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==Mechanism==
Autism's symptoms result from maturation-related changes in various systems of the brain.<!-- ref name=Penn/ --> 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.<ref name=Penn>{{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 }}</ref> The behaviors appear to have multiple pathophysiologies.<ref name=London/>

===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.<ref name=Amaral/>]]
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.<ref name=Geschwind>{{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 }}</ref> Autism appears to result from developmental factors that affect many or all functional brain systems,<ref>{{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 |pmc=3315379}}</ref> and to disturb the timing of brain development more than the final product.<ref name=Amaral>{{vcite journal |journal=Trends Neurosci |year=2008 |volume=31 |issue=3 |pages=137–45 |title=Neuroanatomy of autism |author=[[David Amaral (psychiatrist)|Amaral DG]], Schumann CM, Nordahl CW |doi=10.1016/j.tins.2007.12.005 |pmid=18258309 }}</ref> [[Neuroanatomical]] studies and the associations with [[teratogens]] strongly suggest that autism's mechanism includes alteration of brain development soon after conception.<ref name=Arndt/> This anomaly appears to start a cascade of pathological events in the brain that are significantly influenced by environmental factors.<ref>{{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 }}</ref> 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.<ref name=Geschwind-2009/> 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.<ref>{{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 }}</ref>
* Disturbed [[neuronal migration]] during early [[gestation]].<ref name=Schmitz/><ref name=Persico>{{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 }}</ref>
* Unbalanced excitatory–inhibitory networks.<ref name=Persico/>
* Abnormal formation of [[synapse]]s and [[dendritic spine]]s,<ref name=Persico/> for example, by modulation of the [[neurexin]]–[[neuroligin]] [[Cell adhesion|cell-adhesion]] system,<ref>{{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 }}</ref> or by poorly regulated [[Protein synthesis|synthesis]] of synaptic proteins.<ref>{{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 }}</ref><ref>{{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=10.1038/sj.npp.1301610 }}</ref> Disrupted synaptic development may also contribute to [[epilepsy]], which may explain why the two conditions are associated.<ref>{{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 }}</ref>

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.<ref>{{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 }}</ref> 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.<ref>{{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 }}</ref> As [[autoantibodies]] are found in conditions other than ASD, and are not always present in ASD,<ref>{{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 }}</ref> the relationship between immune disturbances and autism remains unclear and controversial.<ref name=Schmitz>{{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 }}</ref>

====Neurochemical systems====
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.<ref name=Levy>{{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}}</ref> 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.<ref name="pmid18093519">{{vcite 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}}</ref> Some data suggest an increase in several [[growth hormone]]s; other data argue for diminished [[growth factor]]s.<ref>{{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 }}</ref> Also, some [[inborn errors of metabolism]] are associated with autism, but probably account for less than 5% of cases.<ref name=Manzi/>

====Brain systems====

=====Mirror neuron system=====

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.<ref>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 }}</ref> 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.<ref name=Iacoboni>{{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 }}</ref> However, individuals with autism also have abnormal brain activation in many circuits outside the MNS<ref>{{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 }}</ref> and the MNS theory does not explain the normal performance of autistic children on imitation tasks that involve a goal or object.<ref>{{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=<!-- Work around Citation bot bug. --> |last2=<!-- Work around Citation bot bug. --> }}</ref>

[[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).<ref name=Powell>{{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 }}</ref>]]
ASD-related patterns of low function and aberrant activation in the brain differ depending on whether the brain is doing social or nonsocial tasks.<ref>{{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 }}</ref>

