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Autism spectrum
The puzzle ribbon is an often used symbol for the autism spectrum, as it represents the diversity of conditions and people within it.
SpecialtyPsychiatry
Frequency80% (Europe)

Autism spectrum or autistic spectrum describes a range of learning disabilities classified as neurodevelopmental disorders in the fifth and most recent revision of the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders (DSM-5) published in 2013.

The DSM-5 redefined the autism spectrum to encompass the previous (DSM-IV-TR) diagnoses of autism, Asperger syndrome, pervasive developmental disorder not otherwise specified (PDD-NOS), and childhood disintegrative disorder.[1]

Features of these disorders include social deficits and communication difficulties, stereotyped or repetitive behaviors and interests, sensory issues, and in some cases, cognitive delays.

Classification

Further information: Autism § Classification
Autism spectrum disorder video

A revision to autism spectrum disorder (ASD) was presented in the Diagnostic and Statistical Manual of Mental Disorders version 5 (DSM-5), released May 2013.[2] The new diagnosis encompasses previous diagnoses of autistic disorder, Asperger's disorder, childhood disintegrative disorder, and PDD-NOS. Compared with the DSM-4 diagnosis of autistic disorder, the DSM-5 diagnosis of ASD no longer includes communication as a separate criterion, and has merged social interaction and communication into one category.[3]

Rather than categorizing these diagnoses, the DSM-5 has adopted a dimensional approach to diagnosing disorders that fall underneath the autism spectrum umbrella. Some have proposed that individuals on the autism spectrum may be better represented as a single diagnostic category. Within this category, the DSM-5 has proposed a framework of differentiating each individual by dimensions of severity, as well as associated features (i.e., known genetic disorders, and intellectual disability).

Another 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;[4] unlike autism, people with Asperger syndrome have no significant delay in language development, according to the older DSM-4 criteria.[5] 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.[4][6]

Autism, Asperger syndrome, and PDD-NOS are sometimes called the autistic disorders instead of ASD,[7] whereas autism itself is often called autistic disorder, childhood autism, or infantile autism.[8] Although the older term pervasive developmental disorder and the newer term autism spectrum disorder largely or entirely overlap,[6] the former was intended to describe a specific set of diagnostic labels, whereas the latter refers to a postulated spectrum disorder linking various conditions.[9] ASD 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.[8]

Characteristics

Under the DSM-5, autism is characterized by persistent deficits in social communication and interaction across multiple contexts, as well as restricted, repetitive patterns of behavior, interests, or activities. These deficits are present in early childhood, and lead to clinically significant functional impairment.[10] There is also a unique form of autism called autistic savantism, where a child can display outstanding skills in music, art, and numbers with no practice.[11]

Asperger syndrome was distinguished from autism in the DSM-4 by the lack of delay or deviance in early language development.[12] Additionally, individuals diagnosed with Asperger syndrome did not have significant cognitive delays.[13] 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).[14] In the DSM-5, both Asperger syndrome and PDD-NOS have been incorporated into autism spectrum disorder.[10]

Developmental course

Autism spectrum disorders are thought to follow two possible developmental courses, although most parents report that symptom onset occurred within the first year of life.[15][16] One course of development is more gradual in nature, 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.[17]

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.[18][19]

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.[20] While there is conflicting evidence surrounding language outcomes in ASD, some studies have shown that cognitive and language abilities at age 2 1/2 may help predict language proficiency and production after age 5.[21] Overall, the literature stresses the importance of early intervention in achieving positive longitudinal outcomes.[22]

Causes

Main article: Causes of autism

While specific causes of autism spectrum disorders have yet to be found, many risk factors have been identified in the research literature that may contribute to their development. 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.[23]

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.[24] 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.[25] In addition, research suggests that there is a much higher concordance rate among monozygotic twins compared to dizygotic twins.[26] 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 components of the autism spectrum disorders.[27][28][29]

Prenatal and perinatal risk factors

Several 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.[30]

Vaccine controversy

Main article: MMR vaccine controversy

Perhaps the most controversial claim regarding autism etiology was the "vaccine controversy".[31] This conjecture, arising from a case of scientific misconduct,[32] 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.[33] No convincing scientific evidence supports these claims, and further evidence continues to refute them, including the observation that the rate of autism continues to climb despite elimination of thimerosal from routine childhood vaccines.[34] A 2014 meta-analysis examined ten major studies on autism and vaccines involving 1.25 million children worldwide; it concluded that neither the MMR vaccine, which has never contained thimerosal,[35] nor the vaccine components thimerosal or mercury, lead to the development of ASDs.[36]

