CAUSES OF ASPERGER'S SYNDROME

The direct cause, or causes, of Asperger's syndrome are unknown. Even though no consensus exists for the causes of Asperger's syndrome, it is widely accepted that Asperger's syndrome has a hereditary factor. It is suspected that multiple genes play a part in causing Asperger syndrome, since the number and severity of symptoms vary widely among individuals.

Genetics as a principal cause of Asperger Syndrome

Asperger described common symptoms among his patients' family members, especially fathers, and research supports this observation and suggests a genetic contribution to Asperger syndrome. Although no specific gene has yet been identified, multiple factors are believed to play a role in the expression of autism, given the phenotypic variability seen in this group of children.[1][24] Evidence for a genetic link is the tendency for Aspergers syndrome to run in families and an observed higher incidence of family members who have behavioral symptoms similar to Aspergers syndrome but in a more limited form (for example, slight difficulties with social interaction, language, or reading).[4] Most research suggests that all Autism Spectrum Disorders have shared genetic mechanisms, but Aspergers syndrome may have a stronger genetic component than autism.[1] There is probably a common group of genes where particular alleles render an individual vulnerable to developing Aspergers syndrome; if this is the case, the particular combination of alleles would determine the severity and symptoms for each individual with Aspergers syndrome.[4]

Click here to read more about Genetics as a cause of Asperger's syndrome.

teratogens as a possible cause of Asperger Syndrome

A few Autism Spectrum Disorder cases have been linked to exposure to teratogens (agents that cause birth defects) during the first eight weeks from conception. Although this does not exclude the possibility that Autism Spectrum Disorders can be initiated or affected later, it is strong evidence that it arises very early in development.[25] Many environmental factors have been hypothesized to act after birth, but none has been confirmed by scientific investigation.[26]

Mechanism of Asperger's syndrome

Asperger syndrome appears to result from developmental factors that affect many or all functional brain systems, as opposed to localized effects.[27] Although the specific underpinnings of Aspergers syndrome or factors that distinguish it from other Autism Spectrum Disorders are unknown, and no clear pathology common to individuals with Aspergers syndrome has emerged,[1] it is still possible that Aspergers syndrome's mechanism is separate from other Autism Spectrum Disorders.[28]

Neuroanatomical studies and the associations with teratogens strongly suggest that the mechanism includes alteration of brain development soon after conception.[25] Abnormal migration of embryonic cells during fetal development may affect the final structure and connectivity of the brain, resulting in alterations in the neural circuits that control thought and behavior.[29] Several theories of mechanism are available; none are likely to be complete explanations.[30]

underconnectivity and mirror neuron theories

Functional magnetic resonance imaging provides some evidence for both underconnectivity and mirror neuron theories..[31][32] The underconnectivity theory hypothesizes underfunctioning high-level neural connections and synchronization, along with an excess of low-level processes.[31] It maps well to general-processing theories such as weak central coherence theory, which hypothesizes that a limited ability to see the big picture underlies the central disturbance in Autism Spectrum Disorders.[33]

mirror neuron theory

The mirror neuron system (MNS) theory hypothesizes that alterations to the development of the MNS interfere with imitation and lead to Asperger's core feature of social impairment.[32][34] For example, one study found that activation is delayed in the core circuit for imitation in individuals with Aspergers syndrome.[35] This theory maps well to social cognition theories like the theory of mind, which hypothesizes that autistic behavior arises from impairments in ascribing mental states to oneself and others,[36] or hyper-systemizing, which hypothesizes that autistic individuals can systematize internal operation to handle internal events but are less effective at empathizing by handling events generated by other agents.[37] Other possible mechanisms include serotonin dysfunction[38] and cerebellar dysfunction.[39]

Possible environmental causes of Asperger's

The search for environmental triggers has been mostly focused on trying to find a cause for a rapid increase in the alleged increase in autism in recent decades. The prevalence increase would appear to implicate recent changes in human lifestyle, but there is considerable disagreement as to whether the number of cases is actually increasing. Research has focused on possibilities such as:
• Infectious disease
• Heavy metal toxicity
• Certain vaccinations

• Perinatal factors
• Stress.

More information on these is included in the Causes of autism fact sheet.