=====Default Network vs. “Task-positive” Central Executive Network=====

ASD-related patterns of low function and aberrant activation in the brain differ depending on whether the brain is doing social or nonsocial tasks. <ref name =" Di Martino">{{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 }}</ref> A 2008 brain-imaging study found a specific pattern of signals in the [[cingulate cortex]] which differs in individuals with ASD.<ref>{{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 |lay-summary=http://www.technologyreview.com/Biotech/20167/ |lay-source=Technol Rev |lay-date=2007-02-07 }}</ref>Even more recently, evidence suggests that an entire network of brain regions involved in social and emotional processing, the [[default network]] or "Default mode" Network (DMN), shows reduced functional connectivity. In other words, the brain regions do not communicate in the same way that they would in a typical brain. <ref name ="Menon">Menon, V. (2011). Large-scale brain networks and psychopathology: a unifying triple network model. Trends In Cognitive Sciences, 15(10), 483-506. doi:10.1016/j.tics.2011.08.003</ref> Two main hubs of the DMN, the posterior cingulate cortex and medial prefrontal cortex, appear to be hypoactive relative to neurotypical adults, which may disrupt the functioning of the entire network. <ref name="Menon" /> Dysfunction in DMN connectivity is prominent in adolescents and young adults with autism, suggesting that manifestation of DMN dysfunction may occur early in development.<ref name="Menon" /> In contrast to the dysfunction in the DMN network, intact connectivity has been observed in a “central executive” network that is involved in sustained attention, cognitive control, and goal-directed thinking. In people with autism, this network (often called the [[task-positive network]]) and the DMN are not negatively correlated in time (as has been found in typical adults), suggesting a possible imbalance in switching between the two networks, and possibly reflecting a disturbance of [[self-referential]] thought.<ref>{{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 }}</ref>

=====Salience Network=====

The Salience Network (SN) is a network that is anchored in the [[anterior cingulate]] and the anterior [[insula]]. This network is thought to be involved in detecting, integrating, and filtering relevant interoceptive, autonomic, and emotional information to guide attention and action.<ref>Seeley, W.W. et al. (2007) Dissociable intrinsic connectivity networks for
salience processing and executive control. J. Neurosci. 27, 2349–2356
</ref> The SN also includes two important subcortical structures: the [[amygdala]] and the [[substantia nigra]]/[[ventral tegmental area]]. These structures are thought to play a major role in detecting emotional and reward [[salience]]. Both [[functional MRI]] studies of social processing <ref name="Di Martino" /> and MRI studies that measure the size of brain regions<ref name="Menon" /> have shown dysfunction of the SN in individuals with autism. One of the regions consistently showing significant hypoactivity in autism is the right anterior insula<ref name="Menon" />. Dysfunction in this network may result in problems using internal body sensations to guide attention to salient social and other events, with significant consequences for both cognition and self-monitoring <ref>Menon, V. and Uddin, L.Q. (2010) Saliency, switching, attention and
control: a network model of insula function. Brain Struct. Funct. 214,
655–667 </ref>,. 

Recent studies demonstrate that in the typical brain the anterior insula provides an altering signal to initiate appropriate responses to salient stimuli. <ref name="Menon" /> Because the anterior insula is underactive during social processing in individuals with autism,<ref>Uddin, L.Q. and Menon, V. (2009) The anterior insula in autism:
under-connected and under-examined. Neurosci. Biobehav. Rev. 33,
1198–1203</ref> ineffective salience mapping of socially relevant cues may result in atypical social interactions.<ref name="Di Martino" /> In contrast, hyperactivity of the anterior insula has been consistently implicated in [[anxiety]] disorders.<ref name ="Paulus">Paulus, M.P. and Stein, M.B. (2006) An insular view of anxiety. Biol.
Psychiatry 60, 383–387</ref>
<ref>Stein, M.B. et al. (2007) Increased amygdala and insula activation
during emotion processing in anxiety-prone subjects. Am. J.
Psychiatry 164, 318–327</ref> The anterior insula is proposed to play a key role in experiencing negative and worrisome thoughts, as well as coordinating avoidance behaviors in individuals prone to anxiety.<ref name="Paulus" /> These are noteworthy findings because anxiety disorders are a common comorbid feature of many disorders, including autism.<ref name="Menon" /> Therefore, hyperactivity of the anterior insula or other nodes of the SN may lead to pathologically enhanced salience detection in some situations<ref name="Menon" /> (but not others). These findings may give explanation to many of the phenotypic or behavioral presentations of the disorder. For instance, symptoms like stimulatory behavior, increased anxiety, or neuroticism may be consequence of the anterior insula misattributing emotional salience to mundane events.<ref name="Menon" />

