Autism spectrum disorder: Difference between revisions

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{{SI}}
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{{CMG}}; {{AE}} {{KS}}
{{CMG}}; {{AE}} {{KS}}
{{SK}} autism spectrum; autistic spectrum


==Overview==
==Overview==


The '''autism spectrum''' or '''autistic spectrum''' describes a range of conditions classified as [[neurodevelopmental disorder]]s in the fifth revision of the American Psychiatric Association's ''Diagnostic and Statistical Manual of Mental Disorders 5th edition'' ([[DSM-5]]).  The DSM-5, published in 2013, redefined the autism spectrum to encompass the previous ([[DSM-IV-TR]]) diagnoses of [[autism]], [[Asperger syndrome]], [[PDD-NOS|pervasive developmental disorder not otherwise specified]] (PDD-NOS), [[childhood disintegrative disorder]], and [[Rett syndrome]].<ref name=DSM5Autism>{{cite web |url= http://www.dsm5.org/Documents/Autism%20Spectrum%20Disorder%20Fact%20Sheet.pdf |title= Autism spectrum disorder fact sheet |publisher= American Psychiatric Publishing |work= DSM5.org |year= 2013 |accessdate= October 13, 2103}}</ref> These disorders are characterized by social deficits and communication difficulties, stereotyped or repetitive behaviors and interests, and in some cases, cognitive delays.
The autism spectrum disorder describes a range of conditions classified as [[neurodevelopmental disorder]]s in the fifth revision of the American Psychiatric Association's ''Diagnostic and Statistical Manual of Mental Disorders 5th edition'' ([[DSM-5]]).  The DSM-5, published in 2013, redefined the autism spectrum to encompass the previous ([[DSM-IV-TR]]) diagnoses of [[autism]], [[Asperger syndrome]], [[PDD-NOS|pervasive developmental disorder not otherwise specified]] (PDD-NOS), [[childhood disintegrative disorder]], and [[Rett syndrome]].<ref name=DSM5Autism>{{cite web |url= http://www.dsm5.org/Documents/Autism%20Spectrum%20Disorder%20Fact%20Sheet.pdf |title= Autism spectrum disorder fact sheet |publisher= American Psychiatric Publishing |work= DSM5.org |year= 2013 |accessdate= October 13, 2103}}</ref> These disorders are characterized by social deficits and communication difficulties, stereotyped or repetitive behaviors and interests, and in some cases, cognitive delays.


==Historical Perspective==
==Historical Perspective==
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In general, neuroanatomical studies support the notion that autism is linked to a combination of brain enlargement in some areas and brain reduction in other areas.<ref name="Koenig 2001">{{cite book | last1 = Koenig | first1 = Kathleen | last2 = Tsatsanis | first2 = Katherine D. | last3 = Volkmar | first3 = Fred R. | title = Neurobiology and Genetics ofd Autism : A Developmental Perspective | editors = Jacob A Burack, Tony Charman, Nurit Yirmiya, Philip R. Zelazo | work = The development of autism : perspectives from theory and research | publisher = L. Erlbaum, | year = 2001 | location = Mahwah, N.J.  | pages = 73–92 | accessdate = 2013-07-09 | isbn = 9780805832457 | oclc=806185029}}</ref> These studies suggest that autism may be caused by abnormal neuronal growth and pruning during the early stages of prenatal and postnatal brain development, leaving some areas of the brain with too many neurons and other areas with too few neurons.<ref name="Minshew 1996">{{cite journal|last=Minshew|title=Brief report: Brain mechanisms in autism: Functional and structural abnormalities|journal=Journal of Autism and Developmental Disorders|year=1996|volume=26|pages=205–209|doi=10.1007/BF02172013|pmid=8744486|first1=NJ|issue=2}}</ref> Some research has reported an overall brain enlargement in autism while others suggest abnormalities in several areas of the brain, including the frontal lobe, the mirror neuron system, the limbic system, the temporal lobe, and the [[corpus callosum]].
In general, neuroanatomical studies support the notion that autism is linked to a combination of brain enlargement in some areas and brain reduction in other areas.<ref name="Koenig 2001">{{cite book | last1 = Koenig | first1 = Kathleen | last2 = Tsatsanis | first2 = Katherine D. | last3 = Volkmar | first3 = Fred R. | title = Neurobiology and Genetics ofd Autism : A Developmental Perspective | editors = Jacob A Burack, Tony Charman, Nurit Yirmiya, Philip R. Zelazo | work = The development of autism : perspectives from theory and research | publisher = L. Erlbaum, | year = 2001 | location = Mahwah, N.J.  | pages = 73–92 | accessdate = 2013-07-09 | isbn = 9780805832457 | oclc=806185029}}</ref> These studies suggest that autism may be caused by abnormal neuronal growth and pruning during the early stages of prenatal and postnatal brain development, leaving some areas of the brain with too many neurons and other areas with too few neurons.<ref name="Minshew 1996">{{cite journal|last=Minshew|title=Brief report: Brain mechanisms in autism: Functional and structural abnormalities|journal=Journal of Autism and Developmental Disorders|year=1996|volume=26|pages=205–209|doi=10.1007/BF02172013|pmid=8744486|first1=NJ|issue=2}}</ref> Some research has reported an overall brain enlargement in autism while others suggest abnormalities in several areas of the brain, including the frontal lobe, the mirror neuron system, the limbic system, the temporal lobe, and the [[corpus callosum]].


In neuroanatomical studies, when performing [[Theory of Mind]] and facial emotion response tasks, the median person on the autism spectrum exhibits less activation in the primary and secondary somato-sensory cortices than does the median member of a properly sampled control population.  This discrepancy is consistent with reports of abnormal patterns of cortical thickness and grey matter volume in those regions of autistic persons' brains.<ref name="Sugranyes 2011">{{cite journal |author=Sugranyes G, Kyriakopoulos M, Corrigall R, Taylor E, Frangou S |title=Autism spectrum disorders and schizophrenia: meta-analysis of the neural correlates of social cognition |journal=PLoS ONE |volume=6 |issue=10 |pages=e25322 |year=2011 |pmid=21998649 |pmc=3187762 |doi=10.1371/journal.pone.0025322 }}</ref>
In neuroanatomical studies, when performing theory of mind and facial emotion response tasks, the median person on the autism spectrum exhibits less activation in the primary and secondary somato-sensory cortices than does the median member of a properly sampled control population.  This discrepancy is consistent with reports of abnormal patterns of cortical thickness and grey matter volume in those regions of autistic persons' brains.<ref name="Sugranyes 2011">{{cite journal |author=Sugranyes G, Kyriakopoulos M, Corrigall R, Taylor E, Frangou S |title=Autism spectrum disorders and schizophrenia: meta-analysis of the neural correlates of social cognition |journal=PLoS ONE |volume=6 |issue=10 |pages=e25322 |year=2011 |pmid=21998649 |pmc=3187762 |doi=10.1371/journal.pone.0025322 }}</ref>


===Mirror neuron system===
===Mirror Neuron System===


The [[mirror neuron]] system (MNS) consists of a network of brain areas that have been associated with empathy processes in humans.<ref name="Fadiga et al">{{cite journal|last=Fadiga|first=L.|coauthors=Craighero, L. & Olivier, E.|title=Human motor cortex excitability during the perception of others' action|journal=Current Opinion in Neurobiology|year=2005|volume=15|pages=213–218|doi=10.1016/j.conb.2005.03.013|pmid=15831405|issue=2}}</ref> In humans, the MNS has been identified in the inferior frontal gyrus (IFG) and the inferior parietal lobule (IPL) and is thought to be activated during imitation or observation of behaviors.<ref name=Shamy-Tsoory>{{cite journal|last=Shamay-Tsoory|first=S.G.|title=The Neural Bases for Empathy|journal=The Neuroscientist|year=2011|volume=17|issue=1|pages=18–24|doi=10.1177/1073858410379268|pmid=21071616}}</ref>
The [[mirror neuron]] system (MNS) consists of a network of brain areas that have been associated with empathy processes in humans.<ref name="Fadiga et al">{{cite journal|last=Fadiga|first=L.|coauthors=Craighero, L. & Olivier, E.|title=Human motor cortex excitability during the perception of others' action|journal=Current Opinion in Neurobiology|year=2005|volume=15|pages=213–218|doi=10.1016/j.conb.2005.03.013|pmid=15831405|issue=2}}</ref> In humans, the MNS has been identified in the inferior frontal gyrus (IFG) and the inferior parietal lobule (IPL) and is thought to be activated during imitation or observation of behaviors.<ref name=Shamy-Tsoory>{{cite journal|last=Shamay-Tsoory|first=S.G.|title=The Neural Bases for Empathy|journal=The Neuroscientist|year=2011|volume=17|issue=1|pages=18–24|doi=10.1177/1073858410379268|pmid=21071616}}</ref>
It has been proposed that problems with the mirror neuron system may underlie autism;<ref>{{cite journal|last=Nishitani|first=N.|coauthors=Avikainen S. & Hari R.|title=Abnormal imitation-related cortical activation sequences in Asperger's syndrome|journal=Annals of Neurology|year=2004|volume=55|pages=558–562|doi=10.1002/ana.20031|pmid=15048895|issue=4}}</ref><ref>{{cite journal|last=Dapretto|first=M.|title=Understanding emotions in others: mirror neuron dysfunction in children with autism spectrum disorders|journal=Nature Neuroscience|year=2006|volume=9|pages=28–30|author-separator=,|author2=Davies M.S.|author3=Pfeifer J.H.|display-authors=2|doi=10.1038/nn1611|pmid=16327784|last4=Scott|first4=AA|last5=Sigman|first5=M|last6=Bookheimer|first6=SY|last7=Iacoboni|first7=M|issue=1|pmc=3713227}}</ref>  however the connection between mirror neuron dysfunction and autism is tentative and it remains to be seen how mirror neurons may be related to many of the important characteristics of autism.<ref name=Dinstein>{{cite 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 |pmid=18177704 |doi=10.1016/j.cub.2007.11.004 |pmc=2517574}}</ref>
It has been proposed that problems with the mirror neuron system may underlie autism;<ref>{{cite journal|last=Nishitani|first=N.|coauthors=Avikainen S. & Hari R.|title=Abnormal imitation-related cortical activation sequences in Asperger's syndrome|journal=Annals of Neurology|year=2004|volume=55|pages=558–562|doi=10.1002/ana.20031|pmid=15048895|issue=4}}</ref><ref>{{cite journal|last=Dapretto|first=M.|title=Understanding emotions in others: mirror neuron dysfunction in children with autism spectrum disorders|journal=Nature Neuroscience|year=2006|volume=9|pages=28–30|author-separator=,|author2=Davies M.S.|author3=Pfeifer J.H.|display-authors=2|doi=10.1038/nn1611|pmid=16327784|last4=Scott|first4=AA|last5=Sigman|first5=M|last6=Bookheimer|first6=SY|last7=Iacoboni|first7=M|issue=1|pmc=3713227}}</ref>  however the connection between mirror neuron dysfunction and autism is tentative and it remains to be seen how mirror neurons may be related to many of the important characteristics of autism.<ref name=Dinstein>{{cite 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 |pmid=18177704 |doi=10.1016/j.cub.2007.11.004 |pmc=2517574}}</ref>


===Temporal lobe===
===Temporal Lobe===
Functions of the [[temporal lobe]] are related to many of the deficits observed in individuals with ASDs, such as receptive language, social cognition, [[joint attention]], action observation, and empathy. The temporal lobe also contains the [[superior temporal sulcus]] (STS) and the [[fusiform face area]] (FFA), which may mediate facial processing. It has been argued that dysfunction in the STS underlies the social deficits that characterize autism. Compared to typically developing individuals, one fMRI study found that individuals with [[high-functioning autism]] had reduced activity in the FFA when viewing pictures of faces.<ref>{{cite journal|last=Schultz|first=R.|title=Developmental deficits in social perception in autism: The role of amygdala and fusiform face area|journal=International Journal of Developmental Neuroscience|year=2005|volume=23|pages=125–141|doi=10.1016/j.ijdevneu.2004.12.012|pmid=15749240|issue=2–3}}</ref>
Functions of the [[temporal lobe]] are related to many of the deficits observed in individuals with ASDs, such as receptive language, social cognition, [[joint attention]], action observation, and empathy. The temporal lobe also contains the [[superior temporal sulcus]] (STS) and the [[fusiform face area]] (FFA), which may mediate facial processing. It has been argued that dysfunction in the STS underlies the social deficits that characterize autism. Compared to typically developing individuals, one fMRI study found that individuals with [[high-functioning autism]] had reduced activity in the FFA when viewing pictures of faces.<ref>{{cite journal|last=Schultz|first=R.|title=Developmental deficits in social perception in autism: The role of amygdala and fusiform face area|journal=International Journal of Developmental Neuroscience|year=2005|volume=23|pages=125–141|doi=10.1016/j.ijdevneu.2004.12.012|pmid=15749240|issue=2–3}}</ref>


