coping among mothers of children with autism: a population-based study |author=Montes G, Halterman JS |doi=10.1542/peds.2006-2819 |pmid=17473077 |url=http://pediatrics.aappublications.org/cgi/content/full/119/5/e1040 }}&lt;/ref&gt; 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.&lt;ref&gt;{{vcite journal |journal=Ment Retard Dev Disabil Res Rev |year=2007 |volume=13 |issue=4 |pages=313–20 |title=Siblings of individuals with autism spectrum disorders across the life course |author=Orsmond GI, Seltzer MM |doi=10.1002/mrdd.20171 |pmid=17979200 |url=http://www.waisman.wisc.edu/family/pubs/Autism/2007%20siblings_autism_life-course.pdf |format=PDF }}&lt;/ref&gt;

==Classification==

Autism is one of the five [[pervasive developmental disorder]]s (PDD), which are characterized by widespread abnormalities of social interactions and communication, and severely restricted interests and highly repetitive behavior.&lt;ref name=ICD-10-F84.0/&gt; These symptoms do not imply sickness, fragility, or emotional disturbance.&lt;ref name=Rapin/&gt;

Of the five PDD forms, [[Asperger syndrome]] is closest to autism in signs and likely causes; [[Rett syndrome]] and [[childhood disintegrative disorder]] share several signs with autism, but may have unrelated causes; [[PDD not otherwise specified]] (PDD-NOS; also called ''atypical autism'') is diagnosed when the criteria are not met for a more specific disorder.&lt;ref&gt;{{vcite journal |author=Volkmar FR, State M, Klin A |title=Autism and autism spectrum disorders: diagnostic issues for the coming decade |journal=J Child Psychol Psychiatry |volume=50 |issue=1–2 |pages=108–15 |year=2009 |doi=10.1111/j.1469-7610.2008.02010.x |pmid=19220594 }}&lt;/ref&gt; Unlike with autism, people with Asperger syndrome have no substantial delay in [[language development]].&lt;ref name=DSM-IV-TR-299.00/&gt; The terminology of autism can be bewildering, with autism, Asperger syndrome and PDD-NOS often called the ''autism spectrum disorders'' (ASD)&lt;ref name=CCD/&gt; or sometimes the ''autistic disorders'',&lt;ref&gt;{{vcite journal |author=Freitag CM |title=The genetics of autistic disorders and its clinical relevance: a review of the literature |journal=Mol Psychiatry |volume=12 |issue=1 |pages=2–22 |year=2007 |doi=10.1038/sj.mp.4001896 |pmid=17033636 }}&lt;/ref&gt; whereas autism itself is often called ''autistic disorder'', ''childhood autism'', or ''infantile autism''. In this article, ''autism'' refers to the classic autistic disorder; in clinical practice, though, ''autism'', ''ASD'', and ''PDD'' are often used interchangeably.&lt;ref name=Caronna/&gt; ASD, in turn, is a subset of the broader autism [[phenotype]], which describes individuals who may not have ASD but do have autistic-like [[Trait (biology)|traits]], such as avoiding eye contact.&lt;ref&gt;{{vcite journal |author=Piven J, Palmer P, Jacobi D, Childress D, Arndt S |title=Broader autism phenotype: evidence from a family history study of multiple-incidence autism families |journal=Am J Psychiatry |year=1997 |volume=154 |issue=2 |pages=185–90 |pmid=9016266 |url=http://ajp.psychiatryonline.org/cgi/reprint/154/2/185.pdf |format=PDF }}&lt;/ref&gt;

The manifestations of autism cover a wide [[Spectrum disorder|spectrum]], ranging from individuals with severe impairments—who may be silent, [[mentally disabled]], 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, [[pedantic]] communication.&lt;ref&gt;{{vcite journal |author=Happé F |title=Understanding assets and deficits in autism: why success is more interesting than failure |journal=Psychologist |volume=12 |issue=11 |pages=540–7 |year=1999 |url=http://www.thepsychologist.org.uk/archive/archive_home.cfm/volumeID_12-editionID_46-ArticleID_133-getfile_getPDF/thepsychologist/psy_11_99_p540-547_happe.pdf |format=PDF }}&lt;/ref&gt; Because the behavior spectrum is continuous, boundaries between diagnostic categories are necessarily somewhat arbitrary.&lt;ref name=Geschwind-2009/&gt; Sometimes the syndrome is divided into low-, medium- or [[high-functioning autism]] (LFA, MFA, and HFA), based on [[IQ]] thresholds,&lt;ref&gt;{{vcite journal |author=[[Simon Baron-Cohen|Baron-Cohen S]] |title=The hyper-systemizing, assortative mating theory of autism |journal=Prog Neuropsychopharmacol Biol Psychiatry |year=2006 |volume=30 |issue=5 |pages=865–72 |doi=10.1016/j.pnpbp.2006.01.010 |pmid=16519981 |url=http://autismresearchcentre.com/docs/papers/2006_BC_Neuropsychophamacology.pdf |format=PDF }}&lt;/ref&gt; 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 [[Syndrome|syndromal]] and non-syndromal autism; the syndromal autism is associated with severe or profound [[mental retardation]] or a congenital syndrome with physical symptoms, such as [[tuberous sclerosis]].&lt;ref&gt;{{vcite journal |journal=J Autism Dev Disord |year=2005 |volume=35 |issue=1 |pages=103–16 |title=Specific genetic disorders and autism: clinical contribution towards their identification |author=Cohen D, Pichard N, Tordjman S ''et al.'' |author.= |doi=10.1007/s10803-004-1038-2 |pmid=15796126 }}&lt;/ref&gt; Although individuals with Asperger syndrome tend to perform better cognitively than those with autism, the extent of the [[Diagnosis of Asperger syndrome#Differences from high-functioning autism|overlap between Asperger syndrome, HFA, and non-syndromal autism]] is unclear.&lt;ref&gt;Validity of ASD subtypes:
*{{vcite journal |journal=Rev Bras Psiquiatr |year=2006 |volume=28 |issue=suppl 1 |pages=S3–S11 |title=Autism and Asperger syndrome: an overview |author=Klin A |doi=10.1590/S1516-44462006000500002 |pmid=16791390 |url=http://www.scielo.br/scielo.php?script=sci_arttext&amp;pid=S1516-44462006000500002&amp;lng=en&amp;nrm=iso&amp;tlng=en }}
*{{vcite journal |journal=J Autism Dev Disord |volume=38 |issue=9 |pages=1611–24 |year=2008 |title=Examining the validity of autism spectrum disorder subtypes |author=Witwer AN, Lecavalier L |doi=10.1007/s10803-008-0541-2 |pmid=18327636 }}&lt;/ref&gt;

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 [[regressive autism]] is a specific subtype,&lt;ref name=Stefanatos&gt;{{vcite journal |author=Stefanatos GA |title=Regression in autistic spectrum disorders |journal=Neuropsychol Rev |volume=18 |issue=4 |pages=305–19 |year=2008 |pmid=18956241 |doi=10.1007/s11065-008-9073-y }}&lt;/ref&gt;&lt;ref name=Volkmar&gt;{{vcite journal |author=Volkmar F, Chawarska K, Klin A |title=Autism in infancy and early childhood |journal=Annu Rev Psychol |year=2005 |volume=56 |pages=315–36 |doi=10.1146/annurev.psych.56.091103.070159 |pmid=15709938 }} A partial update is in: {{vcite journal |journal=World Psychiatry |year=2008 |volume=7 |issue=1 |pages=19–21 |title=Autism in infants: an update |author=Volkmar FR, Chawarska K |pmid=18458791 |pmc=2366821 }}&lt;/ref&gt;&lt;ref name=Landa/&gt;&lt;ref name=Landa3/&gt; or that there is a continuum of behaviors between autism with and without regression.&lt;ref&gt;{{vcite journal |author=Ozonoff S, Heung K, Byrd R, Hansen R, [[Irva Hertz-Picciotto|Hertz-Picciotto I]] |title=The onset of autism: patterns of symptom emergence in the first years of life |journal=Autism Res |volume=1 |issue=6 |pages=320–328 |year=2008 |pmid=19360687 |doi=10.1002/aur.53 |pmc=2857525}}&lt;/ref&gt;

Research into causes has been hampered by the inability to identify biologically meaningful subpopulations&lt;ref&gt;{{vcite journal |journal=Pediatrics |year=2008 |volume=121 |issue=6 |pages=1225–9 |title=Autism and the environment: challenges and opportunities for research |author=Altevogt BM, Hanson SL, Leshner AI |doi=10.1542/peds.2007-3000 |pmid=18519493 |url=http://pediatrics.aappublications.org/cgi/content/full/121/6/1225 }}&lt;/ref&gt; and by the traditional boundaries between the disciplines of [[psychiatry]], [[psychology]], [[neurology]] and [[pediatrics]].&lt;ref&gt;{{vcite journal |author=Reiss AL |title=Childhood developmental disorders: an academic and clinical convergence point for psychiatry, neurology, psychology and pediatrics |journal=J Child Psychol Psychiatry |volume=50 |issue=1-2 |pages=87–98 |year=2009 |pmid=19220592 |doi=10.1111/j.1469-7610.2008.02046.x }}&lt;/ref&gt; Newer technologies such as [[fMRI]] and [[diffusion tensor imaging]] can help identify biologically relevant [[phenotype]]s (observable traits) that can be viewed on [[brain scan]]s, to help further [[neurogenetic]] studies of autism;&lt;ref&gt;{{vcite journal |author=Piggot J, Shirinyan D, Shemmassian S, Vazirian S, Alarcón M |title=Neural systems approaches to the neurogenetics of autism spectrum disorders |journal=Neuroscience |volume=164 |issue=1 |pages=247–56 |year=2009 |pmid=19482063 |doi=10.1016/j.neuroscience.2009.05.054 }}&lt;/ref&gt; one example is lowered activity in the [[fusiform face area]] of the brain, which is associated with impaired perception of people versus objects.&lt;ref name=Levy/&gt; It has been proposed to classify autism using genetics as well as behavior.&lt;ref&gt;{{vcite journal |journal=Am J Hum Genet |year=2008 |volume=82 |issue=1 |pages=7–9 |title=Unraveling autism |author=Stephan DA |doi=10.1016/j.ajhg.2007.12.003 |pmid=18179879 |pmc=2253980 }}&lt;/ref&gt;

==Causes==
{{main|Causes of autism}}

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.&lt;ref name=Fractionable/&gt; However, there is increasing suspicion that autism is instead a complex disorder whose core aspects have distinct causes that often co-occur.&lt;ref name=Fractionable&gt;{{vcite journal |author=Happé F, Ronald A |title=The 'fractionable autism triad': a review of evidence from behavioural, genetic, cognitive and neural research |journal=[[Neuropsychol Rev]] |volume=18 |issue=4 |pages=287–304 |year=2008 |pmid=18956240 |doi=10.1007/s11065-008-9076-8 }}&lt;/ref&gt;&lt;ref name=HappeTime/&gt;