=====Triple Network Model=====
Because the default mode network, the salience network, and the central executive networks discussed above appear to underlie prominent features of many major psychiatric and neurological disorders (including autism, [[schizophrenia]], [[ADHD]], [[AD]], [[FTD]], [[depression]] and [[epilepsy]]),<ref name ="Kring"> Kring, A. M., Davison, G. C., Neale, J. M., & Johnson, S. (2007). Abnormal psychology. Wiley.</ref> a common framework was recently proposed for understanding dysfunction across disorders: the Triple Network Model.<ref name="Menon" /> This model proposes that deficits in engaging and disengaging these networks play a significant role in many disorders, including autism. By studying networks instead of specific brain regions, it may be possible to gain new insights into understanding dysfunction across a number of disorders.<ref name="Menon" />

A significant number of disorders have symptoms that overlap with autism spectrum disorders, and autism spectrum diagnoses tend to be [[comorbid]] with other disorders. For instance, many individuals with autism may also be diagnosed with or show symptoms of [[depression]], [[anxiety]], [[obsessive-compulsive]] tendencies, and more.<ref name ="Kring" /> The Triple Network Model framework may help us understand why these [[comorbidities]] occur, and allow us to tailor interventions.  Designing individualized interventions is important because autism manifests differently across individuals, often varying from individual to individual. Researchers focusing on the [[etiology]] of autism are beginning to recognize that symptoms cannot be ascribed to the isolated operations of single brain areas.<ref name="Menon" /> The Triple Network Model reflects a shift from studying specific brain region to studying coordinated brain networks. While it may remain unclear what initially causes the disturbances in brain function that characterize autism, understanding how they manifest in large-scale network function may provide insights into predicting dysfunctional behavior patterns and designing appropriate interventions, for autism as well as for a wide range of other psychopathologies.<ref name="Menon" />

=====Additional theories=====

======Underconnectivity theory======

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.<ref>{{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 }}</ref> Evidence for this theory has been found in [[functional neuroimaging]] studies on autistic individuals<ref name=Williams>{{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 }}</ref> and by a [[Electroencephalography|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.<ref>{{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 }}</ref> 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]].<ref>{{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 }}</ref>

======Stimuli processing in Autism======
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, orientation to auditory and visual stimuli, novelty detection, language and face processing, and information storage; several studies have found a preference for nonsocial stimuli.<ref>{{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 }}</ref> For example, [[magnetoencephalography]] studies have found evidence in autistic children of delayed responses in the brain's processing of auditory signals.<ref>{{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 }}</ref>

======Autism and schizophrenia======
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.<ref>{{vcite 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}}</ref>

===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;<ref name=E-S-theory/> this extension is controversial, as many studies contradict the idea that baby boys and girls respond differently to people and objects.<ref>{{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 }}</ref>

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,<ref name=E-S-theory>{{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 |archiveurl=http://web.archive.org/web/20120513020626/http://autismresearchcentre.com/docs/papers/2009_BC_nyas.pdf |archivedate= May 13, 2012}}</ref> and the mirror neuron system theory of autism described in ''[[#Pathophysiology|Pathophysiology]]'' maps well to the hypothesis.<ref name=Iacoboni/> 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.<ref>{{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 }}</ref>

The second category focuses on nonsocial or general processing: the [[executive functions]] such as [[working memory]], planning, [[Inhibition Theory|inhibition]]. In his review, Kenworthy states that "the claim of [[executive dysfunction]] as a causal factor in autism is controversial", however, "it is clear that executive dysfunction plays a role in the social and cognitive deficits observed in individuals with autism".<ref name=Kenworthy/> Tests of core executive processes such as eye movement tasks indicate improvement from late childhood to adolescence, but performance never reaches typical adult levels.<ref>{{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 }}</ref> A strength of the theory is predicting stereotyped behavior and narrow interests;<ref>{{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 }}</ref> two weaknesses are that executive function is hard to measure<ref name=Kenworthy>{{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}}</ref> and that executive function deficits have not been found in young autistic children.<ref name=Sigman/>

[[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.<ref>{{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 }}</ref> A related theory—enhanced perceptual functioning—focuses more on the superiority of locally oriented and [[perceptual]] operations in autistic individuals.<ref>{{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 }}</ref> 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.<ref name=HappeTime>{{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 }}</ref> A combined theory based on multiple deficits may prove to be more useful.<ref>{{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 }}</ref>


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