===Mitochondrial dysfunction===
===Mitochondrial Dysfunction===
It has been noted that children with ASD are afflicted with undiagnosed [[comorbid]] conditions such as abnormalities in the peripheral nervous, immune, gastrointestinal and energy production systems, suggesting that ASD isn't strictly a [[central nervous system]] (CNS) disorder, but rather a systemic one.<ref name=Ming>{{cite journal |journal=J Child Neurol |year=2008 |volume=23 |issue=1 |pages=6–13 |title= Autism spectrum disorders: concurrent clinical disorders |author= Xue Ming, Brimacombe M, Chaaban J, Zimmerman-Bier B, Wagner GC |pmid=18056691 |doi=10.1177/0883073807307102}}</ref> It has been hypothesized that ASD could be linked to a mitochondrial disorder, as it is a basic cellular abnormality that has the potential to cause disturbances in a wide range of body systems.<ref name=Haas>{{cite journal |journal=Pediatrics |year=2007 |volume=120 |issue=6 |pages=1326–1333 |title= Mitochondrial disease: a practical approach for primary care physicians |author= Haas RH, Parikh S, Falk MJ, Saneto RP, Wolf NI, Darin N, Cohen BH |pmid=18055683 |doi=10.1542/peds.2007-0391}}</ref> A recent [[meta-analysis]] study, as well as other population studies have shown that approximately 5% of children with ASD meet the criteria for classical [[mitochondrial disease]] (MD),<ref name=Rossignol>{{cite journal |journal=Mol Psychiatry |year=2010 |volume=17 |issue=3 |pages=290–314 |title= Mitochondrial dysfunction in autism spectrum disorders: a systematic review and meta-analysis |author= [[Dan Rossignol|Rossignol DA]], [[Richard E. Frye|Frye RE]] |pmid=21263444|doi=10.1038/mp.2010.136 |pmc=3285768}}</ref> and that around 7.2 percent of children with ASD present with some variant of mitochondrial dysfunction.<ref name=Oliveira>{{cite journal |journal=Dev Med Child Neurol |year=2005 |volume=47 |issue=3 |pages=185–189 |title= Mitochondrial dysfunction in autism spectrum disorders: a population-based study |author= Oliveira G, Diogo L, Grazina M, Garcia P, Ataíde A, Marquess C, Miguel T, Borges L, Vicente AM, Oliveira CR |pmid=15739723 |doi=10.1017/s0012162205000332}}</ref> It is currently unclear why the mitochondrial dysfunction occurs considering that only 23% of children with both ASD and MD present with mitochondrial DNA ([[mtDNA]]) abnormalities.<ref name="Rossignol" />
It has been noted that children with ASD are afflicted with undiagnosed [[comorbid]] conditions such as abnormalities in the peripheral nervous, immune, gastrointestinal and energy production systems, suggesting that ASD isn't strictly a [[central nervous system]] (CNS) disorder, but rather a systemic one.<ref name=Ming>{{cite journal |journal=J Child Neurol |year=2008 |volume=23 |issue=1 |pages=6–13 |title= Autism spectrum disorders: concurrent clinical disorders |author= Xue Ming, Brimacombe M, Chaaban J, Zimmerman-Bier B, Wagner GC |pmid=18056691 |doi=10.1177/0883073807307102}}</ref> It has been hypothesized that ASD could be linked to a mitochondrial disorder, as it is a basic cellular abnormality that has the potential to cause disturbances in a wide range of body systems.<ref name=Haas>{{cite journal |journal=Pediatrics |year=2007 |volume=120 |issue=6 |pages=1326–1333 |title= Mitochondrial disease: a practical approach for primary care physicians |author= Haas RH, Parikh S, Falk MJ, Saneto RP, Wolf NI, Darin N, Cohen BH |pmid=18055683 |doi=10.1542/peds.2007-0391}}</ref> A recent [[meta-analysis]] study, as well as other population studies have shown that approximately 5% of children with ASD meet the criteria for classical [[mitochondrial disease]] (MD),<ref name=Rossignol>{{cite journal |journal=Mol Psychiatry |year=2010 |volume=17 |issue=3 |pages=290–314 |title= Mitochondrial dysfunction in autism spectrum disorders: a systematic review and meta-analysis |author= [[Dan Rossignol|Rossignol DA]], [[Richard E. Frye|Frye RE]] |pmid=21263444|doi=10.1038/mp.2010.136 |pmc=3285768}}</ref> and that around 7.2 percent of children with ASD present with some variant of mitochondrial dysfunction.<ref name=Oliveira>{{cite journal |journal=Dev Med Child Neurol |year=2005 |volume=47 |issue=3 |pages=185–189 |title= Mitochondrial dysfunction in autism spectrum disorders: a population-based study |author= Oliveira G, Diogo L, Grazina M, Garcia P, Ataíde A, Marquess C, Miguel T, Borges L, Vicente AM, Oliveira CR |pmid=15739723 |doi=10.1017/s0012162205000332}}</ref> It is currently unclear why the mitochondrial dysfunction occurs considering that only 23% of children with both ASD and MD present with mitochondrial DNA ([[mtDNA]]) abnormalities.<ref name="Rossignol" />
==Characteristics==
Under DSM-IV-TR, [[autism]] was characterized by delays or abnormal functioning before the age of three years in one or more of the following domains: (1) social interaction; (2) communication; and (3) restricted, repetitive, and stereotyped patterns of behavior, interests, and activities.<ref name=DSM-IV-TR>{{cite book|title=Diagnostic and Statistical Manual of Mental Disorders (4th ed., text rev.)|year= 2000|publisher=American Psychiatric Association|location=Washington, D.C.}}</ref> There is also a unique form of autism called autistic savantism, where a child can actually display outstanding skills in music, art, and numbers with no practice. (National Institute of Health. U.S. Food and Drug Administration. CDC. Alan G Weintraub, MD May 12, 2013)
[[Asperger syndrome]] was distinguished from autism by the lack of delay or deviance in early language development.<ref name=DSM-IV-TR /> Additionally, individuals with Asperger syndrome did not have significant cognitive delays.<ref>{{cite web|title=NINDS Asperger Syndrome Information Page|url=http://www.ninds.nih.gov/disorders/asperger/asperger.htm|publisher=National Institute of Neurological Disorders and Stroke}}</ref>
[[PDD-NOS]] was considered "subthreshold autism" and "atypical autism" because it was often characterized by milder symptoms of autism or symptoms in only one domain (such as social difficulties).<ref>{{cite journal|last=Mesibov|first=G.B.|title=Ask the Editor: What is PDD-NOS and how is it diagnosed?|journal=Journal of Autism and Developmental Diso|year=1997|volume=27|issue=4}}</ref>
The theory of [[monotropism]] proposes that children on the Autism Spectrum have difficulty shifting their attention out of the individual's attention tunnel.<ref name=Murray>{{cite journal|last=Murray|first=Dinah|coauthors=Lesser, M. & Lawson, W|title=Attention, monotropism and the diagnostic criteria for autism|journal=Autism|date=1 May 2005|volume=9|issue=2|url=http://www.autismusundcomputer.de/english//139.pdf|doi=10.1177/1362361305051398|accessdate=23 September 2013}}</ref>
===Developmental course===
Although autism spectrum disorders are thought to follow two possible developmental courses, most parents report that symptom onset occurred within the first year of life.<ref name="Zwaigenbaum 2009">{{cite journal |author=Zwaigenbaum L, Bryson S, Lord C, et al. |title=Clinical assessment and management of toddlers with suspected autism spectrum disorder: insights from studies of high-risk infants |journal=Pediatrics |volume=123 |issue=5 |pages=1383–91 |date=May 2009 |pmid=19403506 |pmc=2833286 |doi=10.1542/peds.2008-1606}}</ref><ref name="Lord 1995">{{cite journal|last=Lord|first=C|title=Follow-up of two-year-olds referred for possible autism|journal=Journal of Child Psychology and Psychiatry|year=1995| volume=36| pages=1365–1382|doi=10.1111/j.1469-7610.1995.tb01669.x|pmid=8988272|issue=8}}</ref> One course of development follows a gradual course of onset in which parents report concerns in development over the first two years of life and diagnosis is made around 3–4 years of age. Some of the early signs of ASDs in this course include decreased looking at faces, failure to turn when name is called, failure to show interests by showing or pointing, and delayed pretend play.<ref name="Zwaigenbaum 2001">{{cite journal |author=Zwaigenbaum L |title=Autistic spectrum disorders in preschool children |journal=Can Fam Physician |volume=47 |issue= 10|pages=2037–42 |date=October 2001 |pmid=11723598 |pmc=2018435 |url=http://www.cfp.ca/content/47/10/2037.abstract}}</ref> A second course of development is characterized by normal or near-normal development followed by loss of skills or regression in the first 2–3 years. Regression may occur in a variety of domains, including communication, social, cognitive, and self-help skills; however, the most common regression is loss of language.<ref name="Martínez-Pedraza 2009">{{cite journal |author=Martínez-Pedraza Fde L, Carter AS |title=Autism spectrum disorders in young children |journal=Child Adolesc Psychiatr Clin N Am |volume=18 |issue=3 |pages=645–63 |date=July 2009 |pmid=19486843 |pmc=3166636 |doi=10.1016/j.chc.2009.02.002}}</ref><ref name="Werner et al.">{{cite journal|last=Werner|coauthors=Dawson, Munson, & Osterling|title=Variation in early developmental course in autism and its relation with behavioral outcome at 3-4 years of age|journal=Journal of Autism and Developmental Disorders|year=2005|volume=35|issue=3|pages=337–350|doi=10.1007/s10803-005-3301-6|pmid=16119475|first1=E}}</ref> There continues to be a debate over the differential outcomes based on these two developmental courses. Some studies suggest that regression is associated with poorer outcomes and others report no differences between those with early gradual onset and those who experience a regression period.<ref name="Mash & Barkley" /> Overall, the prognosis is poor for persons with classical (Kanner-type) autism with respect to academic achievement and poor to below-average for persons across the autism spectrum with respect to independent living abilities; in each case, a lack of early intervention exacerbates the odds against success.<ref name="Mash & Barkley" /> However, many individuals show improvements as they grow older. The two best predictors of favorable outcome in autism are the absence of intellectual disability and the development of some communicative speech prior to five years of age.{{MEDRS|date=December 2012}}<ref name=Mawhood>{{MEDRS|date=December 2012}} {{cite journal|last=Mawhood|coauthors=Howlin, & Rutter|title=Autism and developmental receptive language disorder: A comparative follow-up in early adult life. I. Cognitive and language outcomes|journal=Journal of Child Psychology and Psychiatry|year=2000|volume=41|pages=547–559|doi=10.1111/1469-7610.00642|pmid=10946748|first1=L|issue=5}}</ref> Overall, the literature stresses the importance of early intervention in achieving positive longitudinal outcomes.<ref name="Dawson & Osterling">{{cite book|last=Dawson & Osterling|title=The effectiveness of early intervention|year=1997|publisher=Brookes|location=Baltimore|pages=307–326}}</ref>


==Causes==
==Causes==
While a specific cause or specific causes of autism spectrum disorders has yet to be found, many risk factors have been identified in the research literature that may contribute to the development of an ASD. These risk factors include genetics, prenatal and perinatal factors, neuroanatomical abnormalities, and environmental factors. It is possible to identify general risk factors, but much more difficult to pinpoint specific factors. In the current state of knowledge, prediction can only be of a global nature and therefore requires the use of general markers.<ref name="Tager-Flusberg 2010">{{cite journal |author=[[Helen Tager-Flusberg|Tager-Flusberg H]] |title=The origins of social impairments in autism spectrum disorder: studies of infants at risk |journal=Neural Netw |volume=23 |issue=8-9 |pages=1072–6 |year=2010 |pmid=20800990 |pmc=2956843 |doi=10.1016/j.neunet.2010.07.008 |url=}}</ref>
While a specific cause or specific causes of autism spectrum disorders has yet to be found, many risk factors have been identified in the research literature that may contribute to the development of an ASD. These risk factors include genetics, prenatal and perinatal factors, neuroanatomical abnormalities, and environmental factors. It is possible to identify general risk factors, but much more difficult to pinpoint specific factors. In the current state of knowledge, prediction can only be of a global nature and therefore requires the use of general markers.<ref name="Tager-Flusberg 2010">{{cite journal |author=[[Helen Tager-Flusberg|Tager-Flusberg H]] |title=The origins of social impairments in autism spectrum disorder: studies of infants at risk |journal=Neural Netw |volume=23 |issue=8-9 |pages=1072–6 |year=2010 |pmid=20800990 |pmc=2956843 |doi=10.1016/j.neunet.2010.07.008 |url=}}</ref>


===Genetic risk factors===
===Associated Conditions===
The results of family and twin studies suggest that genetic factors play a role in the etiology of autism and other pervasive developmental disorders.<ref name="Rutter 2000">{{cite journal|last=Rutter|title=Genetic studies of autism: From the 1970s into the millennium|journal=Journal of Abnormal Child Psychology|year=2000|volume=28|pages=3–14|doi=10.1023/A:1005113900068|pmid=10772346|first1=M|issue=1}}</ref> Studies have consistently found that the prevalence of autism in siblings of autistic children is approximately 15 to 30 times greater than the rate in the general population.<ref name="Szatmari 1999">{{cite journal|last=Szatmari|first=P|title=Heterogeneity and the genetics of autism|journal=Journal of Psychiatry and Neuroscience|year=1999|volume=24|pages=159–165|pmid=10212560|issue=2|pmc=1188998}}</ref> In addition, research suggests that there is a much higher concordance rate among monozygotic twins compared to dizygotic twins.<ref name="Rutter 1990">{{cite journal|last=Rutter|coauthors=Macdonald, Le Couteur, Harrington, Bolton, & Bailey|title=Genetic factors in child psychiatric disorders: II. Empirical findings|journal=Journal of Child Psychology and Psychiatry|year=1990|volume=31|pages=39–83|doi=10.1111/j.1469-7610.1990.tb02273.x|pmid=2179248|first1=M|issue=1}}</ref>  It appears that there is no single gene that can account for autism. Instead, there seem to be multiple genes involved, each of which is a risk factor for part of the autism syndrome through various groups.<ref name="Losh 2008">{{cite journal |author=Losh M, Sullivan PF, Trembath D, Piven J |title=Current developments in the genetics of autism: from phenome to genome |journal=J. Neuropathol. Exp. Neurol. |volume=67 |issue=9 |pages=829–37 |date=September 2008 |pmid=18716561 |pmc=2649757 |doi=10.1097/NEN.0b013e318184482d |url=}}</ref><ref name="=Freitag 2010">{{cite journal |author=Freitag CM, Staal W, Klauck SM, Duketis E, Waltes R |title=Genetics of autistic disorders: review and clinical implications |journal=Eur Child Adolesc Psychiatry |volume=19 |issue=3 |pages=169–78 |date=March 2010 |pmid=19941018 |pmc=2839494 |doi=10.1007/s00787-009-0076-x }}</ref><ref name="Chaste 2012">{{cite journal |author=Chaste P, Leboyer M |title=Autism risk factors: genes, environment, and gene-environment interactions |journal=Dialogues Clin Neurosci |volume=14 |issue=3 |pages=281–92 |date=September 2012 |pmid=23226953 |pmc=3513682  |url=http://www.dialogues-cns.com/publication/dialoguesclinneurosci-14-281-xml/}}</ref>
 
===Associated conditions===
* Intellectual disability<ref name="Obrien & Pearson" />
* Intellectual disability<ref name="Obrien & Pearson" />
* Seizures and epilepsy
* Seizures and epilepsy
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* Smith-Lemli-Opitz syndrome, a cholesterol biosynthesis disorder
* Smith-Lemli-Opitz syndrome, a cholesterol biosynthesis disorder