[[File:Single Chromosome Mutations.png|thumb|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.|Deletion (1), duplication (2) and inversion (3) are all [[chromosome abnormalities]] that have been implicated in autism.&lt;ref name=Beaudet/&gt;]]
Autism has a strong genetic basis, although the [[Heritability of autism|genetics of autism]] are complex and it is unclear whether ASD is explained more by rare [[mutation]]s with major effects, or by rare multigene interactions of common genetic variants.&lt;ref name=Abrahams&gt;{{vcite journal |journal=[[Nature (journal)|Nat Rev Genet]] |year=2008 |volume=9 |issue=5 |pages=341–55 |title=Advances in autism genetics: on the threshold of a new neurobiology |author=Abrahams BS, Geschwind DH |doi=10.1038/nrg2346 |pmid=18414403 |pmc=2756414 }}&lt;/ref&gt;&lt;ref&gt;{{vcite journal |author=Buxbaum JD |title=Multiple rare variants in the etiology of autism spectrum disorders |journal=[[Dialogues Clin Neurosci]] |year=2009 |volume=11 |issue=1 |pages=35–43 |pmid=19432386 |url=http://www.dialogues-cns.org/brochures/40/htm/40_34.asp }}&lt;/ref&gt; Complexity arises due to interactions among multiple genes, the environment, and [[epigenetic]] factors which do not change [[DNA]] but are heritable and influence [[gene expression]].&lt;ref name=Rapin&gt;{{vcite journal |author=Rapin I, Tuchman RF |title=Autism: definition, neurobiology, screening, diagnosis |journal=[[Pediatr Clin North Am]] |volume=55 |issue=5 |pages=1129–46 |year=2008 |pmid=18929056 |doi=10.1016/j.pcl.2008.07.005 }}&lt;/ref&gt; Studies of twins suggest that [[heritability]] is 0.7 for autism and as high as 0.9 for ASD, and siblings of those with autism are about 25 times more likely to be autistic than the general population.&lt;ref name=Geschwind-2009/&gt; However, most of the mutations that increase autism risk have not been identified. Typically, autism cannot be traced to a [[Mendelian]] (single-gene) mutation or to a single [[chromosome abnormality]] like [[fragile X syndrome]], and none of the genetic syndromes associated with ASDs have been shown to selectively cause ASD.&lt;ref name=Abrahams/&gt; Numerous candidate genes have been located, with only small effects attributable to any particular gene.&lt;ref name=Abrahams/&gt; The large number of autistic individuals with unaffected family members may result from [[copy number variation]]s—spontaneous [[Deletion (genetics)|deletions]] or [[Gene duplication|duplications]] in genetic material during [[meiosis]].&lt;ref&gt;{{vcite journal |author=Cook EH, Scherer SW |title=Copy-number variations associated with neuropsychiatric conditions |journal=Nature |volume=455 |issue=7215 |pages=919–23 |year=2008 |pmid=18923514 |doi=10.1038/nature07458 }}&lt;/ref&gt; 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.&lt;ref name=Beaudet&gt;{{vcite journal |author=Beaudet AL |title=Autism: highly heritable but not inherited |journal=Nat Med |year=2007 |volume=13 |issue=5 |pages=534–6 |pmid=17479094 |doi=10.1038/nm0507-534 }}&lt;/ref&gt;

Several lines of evidence point to [[Synapse|synaptic]] dysfunction as a cause of autism.&lt;ref name=Levy/&gt; Some rare mutations may lead to autism by disrupting some synaptic pathways, such as those involved with [[cell adhesion]].&lt;ref name=Betancur&gt;{{vcite journal |author=Betancur C, Sakurai T, Buxbaum JD |title=The emerging role of synaptic cell-adhesion pathways in the pathogenesis of autism spectrum disorders |journal=[[Trends Neurosci]] |volume=32 |issue=7 |pages=402–12 |year=2009 |pmid=19541375 |doi=10.1016/j.tins.2009.04.003 }}&lt;/ref&gt; 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.&lt;ref name=Walsh&gt;{{vcite journal |author=Walsh CA, Morrow EM, Rubenstein JL |title=Autism and brain development |journal=[[Cell (journal)|Cell]] |volume=135 |issue=3 |pages=396–400 |year=2008 |pmid=18984148 |doi=10.1016/j.cell.2008.10.015 |pmc=2701104 }}&lt;/ref&gt; All known [[teratogen]]s (agents that cause [[birth defect]]s) related to the risk of autism appear to act during the first eight weeks from [[Human fertilization|conception]], 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.&lt;ref name=Arndt&gt;{{vcite journal |journal=[[Int J Dev Neurosci]] |year=2005 |volume=23 |issue=2–3 |pages=189–99 |title=The teratology of autism |author=Arndt TL, Stodgell CJ, Rodier PM |doi=10.1016/j.ijdevneu.2004.11.001 |pmid=15749245 }}&lt;/ref&gt;

Although evidence for other environmental causes is anecdotal and has not been confirmed by reliable studies,&lt;ref name=Rutter/&gt; extensive searches are underway.&lt;ref name=Szpir&gt;{{vcite journal |journal=[[Environ Health Perspect]] |year=2006 |volume=114 |issue=7 |pages=A412–8 |title=Tracing the origins of autism: a spectrum of new studies |author=Szpir M |url=http://www.ehponline.org/members/2006/114-7/focus.html |pmid=16835042 |pmc=1513312 |doi=10.1289/ehp.114-a412}}&lt;/ref&gt; [[Environmental factor]]s that have been claimed to contribute to or exacerbate autism, or may be important in future research, include certain foods, [[infectious disease]], [[heavy metals]], [[solvent]]s, [[diesel exhaust]], [[PCBs]], [[phthalates]] and [[phenol]]s used in [[plastic]] products, [[pesticide]]s, [[brominated flame retardant]]s, [[Ethanol|alcohol]], [[smoking]], [[illicit drug]]s, [[vaccine]]s,&lt;ref name=Newschaffer/&gt; and [[prenatal stress]],&lt;ref&gt;{{vcite journal |journal=[[Neurosci Biobehav Rev]] |year=2008 |title=Prenatal stress and risk for autism |author=Kinney DK, Munir KM, Crowley DJ, Miller AM |doi=10.1016/j.neubiorev.2008.06.004 |pmid=18598714 |volume=32 |issue=8 |pages=1519–32 |pmc=2632594 }}&lt;/ref&gt; although no links have been found, and some have been completely disproven.

Parents may first become aware of autistic symptoms in their child around the time of a routine vaccination. This has led to unsupported theories blaming [[Vaccine controversy#Vaccine overload|vaccine &quot;overload&quot;]], a [[Thiomersal controversy|vaccine preservative]], or the [[MMR vaccine controversy|MMR vaccine]] for causing autism.&lt;ref name=GerberOffit2009/&gt; The latter theory was supported by a litigation-funded study that has since been shown to have been &quot;an elaborate fraud&quot;.&lt;ref name=WakefieldarticleBMJ&gt;{{cite journal |year= 2011 |pages= c7452 |volume= 342:c7452 |title= Wakefield's article linking MMR vaccine and autism was fraudulent |author= Godlee F, Smith J, Marcovitch H |journal = [[BMJ]] |url=http://www.bmj.com/content/342/bmj.c7452.full |doi = 10.1136/bmj.c7452}}&lt;/ref&gt; Although these theories lack convincing scientific evidence and are biologically implausible,&lt;ref name=GerberOffit2009/&gt; parental concern about a potential vaccine link with autism has led to lower rates of [[childhood immunizations]], [[MMR vaccine controversy#Disease outbreaks|outbreaks of previously controlled childhood diseases]] in some countries, and the preventable deaths of several children.&lt;ref name=vaccines&gt;Vaccines and autism:
*{{vcite journal |journal=[[Can J Neurol Sci]] |year=2006 |volume=33 |issue=4 |pages=341–6 |title=Immunizations and autism: a review of the literature |author=Doja A, Roberts W |pmid=17168158 }}
*{{vcite journal |author=Gerber JS, [[Paul Offit|Offit PA]] |title=Vaccines and autism: a tale of shifting hypotheses |journal=[[Clin Infect Dis]] |volume=48 |issue=4 |pages=456–61 |year=2009 |pmid=19128068 |pmc= 2908388 |url=http://cid.oxfordjournals.org/content/48/4/456.full|doi=10.1086/596476 }}
*{{vcite journal |author=Gross L |title=A broken trust: lessons from the vaccine–autism wars |journal=PLoS Biol |volume=7 |issue=5 |pages=e1000114 |year=2009 |pmid=19478850 |doi=10.1371/journal.pbio.1000114 |pmc=2682483 }}
*{{vcite journal |author=Paul R |title=Parents ask: am I risking autism if I vaccinate my children? |journal=[[J Autism Dev Disord]] |volume=39 |issue=6 |pages=962–3 |year=2009 |pmid=19363650 |doi=10.1007/s10803-009-0739-y }}
*{{vcite journal |author= Poland GA, Jacobson RM |title= The Age-Old Struggle against the Antivaccinationists |journal= N Engl J Med |volume= 364 |pages= 97–9 |date= 2011-01-13 |url= http://www.nejm.org/doi/full/10.1056/NEJMp1010594 | doi=10.1056/NEJMp1010594 | pmid=21226573}}&lt;/ref&gt;&lt;ref name=dublin&gt;{{vcite journal |author=McBrien J, Murphy J, Gill D, Cronin M, O'Donovan C, Cafferkey MT |title=Measles outbreak in Dublin, 2000 |journal=Pediatr. Infect. Dis. J. |volume=22 |issue=7 |pages=580–4 |year=2003 |month=July |pmid=12867830 |doi=10.1097/00006454-200307000-00002}}&lt;/ref&gt;

==Mechanism==
Autism's symptoms result from maturation-related changes in various systems of the brain.&lt;!-- ref name=Penn/ --&gt; How autism occurs is not well understood. Its mechanism can be divided into two areas: the [[pathophysiology]] of brain structures and processes associated with autism, and the [[neuropsychological]] linkages between brain structures and behaviors.&lt;ref name=Penn&gt;{{vcite journal |author=Penn HE |title=Neurobiological correlates of autism: a review of recent research |journal=Child Neuropsychol |year=2006 |volume=12 |issue=1 |pages=57–79 |doi=10.1080/09297040500253546 |pmid=16484102 }}&lt;/ref&gt; The behaviors appear to have multiple pathophysiologies.&lt;ref name=London/&gt;