Pathophysiology

Main article: Autism § Mechanism

In general, neuroanatomical studies support the concept that autism may involve a combination of brain enlargement in some areas and reduction in others.[37] 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.[38] 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.[39][40]

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 somatosensory cortices of the brain than the median member of a properly sampled control population. This finding coincides with reports demonstrating abnormal patterns of cortical thickness and grey matter volume in those regions of autistic persons' brains.[41]

Mirror neuron system

Main article: Mirror neuron

The mirror neuron system (MNS) consists of a network of brain areas that have been associated with empathy processes in humans.[42] 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.[43] 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.[44][45]

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.[46]

Mitochondrial dysfunction

It has been suggested that ASD could be linked to mitochondrial disease, a basic cellular abnormality with the potential to cause disturbances in a wide range of body systems.[47] 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).[48] It is unclear why the mitochondrial dysfunction occurs considering that only 23% of children with both ASD and MD present with mitochondrial DNA (mtDNA) abnormalities.[48]

Serotonin

It has been hypothesized that increased activity of serotonin in the developing brain may facilitate the onset of autism spectrum disorder, with an association found in six out of eight studies between the use of selective serotonin reuptake inhibitors (SSRIs) by the pregnant mother and the development of ASD by the child exposed to SSRI in the antenatal environment. The study could not definitively conclude SSRIs caused the increased risk for ASDs due to the biases found in those studies, and the authors called for more definitive, better conducted studies.[49]

Diagnosis

Evidence-based assessment

ASD can be detected as early as eighteen months or even younger in some cases.[50] A reliable diagnosis can usually be made by the age of two.[51] 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.[52] Furthermore, clinicians must differentiate among the different pervasive developmental disorders, and may also consider similar conditions, including intellectual disability not associated with a pervasive developmental disorder, specific language disorders, ADHD, anxiety, and psychotic disorders.[53]

Considering the unique challenges in diagnosing ASD, specific practice parameters for its assessment have been published by the American Academy of Neurology,[54] the American Academy of Child and Adolescent Psychiatry,[52] and a consensus panel with representation from various professional societies.[55] 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).[56]

After a child shows initial evidence of ASD tendencies, psychologists administer various psychological assessment tools to assess for ASD.[56] Among 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.[57][58] 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 several opportunities (or "presses") for spontaneous behaviors (e.g., eye contact) in standardized context. Various other questionnaires (e.g., The Childhood Autism Rating Scale, Autism Treatment Evaluation Checklist) 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.[59][60]

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.[61] 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.[62]

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 an intellectual disability,[20] with females more likely to be in the severe range of an intellectual disability. A number of genetic syndromes causing intellectual disability may also be comorbid with ASD, including Fragile X syndrome, Down syndrome, Prader-Willi and Angelman syndromes, and Williams syndrome.[63]

Learning disabilities are also highly comorbid in individuals with an ASD. Approximately 25-75% of individuals with an ASD also have some degree of a learning disability.[64]

Various anxiety disorders tend to co-occur with autism spectrum disorders, with overall comorbidity rates of 7-84%.[20] Rates of comorbid depression in individuals with an ASD range from 4–58%.[65] The relationship between ASD and schizophrenia remains a controversial subject under continued investigation, and recent meta-analyses have examined genetic, environmental, infectious, and immune risk factors that may be shared between the two conditions.[66][67][68]

Deficits in ASD are often linked to behavior problems, such as difficulties following directions, being cooperative, and doing things on other people's terms.[69] Symptoms similar to those of attention deficit hyperactivity disorder (ADHD) can be part of an ASD diagnosis.[70]

Sensory processing disorder is also comorbid with ASD, with comorbidity rates of 42–88%.[71]

Management

Main article: Autism therapies

There is no known cure for autism, although those with Asperger syndrome and other high-functioning forms of autism are more likely to experience a lessening of symptoms over time.[72][73][74] The main goals of treatment are to lessen associated deficits and family distress, and to increase quality of life and functional independence. In general, higher IQs are correlated with greater responsiveness to treatment and improved treatment outcomes.[75][76] Although evidence-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.[77]