===Prenatal and perinatal risk factors===
===Vaccine Controversy===
A number of prenatal and perinatal complications have been reported as possible risk factors for autism. These risk factors include maternal gestational diabetes, maternal and paternal age over 30, bleeding after first trimester, use of prescription medication (e.g. valproate) during pregnancy, and [[meconium]] in the amniotic fluid. While research is not conclusive on the relation of these factors to autism, each of these factors has been identified more frequently in autistic children compared to their non-autistic siblings and other normally developing youth.<ref name="Garder, Spiegelman, Buka">{{cite journal|last=Gardner|coauthors=Spiegelman, & Buka|title=Perinatal and Neonatal Risk Factors for Autism: A Comprehensive Meta-analysis|journal=Pediatrics|year=2011|volume=128|pages=344–355|doi=10.1542/peds.2010-1036|pmid=21746727|first1=H|issue=2|pmc=3387855}}</ref>
 
===Vaccine controversy===


Perhaps the most controversial claim regarding autism etiology was the "[[MMR vaccine controversy|vaccine controversy]]".<ref>{{cite journal|last=Flaherty|first=DK|title=The vaccine-autism connection: a public health crisis caused by unethical medical practices and fraudulent science.|journal=The Annals of pharmacotherapy|year=2011|volume=45|issue=10|pages=1302–4|pmid=21917556|doi=10.1345/aph.1Q318}}</ref>  This conjecture, arising from a case of scientific misconduct,<ref name=Godlee2011>{{cite journal|last=Godlee|first=F|author2=Smith, J|author3= Marcovitch, H|title=Wakefield's article linking MMR vaccine and autism was fraudulent.|journal=BMJ (Clinical research ed.)|year=2011|volume=342|pages=c7452|doi=10.1136/bmj.c7452|pmid=21209060|url=http://www.bmj.com/content/342/bmj.c7452.full}}</ref> suggested that autism results from brain damage caused either by (1) the measles, mumps, rubella (MMR) vaccine itself, or by (2) [[thimerosal]], a vaccine preservative.<ref name="Tan and Parkin 2008">{{cite journal|last=Tan|author2=Parkin|title=Route of decomposition of thimerosal|journal=International Journal of Pharmacy|year=2008|volume=24|pages=13299– 13305}}</ref> No convincing scientific evidence supports these claims, based on various lines of evidence including the observation that the rate of autism continues to climb despite elimination of thimerosal from routine childhood vaccines.<ref name="Waterhouse 2008">{{cite journal|last=Waterhous|title=Autism overflows: Increasing prevalence and proliferating theories|journal=Neuropsychological Review|year=2008|volume=18|pages=273–286|doi=10.1007/s11065-008-9074-x|first1=Lynn|issue=4}}</ref> In 2014 Professor Guy Eslick, an epidemiologist, did a study to help disprove the theories on vaccines causing autism. The vaccine meta analysis examined 10 major studies on autism and vaccines from around the world that involved 1.25 million children and assessed the odds that children would develop autism after vaccination. Professor Eslick stated, “Most of the studies were right on one, there was just no relationship between vaccination and autism. I hope this study goes some way to closing the doors on the connection between vaccination and autism and I want people to vaccinate their children.” <ref>http://www.news.com.au/lifestyle/health/vaccination-versus-autism-study-professor-guy-eslick-tells-why-hes-taking-on-the-scaremongers/story-fneuzlbd-1226929208418</ref>
Perhaps the most controversial claim regarding autism etiology was the "[[MMR vaccine controversy|vaccine controversy]]".<ref>{{cite journal|last=Flaherty|first=DK|title=The vaccine-autism connection: a public health crisis caused by unethical medical practices and fraudulent science.|journal=The Annals of pharmacotherapy|year=2011|volume=45|issue=10|pages=1302–4|pmid=21917556|doi=10.1345/aph.1Q318}}</ref>  This conjecture, arising from a case of scientific misconduct,<ref name=Godlee2011>{{cite journal|last=Godlee|first=F|author2=Smith, J|author3= Marcovitch, H|title=Wakefield's article linking MMR vaccine and autism was fraudulent.|journal=BMJ (Clinical research ed.)|year=2011|volume=342|pages=c7452|doi=10.1136/bmj.c7452|pmid=21209060|url=http://www.bmj.com/content/342/bmj.c7452.full}}</ref> suggested that autism results from brain damage caused either by (1) the measles, mumps, rubella (MMR) vaccine itself, or by (2) [[thimerosal]], a vaccine preservative.<ref name="Tan and Parkin 2008">{{cite journal|last=Tan|author2=Parkin|title=Route of decomposition of thimerosal|journal=International Journal of Pharmacy|year=2008|volume=24|pages=13299– 13305}}</ref> No convincing scientific evidence supports these claims, based on various lines of evidence including the observation that the rate of autism continues to climb despite elimination of thimerosal from routine childhood vaccines.<ref name="Waterhouse 2008">{{cite journal|last=Waterhous|title=Autism overflows: Increasing prevalence and proliferating theories|journal=Neuropsychological Review|year=2008|volume=18|pages=273–286|doi=10.1007/s11065-008-9074-x|first1=Lynn|issue=4}}</ref> In 2014 Professor Guy Eslick, an epidemiologist, did a study to help disprove the theories on vaccines causing autism. The vaccine meta analysis examined 10 major studies on autism and vaccines from around the world that involved 1.25 million children and assessed the odds that children would develop autism after vaccination. Professor Eslick stated, “Most of the studies were right on one, there was just no relationship between vaccination and autism. I hope this study goes some way to closing the doors on the connection between vaccination and autism and I want people to vaccinate their children.” <ref>http://www.news.com.au/lifestyle/health/vaccination-versus-autism-study-professor-guy-eslick-tells-why-hes-taking-on-the-scaremongers/story-fneuzlbd-1226929208418</ref>


==Differential Diagnosis==
==Differential Diagnosis==
*Attention-deficit/hyperactivity disorder
*[[Attention-deficit/hyperactivity disorder]]
*[[Intellectual disability]] (intellectual developmental disorder) without [[autism spectrum disorder]]
*[[Intellectual disability]] (intellectual developmental disorder) without autism spectrum disorder
*Language disorders and [[social (pragmatic) communication disorder]]
*Language disorders and [[social (pragmatic) communication disorder]]
*[[Rett syndrome]]
*[[Rett syndrome]]
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==Epidemiology and Demographics==
==Epidemiology and Demographics==
===Prevalence===
===Prevalence===
The prevalence of [[autism spectrum disorder]] is 1,000 per 100,000 (1%) of the overall population<ref name=DSMV>{{cite book | title = Diagnostic and statistical manual of mental disorders : DSM-5 | publisher = American Psychiatric Association | location = Washington, D.C | year = 2013 | isbn = 0890425558 }}</ref>.
The prevalence of autism spectrum disorder is approximately 1,000 per 100,000 (1%) of the overall population.<ref name=DSMV>{{cite book | title = Diagnostic and statistical manual of mental disorders : DSM-5 | publisher = American Psychiatric Association | location = Washington, D.C | year = 2013 | isbn = 0890425558 }}</ref> However prevalence rates vary for each of the developmental disorders in the spectrum. Autism prevalence has been estimated at 1-2 per 1,000, Asperger syndrome at roughly 0.6 per 1,000, childhood disintegrative disorder at 0.02 per 1,000, and PDD-NOS at 3.7 per 1,000.<ref name="Newschaffer 2007"/> These rates are consistent across cultures and ethnic groups, as autism is considered a universal disorder.<ref name="Mash & Barkley" />
 
===Gender===
While rates of autism spectrum disorders are consistent across cultures, they vary greatly by gender, with boys being affected far more frequently than girls. The average male-to-female ratio for ASDs is 4.2:1,<ref>{{cite journal|last=Fombonne|first=E|title=Epidemiology of Pervasive Developmental Disorders|journal=Pediatric Research|year=2009|volume=65|issue=6|pages=591–598|doi=10.1203/PDR.0b013e31819e7203|pmid=19218885}}</ref> affecting 1 in 70 males, but only 1 in 315 females.<ref>{{cite journal|last=(ADDM) Autism and Developmental Disabilities Monitoring Network Surveillance Year 2006 Principal Investigators|title=Prevalence of autism spectrum disorders-Autism and Developmental Disabilities Monitoring Network|journal=MMWR Surveillance Summary|year=2009|volume=58|pages=1–20}}</ref> Females, however, are more likely to have associated cognitive impairment. Among those with an ASD and intellectual disability, the sex ratio may be closer to 2:1.<ref>{{cite journal|last=Volkmar|first=F|coauthors=Lord, Bailey, Schultz, & Klin|title=Autism and pervasive developmental disorders|journal=Journal of Child Psychology and Psychiatry|year=2004|volume=45|issue=1|pages=135–170|doi=10.1046/j.0021-9630.2003.00317.x|pmid=14959806}}</ref> Prevalence differences might be accounted by gender differences in the expression of clinical symptoms, with females showing less atypical behaviors and, therefore, less likely to receive an ASD diagnosis.<ref name="Tsakanikos Underwood 2011">{{cite journal|last1=Tsakanikos| first1=Elias|last2=Underwood |first2=Lisa|last3=Kravariti|first3=Eugenia|last4=Bouras|first4=Nick|last5=McCarthy|first5=Jane|title=Gender differences in co-morbid psychopathology and clinical management in adults with autism spectrum disorders|journal=Research in Autism Spectrum Disorders|volume=5|issue=2| year=2011| pages=803–808| issn=17509467|doi=10.1016/j.rasd.2010.09.009}}</ref>


==Risk Factors==
==Risk Factors==
 
*Fetal exposure to valproate<ref name=DSMV>{{cite book | title = Diagnostic and statistical manual of mental disorders : DSM-5 | publisher = American Psychiatric Association | location = Washington, D.C | year = 2013 | isbn  0890425558 }}</ref>
*Advanced parental age
*Genetic predisposition<ref name=DSMV>{{cite book | title = Diagnostic and statistical manual of mental disorders : DSM-5 | publisher = American Psychiatric Association | location = Washington, D.C | year = 2013 | isbn  0890425558 }}</ref>
*Fetal exposure to valproate
*[[Low birth weight]]<ref name=DSMV>{{cite book | title = Diagnostic and statistical manual of mental disorders : DSM-5 | publisher = American Psychiatric Association | location = Washington, D.C | year = 2013 | isbn  0890425558 }}</ref>
*Genetic predisposition
*[[Low birth weight]]
*Males<ref name=DSMV>{{cite book | title = Diagnostic and statistical manual of mental disorders : DSM-5 | publisher = American Psychiatric Association | location = Washington, D.C | year = 2013 | isbn  0890425558 }}</ref>
*Males<ref name=DSMV>{{cite book | title = Diagnostic and statistical manual of mental disorders : DSM-5 | publisher = American Psychiatric Association | location = Washington, D.C | year = 2013 | isbn  0890425558 }}</ref>
* Maternal gestational diabetes<ref name="Garder, Spiegelman, Buka">{{cite journal|last=Gardner|coauthors=Spiegelman, & Buka|title=Perinatal and Neonatal Risk Factors for Autism: A Comprehensive Meta-analysis|journal=Pediatrics|year=2011|volume=128|pages=344–355|doi=10.1542/peds.2010-1036|pmid=21746727|first1=H|issue=2|pmc=3387855}}</ref>
* Mternal and paternal age over 30<ref name="Garder, Spiegelman, Buka">{{cite journal|last=Gardner|coauthors=Spiegelman, & Buka|title=Perinatal and Neonatal Risk Factors for Autism: A Comprehensive Meta-analysis|journal=Pediatrics|year=2011|volume=128|pages=344–355|doi=10.1542/peds.2010-1036|pmid=21746727|first1=H|issue=2|pmc=3387855}}</ref>
* Bleeding after first trimester<ref name="Garder, Spiegelman, Buka">{{cite journal|last=Gardner|coauthors=Spiegelman, & Buka|title=Perinatal and Neonatal Risk Factors for Autism: A Comprehensive Meta-analysis|journal=Pediatrics|year=2011|volume=128|pages=344–355|doi=10.1542/peds.2010-1036|pmid=21746727|first1=H|issue=2|pmc=3387855}}</ref>
* Use of prescription medication (e.g. valproate) during pregnancy<ref name="Garder, Spiegelman, Buka">{{cite journal|last=Gardner|coauthors=Spiegelman, & Buka|title=Perinatal and Neonatal Risk Factors for Autism: A Comprehensive Meta-analysis|journal=Pediatrics|year=2011|volume=128|pages=344–355|doi=10.1542/peds.2010-1036|pmid=21746727|first1=H|issue=2|pmc=3387855}}</ref>
* [[Meconium]] in the amniotic fluid<ref name="Garder, Spiegelman, Buka">{{cite journal|last=Gardner|coauthors=Spiegelman, & Buka|title=Perinatal and Neonatal Risk Factors for Autism: A Comprehensive Meta-analysis|journal=Pediatrics|year=2011|volume=128|pages=344–355|doi=10.1542/peds.2010-1036|pmid=21746727|first1=H|issue=2|pmc=3387855}}</ref>


==Natural History,Complications and Prognosis==
===Genetic Risk Factors===
The results of family and twin studies suggest that genetic factors play a role in the etiology of autism and other pervasive developmental disorders.<ref name="Rutter 2000">{{cite journal|last=Rutter|title=Genetic studies of autism: From the 1970s into the millennium|journal=Journal of Abnormal Child Psychology|year=2000|volume=28|pages=3–14|doi=10.1023/A:1005113900068|pmid=10772346|first1=M|issue=1}}</ref> Studies have consistently found that the prevalence of autism in siblings of autistic children is approximately 15 to 30 times greater than the rate in the general population.<ref name="Szatmari 1999">{{cite journal|last=Szatmari|first=P|title=Heterogeneity and the genetics of autism|journal=Journal of Psychiatry and Neuroscience|year=1999|volume=24|pages=159–165|pmid=10212560|issue=2|pmc=1188998}}</ref> In addition, research suggests that there is a much higher concordance rate among monozygotic twins compared to dizygotic twins.<ref name="Rutter 1990">{{cite journal|last=Rutter|coauthors=Macdonald, Le Couteur, Harrington, Bolton, & Bailey|title=Genetic factors in child psychiatric disorders: II. Empirical findings|journal=Journal of Child Psychology and Psychiatry|year=1990|volume=31|pages=39–83|doi=10.1111/j.1469-7610.1990.tb02273.x|pmid=2179248|first1=M|issue=1}}</ref>  It appears that there is no single gene that can account for autism. Instead, there seem to be multiple genes involved, each of which is a risk factor for part of the autism syndrome through various groups.<ref name="Losh 2008">{{cite journal |author=Losh M, Sullivan PF, Trembath D, Piven J |title=Current developments in the genetics of autism: from phenome to genome |journal=J. Neuropathol. Exp. Neurol. |volume=67 |issue=9 |pages=829–37 |date=September 2008 |pmid=18716561 |pmc=2649757 |doi=10.1097/NEN.0b013e318184482d |url=}}</ref><ref name="=Freitag 2010">{{cite journal |author=Freitag CM, Staal W, Klauck SM, Duketis E, Waltes R |title=Genetics of autistic disorders: review and clinical implications |journal=Eur Child Adolesc Psychiatry |volume=19 |issue=3 |pages=169–78 |date=March 2010 |pmid=19941018 |pmc=2839494 |doi=10.1007/s00787-009-0076-x }}</ref><ref name="Chaste 2012">{{cite journal |author=Chaste P, Leboyer M |title=Autism risk factors: genes, environment, and gene-environment interactions |journal=Dialogues Clin Neurosci |volume=14 |issue=3 |pages=281–92 |date=September 2012 |pmid=23226953 |pmc=3513682  |url=http://www.dialogues-cns.com/publication/dialoguesclinneurosci-14-281-xml/}}</ref>