===Pathophysiology===
[[File:Autismbrain.jpg|thumb|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.|Autism affects the [[amygdala]], [[cerebellum]], and many other parts of the brain.&lt;ref name=Amaral/&gt;]]
Unlike many other brain disorders, such as [[Parkinson's]], 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.&lt;ref name=Geschwind&gt;{{vcite journal |author=Geschwind DH |title=Autism: many genes, common pathways? |title.= |journal=Cell |volume=135 |issue=3 |pages=391–5 |year=2008 |pmid=18984147 |doi=10.1016/j.cell.2008.10.016 |pmc=2756410 }}&lt;/ref&gt; Autism appears to result from developmental factors that affect many or all functional brain systems,&lt;ref&gt;{{vcite journal |journal=Ment Retard Dev Disabil Res Rev |year=2007 |volume=13 |issue=1 |pages=85–95 |title=The study of autism as a distributed disorder |author=Müller RA |doi=10.1002/mrdd.20141 |pmid=17326118 }}&lt;/ref&gt; and to disturb the timing of brain development more than the final product.&lt;ref name=Amaral&gt;{{vcite journal |journal=Trends Neurosci |year=2008 |volume=31 |issue=3 |pages=137–45 |title=Neuroanatomy of autism |author=[[David Amaral|Amaral DG]], Schumann CM, Nordahl CW |doi=10.1016/j.tins.2007.12.005 |pmid=18258309 }}&lt;/ref&gt; [[Neuroanatomical]] studies and the associations with [[teratogens]] strongly suggest that autism's mechanism includes alteration of brain development soon after conception.&lt;ref name=Arndt/&gt; This anomaly appears to start a cascade of pathological events in the brain that are significantly influenced by environmental factors.&lt;ref&gt;{{vcite journal |journal=Brain Pathol |year=2007 |volume=17 |issue=4 |pages=422–33 |title=The neuropathology of autism |author=Casanova MF |doi=10.1111/j.1750-3639.2007.00100.x |pmid=17919128 }}&lt;/ref&gt; Just after birth, the brains of autistic children tend to grow faster than usual, followed by normal or relatively slower growth in childhood. It is not known whether early overgrowth occurs in all autistic children. It seems to be most prominent in brain areas underlying the development of higher cognitive specialization.&lt;ref name=Geschwind-2009/&gt; Hypotheses for the cellular and molecular bases of pathological early overgrowth include the following:
* An excess of [[neuron]]s that causes local overconnectivity in key brain regions.&lt;ref&gt;{{vcite journal |journal=Neuron |year=2007 |volume=56 |issue=2 |pages=399–413 |title=Mapping early brain development in autism |author=Courchesne E, Pierce K, Schumann CM ''et al.'' |author.= |doi=10.1016/j.neuron.2007.10.016 |pmid=17964254 }}&lt;/ref&gt;
* Disturbed [[neuronal migration]] during early [[gestation]].&lt;ref name=Schmitz/&gt;&lt;ref name=Persico&gt;{{vcite journal |author=Persico AM, Bourgeron T |title=Searching for ways out of the autism maze: genetic, epigenetic and environmental clues |journal=Trends Neurosci |volume=29 |issue=7 |pages=349–58 |year=2006 |pmid=16808981 |doi=10.1016/j.tins.2006.05.010 }}&lt;/ref&gt;
* Unbalanced excitatory–inhibitory networks.&lt;ref name=Persico/&gt;
* Abnormal formation of [[synapse]]s and [[dendritic spine]]s,&lt;ref name=Persico/&gt; for example, by modulation of the [[neurexin]]–[[neuroligin]] [[Cell adhesion|cell-adhesion]] system,&lt;ref&gt;{{vcite journal |author=Südhof TC |title=Neuroligins and neurexins link synaptic function to cognitive disease |journal=Nature |volume=455 |issue=7215 |pages=903–11 |year=2008 |pmid=18923512 |doi=10.1038/nature07456 |pmc=2673233 }}&lt;/ref&gt; or by poorly regulated [[Protein synthesis|synthesis]] of synaptic proteins.&lt;ref&gt;{{vcite journal |author=Kelleher RJ 3rd, Bear MF |title=The autistic neuron: troubled translation? |title.= |journal=Cell |volume=135 |issue=3 |pages=401–6 |year=2008 |pmid=18984149 |doi=10.1016/j.cell.2008.10.017 }}&lt;/ref&gt;&lt;ref&gt;{{vcite journal |author=Bear MF, Dölen G, Osterweil E, Nagarajan N |title=Fragile X: translation in action. |title.= |journal=Neuropsychopharmacology |volume=33 |issue=1 |pages=84–7 |year=2008 |pmid=17940551 |doi=0.1038/sj.npp.1301610 }}&lt;/ref&gt; Disrupted synaptic development may also contribute to [[epilepsy]], which may explain why the two conditions are associated.&lt;ref&gt;{{vcite journal |author=Tuchman R, Moshé SL, Rapin I |title=Convulsing toward the pathophysiology of autism |journal=Brain Dev |volume=31 |issue=2 |pages=95–103 |year=2009 |pmid=19006654 |doi=10.1016/j.braindev.2008.09.009 |pmc=2734903 }}&lt;/ref&gt;

Interactions between the [[immune system]] and the [[nervous system]] begin early during the [[Human embryogenesis|embryonic stage]] of life, and successful neurodevelopment depends on a balanced immune response. Aberrant immune activity during critical periods of neurodevelopment is possibly part of the mechanism of some forms of ASD.&lt;ref&gt;{{vcite journal |journal=J Leukoc Biol |year=2006 |volume=80 |issue=1 |pages=1–15 |title=The immune response in autism: a new frontier for autism research |author=Ashwood P, Wills S, Van de Water J |doi=10.1189/jlb.1205707 |pmid=16698940 |url=http://www.jleukbio.org/cgi/content/full/80/1/1 }}&lt;/ref&gt; 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.&lt;ref&gt;{{vcite journal |journal=Res Autism Spectr Disord |volume=3 |issue=4 |year=2009 |pages=840–60 |doi=10.1016/j.rasd.2009.01.007 |author=Stigler KA, Sweeten TL, Posey DJ, McDougle CJ |title=Autism and immune factors: a comprehensive review }}&lt;/ref&gt; As [[autoantibodies]] are found in conditions other than ASD, and are not always present in ASD,&lt;ref&gt;{{vcite journal |journal=Ann N Y Acad Sci |year=2007 |volume=1107 |pages=79–91 |title=Autoantibodies in autism spectrum disorders (ASD) |author=Wills S, Cabanlit M, Bennett J, Ashwood P, Amaral D, Van de Water J |doi=10.1196/annals.1381.009 |pmid=17804535 }}&lt;/ref&gt; the relationship between immune disturbances and autism remains unclear and controversial.&lt;ref name=Schmitz&gt;{{vcite journal |journal=Neuropathol Appl Neurobiol |year=2008 |volume=34 |issue=1 |pages=4–11 |title=The neuropathology of autism: where do we stand? |title.= |author=Schmitz C, Rezaie P |doi=10.1111/j.1365-2990.2007.00872.x |pmid=17971078 }}&lt;/ref&gt;

The relationship of [[neurochemical]]s to autism is not well understood; several have been investigated, with the most evidence for the role of [[serotonin]] and of genetic differences in its transport.&lt;ref name=Levy&gt;{{vcite journal |author=Levy SE, Mandell DS, Schultz RT |title=Autism |journal=Lancet |volume=374 |issue=9701 |pages=1627–38 |year=2009 |pmid=19819542 |doi=10.1016/S0140-6736(09)61376-3 |pmc=2863325}}&lt;/ref&gt; The role of group I [[metabotropic glutamate receptors]] (mGluR) in the pathogenesis of [[fragile X syndrome]],  the most common identified genetic cause of autism, has led to interest in the possible implications for future autism research into this pathway.&lt;ref name=&quot;pmid18093519&quot;&gt;{{cite journal |author = Dölen G, Osterweil E, Rao BS, Smith GB, Auerbach BD, Chattarji S, Bear MF | title = Correction of fragile X syndrome in mice | journal = Neuron | volume = 56 | issue = 6 | pages = 955–62| year = 2007 | pmid = 18093519 | doi = 10.1016/j.neuron.2007.12.001 | pmc=2199268}}&lt;/ref&gt; Some data suggest an increase in several [[growth hormone]]s; other data argue for diminished [[growth factor]]s.&lt;ref&gt;{{vcite journal |author=Hughes JR |title=A review of recent reports on autism: 1000 studies published in 2007 |journal=Epilepsy Behav |volume=13 |issue=3 |pages=425–37 |year=2008 |pmid=18627794 |doi=10.1016/j.yebeh.2008.06.015 }}&lt;/ref&gt; Also, some [[inborn errors of metabolism]] are associated with autism, but probably account for less than 5% of cases.&lt;ref name=Manzi/&gt;

The [[mirror neuron system]] (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.&lt;ref&gt;MNS and autism:
*{{vcite journal |journal=Autism Res |year=2008 |volume=1 |issue=2 |pages=73–90 |title=Self–other relations in social development and autism: multiple roles for mirror neurons and other brain bases |author=Williams JHG |doi=10.1002/aur.15 |pmid=19360654 }}
*{{vcite journal |journal=Curr Biol |year=2008 |volume=18 |issue=1 |pages=R13–8 |title=A mirror up to nature |author=Dinstein I, Thomas C, Behrmann M, Heeger DJ |doi=10.1016/j.cub.2007.11.004 |pmid=18177704 |pmc=2517574 }}&lt;/ref&gt; 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.&lt;ref name=Iacoboni&gt;{{vcite journal |journal=Nat Rev Neurosci |year=2006 |volume=7 |issue=12 |pages=942–51 |title=The mirror neuron system and the consequences of its dysfunction |author=Iacoboni M, Dapretto M |doi=10.1038/nrn2024 |pmid=17115076 }}&lt;/ref&gt; However, individuals with autism also have abnormal brain activation in many circuits outside the MNS&lt;ref&gt;{{vcite journal |author=[[Uta Frith|Frith U]], Frith CD |year=2003 |title=Development and neurophysiology of mentalizing |journal=Philos Trans R Soc Lond B Biol Sci |volume=358 |issue=1431 |pages=459–73 |doi=10.1098/rstb.2002.1218 |pmid=12689373 |pmc=1693139 |url=http://rstb.royalsocietypublishing.org/content/358/1431/459.full.pdf |format=PDF }}&lt;/ref&gt; and the MNS theory does not explain the normal performance of autistic children on imitation tasks that involve a goal or object.&lt;ref&gt;{{vcite journal |journal=Q J Exp Psychol |year=2008 |volume=61 |issue=1 |pages=101–15 |title=Emulation and mimicry for social interaction: a theoretical approach to imitation in autism |author=Hamilton AFdC |doi=10.1080/17470210701508798 |pmid=18038342 |first2=&lt;!-- Work around Citation bot bug. --&gt; |last2=&lt;!-- Work around Citation bot bug. --&gt; }}&lt;/ref&gt;

[[File:Powell2004Fig1A.jpeg|thumb|upright|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.|Autistic individuals tend to use different areas of the brain (yellow) for a movement task compared to a control group (blue).&lt;ref name=Powell&gt;{{vcite journal |author=Powell K |title=Opening a window to the autistic brain |journal=PLoS Biol |volume=2 |issue=8 |pages=E267 |year=2004 |pmid=15314667 |pmc=509312 |doi=10.1371/journal.pbio.0020267 |url=http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.0020267 }}&lt;/ref&gt;]]
ASD-related patterns of low function and aberrant activation in the brain differ depending on whether the brain is doing social or nonsocial tasks.&lt;ref&gt;{{vcite journal |journal=Biol Psychiatry |year=2009 |volume=65 |issue=1 |pages=63–74 |doi=10.1016/j.biopsych.2008.09.022 |pmid=18996505 |author=Di Martino A, Ross K, Uddin LQ, Sklar AB, Castellanos FX, Milham MP |title=Functional brain correlates of social and nonsocial processes in autism spectrum disorders: an activation likelihood estimation meta-analysis }}&lt;/ref&gt;
In autism there is evidence for reduced functional connectivity of the [[default network]], a large-scale brain network involved in social and emotional processing, with intact connectivity of the [[task-positive network]], 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 [[self-referential]] thought.&lt;ref&gt;{{vcite journal |author=Broyd SJ, Demanuele C, Debener S, Helps SK, James CJ, Sonuga-Barke EJS |title=Default-mode brain dysfunction in mental disorders: a systematic review |journal=Neurosci Biobehav Rev |year=2009 |volume=33 |issue=3 |pages=279–96 |pmid=18824195 |doi=10.1016/j.neubiorev.2008.09.002 }}&lt;/ref&gt; A 2008 brain-imaging study found a specific pattern of signals in the [[cingulate cortex]] which differs in individuals with ASD.&lt;ref&gt;{{vcite journal |journal=Neuron |year=2008 |volume=57 |issue=3 |pages=463–73 |title=Self responses along cingulate cortex reveal quantitative neural phenotype for high-functioning autism |author=Chiu PH, Kayali MA, Kishida KT ''et al.'' |author.= |doi=10.1016/j.neuron.2007.12.020 |pmid=18255038 |laysummary=http://www.technologyreview.com/Biotech/20167/ |laysource=Technol Rev |laydate=2007-02-07 }}&lt;/ref&gt;