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, developmental models, structured teaching, speech and language therapy, social skills therapy, and occupational therapy.[77] Among these approaches, interventions either treat autistic features comprehensively, or focus treatment on a specific area of deficit.[76]

There has been increasing attention to the development of evidence-based interventions for young children with ASD. Two theoretical frameworks outlined for early childhood intervention include applied behavioral analysis (ABA) and the developmental social-pragmatic model (DSP).[76] Although ABA therapy has a strong evidence base, particularly in regard to early intensive home-based therapy. ABA's effectiveness may be limited by diagnostic severity and IQ of the person effected by ASD.[78] The Journal of Clinical Child and Adolescent Psychology has deemed two early childhood interventions as “well-established”: individual comprehensive ABA, and focused teacher-implemented ABA combined with DSP.[76]

Another evidence-based intervention that has demonstrated efficacy is a parent training model, which teaches parents how to implement various ABA and DSP techniques themselves.[76] Various DSP programs have been developed to explicitly deliver intervention systems through at-home parent implementation.

A multitude of unresearched alternative therapies have also been implemented. Many have resulted in harm to autistic people and should not employed unless proven to be safe.

In October 2015, the American Academy of Pediatrics (AAP) proposed new evidence-based recommendations[79] for early interventions in ASD for children under 3. These recommendations emphasize early involvement with both developmental and behavioral methods, support by and for parents and caregivers, and a focus on both the core and associated symptoms of ASD.

Epidemiology

Main article: Epidemiology of autism

CDC's most recent estimate is that 1 out of every 68 children, or 14.7 per 1,000, have some form of ASD as of 2010.[80] Reviews tend to estimate a prevalence of 6 per 1,000 for autism spectrum disorders as a whole,[81] although 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.[81] These rates are consistent across cultures and ethnic groups, as autism is considered a universal disorder.[20]

While rates of autism spectrum disorders are consistent across cultures, they vary greatly by gender, with boys affected far more frequently than girls. The average male-to-female ratio for ASDs is 4.2:1,[82] affecting 1 in 70 males, but only 1 in 315 females.[83] 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.[84] Prevalence differences may be a result of gender differences in expression of clinical symptoms, with autistic females showing less atypical behaviors and, therefore, less likely to receive an ASD diagnosis.[85]

History

Further information: Autism § History

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.[86] 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. The "refrigerator mother" theory has since continued to be refuted in scientific literature, including a 2015 systematic review which showed no association between caregiver interaction and language outcomes in ASD.[87]

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.[34]

Society and culture

Autism rainbow infinity
The rainbow-colored infinity symbol represents the diversity of the autism spectrum as well as the greater neurodiversity movement.

Caregivers

Families who care for an autistic child face added stress from a number of different causes. One study found that half of parents who had a child with any kind of developmental disability were still caring for their child by age 50, while only 17% of parents that age would typically be caring for children.[88]

Autism rights movement

Further information: Autism rights movement and Neurodiversity

The autism rights movement (ARM) is a social movement within the neurodiversity movement that encourages autistic people, their caregivers, and society to adopt a position of neurodiversity, and to accept autism as a variation in functioning rather than a mental disorder to be cured.[89] The ARM advocates for several goals, including a greater acceptance of autistic behaviors,[90] therapies that teach autistic individuals coping skills rather than therapies focused on imitating behaviors of neurotypical peers,[91] the creation of social networks and events that allow autistic people to socialize on their own terms,[92] and the recognition of the autistic community as a minority group.[93]

Autism rights and neurodiversity advocates believe that the autism spectrum is genetic and should be accepted as a natural expression of the human genome. This perspective is distinct from two other likewise distinct views: (1) the mainstream perspective that autism is caused by a genetic defect and should be addressed by targeting the autism gene(s) and (2) the perspective that autism is caused by environmental factors like vaccines and pollution and could be cured by addressing environmental causes.[89]

The movement is controversial. A common criticism leveled against autistic activists is that many are high-functioning or have Asperger syndrome, and therefore do not represent the views of all autistic people.[94]