===Prognosis===
==Natural History, Complications and Prognosis==


*Good prognostic factor include:<ref name= DSMV>{{cite book | title = Diagnostic and statistical manual of mental disorders : DSM-5 | publisher = American Psychiatric Association |location = Washington, D.C | year = 2013 | isbn = 0890425558 }}</ref>
Although autism spectrum disorders are thought to follow two possible developmental courses, most parents report that symptom onset occurred within the first year of life.<ref name="Zwaigenbaum 2009">{{cite journal |author=Zwaigenbaum L, Bryson S, Lord C, et al. |title=Clinical assessment and management of toddlers with suspected autism spectrum disorder: insights from studies of high-risk infants |journal=Pediatrics |volume=123 |issue=5 |pages=1383–91 |date=May 2009 |pmid=19403506 |pmc=2833286 |doi=10.1542/peds.2008-1606}}</ref><ref name="Lord 1995">{{cite journal|last=Lord|first=C|title=Follow-up of two-year-olds referred for possible autism|journal=Journal of Child Psychology and Psychiatry|year=1995| volume=36| pages=1365–1382|doi=10.1111/j.1469-7610.1995.tb01669.x|pmid=8988272|issue=8}}</ref> One course of development follows a gradual course of onset in which parents report concerns in development over the first two years of life and diagnosis is made around 3–4 years of age. Some of the early signs of ASDs in this course include decreased looking at faces, failure to turn when name is called, failure to show interests by showing or pointing, and delayed pretend play.<ref name="Zwaigenbaum 2001">{{cite journal |author=Zwaigenbaum L |title=Autistic spectrum disorders in preschool children |journal=Can Fam Physician |volume=47 |issue= 10|pages=2037–42 |date=October 2001 |pmid=11723598 |pmc=2018435 |url=http://www.cfp.ca/content/47/10/2037.abstract}}</ref> A second course of development is characterized by normal or near-normal development followed by loss of skills or regression in the first 2–3 years. Regression may occur in a variety of domains, including communication, social, cognitive, and self-help skills; however, the most common regression is loss of language.<ref name="Martínez-Pedraza 2009">{{cite journal |author=Martínez-Pedraza Fde L, Carter AS |title=Autism spectrum disorders in young children |journal=Child Adolesc Psychiatr Clin N Am |volume=18 |issue=3 |pages=645–63 |date=July 2009 |pmid=19486843 |pmc=3166636 |doi=10.1016/j.chc.2009.02.002}}</ref><ref name="Werner et al.">{{cite journal|last=Werner|coauthors=Dawson, Munson, & Osterling|title=Variation in early developmental course in autism and its relation with behavioral outcome at 3-4 years of age|journal=Journal of Autism and Developmental Disorders|year=2005|volume=35|issue=3|pages=337–350|doi=10.1007/s10803-005-3301-6|pmid=16119475|first1=E}}</ref> There continues to be a debate over the differential outcomes based on these two developmental courses. Some studies suggest that regression is associated with poorer outcomes and others report no differences between those with early gradual onset and those who experience a regression period.<ref name="Mash & Barkley" /> Overall, the prognosis is poor for persons with classical (Kanner-type) autism with respect to academic achievement and poor to below-average for persons across the autism spectrum with respect to independent living abilities; in each case, a lack of early intervention exacerbates the odds against success.<ref name="Mash & Barkley" /> However, many individuals show improvements as they grow older. The two best predictors of favorable outcome in autism are the absence of intellectual disability and the development of some communicative speech prior to five years of age.{{MEDRS|date=December 2012}}<ref name=Mawhood>{{MEDRS|date=December 2012}} {{cite journal|last=Mawhood|coauthors=Howlin, & Rutter|title=Autism and developmental receptive language disorder: A comparative follow-up in early adult life. I. Cognitive and language outcomes|journal=Journal of Child Psychology and Psychiatry|year=2000|volume=41|pages=547–559|doi=10.1111/1469-7610.00642|pmid=10946748|first1=L|issue=5}}</ref> Overall, the literature stresses the importance of early intervention in achieving positive longitudinal outcomes.<ref name="Dawson & Osterling">{{cite book|last=Dawson & Osterling|title=The effectiveness of early intervention|year=1997|publisher=Brookes|location=Baltimore|pages=307–326}}</ref>
 
:*Mental health problems
:*Presence or absence of associated intellectual disability and language impairment
 
==Diagnosis==


==Diagnostic Criteria==
==Diagnostic Criteria==
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{{cquote|
{{cquote|


*A. Persistent deficits in social communication and social interaction across multiple contexts,as manifested by the following, currently or by history (examples are illustrative,not exhaustive; see text):
*A. Persistent deficits in social communication and social interaction across multiple contexts,as manifested by the following, currently or by history
:*1. Deficits in social-emotional reciprocity, ranging, for example, from abnormal social approach and failure of normal back-and-forth conversation; to reduced sharing of
:*1. Deficits in social-emotional reciprocity, ranging, for example, from abnormal social approach and failure of normal back-and-forth conversation; to reduced sharing of interests, emotions, or affect; to failure to initiate or respond to social interactions.
interests, emotions, or affect; to failure to initiate or respond to social interactions.


:*2. Deficits in non verbal communicative behaviors used for social interaction, ranging,for example, from poorly integrated verbal and nonverbal communication; to abnormalities
:*2. Deficits in non verbal communicative behaviors used for social interaction, ranging,for example, from poorly integrated verbal and nonverbal communication; to abnormalities in eye contact and body language or deficits in understanding and use of gestures: to a total lack of facial expressions and nonverbal communication.
in eye contact and body language or deficits in understanding and use of gestures: to a total lack of facial expressions and nonverbal communication.


:*3. Deficits in developing, maintaining, and understanding relationships, ranging, for example,from difficulties adjusting behavior to suit various social contexts; to difficulties in sharing imaginative play or in making friends; to absence of interest in peers.
:*3. Deficits in developing, maintaining, and understanding relationships, ranging, for example,from difficulties adjusting behavior to suit various social contexts; to difficulties in sharing imaginative play or in making friends; to absence of interest in peers. Specify current severity: Severity is based on social communication impairments and restricted, repetitive patterns of behavior.
Specify current severity:Severity is based on social communication impairments and restricted, repetitive patterns of behavior.


'''''AND'''''
'''''AND'''''
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*B. Restricted, repetitive patterns of behavior, interests, or activities, as manifested by at least two of the following, currently or by history  
*B. Restricted, repetitive patterns of behavior, interests, or activities, as manifested by at least two of the following, currently or by history  


:*1. Stereotyped or repetitive motor movements, use of objects, or speech (e.g., simple motor stereotypes, lining up toys or flipping objects, echolalia, idiosyncratic
:*1. Stereotyped or repetitive motor movements, use of objects, or speech (e.g., simple motor stereotypes, lining up toys or flipping objects, [[echolalia]], idiosyncratic phrases).
phrases).
:*2. Insistence on sameness, inflexible adherence to routines, or ritualized patterns of verbal or nonverbal behavior (e.g., extreme distress at small changes, difficulties with transitions, rigid thinking patterns, greeting rituals, need to take same route or eat same food every day).
:*2. Insistence on sameness, inflexible adherence to routines, or ritualized patterns of verbal or nonverbal behavior (e.g., extreme distress at small changes, difficulties with transitions, rigid thinking patterns, greeting rituals, need to take same route or eat same food every day).
:*3. Highly restricted, fixated interests that are abnormal in intensity or focus (e.g.,strong attachment to or preoccupation with unusual objects, excessively circumscribed
:*3. Highly restricted, fixated interests that are abnormal in intensity or focus (e.g.,strong attachment to or preoccupation with unusual objects, excessively circumscribed or perseverative interests).
or perseverative interests).
:*4. Hyper- or hyporeactivity to sensory input or unusual interest in sensory aspects of the environment (e.g., apparent indifference to pain/temperature, adverse response to specific sounds or textures, excessive smelling or touching of objects,visual fascination with lights or movement).
:*4. Hyper- or hyporeactivity to sensory input or unusual interest in sensory aspects of the environment (e.g., apparent indifference to pain/temperature, adverse response to specific sounds or textures, excessive smelling or touching of objects,visual fascination with lights or movement).
:*Specify current severity:Severity is based on social communication impairments and restricted, repetitive patterns of behavior.
:*Specify current severity: Severity is based on social communication impairments and restricted, repetitive patterns of behavior.


'''''AND'''''
'''''AND'''''
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'''''AND'''''
'''''AND'''''


*E. These disturbances are not better explained by intellectual disability (intellectual developmental disorder) or global developmental delay. Intellectual disability and autism
*E. These disturbances are not better explained by [[intellectual disability]] (intellectual developmental disorder) or [[global developmental delay]]. Intellectual disability and autism
spectrum disorder frequently co-occur; to make comorbid diagnoses of [[autism spectrum disorder]] and [[intellectual disability]], social communication should be below that expected for general developmental level.
spectrum disorder frequently co-occur; to make comorbid diagnoses of autism spectrum disorder and [[intellectual disability]], social communication should be below that expected for general developmental level.


}}
<SMALL>''Note: Individuals with a well-established DSM-IV diagnosis of autistic disorder, Asperger’s disorder, or pervasive developmental disorder not otherwise specified should be given the diagnosis of autism spectrum disorder. Individuals who have marked deficits in social communication, but whose symptoms do not otherwise meet criteria for autism spectrum disorder, should be evaluated for [[social (pragmatic) communication disorder]].''</SMALL>
 
<SMALL>''Note: Individuals with a well-established DSM-IV diagnosis of autistic disorder, [[Asperger’s disorder]], or pervasive developmental disorder not otherwise specified should be given the diagnosis of [[autism spectrum disorder]]. Individuals who have marked deficits in social communication, but whose symptoms do not otherwise meet criteria for [[autism spectrum disorder]], should be evaluated for [[social (pragmatic) communication disorder]].  
Specify if;  
Specify if;  
*With or without accompanying intellectual impairment
*With or without accompanying intellectual impairment
*With or without accompanying language impairment  
*With or without accompanying language impairment  
*Associated with a known medical or genetic condition or environmental factor.  
*Associated with a known medical or genetic condition or environmental factor.  
*Associated with another neurodevelopmental, mental, or behavioral disorder.''</SMALL>
*Associated with another neurodevelopmental, mental, or behavioral disorder.


===Evidence-based assessment===
}}
 
===Evidence-Based Assessment===
ASD can be detected as early as eighteen months or even younger in some cases.<ref>{{cite web|title=Autism Spectrum Disorder (ASD): Screening and Diagnosis|url=http://www.cdc.gov/ncbddd/autism/screening.html|publisher=Centers for Disease Control and Prevention}}</ref> A reliable diagnosis can usually be made by the age of two.<ref name="Lord 2006">{{cite journal|last=Lord|first=C|author2=Risi, S |author3=DiLavore, PS |author4=Shulman, C |author5=Thurm, A |author6= Pickles, A |title=Autism from 2 to 9 years of age.|journal=Archives of General Psychiatry|date=Jun 2006|volume=63|issue=6|pages=694–701|doi=10.1001/archpsyc.63.6.694|pmid=16754843}}</ref> The diverse expressions of ASD symptoms pose diagnostic challenges to clinicians. Individuals with an ASD may present at various times of development (e.g., toddler, child, or adolescent) and symptom expression may vary over the course of development.<ref name="Volkmar 1999">{{cite journal |author=Volkmar F, Cook EH, Pomeroy J, Realmuto G, Tanguay P |title=Practice parameters for the assessment and treatment of children, adolescents, and adults with autism and other pervasive developmental disorders. American Academy of Child and Adolescent Psychiatry Working Group on Quality Issues |journal=J Am Acad Child Adolesc Psychiatry |volume=38 |issue=12 Suppl |pages=32S–54S |date=December 1999 |pmid=10624084 |doi= 10.1016/s0890-8567(99)80003-3|url=}}</ref> Furthermore, clinicians are required to differentiate among the different pervasive developmental disorders as well as other disorders such as mental retardation not associated with a pervasive developmental disorder, specific developmental disorders (e.g. language), and early onset schizophrenia,{{Citation needed|date=April 2013}} as well as the social-cognitive deficits caused by brain damage from [[alcohol abuse]].<ref name="pmid18412750">{{cite journal |author=Uekermann J, Daum I |title=Social cognition in alcoholism: a link to prefrontal cortex dysfunction? |journal=Addiction |volume=103 |issue=5 |pages=726–35 |date=May 2008 |pmid=18412750 |doi=10.1111/j.1360-0443.2008.02157.x |url=}}</ref>
ASD can be detected as early as eighteen months or even younger in some cases.<ref>{{cite web|title=Autism Spectrum Disorder (ASD): Screening and Diagnosis|url=http://www.cdc.gov/ncbddd/autism/screening.html|publisher=Centers for Disease Control and Prevention}}</ref> A reliable diagnosis can usually be made by the age of two.<ref name="Lord 2006">{{cite journal|last=Lord|first=C|author2=Risi, S |author3=DiLavore, PS |author4=Shulman, C |author5=Thurm, A |author6= Pickles, A |title=Autism from 2 to 9 years of age.|journal=Archives of General Psychiatry|date=Jun 2006|volume=63|issue=6|pages=694–701|doi=10.1001/archpsyc.63.6.694|pmid=16754843}}</ref> The diverse expressions of ASD symptoms pose diagnostic challenges to clinicians. Individuals with an ASD may present at various times of development (e.g., toddler, child, or adolescent) and symptom expression may vary over the course of development.<ref name="Volkmar 1999">{{cite journal |author=Volkmar F, Cook EH, Pomeroy J, Realmuto G, Tanguay P |title=Practice parameters for the assessment and treatment of children, adolescents, and adults with autism and other pervasive developmental disorders. American Academy of Child and Adolescent Psychiatry Working Group on Quality Issues |journal=J Am Acad Child Adolesc Psychiatry |volume=38 |issue=12 Suppl |pages=32S–54S |date=December 1999 |pmid=10624084 |doi= 10.1016/s0890-8567(99)80003-3|url=}}</ref> Furthermore, clinicians are required to differentiate among the different pervasive developmental disorders as well as other disorders such as mental retardation not associated with a pervasive developmental disorder, specific developmental disorders (e.g. language), and early onset schizophrenia,{{Citation needed|date=April 2013}} as well as the social-cognitive deficits caused by brain damage from [[alcohol abuse]].<ref name="pmid18412750">{{cite journal |author=Uekermann J, Daum I |title=Social cognition in alcoholism: a link to prefrontal cortex dysfunction? |journal=Addiction |volume=103 |issue=5 |pages=726–35 |date=May 2008 |pmid=18412750 |doi=10.1111/j.1360-0443.2008.02157.x |url=}}</ref>


