Asperger syndrome pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Pathophysiology
- Asperger syndrome appears to result from developmental factors that affect many or all functional brain systems, as opposed to localized effects.[3] Although the specific underpinnings of AS or factors that distinguish it from other ASDs are unknown, and no clear pathology common to individuals with AS has emerged, it is still possible that AS's mechanism is separate from other ASD.[4] Neuroanatomical studies and the associations with teratogens strongly suggest that the mechanism includes alteration of brain development soon after conception. 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.[5] Several theories of mechanism are available; none are likely to be complete explanations.[6]
- The underconnectivity theory hypothesizes underfunctioning high-level neural connections and synchronization, along with an excess of low-level processes.[1] 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 ASD.[7] A related theory—enhanced perceptual functioning—focuses more on the superiority of locally oriented and perceptual operations in autistic individuals.[8]
- 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.[2][9] For example, one study found that activation is delayed in the core circuit for imitation in individuals with AS.[10] 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,[11] 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.[12]
- Other possible mechanisms include serotonin dysfunction[13] and cerebellar dysfunction.[14]
Associated Conditions
- AS is associated with tics, Tourette syndrome, and bipolar disorder, and the repetitive behaviors of AS have many similarities with the symptoms of obsessive-compulsive disorder and obsessive-compulsive personality disorder.[15] Although many of these studies are based on psychiatric clinic samples without using standardized measures, it seems reasonable to conclude that comorbid conditions are relatively common.
References
- ↑ 1.0 1.1 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.
- ↑ 2.0 2.1 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.
- ↑ 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.
- ↑ 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. doi:10.1046/j.1440-1614.2002.01097.x. PMID 12406118.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ Mottron L, Dawson M, Soulières I, Hubert B, Burack J (2006). "Enhanced perceptual functioning in autism: an update, and eight principles of autistic perception". J Autism Dev Disord. 36 (1): 27–43. doi:10.1007/s10803-005-0040-7. PMID 16453071.
- ↑ Ramachandran VS, Oberman LM (2006). "Broken mirrors: a theory of autism" (PDF). Sci Am. 295 (5): 62–9. PMID 17076085. Retrieved 2008-04-17.
- ↑ 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.
- ↑ 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 2007-06-28.
- ↑ 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.
- ↑ 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.
- ↑ Gowen E, Miall RC (2005). "Behavioural aspects of cerebellar function in adults with Asperger syndrome". Cerebellum. 4 (4): 279–89. doi:10.1080/14734220500355332. PMID 16321884.
- ↑ Gillberg C, Billstedt E (2000). "Autism and Asperger syndrome: coexistence with other clinical disorders". Acta Psychiatr Scand. 102 (5): 321–30. doi:10.1034/j.1600-0447.2000.102005321.x. PMID 11098802.