See also

References

  1. ^ "Autism spectrum disorder fact sheet" (PDF). DSM5.org. American Psychiatric Publishing. 2013. Retrieved October 13, 2013.
  2. ^ "Home | APA DSM-5". Dsm5.org. Retrieved 2012-02-21.
  3. ^ Kulage, Kristine (16 February 2014). "How Will DSM-5 Affect Autism Diagnosis? A Systematic Literature Review and Meta-analysis". Journal of Autism and Developmental Disorders. 44: 1918–32. doi:10.1007/s10803-014-2065-2. PMID 24531932.
  4. ^ a b 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.
  5. ^ 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).
  6. ^ a b National Institute of Mental Health. Autism spectrum disorders (pervasive developmental disorders); 2009 [Retrieved 2009-04-23].
  7. ^ 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.
  8. ^ a b 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. doi:10.1176/ajp.154.2.185. PMID 9016266.
  9. ^ Klin A. Autism and Asperger syndrome: an overview. Rev Bras Psiquiatr. 2006;28(suppl 1):S3–S11. doi:10.1590/S1516-44462006000500002. PMID 16791390.
  10. ^ a b American Psychiatric Association, ed. (2013). "Autism Spectrum Disorder, 299.00 (F84.0)". Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition. American Psychiatric Publishing. pp. 50–59.
  11. ^ Weintraub AG. "Autism: Topic Overview". National Institute of Health. U.S. Food and Drug Administration. CDC. May 12, 2013.
  12. ^ Diagnostic and Statistical Manual of Mental Disorders (4th ed., text rev.). Washington, D.C.: American Psychiatric Association. 2000.
  13. ^ "NINDS Asperger Syndrome Information Page". National Institute of Neurological Disorders and Stroke.
  14. ^ Mesibov GB. Ask the Editor: What is PDD-NOS and how is it diagnosed?. Journal of Autism and Developmental Diso. 1997;27(4).
  15. ^ Zwaigenbaum L, Bryson S, Lord C, et al.. Clinical assessment and management of toddlers with suspected autism spectrum disorder: insights from studies of high-risk infants. Pediatrics. May 2009;123(5):1383–91. doi:10.1542/peds.2008-1606. PMID 19403506.
  16. ^ Lord C. Follow-up of two-year-olds referred for possible autism. Journal of Child Psychology and Psychiatry. 1995;36(8):1365–1382. doi:10.1111/j.1469-7610.1995.tb01669.x. PMID 8988272.
  17. ^ Zwaigenbaum L. Autistic spectrum disorders in preschool children. Can Fam Physician. October 2001;47(10):2037–42. PMID 11723598. PMC 2018435.
  18. ^ Martínez-Pedraza Fde L, Carter AS. Autism spectrum disorders in young children. Child Adolesc Psychiatr Clin N Am. July 2009;18(3):645–63. doi:10.1016/j.chc.2009.02.002. PMID 19486843.
  19. ^ Werner E, Dawson G, Munson J, Osterling J. 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. 2005;35(3):337–350. doi:10.1007/s10803-005-3301-6. PMID 16119475.
  20. ^ a b c d Mash & Barkley (2003). Child Psychopathology. New York: The Guilford Press. pp. 409–454.
  21. ^ Ellis Weismer, Susan; Kover, Sara T. (Jan 3, 2015). "Preschool language variation, growth, and predictors in children on the autism spectrum". Journal of Child Psychology and Psychiatry: 1327–37. doi:10.1111/jcpp.12406. ISSN 1469-7610. PMC 4565784. PMID 25753577.
  22. ^ Dawson & Osterling (1997). The effectiveness of early intervention. Baltimore: Brookes. pp. 307–326.
  23. ^ Tager-Flusberg H. The origins of social impairments in autism spectrum disorder: studies of infants at risk. Neural Netw. 2010;23(8-9):1072–6. doi:10.1016/j.neunet.2010.07.008. PMID 20800990.
  24. ^ Rutter M. Genetic studies of autism: From the 1970s into the millennium. Journal of Abnormal Child Psychology. 2000;28(1):3–14. doi:10.1023/A:1005113900068. PMID 10772346.