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After a child fails an initial screening, psychologists administer various psychological assessment tools to assess for ASD.<ref name="Ozonoff 2005">{{cite journal|last=Ozonoff|first=S.|coauthors=Goodlin-Jones, B.L. & Solomon, M.|title=Evidence-Based Assessment of Autism|journal=Journal of Clinical and Child Adolescent Psychology|year=2005|volume=34|issue=3|pages=523–540|doi=10.1207/s15374424jccp3403_8}}</ref> Amongst these measurements, the Autism Diagnostic Interview-Revised (ADI-R) and the Autism Diagnostic Observation Schedule (ADOS) are considered the "gold standards" for assessing autistic children.<ref name="Corsello 2007">{{cite journal |author=Corsello C, Hus V, Pickles A, et al. |title=Between a ROC and a hard place: decision making and making decisions about using the SCQ |journal=J Child Psychol Psychiatry |volume=48 |issue=9 |pages=932–40 |date=September 2007 |pmid=17714378 |doi=10.1111/j.1469-7610.2007.01762.x |url=}}</ref><ref name="Huerta 2010">{{cite journal |author=Huerta M, Lord C |title=Diagnostic evaluation of autism spectrum disorders |journal=Pediatr. Clin. North Am. |volume=59 |issue=1 |pages=103–11, xi |date=February 2012 |pmid=22284796 |pmc=3269006 |doi=10.1016/j.pcl.2011.10.018 |url=}}</ref> The ADI-R is a semi-structured parent interview that probes for symptoms of autism by evaluating a child's current behavior and developmental history. The ADOS is a semistructured interactive evaluation of ASD symptoms that is used to measure social and communication abilities by eliciting a number of opportunities (or "presses") for spontaneous behaviors (e.g., eye contact) in standardized context. Various other questionnaires (e.g., The Childhood Autism Rating Scale) and tests of cognitive functioning (e.g., The Peabody Picture Vocabulary Test) are typically included in an ASD assessment battery.
After a child fails an initial screening, psychologists administer various psychological assessment tools to assess for ASD.<ref name="Ozonoff 2005">{{cite journal|last=Ozonoff|first=S.|coauthors=Goodlin-Jones, B.L. & Solomon, M.|title=Evidence-Based Assessment of Autism|journal=Journal of Clinical and Child Adolescent Psychology|year=2005|volume=34|issue=3|pages=523–540|doi=10.1207/s15374424jccp3403_8}}</ref> Amongst these measurements, the Autism Diagnostic Interview-Revised (ADI-R) and the Autism Diagnostic Observation Schedule (ADOS) are considered the "gold standards" for assessing autistic children.<ref name="Corsello 2007">{{cite journal |author=Corsello C, Hus V, Pickles A, et al. |title=Between a ROC and a hard place: decision making and making decisions about using the SCQ |journal=J Child Psychol Psychiatry |volume=48 |issue=9 |pages=932–40 |date=September 2007 |pmid=17714378 |doi=10.1111/j.1469-7610.2007.01762.x |url=}}</ref><ref name="Huerta 2010">{{cite journal |author=Huerta M, Lord C |title=Diagnostic evaluation of autism spectrum disorders |journal=Pediatr. Clin. North Am. |volume=59 |issue=1 |pages=103–11, xi |date=February 2012 |pmid=22284796 |pmc=3269006 |doi=10.1016/j.pcl.2011.10.018 |url=}}</ref> The ADI-R is a semi-structured parent interview that probes for symptoms of autism by evaluating a child's current behavior and developmental history. The ADOS is a semistructured interactive evaluation of ASD symptoms that is used to measure social and communication abilities by eliciting a number of opportunities (or "presses") for spontaneous behaviors (e.g., eye contact) in standardized context. Various other questionnaires (e.g., The Childhood Autism Rating Scale) and tests of cognitive functioning (e.g., The Peabody Picture Vocabulary Test) are typically included in an ASD assessment battery.
There has been no current medical testing, such as blood work or brain scan, to diagnose autism (Gale Encyclopedia of Genetic Disorder), but there is some developmental screening that should be done during regular well-child doctor visits. These screenings should be done at every visit starting at nine months to twenty-four or thirty months and continue in children at high risk for developmental problems due to preterm birth, low birth weight, or other reasons (CDC).
According to the Gale Encyclopedia of Mental Health, Nursing and Allied Health, Genetic Disorders, (CDC) the Centers for Disease Control and Prevention, and WebMD there are three main developmental markers that are directly affected by (ASD) autism Spectrum disorder. The severity of the impairments varies individually, but the same markers are always considered. The three developmental areas that are affected in someone that has (ASD) are their social interactions and relationships, verbal and nonverbal communication skills, and behavioral issues and there are also a few other aspects other than developmental that are affected in people with (ASD) autism spectrum disorder, such as sensory problems.
One of the markers mentioned above used to help diagnose autism spectrum disorder is social interactions and relationships. This developmental marker is basically how someone can connect with others (Gale Encyclopedia of Nursing and Allied Health). In infants, (ASD) autism spectrum disorder is first demonstrated in social interactions and relationships when the infant fails to maintain eye contact, or seems uncomfortable when being picked up or held. They may cry, or become limp or tense. They may also seem to have no bond with parents or caregivers. (ASD) prevents them from having the ability to pick up on social cues. This lack can sometimes cause uncontrolled emotional outbursts. It will affect their relationships with others their own ages and they may not be able to express themselves appropriately (WebMD). Autism spectrum disorder also has an effect on the sense of empathy and this lack can challenge the full understanding of someone else’s emotions, such as pain and sorrow (WebMD).
According to Gale Encyclopedia of Nursing and Allied Health, and the Gale Encyclopedia of Genetic Disorder, and also by WebMD is that verbal and non-verbal communication varies on an individual basis, and is one of the first warning signs of this disorder. Warning signs listed by WebMD are your child does not babble or coo by twelve months, does not gesture, such as point or wave by twelve months, does not say single words by sixteen months, does not say two-word phrases on his or her own, and does not make a facial expressions or respond to your facial expression. Common signs are different in each case. Some children may not speak at all, can only use two words at a time, or they can have a large range of words but cannot hold a full conversation (Gale Encyclopedia of Nursing and Allied Health). According to Gale Encyclopedia of Genetic Disorders, another aspect that has appeared in children is the constant repeating of meaningless words or phrases.
One of the other developmental markers highlighted in the detection of (ASD) are behavioral issues.  In children, detecting autism, can manifest itself in the unique ways they play with toys and other objects, such as repetitive lining of the toy in certain ways (WebMD). They also need to have strict routine and constant familiarity, and are very resistant to change. They have continuous body movements or patterns of behavior, such as hand flapping, spinning, or body rocking (WebMD) and other characteristics, such as temper tantrums or screaming fits, hyperactivity, and inappropriate laughing or giggling, are shown (Gale Encyclopedia of Genetic Disorders). One of the other behavioral issues is the fixation or obsessive interest in an activity, idea, or person (Gale Encyclopedia of Genetic Disorders).
Even though there are three major components that are affected by (ASD) autism spectrum disorder, there are other symptoms that factor in as well, such as sensory issues. A large percentage of children seem overwhelmed by these senses and react badly to certain sounds by sometimes banging their heads and obsessing with how objects feel under their fingers.
There is no cure for this disorder at this time, but early detection, intensive therapy, and knowledge are the best forms of treatments. Medication can be helpful, also. One form of therapy is behavioral training and management where positive reinforcement, self-help, and social skills training are used to improve behavioral and communication skills (WebMD) and other treatments, such as speech therapy can be used to develop and improve language skills. Occupational therapy can help develop motor skills and teaches self-help and functional skills like grooming. There are many other therapies that can be used to manage the symptoms of (ASD) autism spectrum disorder such as applied behavioral analysis, auditory integration training, dietary interventions, music therapy, physical therapy, sensory integration, and vision therapy(Gale Encyclopedia of Nursing and allied Health). No medication has been developed that will cure (ASD) autism spectrum disorder, but they have found some drugs have an effect on the symptoms (CDC). These medications are used to treat things like anxiety, depression, hyperactivity, anger and aggression. Ritalin, Luvox, ReVia, Methylphenidate, and lithium are types of remedies (Gale Encyclopedia of Mental Health). Treatment, whether it’s therapy or medication must be consistent and with family support (Gale Encyclopedia of Nursing and Allied Health).The knowledge of the symptoms of (ASD) is key to the effectiveness of home treatment (WebMD). Families must educate themselves as well as stay in constant communication with others that are involved in the care of the child (WebMD).  According to Gale Encyclopedia of Mental health the most popular alternative treatment is megavitamin therapy because some studies have shown that Vitamin B6 with Magnesium can improve eye contact and speech, and lessen tantrums behavior.


===Comorbidity===
===Comorbidity===
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Deficits in ASD are often linked to behavior problems, such as difficulties following directions, being cooperative, and doing things on other people's terms.<ref name="Tsakanikos 2007">{{cite journal |author=Tsakanikos E, Costello H, Holt G, Sturmey P, Bouras N |title=Behaviour management problems as predictors of psychotropic medication and use of psychiatric services in adults with autism |journal=J Autism Dev Disord |volume=37 |issue=6 |pages=1080–5 |date=July 2007 |pmid=17053989 |doi=10.1007/s10803-006-0248-1 |url=http://cogprints.org/6268/2/JADD_2007.pdf}}</ref> [[Attention Deficit Hyperactivity Disorder]] (ADHD)-like symptoms are seen to be part of the ASD diagnosis.<ref name="Rommelse et al.">{{cite journal|last=Rommelse|coauthors=Franke, Geurts, Hartman, & Buitelaar|title=Shared heritability of attention-deficit/hyperactivity disorder and autism spectrum disorder|journal=European Child and Adolescent Psychiatry|year=2010|volume=19|pages=281–295|doi=10.1007/s00787-010-0092-x|pmid=20148275|first1=NN|issue=3|pmc=2839489}}</ref>
Deficits in ASD are often linked to behavior problems, such as difficulties following directions, being cooperative, and doing things on other people's terms.<ref name="Tsakanikos 2007">{{cite journal |author=Tsakanikos E, Costello H, Holt G, Sturmey P, Bouras N |title=Behaviour management problems as predictors of psychotropic medication and use of psychiatric services in adults with autism |journal=J Autism Dev Disord |volume=37 |issue=6 |pages=1080–5 |date=July 2007 |pmid=17053989 |doi=10.1007/s10803-006-0248-1 |url=http://cogprints.org/6268/2/JADD_2007.pdf}}</ref> [[Attention Deficit Hyperactivity Disorder]] (ADHD)-like symptoms are seen to be part of the ASD diagnosis.<ref name="Rommelse et al.">{{cite journal|last=Rommelse|coauthors=Franke, Geurts, Hartman, & Buitelaar|title=Shared heritability of attention-deficit/hyperactivity disorder and autism spectrum disorder|journal=European Child and Adolescent Psychiatry|year=2010|volume=19|pages=281–295|doi=10.1007/s00787-010-0092-x|pmid=20148275|first1=NN|issue=3|pmc=2839489}}</ref>


[[Sensory processing disorder]] is also comorbid with ASD, with comorbidity rates of 42-88%.<ref name="Baranek 2002">{{cite journal|last=Baranek|first=G|title=Efficacy of sensory and motor interventions in children with autism|journal=Journal of Autism and Developmental Disorders|year=2002|volume=32|issue=5|pages=397–422|doi=10.1023/A:1020541906063|pmid=12463517}}</ref>
Sensory processing disorder is also comorbid with ASD, with comorbidity rates of 42-88%.<ref name="Baranek 2002">{{cite journal|last=Baranek|first=G|title=Efficacy of sensory and motor interventions in children with autism|journal=Journal of Autism and Developmental Disorders|year=2002|volume=32|issue=5|pages=397–422|doi=10.1023/A:1020541906063|pmid=12463517}}</ref>