The poor parenting myth

Since the 1950s up to the 1970s it was believed that autism, and by association Aspergers syndrome, was the result of the faulty environment provided by uncaring “refrigerator mothers", a theory that went largely unchallenged by psychologists at the time. This theory is discredited now, along with its main champion, Bruno Bettelheim. The Folstein-Rutter (1977) twin study is credited with shifting the focus from psychological factors to genetics. Click here to read a fact sheet on the "refrigerator mother" theory as a cause of autism.

References

1. 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.
4. National Institute of Neurological Disorders and Stroke (NINDS) (2007-07-31). Asperger syndrome fact sheet. Retrieved on 2007-08-24. NIH Publication No. 05-5624.
24. ^ a b c d e f Foster B, King BH (2003). "Asperger syndrome: to be or not to be?". Curr Opin Pediatr 15 (5): 491–4. PMID 14508298.
25. ^ a b Arndt TL, Stodgell CJ, Rodier PM (2005). "The teratology of autism". Int J Dev Neurosci 23 (2–3): 189–99. doi:10.1016/j.ijdevneu.2004.11.001. PMID 15749245.
26. ^ Rutter M (2005). "Incidence of Autism Spectrum Disorders: changes over time and their meaning". Acta Paediatr 94 (1): 2–15. PMID 15858952.
27. ^ Müller RA (2007). "The study of autism as a distributed disorder". Ment Retard Dev Disabil Res Rev 13 (1): 85–95. doi:10.1002/mrdd.20141. PMID 17326118.
28. ^ Rinehart NJ, Bradshaw JL, Brereton AV, Tonge BJ (2002). "A clinical and neurobehavioural review of high-functioning autism and Asperger's disorder". Aust N Z J Psychiatry 36 (6): 762–70. PMID 12406118.
29. ^ Berthier ML, Starkstein SE, Leiguarda R (1990). "Developmental cortical anomalies in Asperger's syndrome: neuroradiological findings in two patients". J Neuropsychiatry Clin Neurosci 2 (2): 197–201. PMID 2136076.
30. ^ Happé F, Ronald A, Plomin R (2006). "Time to give up on a single explanation for autism". Nat Neurosci 9 (10): 1218–20. doi:10.1038/nn1770. PMID 17001340.
31. ^ a b Just MA, Cherkassky VL, Keller TA, Kana RK, Minshew NJ (2007). "Functional and anatomical cortical underconnectivity in autism: evidence from an FMRI study of an executive function task and corpus callosum morphometry". Cereb Cortex 17 (4): 951-61. doi:10.1093/cercor/bhl006. PMID 16772313.
32. ^ a b Iacoboni M, Dapretto M (2006). "The mirror neuron system and the consequences of its dysfunction". Nat Rev Neurosci 7 (12): 942–51. doi:10.1038/nrn2024. PMID 17115076.
33. ^ Happé F, Frith U (2006). "The weak coherence account: detail-focused cognitive style in Autism Spectrum Disorders". J Autism Dev Disord 36 (1): 5–25. doi:10.1007/s10803-005-0039-0. PMID 16450045.
34. ^ Ramachandran VS, Oberman LM (2006). "Broken mirrors: a theory of autism". Sci Am 295 (5): 62–9. PMID 17076085.
35. ^ Nishitani N, Avikainen S, Hari R (2004). "Abnormal imitation-related cortical activation sequences in Asperger's syndrome". Ann Neurol 55 (4): 558–62. doi:10.1002/ana.20031. PMID 15048895.
36. ^ Baron-Cohen S, Leslie AM, Frith U (1985). "Does the autistic child have a 'theory of mind'?" (PDF). Cognition 21 (1): 37–46. doi:10.1016/0010-0277(85)90022-8. PMID 2934210. Retrieved on 2007-06-28.
37. ^ Baron-Cohen S (2006). "The hyper-systemizing, assortative mating theory of autism". Prog Neuropsychopharmacol Biol Psychiatry 30 (5): 865–72. doi:10.1016/j.pnpbp.2006.01.010. PMID 16519981.
38. ^ Murphy DG, Daly E, Schmitz N et al. (2006). "Cortical serotonin 5-HT2A receptor binding and social communication in adults with Asperger's syndrome: an in vivo SPECT study". Am J Psychiatry 163 (5): 934–6. doi:10.1176/appi.ajp.163.5.934. PMID 16648340.
39. ^ Gowen E, Miall RC (2005). "Behavioral aspects of cerebellar function in adults with Asperger syndrome". Cerebellum 4 (4): 279–89. doi:10.1080/14734220500355332. PMID 16321884.

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