  25. ^ Heterogeneity and the genetics of autism. Journal of Psychiatry and Neuroscience. 1999;24(2):159–165. PMID 10212560.
  26. ^ Rutter M, Macdonald H, Le Couteur A, et al. Genetic factors in child psychiatric disorders: II. Empirical findings. Journal of Child Psychology and Psychiatry. 1990;31(1):39–83. doi:10.1111/j.1469-7610.1990.tb02273.x. PMID 2179248.
  27. ^ Losh M, Sullivan PF, Trembath D, Piven J. Current developments in the genetics of autism: from phenome to genome. J. Neuropathol. Exp. Neurol.. September 2008;67(9):829–37. doi:10.1097/NEN.0b013e318184482d. PMID 18716561.
  28. ^ Freitag CM, Staal W, Klauck SM, Duketis E, Waltes R. Genetics of autistic disorders: review and clinical implications. Eur Child Adolesc Psychiatry. March 2010;19(3):169–78. doi:10.1007/s00787-009-0076-x. PMID 19941018.
  29. ^ Chaste P, Leboyer M. Autism risk factors: genes, environment, and gene-environment interactions. Dialogues Clin Neurosci. September 2012;14(3):281–92. PMID 23226953. PMC 3513682.
  30. ^ Gardener H, Spiegelman D, Buka SL. Perinatal and Neonatal Risk Factors for Autism: A Comprehensive Meta-analysis. Pediatrics. 2011;128(2):344–355. doi:10.1542/peds.2010-1036. PMID 21746727.
  31. ^ 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.
  32. ^ Godlee F, Smith J, Marcovitch H. Wakefield's article linking MMR vaccine and autism was fraudulent. BMJ (Clinic al research ed.). 2011;342:c7452. doi:10.1136/bmj.c7452. PMID 21209060.
  33. ^ Tan M, Parkin JE. Route of decomposition of thimerosal. International Journal of Pharmacy. 2008;208:23–34. PMID 11064208.
  34. ^ a b Autism overflows: Increasing prevalence and proliferating theories. Neuropsychological Review. 2008;18(4):273–286. doi:10.1007/s11065-008-9074-x. PMID 19015994.
  35. ^ http://www.cdc.gov/vaccinesafety/Concerns/thimerosal/thimerosal_faqs.html
  36. ^ Taylor LE, Swerdfeger AL, Eslick GD. Vaccines are not associated with autism: an evidence-based meta-analysis of case-control and cohort studies. Vaccine. 2014;32(29):3623–9. doi:10.1016/j.vaccine.2014.04.085. PMID 24814559.
  37. ^ Koenig K, Tsatsanis KD, Volkmar FR (2001). Neurobiology and Genetics ofd Autism : A Developmental Perspective. Mahwah, N.J.: L. Erlbaum,. pp. 73–92. ISBN 9780805832457. OCLC 806185029. {{cite book}}: |work= ignored (help); Unknown parameter |editors= ignored (|editor= suggested) (help)CS1 maint: extra punctuation (link)
  38. ^ Minshew NJ. Brief report: Brain mechanisms in autism: Functional and structural abnormalities. Journal of Autism and Developmental Disorders. 1996;26(2):205–209. doi:10.1007/BF02172013. PMID 8744486.
  39. ^ Stanfield, Andrew C.; McIntosh, Andrew M.; Spencer, Michael D.; Philip, Ruth; Gaur, Sonia; Lawrie, Stephen M. (2008-06-01). "Towards a neuroanatomy of autism: a systematic review and meta-analysis of structural magnetic resonance imaging studies". European Psychiatry: The Journal of the Association of European Psychiatrists. 23 (4): 289–299. doi:10.1016/j.eurpsy.2007.05.006. ISSN 0924-9338. PMID 17765485.
  40. ^ Lefebvre, Aline; Beggiato, Anita; Bourgeron, Thomas; Toro, Roberto. "Neuroanatomical Diversity of Corpus Callosum and Brain Volume in Autism: Meta-analysis, Analysis of the Autism Brain Imaging Data Exchange Project, and Simulation". Biological Psychiatry. 78 (2): 126–134. doi:10.1016/j.biopsych.2015.02.010.
  41. ^ Sugranyes G, Kyriakopoulos M, Corrigall R, Taylor E, Frangou S. Autism spectrum disorders and schizophrenia: meta-analysis of the neural correlates of social cognition. PLoS ONE. 2011;6(10):e25322. doi:10.1371/journal.pone.0025322. PMID 21998649.