==Management==
==Management==
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Although (ASD) autism spectrum disorder is lifelong, it can be treated. A family with a child that suffers this ailment must know and understand the aspects of it, as well as being consistent with the treatment plan. A key point is to learn how to handle the normal range of emotions that comes from raising a child with this disorder (WebMD) and another facet that a family should consider is finding a support group for both the child as well as themselves.   
Although (ASD) autism spectrum disorder is lifelong, it can be treated. A family with a child that suffers this ailment must know and understand the aspects of it, as well as being consistent with the treatment plan. A key point is to learn how to handle the normal range of emotions that comes from raising a child with this disorder (WebMD) and another facet that a family should consider is finding a support group for both the child as well as themselves.   
According to WebMD there are many places to get help for either the family or to find treatment plans for the child. The National Institute of Neurological Disorders and Stroke which is the leading U.S. federal government agency supporting research on brain and nervous system disorders is one such organization. It provides the public with educational materials and information about these disorders. The Centers for Disease Control and Prevention (CDC) is another agency whose aim is to find the cause of and prevent birth defects and developmental disabilities. This group works to help people of all ages with the disabilities live to the fullest.
According to WebMD there are many places to get help for either the family or to find treatment plans for the child. The National Institute of Neurological Disorders and Stroke which is the leading U.S. federal government agency supporting research on brain and nervous system disorders is one such organization. It provides the public with educational materials and information about these disorders. The Centers for Disease Control and Prevention (CDC) is another agency whose aim is to find the cause of and prevent birth defects and developmental disabilities. This group works to help people of all ages with the disabilities live to the fullest.
===Epidemiology and Demographics===
==Epidemiology==
Reviews tend to estimate a prevalence of 6 per 1,000 for autism spectrum disorders as a whole,<ref name="Newschaffer 2007">{{cite journal |author=Newschaffer CJ, Croen LA, Daniels J, et al. |title=The epidemiology of autism spectrum disorders |journal=Annu Rev Public Health |volume=28 |issue= |pages=235–58 |year=2007 |pmid=17367287 |doi=10.1146/annurev.publhealth.28.021406.144007 }}</ref> however prevalence rates vary for each of the developmental disorders in the spectrum. Autism prevalence has been estimated at 1-2 per 1,000, Asperger syndrome at roughly 0.6 per 1,000, childhood disintegrative disorder at 0.02 per 1,000, and PDD-NOS at 3.7 per 1,000.<ref name="Newschaffer 2007"/> These rates are consistent across cultures and ethnic groups, as autism is considered a universal disorder.<ref name="Mash & Barkley" />
While rates of autism spectrum disorders are consistent across cultures, they vary greatly by gender, with boys being affected far more frequently than girls. The average male-to-female ratio for ASDs is 4.2:1,<ref>{{cite journal|last=Fombonne|first=E|title=Epidemiology of Pervasive Developmental Disorders|journal=Pediatric Research|year=2009|volume=65|issue=6|pages=591–598|doi=10.1203/PDR.0b013e31819e7203|pmid=19218885}}</ref> affecting 1 in 70 males, but only 1 in 315 females.<ref>{{cite journal|last=(ADDM) Autism and Developmental Disabilities Monitoring Network Surveillance Year 2006 Principal Investigators|title=Prevalence of autism spectrum disorders-Autism and Developmental Disabilities Monitoring Network|journal=MMWR Surveillance Summary|year=2009|volume=58|pages=1–20}}</ref> Females, however, are more likely to have associated cognitive impairment. Among those with an ASD and intellectual disability, the sex ratio may be closer to 2:1.<ref>{{cite journal|last=Volkmar|first=F|coauthors=Lord, Bailey, Schultz, & Klin|title=Autism and pervasive developmental disorders|journal=Journal of Child Psychology and Psychiatry|year=2004|volume=45|issue=1|pages=135–170|doi=10.1046/j.0021-9630.2003.00317.x|pmid=14959806}}</ref> Prevalence differences might be
accounted by gender differences in the expression of clinical symptoms, with females showing less atypical behaviors and, therefore, less likely to receive an ASD diagnosis.<ref name="Tsakanikos Underwood 2011">{{cite journal|last1=Tsakanikos| first1=Elias|last2=Underwood |first2=Lisa|last3=Kravariti|first3=Eugenia|last4=Bouras|first4=Nick|last5=McCarthy|first5=Jane|title=Gender differences in co-morbid psychopathology and clinical management in adults with autism spectrum disorders|journal=Research in Autism Spectrum Disorders|volume=5|issue=2| year=2011| pages=803–808| issn=17509467|doi=10.1016/j.rasd.2010.09.009}}</ref>
===Prevalence===
The prevalence of intellectual disability is approximately 1,000 per 100,000 (1%) of the overall population<ref>{{cite book | title = Diagnostic and statistical manual of mental disorders : DSM-5 | publisher = American Psychiatric Association | location = Washington, D.C | year = 2013 | isbn = 0890425558 }}</ref>.
==Schools==
There are a number of [[List of schools for people on the autistic spectrum|schools for students on the autism spectrum]].
==See also==
* [[Asperger syndrome and neuroscience]]
* [[Autism and memory]]
* [[Autism and working memory]]
* [[Lorna Wing]]
* [[Global perceptions of autism]]


==References==
==References==
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{{Pervasive developmental disorders}}
{{Pervasive developmental disorders}}
{{Autism resources}}
{{Autism films}}
{{Portal bar|Pervasive developmental disorders}}


[[Category:Autism]]
[[Category:Autism]]
[[Category:Developmental psychology]]
[[Category:Developmental psychology]]
[[Category:Developmental neuroscience]]
[[Category:Developmental neuroscience]]
[[Category:Psychiatric diagnosis]]
[[Category:Learning disabilities]]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Kiran Singh, M.D. [2]

Synonyms and keywords: autism spectrum; autistic spectrum

Overview

The autism spectrum disorder describes a range of conditions classified as neurodevelopmental disorders in the fifth revision of the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders 5th edition (DSM-5). The DSM-5, published in 2013, redefined the autism spectrum to encompass the previous (DSM-IV-TR) diagnoses of autism, Asperger syndrome, pervasive developmental disorder not otherwise specified (PDD-NOS), childhood disintegrative disorder, and Rett syndrome.[1] These disorders are characterized by social deficits and communication difficulties, stereotyped or repetitive behaviors and interests, and in some cases, cognitive delays.

Historical Perspective

Controversies have surrounded various claims regarding the etiology of autism spectrum disorders. In the 1950s, the "refrigerator mother theory" emerged as an explanation for autism. The hypothesis was based on the idea that autistic behaviors stem from the emotional frigidity, lack of warmth, and cold, distant, rejecting demeanor of a child's mother.[2] Naturally, parents of children with an autism spectrum disorder suffered from blame, guilt, and self-doubt, especially as the theory was embraced by the medical establishment and went largely unchallenged into the mid-1960s. While the "refrigerator mother theory" has been rejected in the research literature, its effects have lingered into the 21st century. Another controversial claim suggests that watching extensive amounts of television may cause autism. This hypothesis was largely based on research suggesting that the increasing rates of autism in the 1970s and 1980s were linked to the growth of cable television at this time.[3] This conjecture has not been supported in the research literature.[citation needed]

Classification

A revision to autism spectrum disorder (ASD) was proposed in the Diagnostic and Statistical Manual of Mental Disorders version 5 (DSM-5), released May 2013.[4] The new diagnosis encompasses previous diagnoses of autistic disorder, Asperger's disorder, childhood disintegrative disorder, and PDD-NOS. Rather than categorizing these diagnoses, the DSM-5 will adopt a dimensional approach to diagnosing disorders that fall underneath the autism spectrum umbrella. It is thought that individuals with ASDs are best represented as a single diagnostic category because they demonstrate similar types of symptoms and are better differentiated by clinical specifiers (i.e., dimensions of severity) and associated features (i.e., known genetic disorders, epilepsy and intellectual disability). An additional change to the DSM includes collapsing social and communication deficits into one domain. Thus, an individual with an ASD diagnosis will be described in terms of severity of social communication symptoms, severity of fixated or restricted behaviors or interests and associated features. The restriction of onset age has also been loosened from 3 years of age to "early developmental period", with a note that symptoms may manifest later when demands exceed capabilities.

Autism forms the core of the autism spectrum disorders. Asperger syndrome is closest to autism in signs and likely causes;[5] unlike autism, people with Asperger syndrome have no significant delay in language development.[6] PDD-NOS is diagnosed when the criteria are not met for a more specific disorder. Some sources also include Rett syndrome and childhood disintegrative disorder, which share several signs with autism but may have unrelated causes; other sources differentiate them from ASD, but group all of the above conditions into the pervasive developmental disorders.[5][7]

The terminology of autism can be bewildering. Autism, Asperger syndrome, and PDD-NOS are sometimes called the autistic disorders instead of ASD,[8] whereas autism itself is often called autistic disorder, childhood autism, or infantile autism.[9] Although the older term pervasive developmental disorder and the newer term autism spectrum disorder largely or entirely overlap,[7] the former was intended to describe a specific set of diagnostic labels, whereas the latter refers to a postulated spectrum disorder linking various conditions.[10] ASD, in turn, is a subset of the broader autism phenotype (BAP), which describes individuals who may not have ASD but do have autistic-like traits, such as avoiding eye contact.[9]

Pathophysiology

In general, neuroanatomical studies support the notion that autism is linked to a combination of brain enlargement in some areas and brain reduction in other areas.[11] These studies suggest that autism may be caused by abnormal neuronal growth and pruning during the early stages of prenatal and postnatal brain development, leaving some areas of the brain with too many neurons and other areas with too few neurons.[12] Some research has reported an overall brain enlargement in autism while others suggest abnormalities in several areas of the brain, including the frontal lobe, the mirror neuron system, the limbic system, the temporal lobe, and the corpus callosum.

In neuroanatomical studies, when performing theory of mind and facial emotion response tasks, the median person on the autism spectrum exhibits less activation in the primary and secondary somato-sensory cortices than does the median member of a properly sampled control population. This discrepancy is consistent with reports of abnormal patterns of cortical thickness and grey matter volume in those regions of autistic persons' brains.[13]

Mirror Neuron System

The mirror neuron system (MNS) consists of a network of brain areas that have been associated with empathy processes in humans.[14] In humans, the MNS has been identified in the inferior frontal gyrus (IFG) and the inferior parietal lobule (IPL) and is thought to be activated during imitation or observation of behaviors.[15] It has been proposed that problems with the mirror neuron system may underlie autism;[16][17] however the connection between mirror neuron dysfunction and autism is tentative and it remains to be seen how mirror neurons may be related to many of the important characteristics of autism.[18]

Temporal Lobe

Functions of the temporal lobe are related to many of the deficits observed in individuals with ASDs, such as receptive language, social cognition, joint attention, action observation, and empathy. The temporal lobe also contains the superior temporal sulcus (STS) and the fusiform face area (FFA), which may mediate facial processing. It has been argued that dysfunction in the STS underlies the social deficits that characterize autism. Compared to typically developing individuals, one fMRI study found that individuals with high-functioning autism had reduced activity in the FFA when viewing pictures of faces.[19]

Mitochondrial Dysfunction

It has been noted that children with ASD are afflicted with undiagnosed comorbid conditions such as abnormalities in the peripheral nervous, immune, gastrointestinal and energy production systems, suggesting that ASD isn't strictly a central nervous system (CNS) disorder, but rather a systemic one.[20] It has been hypothesized that ASD could be linked to a mitochondrial disorder, as it is a basic cellular abnormality that has the potential to cause disturbances in a wide range of body systems.[21] A recent meta-analysis study, as well as other population studies have shown that approximately 5% of children with ASD meet the criteria for classical mitochondrial disease (MD),[22] and that around 7.2 percent of children with ASD present with some variant of mitochondrial dysfunction.[23] It is currently unclear why the mitochondrial dysfunction occurs considering that only 23% of children with both ASD and MD present with mitochondrial DNA (mtDNA) abnormalities.[22]

Causes

While a specific cause or specific causes of autism spectrum disorders has yet to be found, many risk factors have been identified in the research literature that may contribute to the development of an ASD. These risk factors include genetics, prenatal and perinatal factors, neuroanatomical abnormalities, and environmental factors. It is possible to identify general risk factors, but much more difficult to pinpoint specific factors. In the current state of knowledge, prediction can only be of a global nature and therefore requires the use of general markers.[24]

Associated Conditions

Vaccine Controversy

Perhaps the most controversial claim regarding autism etiology was the "vaccine controversy".[26] This conjecture, arising from a case of scientific misconduct,[27] suggested that autism results from brain damage caused either by (1) the measles, mumps, rubella (MMR) vaccine itself, or by (2) thimerosal, a vaccine preservative.[28] No convincing scientific evidence supports these claims, based on various lines of evidence including the observation that the rate of autism continues to climb despite elimination of thimerosal from routine childhood vaccines.[3] In 2014 Professor Guy Eslick, an epidemiologist, did a study to help disprove the theories on vaccines causing autism. The vaccine meta analysis examined 10 major studies on autism and vaccines from around the world that involved 1.25 million children and assessed the odds that children would develop autism after vaccination. Professor Eslick stated, “Most of the studies were right on one, there was just no relationship between vaccination and autism. I hope this study goes some way to closing the doors on the connection between vaccination and autism and I want people to vaccinate their children.” [29]

Differential Diagnosis

Epidemiology and Demographics

Prevalence

The prevalence of autism spectrum disorder is approximately 1,000 per 100,000 (1%) of the overall population.[30] However prevalence rates vary for each of the developmental disorders in the spectrum. Autism prevalence has been estimated at 1-2 per 1,000, Asperger syndrome at roughly 0.6 per 1,000, childhood disintegrative disorder at 0.02 per 1,000, and PDD-NOS at 3.7 per 1,000.[31] These rates are consistent across cultures and ethnic groups, as autism is considered a universal disorder.[32]

Gender

While rates of autism spectrum disorders are consistent across cultures, they vary greatly by gender, with boys being affected far more frequently than girls. The average male-to-female ratio for ASDs is 4.2:1,[33] affecting 1 in 70 males, but only 1 in 315 females.[34] Females, however, are more likely to have associated cognitive impairment. Among those with an ASD and intellectual disability, the sex ratio may be closer to 2:1.[35] Prevalence differences might be accounted by gender differences in the expression of clinical symptoms, with females showing less atypical behaviors and, therefore, less likely to receive an ASD diagnosis.[36]

Risk Factors

Genetic Risk Factors

The results of family and twin studies suggest that genetic factors play a role in the etiology of autism and other pervasive developmental disorders.[38] Studies have consistently found that the prevalence of autism in siblings of autistic children is approximately 15 to 30 times greater than the rate in the general population.[39] In addition, research suggests that there is a much higher concordance rate among monozygotic twins compared to dizygotic twins.[40] It appears that there is no single gene that can account for autism. Instead, there seem to be multiple genes involved, each of which is a risk factor for part of the autism syndrome through various groups.[41][42][43]

Natural History, Complications and Prognosis

Although autism spectrum disorders are thought to follow two possible developmental courses, most parents report that symptom onset occurred within the first year of life.[44][45] One course of development follows a gradual course of onset in which parents report concerns in development over the first two years of life and diagnosis is made around 3–4 years of age. Some of the early signs of ASDs in this course include decreased looking at faces, failure to turn when name is called, failure to show interests by showing or pointing, and delayed pretend play.[46] A second course of development is characterized by normal or near-normal development followed by loss of skills or regression in the first 2–3 years. Regression may occur in a variety of domains, including communication, social, cognitive, and self-help skills; however, the most common regression is loss of language.[47][48] There continues to be a debate over the differential outcomes based on these two developmental courses. Some studies suggest that regression is associated with poorer outcomes and others report no differences between those with early gradual onset and those who experience a regression period.[32] Overall, the prognosis is poor for persons with classical (Kanner-type) autism with respect to academic achievement and poor to below-average for persons across the autism spectrum with respect to independent living abilities; in each case, a lack of early intervention exacerbates the odds against success.[32] However, many individuals show improvements as they grow older. The two best predictors of favorable outcome in autism are the absence of intellectual disability and the development of some communicative speech prior to five years of age.[unreliable medical source?][49] Overall, the literature stresses the importance of early intervention in achieving positive longitudinal outcomes.[50]

Diagnostic Criteria

DSM-V Diagnostic Criteria for Autism Spectrum Disorder[30]

“
  • A. Persistent deficits in social communication and social interaction across multiple contexts,as manifested by the following, currently or by history
  • 1. Deficits in social-emotional reciprocity, ranging, for example, from abnormal social approach and failure of normal back-and-forth conversation; to reduced sharing of interests, emotions, or affect; to failure to initiate or respond to social interactions.
  • 2. Deficits in non verbal communicative behaviors used for social interaction, ranging,for example, from poorly integrated verbal and nonverbal communication; to abnormalities in eye contact and body language or deficits in understanding and use of gestures: to a total lack of facial expressions and nonverbal communication.
  • 3. Deficits in developing, maintaining, and understanding relationships, ranging, for example,from difficulties adjusting behavior to suit various social contexts; to difficulties in sharing imaginative play or in making friends; to absence of interest in peers. Specify current severity: Severity is based on social communication impairments and restricted, repetitive patterns of behavior.