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.&lt;ref&gt;{{vcite journal |journal=Cereb Cortex |year=2007 |volume=17 |issue=4 |pages=951–61 |title=Functional and anatomical cortical underconnectivity in autism: evidence from an FMRI study of an executive function task and corpus callosum morphometry |author=Just MA, Cherkassky VL, Keller TA, Kana RK, Minshew NJ |doi=10.1093/cercor/bhl006 |pmid=16772313 |url=http://cercor.oxfordjournals.org/cgi/content/full/17/4/951 }}&lt;/ref&gt; Evidence for this theory has been found in [[functional neuroimaging]] studies on autistic individuals&lt;ref name=Williams&gt;{{vcite journal |author=Williams DL, Goldstein G, Minshew NJ |title=Neuropsychologic functioning in children with autism: further evidence for disordered complex information-processing |journal=Child Neuropsychol |volume=12 |issue=4–5 |pages=279–98 |year=2006 |pmid=16911973 |doi=10.1080/09297040600681190 |pmc=1803025 }}&lt;/ref&gt; and by a [[brainwave]] study that suggested that adults with ASD have local overconnectivity in the [[Cerebral cortex|cortex]] and weak functional connections between the [[frontal lobe]] and the rest of the cortex.&lt;ref&gt;{{vcite journal |author=Murias M, Webb SJ, Greenson J, Dawson G |title=Resting state cortical connectivity reflected in EEG coherence in individuals with autism |journal=Biol Psychiatry |volume=62 |issue=3 |pages=270–3 |year=2007 |pmid=17336944 |doi=10.1016/j.biopsych.2006.11.012 |pmc=2001237 }}&lt;/ref&gt; Other evidence suggests the underconnectivity is mainly within each [[Cerebral hemisphere|hemisphere]] of the cortex and that autism is a disorder of the [[Association areas|association cortex]].&lt;ref&gt;{{vcite journal |journal=Arch Neurol |year=2007 |volume=64 |issue=7 |pages=945–50 |title=The new neurobiology of autism: cortex, connectivity, and neuronal organization |author=Minshew NJ, Williams DL |pmid=17620483 |doi=10.1001/archneur.64.7.945 |pmc=2597785 }}&lt;/ref&gt;

From studies based on [[event-related potential]]s, 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 nonsocial stimuli.&lt;ref&gt;{{vcite journal |author=Jeste SS, Nelson CA 3rd |title=Event related potentials in the understanding of autism spectrum disorders: an analytical review |journal=J Autism Dev Disord |volume=39 |issue=3 |pages=495–510 |year=2009 |pmid=18850262 |doi=10.1007/s10803-008-0652-9 }}&lt;/ref&gt; For example, [[magnetoencephalography]] studies have found evidence in autistic children of delayed responses in the brain's processing of auditory signals.&lt;ref&gt;{{vcite journal |author=Roberts TP, Schmidt GL, Egeth M ''et al.'' |author.= |title=Electrophysiological signatures: magnetoencephalographic studies of the neural correlates of language impairment in autism spectrum disorders |journal=Int J Psychophysiol |volume=68 |issue=2 |pages=149–60 |year=2008 |pmid=18336941 |doi=10.1016/j.ijpsycho.2008.01.012 |pmc=2397446 }}&lt;/ref&gt;

In the genetic area, relations have been found between autism and [[schizophrenia]] based on duplications and deletions of chromosomes; research showed that schizophrenia and autism are significantly more common in combination with [[1q21.1 deletion syndrome]].  Research on autism/schizophrenia relations for chromosome 15 (15q13.3), chromosome 16 (16p13.1) and chromosome 17 (17p12) are inconclusive.&lt;ref&gt;{{cite journal |author=Crespi B, Stead P, Elliot M |title=Evolution in health and medicine Sackler colloquium: Comparative genomics of autism and schizophrenia |journal=Proc. Natl. Acad. Sci. U.S.A. |volume=107 | issue= Suppl 1 |pages=1736–41 |year=2010 |month=January |pmid=19955444 |pmc=2868282 |doi=10.1073/pnas.0906080106}}&lt;/ref&gt;

===Neuropsychology===
Two major categories of [[cognitive]] theories have been proposed about the links between autistic brains and behavior.

The first category focuses on deficits in [[social cognition]]. The [[empathizing–systemizing theory]] 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;&lt;ref name=E-S-theory/&gt; this extension is controversial, as many studies contradict the idea that baby boys and girls respond differently to people and objects.&lt;ref&gt;{{vcite journal |author=Spelke ES |title=Sex differences in intrinsic aptitude for mathematics and science?: a critical review |journal=Am Psychol |volume=60 |issue=9 |pages=950–8 |year=2005 |pmid=16366817 |doi=10.1037/0003-066X.60.9.950 |url=http://www.wjh.harvard.edu/~lds/pdfs/spelke2005.pdf |format=PDF }}&lt;/ref&gt;

These theories are somewhat related to the earlier [[theory of mind]] 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 [[Sally–Anne test]] for reasoning about others' motivations,&lt;ref name=E-S-theory&gt;{{vcite journal |author=Baron-Cohen S |title=Autism: the empathizing–systemizing (E-S) theory |journal=Ann N Y Acad Sci |volume=1156 |pages=68–80 |year=2009 |pmid=19338503 |doi=10.1111/j.1749-6632.2009.04467.x |url=http://autismresearchcentre.com/docs/papers/2009_BC_nyas.pdf |format=PDF }}&lt;/ref&gt; and the mirror neuron system theory of autism described in ''[[#Pathophysiology|Pathophysiology]]'' maps well to the hypothesis.&lt;ref name=Iacoboni/&gt; However, most studies have found no evidence of impairment in autistic individuals' ability to understand other people's basic intentions or goals; instead, data suggests that impairments are found in understanding more complex social emotions or in considering others' viewpoints.&lt;ref&gt;{{vcite journal |author=Hamilton AFdC |title=Goals, intentions and mental states: challenges for theories of autism |journal=J Child Psychol Psychiatry |volume=50 |issue=8 |pages=881–92 |year=2009 |pmid=19508497 |doi=10.1111/j.1469-7610.2009.02098.x }}&lt;/ref&gt;

The second category focuses on nonsocial or general processing. [[Executive dysfunction]] hypothesizes that autistic behavior results in part from deficits in [[working memory]], planning, [[Inhibition Theory|inhibition]], and other forms of executive function.&lt;ref name=Kenworthy/&gt; Tests of core executive processes such as eye movement tasks indicate improvement from late childhood to adolescence, but performance never reaches typical adult levels.&lt;ref&gt;{{vcite journal |author=O'Hearn K, Asato M, Ordaz S, Luna B |title=Neurodevelopment and executive function in autism |journal=Dev Psychopathol |volume=20 |issue=4 |pages=1103–32 |year=2008 |pmid=18838033 |doi=10.1017/S0954579408000527 }}&lt;/ref&gt; A strength of the theory is predicting stereotyped behavior and narrow interests;&lt;ref&gt;{{vcite journal |author=Hill EL |title=Executive dysfunction in autism |journal=Trends Cogn Sci |year=2004 |volume=8 |issue=1 |pages=26–32 |doi=10.1016/j.dr.2004.01.001 |pmid=14697400 }}&lt;/ref&gt; two weaknesses are that executive function is hard to measure&lt;ref name=Kenworthy&gt;{{vcite journal |author=Kenworthy L, Yerys BE, Anthony LG, Wallace GL |title=Understanding executive control in autism spectrum disorders in the lab and in the real world |journal=Neuropsychol Rev |volume=18 |issue=4 |pages=320–38 |year=2008 |pmid=18956239 |doi=10.1007/s11065-008-9077-7 |pmc=2856078}}&lt;/ref&gt; and that executive function deficits have not been found in young autistic children.&lt;ref name=Sigman/&gt;

[[Weak central coherence theory]] 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.&lt;ref&gt;{{vcite journal |author=Happé F, Frith U |title=The weak coherence account: detail-focused cognitive style in autism spectrum disorders |journal=J Autism Dev Disord |year=2006 |volume=36 |issue=1 |pages=5–25 |doi=10.1007/s10803-005-0039-0 |pmid=16450045 }}&lt;/ref&gt; A related theory—enhanced perceptual functioning—focuses more on the superiority of locally oriented and [[perceptual]] operations in autistic individuals.&lt;ref&gt;{{vcite journal |journal=J Autism Dev Disord |year=2006 |volume=36 |issue=1 |pages=27–43 |title=Enhanced perceptual functioning in autism: an update, and eight principles of autistic perception |author=Mottron L, [[Michelle Dawson|Dawson M]], Soulières I, Hubert B, Burack J |doi=10.1007/s10803-005-0040-7 |pmid=16453071 }}&lt;/ref&gt; These theories map well from the underconnectivity theory of autism.

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.&lt;ref name=HappeTime&gt;{{vcite journal |author=Happé F, Ronald A, [[Robert Plomin|Plomin R]] |title=Time to give up on a single explanation for autism |journal=Nat Neurosci |year=2006 |volume=9 |issue=10 |pages=1218–20 |doi=10.1038/nn1770 |pmid=17001340 }}&lt;/ref&gt; A combined theory based on multiple deficits may prove to be more useful.&lt;ref&gt;{{vcite journal |journal=Dev Rev |year=2007 |volume=27 |issue=2 |pages=224–60 |title=Cognitive theories of autism |author=Rajendran G, Mitchell P |doi=10.1016/j.dr.2007.02.001 }}&lt;/ref&gt;

==Screening==
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.&lt;ref name=Landa3/&gt; According to an article in the ''Journal of Autism and Developmental Disorders'', failure to meet any of the following milestones ''&quot;is an absolute indication to proceed with further evaluations. Delay in referral for such testing may delay early diagnosis and treatment and affect the long-term outcome.&quot;''&lt;ref name=Filipek/&gt;
*No [[babbling]] by 12 months.
*No [[Gesture|gesturing]] (pointing, waving bye-bye, etc.) by 12 months.
*No single words by 16 months.
*No two-word spontaneous (''not just [[echolalia|echolalic]]'') phrases by 24 months.
*''Any'' loss of ''any'' language or social skills, ''at any age''.
US and Japanese practice is to [[Screening (medicine)|screen]] all children for ASD at 18 and 24 months, using autism-specific formal screening tests. In contrast, in the UK, children whose families or doctors recognize possible signs of autism are screened. It is not known which approach is more effective.&lt;ref name=Levy/&gt; 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 [[Sensitivity (tests)|sensitivity]] (many false-negatives) but good [[Specificity (tests)|specificity]] (few false-positives).&lt;ref name=Landa3/&gt; It may be more accurate to precede these tests with a broadband screener that does not distinguish ASD from other developmental disorders.&lt;ref&gt;{{vcite journal |author=Wetherby AM, Brosnan-Maddox S, Peace V, Newton L |title=Validation of the Infant–Toddler Checklist as a broadband screener for autism spectrum disorders from 9 to 24 months of age |journal=Autism |volume=12 |issue=5 |pages=487–511 |year=2008 |pmid=18805944 |doi=10.1177/1362361308094501 |pmc=2663025 }}&lt;/ref&gt; Screening tools designed for one culture's norms for behaviors like eye contact may be inappropriate for a different culture.&lt;ref&gt;{{vcite journal |journal=Acta Paediatr |year=2008 |volume=97 |issue=5 |pages=539–40 |title=The challenge of screening for autism spectrum disorder in a culturally diverse society |author=Wallis KE, Pinto-Martin J |doi=10.1111/j.1651-2227.2008.00720.x |pmid=18373717 }}&lt;/ref&gt; Although [[genetic screening]] for autism is generally still impractical, it can be considered in some cases, such as children with neurological symptoms and [[dysmorphic feature]]s.&lt;ref&gt;{{vcite journal |author=Lintas C, Persico AM |title=Autistic phenotypes and genetic testing: state-of-the-art for the clinical geneticist |journal=J Med Genet |volume=46 |issue=1 |pages=1–8 |year=2009 |pmid=18728070 |pmc=2603481 |doi=10.1136/jmg.2008.060871 |url=http://jmg.bmj.com/content/46/1/1.long }}&lt;/ref&gt;