  42. ^ Fadiga L, Craighero L, Olivier E. Human motor cortex excitability during the perception of others' action. Current Opinion in Neurobiology. 2005;15(2):213–218. doi:10.1016/j.conb.2005.03.013. PMID 15831405.
  43. ^ Shamay-Tsoory SG. The Neural Bases for Empathy. The Neuroscientist. 2011;17(1):18–24. doi:10.1177/1073858410379268. PMID 21071616.
  44. ^ Dinstein I, Thomas C, Behrmann M, Heeger DJ. A mirror up to nature. Curr Biol. 2008;18(1):R13–8. doi:10.1016/j.cub.2007.11.004. PMID 18177704.
  45. ^ Kalat J (2009). Biological Psychology (Tenth ed.). pp. 237–8. ISBN 978-0-495-60300-9.
  46. ^ Schultz R. Developmental deficits in social perception in autism: The role of amygdala and fusiform face area. International Journal of Developmental Neuroscience. 2005;23(2–3):125–141. doi:10.1016/j.ijdevneu.2004.12.012. PMID 15749240.
  47. ^ Haas RH, Parikh S, Falk MJ, et al. Mitochondrial disease: a practical approach for primary care physicians. Pediatrics. 2007;120(6):1326–1333. doi:10.1542/peds.2007-0391. PMID 18055683.
  48. ^ a b Rossignol DA, Frye RE. Mitochondrial dysfunction in autism spectrum disorders: a systematic review and meta-analysis. Mol Psychiatry. 2010;17(3):290–314. doi:10.1038/mp.2010.136. PMID 21263444.
  49. ^ Gentile, S (15 August 2015). "Prenatal antidepressant exposure and the risk of autism spectrum disorders in children. Are we looking at the fall of Gods?". Journal of Affective Disorders. 182: 132–7. doi:10.1016/j.jad.2015.04.048. PMID 25985383.
  50. ^ "Autism Spectrum Disorder (ASD): Screening and Diagnosis". Centers for Disease Control and Prevention.
  51. ^ Lord C, Risi S, DiLavore PS, Shulman C, Thurm A, Pickles A. Autism from 2 to 9 years of age.. Archives of General Psychiatry. Jun 2006;63(6):694–701. doi:10.1001/archpsyc.63.6.694. PMID 16754843.
  52. ^ a b Volkmar F, Cook EH, Pomeroy J, Realmuto G, Tanguay P. 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. December 1999;38(12 Suppl):32S–54S. doi:10.1016/s0890-8567(99)80003-3. PMID 10624084.
  53. ^ "Diagnosis of autism spectrum disorder: reconciling the syndrome, its diverse origins, and variation in expression - The Lancet Neurology". The Lancet Neurology. 15: 279–291. doi:10.1016/s1474-4422(15)00151-9.
  54. ^ Filipek PA, Accardo PJ, Ashwal S, et al.. 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. August 2000;55(4):468–79. doi:10.1212/wnl.55.4.468. PMID 10953176.
  55. ^ Filipek PA, Accardo PJ, Baranek GT, et al.. The screening and diagnosis of autistic spectrum disorders. J Autism Dev Disord. December 1999;29(6):439–84. doi:10.1023/A:1021943802493. PMID 10638459.
  56. ^ a b Ozonoff S, Goodlin-Jones BL, Solomon M. Evidence-Based Assessment of Autism. Journal of Clinical and Child Adolescent Psychology. 2005;34(3):523–540. doi:10.1207/s15374424jccp3403_8.
  57. ^ Corsello C, Hus V, Pickles A, et al.. Between a ROC and a hard place: decision making and making decisions about using the SCQ. J Child Psychol Psychiatry. September 2007;48(9):932–40. doi:10.1111/j.1469-7610.2007.01762.x. PMID 17714378.
  58. ^ Huerta M, Lord C. Diagnostic evaluation of autism spectrum disorders. Pediatr. Clin. North Am.. February 2012;59(1):103–11, xi. doi:10.1016/j.pcl.2011.10.018. PMID 22284796.
  59. ^ Helverschou SB, Bakken TL, Martinsen H (2011). Psychiatric Disorders in People with Autism Spectrum Disorders: Phenomenology and Recognition. New York: Springer,. pp. 53–74. ISBN 9781441980649. OCLC 746203105. {{cite book}}: |work= ignored (help); Unknown parameter |editors= ignored (|editor= suggested) (help)CS1 maint: extra punctuation (link)