AND

  • B. Restricted, repetitive patterns of behavior, interests, or activities, as manifested by at least two of the following, currently or by history
  • 1. Stereotyped or repetitive motor movements, use of objects, or speech (e.g., simple motor stereotypes, lining up toys or flipping objects, echolalia, idiosyncratic phrases).
  • 2. Insistence on sameness, inflexible adherence to routines, or ritualized patterns of verbal or nonverbal behavior (e.g., extreme distress at small changes, difficulties with transitions, rigid thinking patterns, greeting rituals, need to take same route or eat same food every day).
  • 3. Highly restricted, fixated interests that are abnormal in intensity or focus (e.g.,strong attachment to or preoccupation with unusual objects, excessively circumscribed or perseverative interests).
  • 4. Hyper- or hyporeactivity to sensory input or unusual interest in sensory aspects of the environment (e.g., apparent indifference to pain/temperature, adverse response to specific sounds or textures, excessive smelling or touching of objects,visual fascination with lights or movement).
  • Specify current severity: Severity is based on social communication impairments and restricted, repetitive patterns of behavior.

AND

  • C. Symptoms must be present in the early developmental period (but may not become fully manifest until social demands exceed limited capacities, or may be masked by learned strategies in later life).

AND

  • D. Symptoms cause clinically significant impairment in social, occupational, or other important areas of current functioning.

AND

spectrum disorder frequently co-occur; to make comorbid diagnoses of autism spectrum disorder and intellectual disability, social communication should be below that expected for general developmental level.

Note: Individuals with a well-established DSM-IV diagnosis of autistic disorder, Asperger’s disorder, or pervasive developmental disorder not otherwise specified should be given the diagnosis of autism spectrum disorder. Individuals who have marked deficits in social communication, but whose symptoms do not otherwise meet criteria for autism spectrum disorder, should be evaluated for social (pragmatic) communication disorder.

Specify if;

  • With or without accompanying intellectual impairment
  • With or without accompanying language impairment
  • Associated with a known medical or genetic condition or environmental factor.
  • Associated with another neurodevelopmental, mental, or behavioral disorder.


 ”

Evidence-Based Assessment

ASD can be detected as early as eighteen months or even younger in some cases.[51] A reliable diagnosis can usually be made by the age of two.[52] The diverse expressions of ASD symptoms pose diagnostic challenges to clinicians. Individuals with an ASD may present at various times of development (e.g., toddler, child, or adolescent) and symptom expression may vary over the course of development.[53] Furthermore, clinicians are required to differentiate among the different pervasive developmental disorders as well as other disorders such as mental retardation not associated with a pervasive developmental disorder, specific developmental disorders (e.g. language), and early onset schizophrenia,[citation needed] as well as the social-cognitive deficits caused by brain damage from alcohol abuse.[54]

Considering the unique challenges associated with diagnosing ASD, specific practice parameters for the assessment of ASD have been published by the American Academy of Neurology,[55] the American Academy of Child and Adolescent Psychiatry,[53] and a consensus panel with representation from various professional societies.[56] The practice parameters outlined by these societies include an initial screening of children by general practitioners (i.e., "Level 1 screening") and for children who fail the initial screening, a comprehensive diagnostic assessment by experienced clinicians (i.e. "Level 2 evaluation"). Furthermore, it has been suggested that assessments of children with suspected ASD be evaluated within a developmental framework, include multiple informants (e.g., parents and teachers) from diverse contexts (e.g., home and school), and employ a multidisciplinary team of professionals (e.g., clinical psychologists, neuropsychologists, and psychiatrists).[57]

After a child fails an initial screening, psychologists administer various psychological assessment tools to assess for ASD.[57] Amongst these measurements, the Autism Diagnostic Interview-Revised (ADI-R) and the Autism Diagnostic Observation Schedule (ADOS) are considered the "gold standards" for assessing autistic children.[58][59] The ADI-R is a semi-structured parent interview that probes for symptoms of autism by evaluating a child's current behavior and developmental history. The ADOS is a semistructured interactive evaluation of ASD symptoms that is used to measure social and communication abilities by eliciting a number of opportunities (or "presses") for spontaneous behaviors (e.g., eye contact) in standardized context. Various other questionnaires (e.g., The Childhood Autism Rating Scale) and tests of cognitive functioning (e.g., The Peabody Picture Vocabulary Test) are typically included in an ASD assessment battery.

Comorbidity

Main article: Conditions comorbid to autism spectrum disorders

Autism spectrum disorders tend to be highly comorbid with other disorders. Comorbidity may increase with age and may worsen the course of youth with ASDs and make intervention/treatment more difficult. Distinguishing between ASDs and other diagnoses can be challenging because the traits of ASDs often overlap with symptoms of other disorders and the characteristics of ASDs make traditional diagnostic procedures difficult.[60][61]

The most common medical condition occurring in individuals with autism spectrum disorders is seizure disorder or epilepsy, which occurs in 11-39% of individuals with ASD.[62] Tuberous sclerosis, a medical condition in which non-malignant tumors grow in the brain and on other vital organs, occurs in 1-4% of individuals with ASDs.[63]

Intellectual disabilities are some of the most common comorbid disorders with ASDs. Recent estimates suggest that 40-69% of individuals with ASD have some degree of mental retardation,[32] with females more likely to be in severe range of mental retardation. Learning disabilities are also highly comorbid in individuals with an ASD. Approximately 25-75% of individuals with an ASD also have some degree of learning disability.[25]

A variety of anxiety disorders tend to co-occur with autism spectrum disorders, with overall comorbidity rates of 7-84%.[32] Rates of comorbid depression in individuals with an ASD range from 4–58%.[64]

Deficits in ASD are often linked to behavior problems, such as difficulties following directions, being cooperative, and doing things on other people's terms.[65] Attention Deficit Hyperactivity Disorder (ADHD)-like symptoms are seen to be part of the ASD diagnosis.[66]

Sensory processing disorder is also comorbid with ASD, with comorbidity rates of 42-88%.[67]

Management

The main goals of treatment are to lessen associated deficits and family distress, and to increase quality of life and functional independence. No single treatment is best and treatment is typically tailored to the child's needs. Intensive, sustained special education programs and behavior therapy early in life can help children acquire self-care, social, and job skills. Available approaches include applied behavior analysis (ABA), developmental models, structured teaching, speech and language therapy, social skills therapy, and occupational therapy.[68] There has been increasing attention to the development of evidenced-based interventions for young children with ASDs. Unresearched alternative therapies have also been implemented (for example, vitamin therapy and acupuncture). Although evidenced-based interventions for autistic children vary in their methods, many adopt a psychoeducational approach to enhancing cognitive, communication and social skills while minimizing problem behaviors. It has been argued that no single treatment is best and treatment is typically tailored to the child's needs.[68]

One of the most empirically supported intervention approaches is applied behavioral analysis, particularly in regard to early intensive home-based therapy. Although ABA therapy has a strong research base, other studies have found that this approach may be limited by diagnostic severity and IQ.[69]

Early Intensive Behavioral Intervention (EIBI), through the use of Applied Behavioral Analysis (ABA), has been researched for over 40 years in its effectiveness. Most EIBI programs recognize that all skills appropriate for each specific age are teachable and should be taught. General curriculum areas that are addressed are language, social skills, play skills, motor skills, pre-academic and academic skills, and independent living skills. ABA models of intervention for preschool age include two main approaches to teaching. "Discrete Trial Teaching" or DTT, includes multiple discrete opportunities that are presented across the day or session. A discrete trial consists of the therapist presenting an instruction, the child responding, and the therapist responding to that by presenting a consequence. If the child responds incorrectly, the reinforcer is not given and the therapist will follow up with an error correction procedure, followed by another trial. A strength of this way of teaching is the child receives a large number of trials in a short time, allowing for a large amount of learning opportunities. A potential weakness may be that the skills learned in this structured setting are not easily generalized in less strict settings. "Natural Environment Teaching" consists of maximizing naturally occurring learning opportunities. It involves a more child-directed format that allows for the child to initiate learning, and the therapist to recognize this and follow it by prompting the child for a desired behavior before giving the reinforcer.[70] Although (ASD) autism spectrum disorder is lifelong, it can be treated. A family with a child that suffers this ailment must know and understand the aspects of it, as well as being consistent with the treatment plan. A key point is to learn how to handle the normal range of emotions that comes from raising a child with this disorder (WebMD) and another facet that a family should consider is finding a support group for both the child as well as themselves. According to WebMD there are many places to get help for either the family or to find treatment plans for the child. The National Institute of Neurological Disorders and Stroke which is the leading U.S. federal government agency supporting research on brain and nervous system disorders is one such organization. It provides the public with educational materials and information about these disorders. The Centers for Disease Control and Prevention (CDC) is another agency whose aim is to find the cause of and prevent birth defects and developmental disabilities. This group works to help people of all ages with the disabilities live to the fullest.