==Diagnosis==
[[Medical diagnosis|Diagnosis]] is based on behavior, not cause or mechanism.&lt;ref name=London&gt;{{vcite journal |journal=Brain Pathol |year=2007 |volume=17 |issue=4 |pages=408–11 |title=The role of the neurobiologist in redefining the diagnosis of autism |author=London E |doi=10.1111/j.1750-3639.2007.00103.x |pmid=17919126 }}&lt;/ref&gt;&lt;ref&gt;{{vcite journal |journal=BMJ |year=2003 |volume=327 |issue=7413 |pages=488–93 |title=Diagnosis of autism |author=Baird G, Cass H, Slonims V |doi=10.1136/bmj.327.7413.488 |pmid=12946972 |pmc=188387 |url=http://www.bmj.com/cgi/content/full/327/7413/488 }}&lt;/ref&gt; Autism is defined in the [[DSM-IV-TR]] 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 [[Rett syndrome]] or [[childhood disintegrative disorder]].&lt;ref name=DSM-IV-TR-299.00&gt;{{vcite book |title=Diagnostic and Statistical Manual of Mental Disorders |edition=4th, text revision ([[DSM-IV-TR]]) |author=American Psychiatric Association |year=2000 |isbn=0-89042-025-4 |chapter=Diagnostic criteria for 299.00 Autistic Disorder |chapterurl=http://cdc.gov/ncbddd/autism/hcp-dsm.html |publisher=&lt;!--comment to foil Citation bot--&gt; |location=&lt;!--comment to foil Citation bot--&gt; }}&lt;/ref&gt; [[ICD-10]] uses essentially the same definition.&lt;ref name=ICD-10-F84.0&gt;{{vcite web |url=http://apps.who.int/classifications/apps/icd/icd10online/?gf80.htm+f84 |year=2007 |accessdate=2009-10-10 |work=ICD-10: International Statistical Classification of Diseases and Related Health Problems: Tenth Revision |publisher=World Health Organization |title=F84. Pervasive developmental disorders }}&lt;/ref&gt;

Several diagnostic instruments are available. Two are commonly used in autism research: the [[Autism Diagnostic Interview-Revised]] (ADI-R) is a semistructured parent interview, and the [[Autism Diagnostic Observation Schedule]] (ADOS) uses observation and interaction with the child. The [[Childhood Autism Rating Scale]] (CARS) is used widely in clinical environments to assess severity of autism based on observation of children.&lt;ref name=Volkmar/&gt;

A [[pediatrician]] 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 [[medical conditions]].&lt;ref name=Dover/&gt; A pediatric [[neuropsychologist]] is often asked to assess behavior and cognitive skills, both to aid diagnosis and to help recommend educational interventions.&lt;ref name=Kanne&gt;{{vcite journal |author=Kanne SM, Randolph JK, Farmer JE |title=Diagnostic and assessment findings: a bridge to academic planning for children with autism spectrum disorders |journal=Neuropsychol Rev |volume=18 |issue=4 |pages=367–84 |year=2008 |pmid=18855144 |doi=10.1007/s11065-008-9072-z }}&lt;/ref&gt; A [[differential diagnosis]] for ASD at this stage might also consider [[mental retardation]], [[hearing impairment]], and a [[specific language impairment]]&lt;ref name=Dover/&gt; such as [[Landau–Kleffner syndrome]].&lt;ref&gt;{{vcite journal |journal=Dev Med Child Neurol |year=2000 |volume=42 |issue=5 |pages=349–53 |title=Autistic regression and Landau–Kleffner syndrome: progress or confusion? |title.= |author=Mantovani JF |doi=10.1017/S0012162200210621 |pmid=10855658 }}&lt;/ref&gt; The presence of autism can make it harder to diagnose coexisting psychiatric disorders such as [[Mood disorder|depression]].&lt;ref&gt;{{vcite journal |author=Matson JL, Neal D |title=Cormorbidity: diagnosing comorbid psychiatric conditions |journal=Psychiatr Times |volume=26 |issue=4 |year=2009 |url=http://www.psychiatrictimes.com/display/article/10168/1403043 }}&lt;/ref&gt;

[[Clinical genetics]] evaluations are often done once ASD is diagnosed, particularly when other symptoms already suggest a genetic cause.&lt;ref name=Caronna/&gt; Although genetic technology allows clinical geneticists to link an estimated 40% of cases to genetic causes,&lt;ref&gt;{{vcite journal |journal=Genet Med |year=2008 |volume=10 |issue=1 |pages=4–12 |title=Genetics evaluation for the etiologic diagnosis of autism spectrum disorders |author=Schaefer GB, Mendelsohn NJ |doi=10.1097/GIM.0b013e31815efdd7 |pmid=18197051 |laysummary=http://www.medicalnewstoday.com/articles/96448.php |laysource=Medical News Today |laydate=2008-02-07 }}&lt;/ref&gt; consensus guidelines in the US and UK are limited to high-resolution chromosome and [[fragile X]] testing.&lt;ref name=Caronna/&gt; A [[genotype]]-first model of diagnosis has been proposed, which would routinely assess the genome's copy number variations.&lt;ref&gt;{{vcite journal |author=Ledbetter DH |title=Cytogenetic technology—genotype and phenotype |journal=N Engl J Med |volume=359 |issue=16 |pages=1728–30 |year=2008 |pmid=18784093 |doi=10.1056/NEJMe0806570 }}&lt;/ref&gt;  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.&lt;ref&gt;{{vcite journal |journal=Am J Med Genet C Semin Med Genet |year=2006 |volume=142C |issue=1 |pages=52–7 |title=Genetic counseling and ethical issues for autism |author=McMahon WM, Baty BJ, Botkin J |doi=10.1002/ajmg.c.30082 |pmid=16419100 }}&lt;/ref&gt; [[Metabolic]] and [[neuroimaging]] tests are sometimes helpful, but are not routine.&lt;ref name=Caronna/&gt;

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.&lt;ref name=Landa3&gt;{{vcite journal |journal=Nat Clin Pract Neurol |year=2008 |volume=4 |issue=3 |pages=138–47 |title=Diagnosis of autism spectrum disorders in the first 3 years of life |author=Landa RJ |doi=10.1038/ncpneuro0731 |pmid=18253102 }}&lt;/ref&gt; 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.&lt;ref name=Dover&gt;{{vcite journal |journal=Arch Dis Child |year=2007 |volume=92 |issue=6 |pages=540–5 |title=How to diagnose autism |author=Dover CJ, Le Couteur A |doi=10.1136/adc.2005.086280 |pmid=17515625 }}&lt;/ref&gt; A 2009 US 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.&lt;ref&gt;{{vcite journal |author=Shattuck PT, Durkin M, Maenner M ''et al.'' |author.= |title=Timing of identification among children with an autism spectrum disorder: findings from a population-based surveillance study |journal=J Am Acad Child Adolesc Psychiatry |volume=48 |issue=5 |pages=474–83 |year=2009 |pmid=19318992 |doi=10.1097/CHI.0b013e31819b3848 }}&lt;/ref&gt; 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.&lt;ref&gt;{{vcite web |publisher=National Autistic Society |title=Diagnosis: how can it benefit me as an adult? |title.= |year=2005 |url=http://www.autism.org.uk/about-autism/all-about-diagnosis/diagnosis-the-process-for-adults/diagnosis-how-can-it-benefit-me-as-an-adult.aspx |accessdate=2008-03-24 }}&lt;/ref&gt;

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.&lt;ref&gt;{{vcite journal |author=Shattuck PT, Grosse SD |title=Issues related to the diagnosis and treatment of autism spectrum disorders |journal=Ment Retard Dev Disabil Res Rev |year=2007 |volume=13 |issue=2 |pages=129–35 |doi=10.1002/mrdd.20143 |pmid=17563895 }}&lt;/ref&gt; It is particularly hard to diagnose autism among the [[visually impaired]], partly because some of its diagnostic criteria depend on vision, and partly because autistic symptoms overlap with those of common blindness syndromes or [[blindism]]s.&lt;ref&gt;{{vcite journal |title=Visual impairment and autism: current questions and future research |author=Cass H |journal=Autism |year=1998 |volume=2 |issue=2 |pages=117–38 |doi=10.1177/1362361398022002 }}&lt;/ref&gt;

==Management==
{{main|Autism therapies}}
[[File:Opening a window to the autistic brain.jpg|thumb|alt=A young child points, in front of a woman who smiles and points in the same direction.|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.&lt;ref name=Powell/&gt;]]
The main goals when treating children with autism 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.&lt;ref name=CCD/&gt; Families and the educational system are the main resources for treatment.&lt;ref name=Levy/&gt; Studies of interventions have methodological problems that prevent definitive conclusions about [[efficacy]].&lt;ref&gt;{{vcite journal |author=Ospina MB, Krebs Seida J, Clark B ''et al.'' |author.= |title=Behavioural and developmental interventions for autism spectrum disorder: a clinical systematic review |journal=PLoS ONE |volume=3 |issue=11 |pages=e3755 |year=2008 |pmid=19015734 |pmc=2582449 |doi=10.1371/journal.pone.0003755 |url=http://www.plosone.org/article/info:doi/10.1371/journal.pone.0003755 }}&lt;/ref&gt; Although many [[psychosocial]] interventions have some positive evidence, suggesting that some form of treatment is preferable to no treatment, the methodological quality of [[systematic review]]s 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.&lt;ref&gt;{{vcite journal |author=Krebs Seida J, Ospina MB, Karkhaneh M, Hartling L, Smith V, Clark B |title=Systematic reviews of psychosocial interventions for autism: an umbrella review |journal=Dev Med Child Neurol |volume=51 |issue=2 |pages=95–104 |year=2009 |pmid=19191842 |doi=10.1111/j.1469-8749.2008.03211.x }}&lt;/ref&gt; Intensive, sustained [[special education]] programs and [[behavior therapy]] early in life can help children acquire self-care, social, and job skills,&lt;ref name=CCD&gt;{{vcite journal |journal=Pediatrics |year=2007 |volume=120 |issue=5 |pages=1162–82 |title=Management of children with autism spectrum disorders |author=Myers SM, Johnson CP, Council on Children with Disabilities |doi=10.1542/peds.2007-2362 |pmid=17967921 |url=http://pediatrics.aappublications.org/cgi/content/full/120/5/1162 |laysummary=http://aap.org/advocacy/releases/oct07autism.htm |laysource=AAP |laydate=2007-10-29 }}&lt;/ref&gt; and often improve functioning and decrease symptom severity and maladaptive behaviors;&lt;ref name=Rogers&gt;{{vcite journal |journal=J Clin Child Adolesc Psychol |year=2008 |volume=37 |issue=1 |pages=8–38 |title=Evidence-based comprehensive treatments for early autism |author=Rogers SJ, Vismara LA |doi=10.1080/15374410701817808 |pmid=18444052 |pmc=2943764}}&lt;/ref&gt; claims that intervention by around age three years is crucial are not substantiated.&lt;ref name=HowlinCharman&gt;{{vcite journal |author=Howlin P, Magiati I, Charman T |title=Systematic review of early intensive behavioral interventions for children with autism |journal=Am J Intellect Dev Disabil |volume=114 |issue=1 |pages=23–41 |year=2009 |pmid=19143460 |doi=10.1352/2009.114:23-41 }}&lt;/ref&gt; Available approaches include [[applied behavior analysis]] (ABA), developmental models, [[TEACCH|structured teaching]], [[speech and language therapy]], [[social skills]] therapy, and [[occupational therapy]].&lt;ref name=CCD/&gt;