  60. ^ Underwood L, McCarthy J, Tsakanikos E. Mental health of adults with autism spectrum disorders and intellectual disability. Current Opinion in Psychiatry. September 2010;23(5):421–6. doi:10.1097/YCO.0b013e32833cfc18. PMID 20613532.
  61. ^ Ballaban-Gil K, Tuchman R. Epilepsy and epileptiform EEG: Association with autism and language disorders. Mental Retardation and Developmental Disabilities Research Reviews. 2000;6(4):300–308. doi:10.1002/1098-2779(2000)6:4<300::AID-MRDD9>3.0.CO;2-R. PMID 11107195.
  62. ^ Wiznitzer M. Autism and tuberous sclerosis. Journal of Child Neurology. 2004;19(9):675–679. doi:10.1177/08830738040190090701. PMID 15563013.
  63. ^ "Childhood autism and associated comorbidities - Brain and Development". www.brainanddevelopment.com. Retrieved 2015-11-15.
  64. ^ O'Brien G, Pearson J. Autism and learning disability. Autism. 2004;8(2):125–140. doi:10.1177/1362361304042718. PMID 15165430.
  65. ^ Lainhart J. Psychiatric problems in individuals with autism, their parents and siblings. International Review of Psychiatry. 1999;11(4):278–298. doi:10.1080/09540269974177.
  66. ^ Chisholm, Katharine; Lin, Ashleigh; Abu-Akel, Ahmad; Wood, Stephen J. (2015-08-01). "The association between autism and schizophrenia spectrum disorders: A review of eight alternate models of co-occurrence". Neuroscience & Biobehavioral Reviews. 55: 173–183. doi:10.1016/j.neubiorev.2015.04.012.
  67. ^ Hamlyn, Jess; Duhig, Michael; McGrath, John; Scott, James. "Modifiable risk factors for schizophrenia and autism — Shared risk factors impacting on brain development". Neurobiology of Disease. 53: 3–9. doi:10.1016/j.nbd.2012.10.023.
  68. ^ Crespi, B. J.; Thiselton, D. L. (2011-10-01). "Comparative immunogenetics of autism and schizophrenia". Genes, Brain and Behavior. 10 (7): 689–701. doi:10.1111/j.1601-183X.2011.00710.x. ISSN 1601-183X.
  69. ^ Tsakanikos E, Costello H, Holt G, Sturmey P, Bouras N. Behaviour management problems as predictors of psychotropic medication and use of psychiatric services in adults with autism. J Autism Dev Disord. July 2007;37(6):1080–5. doi:10.1007/s10803-006-0248-1. PMID 17053989.
  70. ^ Rommelse NN, Franke B, Geurts HM, Hartman CA, Buitelaar JK. Shared heritability of attention-deficit/hyperactivity disorder and autism spectrum disorder. European Child and Adolescent Psychiatry. 2010;19(3):281–295. doi:10.1007/s00787-010-0092-x. PMID 20148275.
  71. ^ Baranek G. Efficacy of sensory and motor interventions in children with autism. Journal of Autism and Developmental Disorders. 2002;32(5):397–422. doi:10.1023/A:1020541906063. PMID 12463517.
  72. ^ McPartland J, Klin A (2006). "Asperger's syndrome". Adolesc Med Clin. 17 (3): 771–88. doi:10.1016/j.admecli.2006.06.010. PMID 17030291.
  73. ^ Woodbury-Smith MR, Volkmar FR (January 2009). "Asperger syndrome". Eur Child Adolesc Psychiatry. 18 (1): 2–11. doi:10.1007/s00787-008-0701-0. PMID 18563474.
  74. ^ Coplan J, Jawad AF (2005). "Modeling clinical outcome of children with autistic spectrum disorders". Pediatrics. 116 (1): 117–22. doi:10.1542/peds.2004-1118. PMID 15995041. {{cite journal}}: Unknown parameter |laydate= ignored (help); Unknown parameter |laysource= ignored (help); Unknown parameter |laysummary= ignored (help)