References

  1. ↑ "Autism spectrum disorder fact sheet" (PDF). DSM5.org. American Psychiatric Publishing. 2013. Retrieved October 13, 2103. Check date values in: |accessdate= (help)
  2. ↑ Kanner, L (1949). "Problems of nosology and psychodynamics in early childhood autism". American Journal of Orthopsychiatry. 19 (3): 416–426. doi:10.1111/j.1939-0025.1949.tb05441.x. PMID 18146742.
  3. ↑ 3.0 3.1 Waterhouse, Lynn (2008). "Autism overflows: Increasing prevalence and proliferating theories". Neuropsychological Review. 18 (4): 273–286. doi:10.1007/s11065-008-9074-x.
  4. ↑ "Home | APA DSM-5". Dsm5.org. Retrieved 2012-02-21.
  5. ↑ 5.0 5.1 Lord C, Cook EH, Leventhal BL, Amaral DG. Autism spectrum disorders. Neuron. 2000;28(2):355–63. doi:10.1016/S0896-6273(00)00115-X. PMID 11144346.
  6. ↑ American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 4th ed., text revision (DSM-IV-TR). 2000. ISBN 0890420254. Diagnostic criteria for 299.80 Asperger's Disorder (AD).
  7. ↑ 7.0 7.1 National Institute of Mental Health. Autism spectrum disorders (pervasive developmental disorders); 2009 [Retrieved 2009-04-23].
  8. ↑ Freitag CM. The genetics of autistic disorders and its clinical relevance: a review of the literature. Mol Psychiatry. 2007;12(1):2–22. doi:10.1038/sj.mp.4001896. PMID 17033636.
  9. ↑ 9.0 9.1 Piven J, Palmer P, Jacobi D, Childress D, Arndt S. Broader autism phenotype: evidence from a family history study of multiple-incidence autism families [PDF]. Am J Psychiatry. 1997;154(2):185–90. PMID 9016266.
  10. ↑ Klin A. Autism and Asperger syndrome: an overview. Rev Bras Psiquiatr. 2006;28(suppl 1):S3–S11. doi:10.1590/S1516-44462006000500002. PMID 16791390.
  11. ↑ Koenig, Kathleen; Tsatsanis, Katherine D.; Volkmar, Fred R. (2001). Jacob A Burack, Tony Charman, Nurit Yirmiya, Philip R. Zelazo, eds. Neurobiology and Genetics ofd Autism : A Developmental Perspective. The development of autism : perspectives from theory and research. Mahwah, N.J.: L. Erlbaum,. pp. 73–92. ISBN 9780805832457. OCLC 806185029. |access-date= requires |url= (help)
  12. ↑ Minshew, NJ (1996). "Brief report: Brain mechanisms in autism: Functional and structural abnormalities". Journal of Autism and Developmental Disorders. 26 (2): 205–209. doi:10.1007/BF02172013. PMID 8744486.
  13. ↑ Sugranyes G, Kyriakopoulos M, Corrigall R, Taylor E, Frangou S (2011). "Autism spectrum disorders and schizophrenia: meta-analysis of the neural correlates of social cognition". PLoS ONE. 6 (10): e25322. doi:10.1371/journal.pone.0025322. PMC 3187762. PMID 21998649.
  14. ↑ Fadiga, L. (2005). "Human motor cortex excitability during the perception of others' action". Current Opinion in Neurobiology. 15 (2): 213–218. doi:10.1016/j.conb.2005.03.013. PMID 15831405. Unknown parameter |coauthors= ignored (help)
  15. ↑ Shamay-Tsoory, S.G. (2011). "The Neural Bases for Empathy". The Neuroscientist. 17 (1): 18–24. doi:10.1177/1073858410379268. PMID 21071616.
  16. ↑ Nishitani, N. (2004). "Abnormal imitation-related cortical activation sequences in Asperger's syndrome". Annals of Neurology. 55 (4): 558–562. doi:10.1002/ana.20031. PMID 15048895. Unknown parameter |coauthors= ignored (help)
  17. ↑ Dapretto, M.; Davies M.S.; et al. (2006). "Understanding emotions in others: mirror neuron dysfunction in children with autism spectrum disorders". Nature Neuroscience. 9 (1): 28–30. doi:10.1038/nn1611. PMC 3713227. PMID 16327784. Unknown parameter |author-separator= ignored (help)
  18. ↑ Dinstein I, Thomas C, Behrmann M, Heeger DJ (2008). "A mirror up to nature". Curr Biol. 18 (1): R13–8. doi:10.1016/j.cub.2007.11.004. PMC 2517574. PMID 18177704.
  19. ↑ Schultz, R. (2005). "Developmental deficits in social perception in autism: The role of amygdala and fusiform face area". International Journal of Developmental Neuroscience. 23 (2–3): 125–141. doi:10.1016/j.ijdevneu.2004.12.012. PMID 15749240.
  20. ↑ Xue Ming, Brimacombe M, Chaaban J, Zimmerman-Bier B, Wagner GC (2008). "Autism spectrum disorders: concurrent clinical disorders". J Child Neurol. 23 (1): 6–13. doi:10.1177/0883073807307102. PMID 18056691.
  21. ↑ Haas RH, Parikh S, Falk MJ, Saneto RP, Wolf NI, Darin N, Cohen BH (2007). "Mitochondrial disease: a practical approach for primary care physicians". Pediatrics. 120 (6): 1326–1333. doi:10.1542/peds.2007-0391. PMID 18055683.
  22. ↑ 22.0 22.1 Rossignol DA, Frye RE (2010). "Mitochondrial dysfunction in autism spectrum disorders: a systematic review and meta-analysis". Mol Psychiatry. 17 (3): 290–314. doi:10.1038/mp.2010.136. PMC 3285768. PMID 21263444.
  23. ↑ Oliveira G, Diogo L, Grazina M, Garcia P, Ataíde A, Marquess C, Miguel T, Borges L, Vicente AM, Oliveira CR (2005). "Mitochondrial dysfunction in autism spectrum disorders: a population-based study". Dev Med Child Neurol. 47 (3): 185–189. doi:10.1017/s0012162205000332. PMID 15739723.
  24. ↑ Tager-Flusberg H (2010). "The origins of social impairments in autism spectrum disorder: studies of infants at risk". Neural Netw. 23 (8–9): 1072–6. doi:10.1016/j.neunet.2010.07.008. PMC 2956843. PMID 20800990.
  25. ↑ 25.0 25.1 O'Brien, G; Pearson (2004). "Autism and learning disability". Autism. 8 (2): 125–140. doi:10.1177/1362361304042718. PMID 15165430.
  26. ↑ Flaherty, DK (2011). "The vaccine-autism connection: a public health crisis caused by unethical medical practices and fraudulent science". The Annals of pharmacotherapy. 45 (10): 1302–4. doi:10.1345/aph.1Q318. PMID 21917556.
  27. ↑ Godlee, F; Smith, J; Marcovitch, H (2011). "Wakefield's article linking MMR vaccine and autism was fraudulent". BMJ (Clinical research ed.). 342: c7452. doi:10.1136/bmj.c7452. PMID 21209060.
  28. ↑ Tan; Parkin (2008). "Route of decomposition of thimerosal". International Journal of Pharmacy. 24: 13299–13305.
  29. ↑ http://www.news.com.au/lifestyle/health/vaccination-versus-autism-study-professor-guy-eslick-tells-why-hes-taking-on-the-scaremongers/story-fneuzlbd-1226929208418
  30. ↑ 30.0 30.1 30.2 30.3 30.4 30.5 30.6 Diagnostic and statistical manual of mental disorders : DSM-5. Washington, D.C: American Psychiatric Association. 2013. ISBN 0890425558.
  31. ↑
  32. ↑ 32.0 32.1 32.2 32.3 32.4 Mash & Barkley (2003). Child Psychopathology. New York: The Guilford Press. pp. 409–454.
  33. ↑ Fombonne, E (2009). "Epidemiology of Pervasive Developmental Disorders". Pediatric Research. 65 (6): 591–598. doi:10.1203/PDR.0b013e31819e7203. PMID 19218885.
  34. ↑ (ADDM) Autism and Developmental Disabilities Monitoring Network Surveillance Year 2006 Principal Investigators (2009). "Prevalence of autism spectrum disorders-Autism and Developmental Disabilities Monitoring Network". MMWR Surveillance Summary. 58: 1–20.
  35. ↑ Volkmar, F (2004). "Autism and pervasive developmental disorders". Journal of Child Psychology and Psychiatry. 45 (1): 135–170. doi:10.1046/j.0021-9630.2003.00317.x. PMID 14959806. Unknown parameter |coauthors= ignored (help)
  36. ↑ Tsakanikos, Elias; Underwood, Lisa; Kravariti, Eugenia; Bouras, Nick; McCarthy, Jane (2011). "Gender differences in co-morbid psychopathology and clinical management in adults with autism spectrum disorders". Research in Autism Spectrum Disorders. 5 (2): 803–808. doi:10.1016/j.rasd.2010.09.009. ISSN 1750-9467.
  37. ↑ 37.0 37.1 37.2 37.3 37.4 Gardner, H (2011). "Perinatal and Neonatal Risk Factors for Autism: A Comprehensive Meta-analysis". Pediatrics. 128 (2): 344–355. doi:10.1542/peds.2010-1036. PMC 3387855. PMID 21746727. Unknown parameter |coauthors= ignored (help)
  38. ↑ Rutter, M (2000). "Genetic studies of autism: From the 1970s into the millennium". Journal of Abnormal Child Psychology. 28 (1): 3–14. doi:10.1023/A:1005113900068. PMID 10772346.
  39. ↑ Szatmari, P (1999). "Heterogeneity and the genetics of autism". Journal of Psychiatry and Neuroscience. 24 (2): 159–165. PMC 1188998. PMID 10212560.
  40. ↑ Rutter, M (1990). "Genetic factors in child psychiatric disorders: II. Empirical findings". Journal of Child Psychology and Psychiatry. 31 (1): 39–83. doi:10.1111/j.1469-7610.1990.tb02273.x. PMID 2179248. Unknown parameter |coauthors= ignored (help)
  41. ↑ Losh M, Sullivan PF, Trembath D, Piven J (September 2008). "Current developments in the genetics of autism: from phenome to genome". J. Neuropathol. Exp. Neurol. 67 (9): 829–37. doi:10.1097/NEN.0b013e318184482d. PMC 2649757. PMID 18716561.
  42. ↑ Freitag CM, Staal W, Klauck SM, Duketis E, Waltes R (March 2010). "Genetics of autistic disorders: review and clinical implications". Eur Child Adolesc Psychiatry. 19 (3): 169–78. doi:10.1007/s00787-009-0076-x. PMC 2839494. PMID 19941018.
  43. ↑ Chaste P, Leboyer M (September 2012). "Autism risk factors: genes, environment, and gene-environment interactions". Dialogues Clin Neurosci. 14 (3): 281–92. PMC 3513682. PMID 23226953.
  44. ↑ Zwaigenbaum L, Bryson S, Lord C; et al. (May 2009). "Clinical assessment and management of toddlers with suspected autism spectrum disorder: insights from studies of high-risk infants". Pediatrics. 123 (5): 1383–91. doi:10.1542/peds.2008-1606. PMC 2833286. PMID 19403506.
  45. ↑ Lord, C (1995). "Follow-up of two-year-olds referred for possible autism". Journal of Child Psychology and Psychiatry. 36 (8): 1365–1382. doi:10.1111/j.1469-7610.1995.tb01669.x. PMID 8988272.
  46. ↑ Zwaigenbaum L (October 2001). "Autistic spectrum disorders in preschool children". Can Fam Physician. 47 (10): 2037–42. PMC 2018435. PMID 11723598.
  47. ↑ Martínez-Pedraza Fde L, Carter AS (July 2009). "Autism spectrum disorders in young children". Child Adolesc Psychiatr Clin N Am. 18 (3): 645–63. doi:10.1016/j.chc.2009.02.002. PMC 3166636. PMID 19486843.
  48. ↑ Werner, E (2005). "Variation in early developmental course in autism and its relation with behavioral outcome at 3-4 years of age". Journal of Autism and Developmental Disorders. 35 (3): 337–350. doi:10.1007/s10803-005-3301-6. PMID 16119475. Unknown parameter |coauthors= ignored (help)
  49. ↑ [unreliable medical source?] Mawhood, L (2000). "Autism and developmental receptive language disorder: A comparative follow-up in early adult life. I. Cognitive and language outcomes". Journal of Child Psychology and Psychiatry. 41 (5): 547–559. doi:10.1111/1469-7610.00642. PMID 10946748. Unknown parameter |coauthors= ignored (help)
  50. ↑ Dawson & Osterling (1997). The effectiveness of early intervention. Baltimore: Brookes. pp. 307–326.
  51. ↑ "Autism Spectrum Disorder (ASD): Screening and Diagnosis". Centers for Disease Control and Prevention.
  52. ↑ Lord, C; Risi, S; DiLavore, PS; Shulman, C; Thurm, A; Pickles, A (Jun 2006). "Autism from 2 to 9 years of age". Archives of General Psychiatry. 63 (6): 694–701. doi:10.1001/archpsyc.63.6.694. PMID 16754843.
  53. ↑ 53.0 53.1 Volkmar F, Cook EH, Pomeroy J, Realmuto G, Tanguay P (December 1999). "Practice parameters for the assessment and treatment of children, adolescents, and adults with autism and other pervasive developmental disorders. American Academy of Child and Adolescent Psychiatry Working Group on Quality Issues". J Am Acad Child Adolesc Psychiatry. 38 (12 Suppl): 32S–54S. doi:10.1016/s0890-8567(99)80003-3. PMID 10624084.
  54. ↑ Uekermann J, Daum I (May 2008). "Social cognition in alcoholism: a link to prefrontal cortex dysfunction?". Addiction. 103 (5): 726–35. doi:10.1111/j.1360-0443.2008.02157.x. PMID 18412750.
  55. ↑ Filipek PA, Accardo PJ, Ashwal S; et al. (August 2000). "Practice parameter: screening and diagnosis of autism: report of the Quality Standards Subcommittee of the American Academy of Neurology and the Child Neurology Society". Neurology. 55 (4): 468–79. doi:10.1212/wnl.55.4.468. PMID 10953176.
  56. ↑ Filipek PA, Accardo PJ, Baranek GT; et al. (December 1999). "The screening and diagnosis of autistic spectrum disorders". J Autism Dev Disord. 29 (6): 439–84. doi:10.1023/A:1021943802493. PMID 10638459.
  57. ↑ 57.0 57.1 Ozonoff, S. (2005). "Evidence-Based Assessment of Autism". Journal of Clinical and Child Adolescent Psychology. 34 (3): 523–540. doi:10.1207/s15374424jccp3403_8. Unknown parameter |coauthors= ignored (help)
  58. ↑ Corsello C, Hus V, Pickles A; et al. (September 2007). "Between a ROC and a hard place: decision making and making decisions about using the SCQ". J Child Psychol Psychiatry. 48 (9): 932–40. doi:10.1111/j.1469-7610.2007.01762.x. PMID 17714378.
  59. ↑ Huerta M, Lord C (February 2012). "Diagnostic evaluation of autism spectrum disorders". Pediatr. Clin. North Am. 59 (1): 103–11, xi. doi:10.1016/j.pcl.2011.10.018. PMC 3269006. PMID 22284796.
  60. ↑ Helverschou,, S.B.; Bakken, T.L.; Martinsen., H. (2011). Johnny L Matson; Peter Sturmey, eds. Psychiatric Disorders in People with Autism Spectrum Disorders: Phenomenology and Recognition. International handbook of autism and pervasive developmental disorders. New York: Springer,. pp. 53–74. ISBN 9781441980649. OCLC 746203105. |access-date= requires |url= (help)
  61. ↑ Underwood L, McCarthy J, Tsakanikos E (September 2010). "Mental health of adults with autism spectrum disorders and intellectual disability". Current Opinion in Psychiatry. 23 (5): 421–6. doi:10.1097/YCO.0b013e32833cfc18. PMID 20613532.
  62. ↑ Ballaban-Gil, K; Tuchman (2000). "Epilepsy and epileptiform EEG: Association with autism and language disorders". Mental Retardation and Developmental Disabilities Research Reviews. 6 (4): 300–308. doi:10.1002/1098-2779(2000)6:4<300::AID-MRDD9>3.0.CO;2-R. PMID 11107195.
  63. ↑ Wiznitzer, M (2004). "Autism and tuberous sclerosis". Journal of Child Neurology. 19 (9): 675–679. PMID 15563013.
  64. ↑ Lainhart, J (1999). "Psychiatric problems in individuals with autism, their parents and siblings". International Review of Psychiatry. 11 (4): 278–298. doi:10.1080/09540269974177.
  65. ↑ Tsakanikos E, Costello H, Holt G, Sturmey P, Bouras N (July 2007). "Behaviour management problems as predictors of psychotropic medication and use of psychiatric services in adults with autism" (PDF). J Autism Dev Disord. 37 (6): 1080–5. doi:10.1007/s10803-006-0248-1. PMID 17053989.
  66. ↑ Rommelse, NN (2010). "Shared heritability of attention-deficit/hyperactivity disorder and autism spectrum disorder". European Child and Adolescent Psychiatry. 19 (3): 281–295. doi:10.1007/s00787-010-0092-x. PMC 2839489. PMID 20148275. Unknown parameter |coauthors= ignored (help)
  67. ↑ Baranek, G (2002). "Efficacy of sensory and motor interventions in children with autism". Journal of Autism and Developmental Disorders. 32 (5): 397–422. doi:10.1023/A:1020541906063. PMID 12463517.
  68. ↑ 68.0 68.1 Myers SM, Johnson CP, Council on Children with Disabilities. Management of children with autism spectrum disorders. Pediatrics. 2007;120(5):1162–82. doi:10.1542/peds.2007-2362. PMID 17967921. Lay summary: AAP, 2007-10-29.
  69. ↑ Rogers SJ, Vismara LA (January 2008). "Evidence-based comprehensive treatments for early autism". J Clin Child Adolesc Psychol. 37 (1): 8–38. doi:10.1080/15374410701817808. PMC 2943764. PMID 18444052.
  70. ↑ Granpeesheh, PhD, BCBA, Doreen. "Applied behavior analytic interventions for children with autism: A description and review of treatment research". The Journal of Family Practice. Retrieved February 20, 2011.

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