Educational interventions can be effective to varying degrees in most children: intensive ABA treatment has demonstrated effectiveness in enhancing global functioning in preschool children&lt;ref name=Eikeseth&gt;{{vcite journal |journal=Res Dev Disabil |year=2009 |title=Outcome of comprehensive psycho-educational interventions for young children with autism |author=Eikeseth S |doi=10.1016/j.ridd.2008.02.003 |pmid=18385012 |volume=30 |issue=1 |pages=158–78 }}&lt;/ref&gt; and is well-established for improving intellectual performance of young children.&lt;ref name=Rogers/&gt; Neuropsychological reports are often poorly communicated to educators, resulting in a gap between what a report recommends and what education is provided.&lt;ref name=Kanne/&gt; It is not known whether treatment programs for children lead to significant improvements after the children grow up,&lt;ref name=Rogers/&gt; and the limited research on the effectiveness of adult residential programs shows mixed results.&lt;ref&gt;{{vcite journal |journal=J Autism Dev Disord |year=2003 |volume=33 |issue=2 |pages=131–40 |title=Effects of a model treatment approach on adults with autism |author=Van Bourgondien ME, Reichle NC, [[Eric Schopler|Schopler E]] |doi=10.1023/A:1022931224934 |pmid=12757352 }}&lt;/ref&gt; The appropriateness of including children with varying severity of autism spectrum disorders in the general education population is a subject of current debate among educators and researchers.&lt;ref&gt;{{vcite journal |journal=Topics in Language Disorders |year=2003 |volume=23 |issue=2 |pages=116–133 |title=Inclusion of Learners with Autism Spectrum Disorders in General Education Settings |authors= Simpson RL, de Boer-Ott SR, Smith-Myles B|url=http://www.nursingcenter.com/pdf.asp?AID=520301 }}&lt;/ref&gt;

Many medications are used to treat ASD symptoms that interfere with integrating a child into home or school when behavioral treatment fails.&lt;ref name=Rapin/&gt;&lt;ref&gt;{{vcite journal |journal=Harv Rev Psychiatry |year=2008 |volume=16 |issue=2 |pages=97–112 |title=Pharmacological treatment options for autism spectrum disorders in children and adolescents |author=Leskovec TJ, Rowles BM, Findling RL |doi=10.1080/10673220802075852 |pmid=18415882 }}&lt;/ref&gt; More than half of US children diagnosed with ASD are prescribed [[psychoactive drug]]s or [[anticonvulsant]]s, with the most common drug classes being [[antidepressant]]s, [[stimulant]]s, and [[antipsychotic]]s.&lt;ref&gt;{{vcite journal |journal=J Child Adolesc Psychopharmacol |year=2007 |volume=17 |issue=3 |pages=348–55 |title=Medication use among children with autism spectrum disorders |author=Oswald DP, Sonenklar NA |doi=10.1089/cap.2006.17303 |pmid=17630868 }}&lt;/ref&gt; Aside from antipsychotics,&lt;ref&gt;{{vcite journal |journal=J Clin Invest |year=2008 |volume=118 |issue=1 |pages=6–14 |title=Antipsychotics in the treatment of autism |author=Posey DJ, Stigler KA, Erickson CA, McDougle CJ |doi=10.1172/JCI32483 |pmid=18172517 |pmc=2171144 |url=http://www.jci.org/articles/view/32483/version/1 }}&lt;/ref&gt; there is scant reliable research about the effectiveness or safety of drug treatments for adolescents and adults with ASD.&lt;ref&gt;Lack of research on drug treatments:
*{{vcite journal |journal=Aust Fam Physician |year=2007 |volume=36 |issue=9 |pages=741–4 |title=Children and autism—part 1—recognition and pharmacological management |author=Angley M, Young R, Ellis D, Chan W, McKinnon R |pmid=17915375 |url=http://www.racgp.org.au/afp/200709/200709angley.pdf |format=PDF }}
*{{vcite journal |journal=Autism |year=2007 |volume=11 |issue=4 |pages=335–48 |title=Systematic review of the effectiveness of pharmacological treatments for adolescents and adults with autism spectrum disorder |author=Broadstock M, Doughty C, Eggleston M |doi=10.1177/1362361307078132 |pmid=17656398 }}&lt;/ref&gt; A person with ASD may respond atypically to medications, the medications can have [[Adverse effect (medicine)|adverse effects]],&lt;ref name=CCD/&gt; and no known medication relieves autism's core symptoms of social and communication impairments.&lt;ref&gt;{{vcite journal |journal=Novartis Found Symp |year=2003 |volume=251 |pages=235–44; discussion 245–9, 281–97 |title=Why have drug treatments been so disappointing? |title.= |author=Buitelaar JK |doi=10.1002/0470869380.ch14 |pmid=14521196 }}&lt;/ref&gt; Experiments in mice have reversed or reduced some symptoms related to autism by replacing or modulating gene function,&lt;ref name=Walsh/&gt;&lt;ref name=&quot;pmid18093519&quot;/&gt; suggesting the possibility of targeting therapies to specific rare mutations known to cause autism.&lt;ref name=Betancur/&gt;&lt;ref name=&quot;pmid20303363&quot;&gt;{{cite journal |author = Dölen G, Carpenter RL, Ocain TD, Bear MF | title = Mechanism-based approaches to treating fragile X | journal = Pharmacol Ther | volume = 127 | issue = 1 | pages = 78–93| year = 2010 | pmid = 20303363 | doi = 10.1016/j.pharmthera.2010.02.008}}&lt;/ref&gt;

Although many [[Alternative therapies for developmental and learning disabilities|alternative therapies and interventions]] are available, few are supported by scientific studies.&lt;ref name=Sigman/&gt;&lt;ref&gt;Lack of support for interventions:
*{{vcite journal |journal=Dev Med Child Neurol |year=2005 |volume=47 |issue=7 |pages=493–9 |title=Autism interventions: a critical update |author=Francis K |doi=10.1017/S0012162205000952 |pmid=15991872 |url=http://journals.cambridge.org/production/action/cjoGetFulltext?fulltextid=313204 |format=PDF }}
*{{vcite journal |author=Levy SE, Hyman SL |title=Complementary and alternative medicine treatments for children with autism spectrum disorders |journal=Child Adolesc Psychiatr Clin N Am |volume=17 |issue=4 |pages=803–20, ix |year=2008 |pmid=18775371 |pmc=2597185 |doi=10.1016/j.chc.2008.06.004 }}
*{{vcite journal |journal=J Autism Dev Disord |year=2008 |volume=38 |issue=2 |pages=353–61 |title=Social skills interventions for children with Asperger's syndrome or high-functioning autism: a review and recommendations |author=Rao PA, Beidel DC, Murray MJ |doi=10.1007/s10803-007-0402-4 |pmid=17641962 }}
&lt;/ref&gt; Treatment approaches have little empirical support in [[Quality of life|quality-of-life]] contexts, and many programs focus on success measures that lack predictive validity and real-world relevance.&lt;ref name=Burgess/&gt; Scientific evidence appears to matter less to service providers than program marketing, training availability, and parent requests.&lt;ref&gt;{{vcite journal |journal=Focus Autism Other Dev Disabl |year=2005 |volume=20 |issue=2 |pages=66–79 |title=Early intervention practices for children with autism: descriptions from community providers |author=Stahmer AC, Collings NM, Palinkas LA |pmid=16467905 |pmc=1350798 |doi=10.1177/10883576050200020301 }}&lt;/ref&gt;  Some alternative treatments may place the child at risk. A 2008 study found that compared to their peers, autistic boys have significantly thinner bones if on [[Casein-free diet|casein-free diets]];&lt;ref&gt;{{vcite journal |journal=J Autism Dev Disord |year=2008 |volume=38 |issue=5 |pages=848–56 |title=Reduced bone cortical thickness in boys with autism or autism spectrum disorder |author=Hediger ML, England LJ, Molloy CA, Yu KF, Manning-Courtney P, Mills JL |doi=10.1007/s10803-007-0453-6 |pmid=17879151 |laysummary=http://www.nih.gov/news/health/jan2008/nichd-29.htm |laysource=NIH News |laydate=2008-01-29 }}&lt;/ref&gt; in 2005, botched [[chelation therapy]] killed a five-year-old child with autism.&lt;ref&gt;{{vcite journal |journal=Pediatrics |year=2006 |volume=118 |issue=2 |pages=e534–6 |title=Deaths resulting from hypocalcemia after administration of edetate disodium: 2003–2005 |author=Brown MJ, Willis T, Omalu B, Leiker R |doi=10.1542/peds.2006-0858 |pmid=16882789 |url=http://pediatrics.aappublications.org/cgi/content/full/118/2/e534 }}&lt;/ref&gt;

Treatment is expensive; indirect costs are more so. For someone born in 2000, a US study estimated an average lifetime cost of ${{formatprice|{{inflation|US|3160384|2003}}}} ([[net present value]] in {{CURRENTYEAR}} dollars, inflation-adjusted from 2003 estimate),{{inflation-fn|US}} with about 10% [[medical care]], 30% extra education and other care, and 60% lost economic productivity.&lt;ref&gt;{{vcite journal |journal=Arch Pediatr Adolesc Med |year=2007 |volume=161 |issue=4 |pages=343–9 |title=The lifetime distribution of the incremental societal costs of autism |author=Ganz ML |pmid=17404130 |url=http://archpedi.ama-assn.org/cgi/content/full/161/4/343 |laysummary=http://www.hsph.harvard.edu/news/press-releases/2006-releases/press04252006.html |laysource=Harvard School of Public Health |laydate=2006-04-25 |doi=10.1001/archpedi.161.4.343 }}&lt;/ref&gt; 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;&lt;ref&gt;{{vcite journal |journal=J Fam Econ Iss |year=2007 |volume=28 |issue=2 |pages=247–64 |doi=10.1007/s10834-007-9059-6 |title=Financial issues associated with having a child with autism |author=Sharpe DL, Baker DL }}&lt;/ref&gt; one 2008 US study found a 14% average loss of annual income in families of children with ASD,&lt;ref&gt;{{vcite journal |journal=Pediatrics |year=2008 |volume=121 |issue=4 |pages=e821–6 |title=Association of childhood autism spectrum disorders and loss of family income |author=Montes G, Halterman JS |doi=10.1542/peds.2007-1594 |pmid=18381511 |url=http://pediatrics.aappublications.org/cgi/content/full/121/4/e821 }}&lt;/ref&gt; and a related study found that ASD is associated with higher probability that [[child care]] problems will greatly affect parental employment.&lt;ref&gt;{{vcite journal |journal=Pediatrics |year=2008 |volume=122 |issue=1 |pages=e202–8 |title=Child care problems and employment among families with preschool-aged children with autism in the United States |author=Montes G, Halterman JS |doi=10.1542/peds.2007-3037 |pmid=18595965 |url=http://pediatrics.aappublications.org/cgi/content/full/122/1/e202 }}&lt;/ref&gt; US states increasingly require private health insurance to cover autism services, shifting costs from publicly funded education programs to privately funded health insurance.&lt;ref&gt;{{vcite journal |journal=Manag Care |year=2008 |volume=17 |issue=8 |pages=35–6, 39 |title=States increasingly mandate special autism services |author=Reinke T |pmid=18777788 |url=http://managedcaremag.com/archives/0808/0808.autism.html }}&lt;/ref&gt; After childhood, key treatment issues include residential care, job training and placement, sexuality, social skills, and [[estate planning]].&lt;ref&gt;{{vcite journal |journal=J Clin Psychiatry |year=2005 |volume=66 |issue=Suppl 10 |pages=38–45 |title=Treatment planning for patients with autism spectrum disorders |author=Aman MG |pmid=16401149 }}&lt;/ref&gt;