  75. ^ Eldevik, Sigmund; Hastings, Richard P.; Hughes, J. Carl; Jahr, Erik; Eikeseth, Svein; Cross, Scott (2009-05-19). "Meta-Analysis of Early Intensive Behavioral Intervention for Children With Autism". Journal of Clinical Child & Adolescent Psychology. 38 (3): 439–450. doi:10.1080/15374410902851739. ISSN 1537-4416. PMID 19437303.
  76. ^ a b c d e Smith, T; Iadarola, S (2015). "Evidence Base Update for Autism Spectrum Disorder". Journal of Clinical Child and Adolescent Psychology. 44 (6): 897–922. doi:10.1080/15374416.2015.1077448. PMID 26430947.
  77. ^ a b 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.
  78. ^ Rogers SJ, Vismara LA. Evidence-based comprehensive treatments for early autism. J Clin Child Adolesc Psychol. January 2008;37(1):8–38. doi:10.1080/15374410701817808. PMID 18444052.
  79. ^ Zwaigenbaum, Lonnie; Bauman, Margaret L.; Choueiri, Roula; Kasari, Connie; Carter, Alice; Granpeesheh, Doreen; Mailloux, Zoe; Roley, Susanne Smith; Wagner, Sheldon (2015-10-01). "Early Intervention for Children With Autism Spectrum Disorder Under 3 Years of Age: Recommendations for Practice and Research". Pediatrics. 136 (Supplement 1): S60–S81. doi:10.1542/peds.2014-3667E. ISSN 0031-4005. PMID 26430170.
  80. ^ http://www.cdc.gov/ncbddd/autism/index.html
  81. ^ a b Newschaffer CJ, Croen LA, Daniels J, et al.. The epidemiology of autism spectrum disorders. Annu Rev Public Health. 2007;28:235–58. doi:10.1146/annurev.publhealth.28.021406.144007. PMID 17367287.
  82. ^ Fombonne E. Epidemiology of Pervasive Developmental Disorders. Pediatric Research. 2009;65(6):591–598. doi:10.1203/PDR.0b013e31819e7203. PMID 19218885.
  83. ^ Prevalence of autism spectrum disorders-Autism and Developmental Disabilities Monitoring Network. MMWR Surveillance Summary. 2009;58:1–20.
  84. ^ Volkmar FR, Lord C, Bailey A, Schultz RT, Klin A. Autism and pervasive developmental disorders. Journal of Child Psychology and Psychiatry. 2004;45(1):135–170. doi:10.1046/j.0021-9630.2003.00317.x. PMID 14959806.
  85. ^ Tsakanikos E, Underwood L, Kravariti E, Bouras N, McCarthy J. Gender differences in co-morbid psychopathology and clinical management in adults with autism spectrum disorders. Research in Autism Spectrum Disorders. 2011;5(2):803–808. doi:10.1016/j.rasd.2010.09.009.
  86. ^ Kanner L. Problems of nosology and psychodynamics in early childhood autism. American Journal of Orthopsychiatry. 1949;19(3):416–426. doi:10.1111/j.1939-0025.1949.tb05441.x. PMID 18146742.
  87. ^ Tager-Flusberg, Helen. "Risk Factors Associated with Language in Autism Spectrum Disorder: Clues to Underlying Mechanisms". Journal of Speech Language and Hearing Research. doi:10.1044/2015_jslhr-l-15-0146.
  88. ^ Karst JS, Van Hecke AV. Parent and family impact of autism spectrum disorders: a review and proposed model for intervention evaluation. Clin Child Fam Psychol Rev. 2012;15(3):247–77. doi:10.1007/s10567-012-0119-6. PMID 22869324.
  89. ^ a b Solomon A (2008-05-25). "The autism rights movement". New York. Archived from the original on 27 May 2008. Retrieved 2008-05-27. {{cite news}}: Unknown parameter |deadurl= ignored (|url-status= suggested) (help)
  90. ^ Mission Statement. Autism Acceptance Project. Retrieved on 2008-11-24.
  91. ^ Mission Statement. Aspies for Freedom. Retrieved on 2008-11-24.
  92. ^ Autism Network International presents Autreat. (2008-05-23) AIN.
  93. ^ "Declaration From the Autism Community That They Are a Minority Group" (Press release). PRWeb, Press Release Newswire. 2004-11-18. Retrieved 2007-11-07.
  94. ^ "The autism rights movement". Synapse.org.au.

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