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Autism & Pathophysiology

Autism appears to result from developmental factors that affect many or all functional brain systems. Neuroanatomical studies and the associations with teratogens strongly suggest that Autism's mechanism includes alteration of brain development soon after conception. This localized anomaly appears to start a cascade of pathological events in the brain that are significantly influenced by environmental factors. Many major structures of the human brain have been implicated. Consistent abnormalities have been found in the development of the cerebral cortex; and in the cerebellum and related inferior olive, which have a significant decrease in the number of Purkinje cells. Brain weight and volume and head circumference tend to be greater in autistic children. The cellular and molecular bases of pathological early overgrowth are not known, nor is it known whether the overgrown neural systems cause Autism's characteristic signs. Current hypotheses include:-





Interactions between the immune system and the nervous system begin early during embryogenesis, and successful neurodevelopment depends on a balanced immune response. Several symptoms consistent with a poorly regulated immune response have been reported in autistic children. It is possible that aberrant immune activity during critical periods of neurodevelopment is part of the mechanism of some forms of Autistic Spectrum Disorder (ASD). As autoantibodies have not been associated with pathology, are found in diseases other than ASD, and are not always present in ASD, the relationship between immune disturbances and Autism remains unclear and controversial.

Several
neurotransmitter abnormalities have been detected in Autism, notably increased blood levels of serotonin . Whether these lead to structural or behavioural abnormalities is unclear.


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