==Prognosis==
There is no known cure.&lt;ref name=Levy/&gt;&lt;ref name=CCD/&gt; Children recover occasionally, so that they lose their diagnosis of ASD;&lt;ref name=Helt/&gt; this occurs sometimes after intensive treatment and sometimes not. It is not known how often recovery happens;&lt;ref name=Rogers/&gt; reported rates in unselected samples of children with ASD have ranged from 3% to 25%.&lt;ref name=Helt&gt;{{vcite journal |author=Helt M, Kelley E, Kinsbourne M ''et al.'' |author.= |title=Can children with autism recover? if so, how? |title.= |journal=Neuropsychol Rev |volume=18 |issue=4 |pages=339–66 |year=2008 |pmid=19009353 |doi=10.1007/s11065-008-9075-9 }}&lt;/ref&gt; Most autistic children can acquire language by age 5 or younger, though a few have developed communication skills in later years.&lt;ref&gt;{{vcite journal |author=Pickett E, Pullara O, O'Grady J, Gordon B |title=Speech acquisition in older nonverbal individuals with autism: a review of features, methods, and prognosis |journal=Cogn Behav Neurol |volume=22 |issue=1 |pages=1–21 |year=2009 |pmid=19372766 |doi=10.1097/WNN.0b013e318190d185 }}&lt;/ref&gt; Most children with autism lack [[social support]], meaningful relationships, future employment opportunities or [[Self-determination theory|self-determination]].&lt;ref name=Burgess&gt;{{vcite journal |author=Burgess AF, Gutstein SE |year=2007 |title=Quality of life for people with autism: raising the standard for evaluating successful outcomes |journal=Child Adolesc Ment Health |volume=12 |issue=2 |pages=80–6 |doi=10.1111/j.1475-3588.2006.00432.x |url=http://www3.interscience.wiley.com/cgi-bin/fulltext/118546008/HTMLSTART}}&lt;/ref&gt; Although core difficulties tend to persist, symptoms often become less severe with age.&lt;ref name=Rapin/&gt; Few high-quality studies address long-term [[prognosis]]. Some adults show modest improvement in communication skills, but a few decline; no study has focused on autism after midlife.&lt;ref&gt;{{vcite journal |journal=Ment Retard Dev Disabil Res Rev |volume=10 |issue=4 |pages=234–47 |year=2004 |title=Trajectory of development in adolescents and adults with autism |author=Seltzer MM, Shattuck P, Abbeduto L, Greenberg JS |doi=10.1002/mrdd.20038 |pmid=15666341 }}&lt;/ref&gt; Acquiring language before age six, having an [[IQ]] above 50, and having a marketable skill all predict better outcomes; [[independent living]] is unlikely with severe autism.&lt;ref&gt;{{vcite journal |author=Tidmarsh L, Volkmar FR |title=Diagnosis and epidemiology of autism spectrum disorders |journal=Can J Psychiatry |volume=48 |issue=8 |pages=517–25 |year=2003 |pmid=14574827 |url=http://ww1.cpa-apc.org:8080/Publications/Archives/CJP/2003/september/tidmarsh.asp }}&lt;/ref&gt; 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.&lt;ref name=Howlin&gt;{{vcite journal |author=Howlin P, Goode S, Hutton J, Rutter M |title=Adult outcome for children with autism |journal=J Child Psychol Psychiatry |year=2004 |volume=45 |issue=2 |pages=212–29 |pmid=14982237 |doi=10.1111/j.1469-7610.2004.00215.x }}&lt;/ref&gt; A 2005 Swedish study of 78 adults that did not exclude low IQ found worse prognosis; for example, only 4% achieved independence.&lt;ref&gt;{{vcite journal |journal=J Autism Dev Disord |year=2005 |volume=35 |issue=3 |pages=351–60 |title=Autism after adolescence: population-based 13- to 22-year follow-up study of 120 individuals with autism diagnosed in childhood |author=Billstedt E, Gillberg C, Gillberg C |doi=10.1007/s10803-005-3302-5 |pmid=16119476 }}&lt;/ref&gt; 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 [[part-time]] work.&lt;ref&gt;{{vcite journal |journal=J Autism Dev Disord |year=2008 |volume=38 |issue=4 |pages=739–47 |title=Young adult outcome of autism spectrum disorders |author=Eaves LC, Ho HH |doi=10.1007/s10803-007-0441-x |pmid=17764027 }}&lt;/ref&gt; Changes in diagnostic practice and increased availability of effective early intervention make it unclear whether these findings can be generalized to recently diagnosed children.&lt;ref name=Newschaffer/&gt;

==Epidemiology==
{{Main|Epidemiology of autism}}
[[File:US-autism-6-17-1996-2007.png|thumb|left|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.|Reports of autism cases per 1,000 children grew dramatically in the US from 1996 to 2007. It is unknown how much, if any, growth came from changes in autism's [[prevalence]].]]
Most recent [[review]]s tend to estimate a prevalence of 1–2 per 1,000 for autism and close to 6 per 1,000 for ASD;&lt;ref name=Newschaffer&gt;{{vcite journal |author=Newschaffer CJ, Croen LA, Daniels J ''et al.'' |author.= |title=The epidemiology of autism spectrum disorders |journal=Annu Rev Public Health |year=2007 |volume=28 |pages=235–58 |pmid=17367287 |doi=10.1146/annurev.publhealth.28.021406.144007 |url=http://idea.library.drexel.edu/bitstream/1860/2632/1/2006175339.pdf |format=PDF }}&lt;/ref&gt; because of inadequate data, these numbers may underestimate ASD's true prevalence.&lt;ref name=Caronna&gt;{{vcite journal |journal=Arch Dis Child |year=2008 |volume=93 |issue=6 |pages=518–23 |title=Autism spectrum disorders: clinical and research frontiers |author=Caronna EB, Milunsky JM, Tager-Flusberg H |doi=10.1136/adc.2006.115337 |pmid=18305076 }}&lt;/ref&gt; [[PDD-NOS]]'s prevalence has been estimated at 3.7 per 1,000, Asperger syndrome at roughly 0.6 per 1,000, and [[childhood disintegrative disorder]] at 0.02 per 1,000.&lt;ref name=Fombonne-2009&gt;{{vcite journal |author=Fombonne E |title=Epidemiology of pervasive developmental disorders |journal=Pediatr Res |volume=65 |issue=6 |pages=591–8 |year=2009 |pmid=19218885 |doi=10.1203/PDR.0b013e31819e7203 }}&lt;/ref&gt; 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,&lt;ref name=Fombonne-2009/&gt;&lt;ref&gt;{{vcite journal |author=Wing L, Potter D |title=The epidemiology of autistic spectrum disorders: is the prevalence rising? |title.= |journal=Ment Retard Dev Disabil Res Rev |volume=8 |issue=3 |year=2002 |pages=151–61 |pmid=12216059 |doi=10.1002/mrdd.10029 }}&lt;/ref&gt; though unidentified environmental risk factors cannot be ruled out.&lt;ref name=Rutter&gt;{{vcite journal |author=Rutter M |title=Incidence of autism spectrum disorders: changes over time and their meaning |journal=Acta Paediatr |volume=94 |issue=1 |year=2005 |pages=2–15 |pmid=15858952 |doi=10.1111/j.1651-2227.2005.tb01779.x }}&lt;/ref&gt; The available evidence does not rule out the possibility that autism's true prevalence has increased;&lt;ref name=Fombonne-2009/&gt; a real increase would suggest directing more attention and funding toward changing environmental factors instead of continuing to focus on genetics.&lt;ref name=Szpir/&gt;

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.&lt;ref name=Newschaffer/&gt; 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.&lt;ref&gt;{{vcite journal |author=Gardener H, Spiegelman D, Buka SL |title=Prenatal risk factors for autism: comprehensive meta-analysis |journal=Br J Psychiatry |volume=195 |issue=1 |pages=7–14 |year=2009 |pmid=19567888 |doi=10.1192/bjp.bp.108.051672 }}&lt;/ref&gt; 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.&lt;ref name=Geschwind-2009/&gt; Most professionals believe that race, ethnicity, and socioeconomic background do not affect the occurrence of autism.&lt;ref&gt;{{vcite journal |author=Bertoglio K, Hendren RL |title=New developments in autism |journal=Psychiatr Clin North Am |volume=32 |issue=1 |pages=1–14 |year=2009 |pmid=19248913 |doi=10.1016/j.psc.2008.10.004 }}&lt;/ref&gt;

Several other conditions are common in children with autism.&lt;ref name=Levy/&gt; They include:
*'''[[Genetic disorder]]s'''. About 10–15% of autism cases have an identifiable [[Mendelian]] (single-gene) condition, [[chromosome abnormality]], or other genetic syndrome,&lt;ref&gt;{{vcite journal |author=Folstein SE, Rosen-Sheidley B |title=Genetics of autism: complex aetiology for a heterogeneous disorder |journal=Nat Rev Genet |year=2001 |volume=2 |issue=12 |pages=943–55 |doi=10.1038/35103559 |pmid=11733747 }}&lt;/ref&gt; and ASD is associated with several genetic disorders.&lt;ref&gt;{{vcite journal |journal=Brain Dev |year=2007 |volume=29 |issue=5 |pages=257–72 |title=Childhood autism and associated comorbidities |author=Zafeiriou DI, Ververi A, Vargiami E |doi=10.1016/j.braindev.2006.09.003 |pmid=17084999 }}&lt;/ref&gt;
*'''[[Mental retardation]]'''. 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.&lt;ref&gt;{{vcite book |chapter=Learning in autism |author=Dawson M, Mottron L, Gernsbacher MA |title=Learning and Memory: A Comprehensive Reference |volume=2 |pages=759–72 |editor=Byrne JH, editor-in-chief, Roediger HL 3rd, volume editor |publisher=Academic Press |year=2008 |doi=10.1016/B978-012370509-9.00152-2 |isbn=0-12-370504-5 |chapterurl=http://psych.wisc.edu/lang/pdf/Dawson_AutisticLearning.pdf |chapterformat=PDF }}&lt;/ref&gt; For ASD other than autism, the association with mental retardation is much weaker.&lt;ref&gt;{{vcite journal |author=Chakrabarti S, Fombonne E |title=Pervasive developmental disorders in preschool children |journal=JAMA |year=2001 |volume=285 |issue=24 |pages=3093–9 |pmid=11427137 |url=http://jama.ama-assn.org/cgi/content/full/285/24/3093 |doi=10.1001/jama.285.24.3093 }}&lt;/ref&gt;
*'''[[Anxiety disorder]]s''' 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.&lt;ref&gt;{{vcite journal |author=White SW, Oswald D, Ollendick T, Scahill L |title=Anxiety in children and adolescents with autism spectrum disorders |journal=Clin Psychol Rev |volume=29 |issue=3 |pages=216–29 |year=2009 |pmid=19223098 |doi=10.1016/j.cpr.2009.01.003 |pmc=2692135 }}&lt;/ref&gt;
*'''[[Epilepsy]]''', with variations in risk of epilepsy due to age, cognitive level, and type of [[language disorder]].&lt;ref&gt;{{vcite journal |journal=Pediatr Res |year=2009 |volume=65 |issue=6 |pages=599–606 |title=The role of epilepsy and epileptiform EEGs in autism spectrum disorders |author=Spence SJ, Schneider MT |doi=10.1203/PDR.0b013e31819e7168 |pmid=19454962 |pmc=2692092}}&lt;/ref&gt;
*Several '''[[metabolic defect]]s''', such as [[phenylketonuria]], are associated with autistic symptoms.&lt;ref name=Manzi&gt;{{vcite journal |journal=J Child Neurol |year=2008 |volume=23 |issue=3 |pages=307–14 |title=Autism and metabolic diseases |author=Manzi B, Loizzo AL, Giana G, Curatolo P |doi=10.1177/0883073807308698 |pmid=18079313 }}&lt;/ref&gt;
*'''[[Minor physical anomalies]]''' are significantly increased in the autistic population.&lt;ref&gt;{{vcite journal |journal=Mol Psychiatry |year=2010 |volume=15 |issue=3 |pages=300–7 |title=Minor physical anomalies in autism: a meta-analysis |author=Ozgen HM, Hop JW, Hox JJ, Beemer FA, van Engeland H |doi=10.1038/mp.2008.75 |pmid=18626481 }}&lt;/ref&gt;
*'''Preempted diagnoses'''. Although the DSM-IV rules out concurrent diagnosis of many other conditions along with autism, the full criteria for [[ADHD]], [[Tourette syndrome]], and other of these conditions are often present and these [[Conditions comorbid to autism spectrum disorders|comorbid diagnoses]] are increasingly accepted.&lt;ref&gt;{{vcite journal |journal=Eur J Pediatr |year=2008 |title=What's new in autism? |title.= |author=Steyaert JG, De La Marche W |doi=10.1007/s00431-008-0764-4 |pmid=18597114 |volume=167 |issue=10 |pages=1091–101 }}&lt;/ref&gt;
*'''Sleep problems''' affect about two-thirds of individuals with ASD at some point in childhood. These most commonly include symptoms of [[insomnia]] such as difficulty in falling asleep, frequent [[middle-of-the-night insomnia|nocturnal awakenings]], 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.&lt;ref&gt;{{vcite journal |author=Richdale AL, Schreck KA |title=Sleep problems in autism spectrum disorders: prevalence, nature, &amp; possible biopsychosocial aetiologies |journal=Sleep Med Rev |volume=13 |issue=6 |pages=403–11 |year=2009 |pmid=19398354 |doi=10.1016/j.smrv.2009.02.003 }}&lt;/ref&gt;

==History==
{{see|History of Asperger syndrome|Sociological and cultural aspects of autism}}
[[File:Leo-Kanner.jpeg|thumb|upright|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.|[[Leo Kanner]] introduced the label ''early infantile autism'' in 1943.]]
A few examples of autistic symptoms and treatments were described long before autism was named. The ''[[Table Talk (Luther)|Table Talk]]'' of [[Martin Luther]], compiled by his notetaker, Mathesius, contains the story of a 12-year-old boy who may have been severely autistic.&lt;ref&gt;{{vcite journal |journal=Autism |volume=1 |issue=1 |pages=13–23 |year=1997 |doi=10.1177/1362361397011004 |title=The history of ideas on autism: legends, myths and reality |author=[[Lorna Wing|Wing L]]}}&lt;/ref&gt; Luther reportedly thought the boy was a soulless mass of flesh possessed by the devil, and suggested that he be suffocated, although a later critic has cast doubt on the veracity of this report.&lt;ref&gt;{{vcite web |author=Miles M |year=2005 |title=Martin Luther and childhood disability in 16th century Germany: what did he write? what did he say? |title.= |publisher=Independent Living Institute |url=http://www.independentliving.org/docs7/miles2005b.html |accessdate=2008-12-23 }}&lt;/ref&gt; 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.&lt;ref&gt;{{vcite book |author=Houston R, Frith U |title=Autism in History: The Case of Hugh Blair of Borgue |year=2000 |publisher=Blackwell |isbn=0-631-22089-5 }}&lt;/ref&gt; The [[Wild Boy of Aveyron]], a [[feral child]] caught in 1798, showed several signs of autism; the medical student [[Jean Marc Gaspard Itard|Jean Itard]] treated him with a behavioral program designed to help him form social attachments and to induce speech via imitation.&lt;ref name=Wolff&gt;{{vcite journal |journal=Eur Child Adolesc Psychiatry |year=2004 |volume=13 |issue=4 |pages=201–8 |title=The history of autism |author=Wolff S |doi=10.1007/s00787-004-0363-5 |pmid=15365889 }}&lt;/ref&gt;

The [[New Latin]] word ''autismus'' (English translation ''autism'') was coined by the [[Swiss]] psychiatrist [[Eugen Bleuler]] in 1910 as he was defining symptoms of [[schizophrenia]]. He derived it from the Greek word ''autós'' (αὐτός, meaning ''self''), and used it to mean morbid self-admiration, referring to &quot;autistic withdrawal of the patient to his fantasies, against which any influence from outside becomes an intolerable disturbance&quot;.&lt;ref&gt;{{vcite journal |author=Kuhn R; tr. Cahn CH |title=Eugen Bleuler's concepts of psychopathology |journal=Hist Psychiatry |volume=15 |issue=3 |year=2004 |pages=361–6 |doi=10.1177/0957154X04044603 |pmid=15386868 }} The quote is a translation of Bleuler's 1910 original.&lt;/ref&gt;

The word ''autism'' first took its modern sense in 1938 when [[Hans Asperger]] of the [[Vienna General Hospital|Vienna University Hospital]] adopted Bleuler's terminology ''autistic psychopaths'' in a lecture in German about [[child psychology]].&lt;ref&gt;{{vcite journal |journal=Wien Klin Wochenschr |year=1938 |volume=51 |pages=1314–7 |trans_title=The psychically abnormal child |author=[[Hans Asperger|Asperger H]] |language=German }}&lt;/ref&gt; Asperger was investigating an ASD now known as [[Asperger syndrome]], though for various reasons it was not widely recognized as a separate diagnosis until 1981.&lt;ref name=Wolff/&gt; [[Leo Kanner]] of the [[Johns Hopkins Hospital]] first used ''autism'' in its modern sense in English when he introduced the label ''early infantile autism'' in a 1943 report of 11 children with striking behavioral similarities.&lt;ref name=Kanner1943&gt;{{vcite journal |author=[[Leo Kanner|Kanner L]] |title=Autistic disturbances of affective contact |journal=Nerv Child |volume=2 |pages=217–50 |year=1943 }} Reprinted in {{vcite journal |year=1968 |journal=Acta Paedopsychiatr |volume=35 |issue=4 |pages=100–36 |pmid=4880460 |author=&lt;!-- Pacify Citation bot. --&gt; |title=&lt;!-- Pacify Citation bot. --&gt; }}&lt;/ref&gt; Almost all the characteristics described in Kanner's first paper on the subject, notably &quot;autistic aloneness&quot; and &quot;insistence on sameness&quot;, are still regarded as typical of the autistic spectrum of disorders.&lt;ref name=HappeTime/&gt; It is not known whether Kanner derived the term independently of Asperger.&lt;ref name=Lyons&gt;{{vcite journal |journal=J Autism Dev Disord |year=2007 |volume=37 |issue=10 |pages=2022–3 |title=Asperger (1906–1980) and Kanner (1894–1981), the two pioneers of autism |author=Lyons V, Fitzgerald M |doi=10.1007/s10803-007-0383-3 |pmid=17922179 }}&lt;/ref&gt;

Kanner's reuse of ''autism'' led to decades of confused terminology like ''infantile schizophrenia'', and child psychiatry's focus on maternal deprivation led to misconceptions of autism as an infant's response to &quot;[[refrigerator mother]]s&quot;. 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.&lt;ref&gt;{{vcite journal |journal=Can J Psychiatry |year=2003 |volume=48 |issue=8 |pages=503–5 |title=Modern views of autism |author=Fombonne E |pmid=14574825 |url=http://ww1.cpa-apc.org:8080/Publications/Archives/CJP/2003/september/guesteditorial.asp }}&lt;/ref&gt; 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.&lt;ref&gt;{{vcite book |chapter=Genetic epidemiology of autism spectrum disorders |author=[[Peter Szatmari|Szatmari P]], Jones MB |pages=157–78 |title=Autism and Pervasive Developmental Disorders |edition=2nd |editor=Volkmar FR |publisher=Cambridge University Press |year=2007 |isbn=0-521-54957-4 }}&lt;/ref&gt; Although the rise of parent organizations and the destigmatization of childhood ASD have deeply affected how we view ASD,&lt;ref name=Wolff/&gt; parents continue to feel [[social stigma]] in situations where their autistic children's behaviors are perceived negatively by others,&lt;ref&gt;{{vcite journal |journal=J Autism Dev Disord |year=2008 |title=Adult attitudes toward behaviors of a six-year-old boy with autism |author=Chambres P, Auxiette C, Vansingle C, Gil S |doi=10.1007/s10803-007-0519-5 |pmid=18297387 |volume=38 |issue=7 |pages=1320–7 }}&lt;/ref&gt; and many [[primary care physician]]s and [[medical specialist]]s still express some beliefs consistent with outdated autism research.&lt;ref&gt;{{vcite journal |journal=J Autism Dev Disord |year=2005 |volume=35 |issue=3 |pages=323–30 |title=A survey of autism knowledge in a health care setting |author=Heidgerken AD, Geffken G, Modi A, Frakey L |doi=10.1007/s10803-005-3298-x |pmid=16119473 }}&lt;/ref&gt;

The [[Internet]] 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.&lt;ref&gt;{{vcite journal |author=Biever C |title=Web removes social barriers for those with autism |journal=New Sci |issue=2610 |pages=26–7 |date=2007 |url=http://www.newscientist.com/article/mg19426106.100 }}&lt;/ref&gt; [[Sociological and cultural aspects of autism]] have developed: some in the community seek a cure, while others believe that autism is simply another way of being.&lt;ref name=Silverman&gt;{{vcite journal |journal=Biosocieties |year=2008 |volume=3 |issue=3 |pages=325–41 |title=Fieldwork on another planet: social science perspectives on the autism spectrum |author=Silverman C |doi=10.1017/S1745855208006236 }}&lt;/ref&gt;&lt;ref&gt;{{vcite news |author=Harmon A |title=How about not 'curing' us, some autistics are pleading |date=2004-12-20 |work=New York Times |url=http://www.nytimes.com/2004/12/20/health/20autism.html }}&lt;/ref&gt;

==References==
{{reflist|35em}}

==External links==
{{portal|Pervasive Developmental Disorders}}
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{{Commons category-inline|Autism}}
* {{dmoz|Health/Mental_Health/Disorders/Neurodevelopmental/Autism_Spectrum}}
{{featured article}}
{{Pervasive developmental disorders}}
{{Mental and behavioural disorders|selected = childhood}}
[[Category:Autism| ]]
[[Category:Communication disorders]]
[[Category:Mental and behavioural disorders]]
[[Category:Neurological disorders]]
[[Category:Neurological disorders in children]]
[[Category:Pervasive developmental disorders]]

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[[kk:Аутизм]]
[[sw:Autism]]
[[ku:Otîzm]]
[[la:Autismus]]
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[[ms:Autisme]]
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`

func TestParserBroken(t *testing.T) {
	p, err := NewParser(bytes.NewReader(nil))
	if err == nil {
		t.Fatalf("Expected failure opening bad xml, got %v", p)
	}
}

func TestParserSemiBroken(t *testing.T) {
	p, err := NewParser(strings.NewReader(`<?xml version="1.0"?>`))
	if err == nil {
		t.Fatalf("Expected failure opening bad xml, got %v", p)
	}
}

func TestParserSuccess(t *testing.T) {
	p, err := NewParser(strings.NewReader(exemplar))
	if err != nil {
		t.Fatalf("Error making parser: %v", err)
	}
	if p.SiteInfo().SiteName != "Wikipedia" {
		t.Fatalf("Got the wrong site name: %q", p.SiteInfo().SiteName)
	}
	pages := 0
	for {
		_, err = p.Next()
		if err != nil {
			break
		}
		pages++
	}
	if pages != 1 {
		t.Fatalf("Expected one page, got %v", pages)
	}
}

func xmld(b *testing.B, doc []byte) {
	b.SetBytes(int64(len(doc)))
	br := bytes.NewReader(doc)
	for i := 0; i < b.N; i++ {
		br.Seek(0, 0)
		d := xml.NewDecoder(br)
		page := Page{}
		err := d.Decode(&page)
		if err != nil {
			b.Fatalf("Error parsing: %v", err)
		}
	}
}

func BenchmarkSmallParsing(b *testing.B) {
	xmld(b, []byte(smaller))
}

func BenchmarkLargeParsing(b *testing.B) {
	xmld(b, []byte(larger))
}

func tokening(b *testing.B, doc []byte) {
	b.SetBytes(int64(len(doc)))
	br := bytes.NewReader(doc)
	for i := 0; i < b.N; i++ {
		br.Seek(0, 0)
		d := xml.NewDecoder(br)
		var page Page
		done := false
		for !done {
			t, err := d.Token()
			if err != nil {
				b.Fatalf("Error parsing %v: %v", page, err)
			}
			if ee, ok := t.(xml.EndElement); ok && ee.Name.Local == "page" {
				done = true
			}
		}
	}
}

func BenchmarkSmallTokening(b *testing.B) {
	tokening(b, []byte(smaller))
}

func BenchmarkLargeTokening(b *testing.B) {
	tokening(b, []byte(larger))
}