November, 09, 2010
"Autism is a lifelong developmental disability. It is part of the autism spectrum and is sometimes referred to as an autism spectrum disorder, or an ASD. The word 'spectrum' is used because, while all people with autism share three main areas of difficulty, their condition will affect them in very different ways. Some are able to live relatively 'everyday' lives; others will require a lifetime of specialist support (Hesmondhalgh, 2010). This thesis intends to investigate this behavioural disorder through its mechanisms of pathophysiology of brain structures and processes associated with autism, and the neuropsychological linkages between brain structures and behaviours also treatment for the disease through behavioural and cognitive approaches. In contrast to Neurodegenerative diseases such as Alzheimer’s diseases, autism lacks any clear unifying pathology at the molecular, cellular, or systems level (Geschwind, 2008). Autism appears to result from developmental factors that affect many or all functional brain systems. “Several recent functional neuro-imaging studies provide evidence of a lower degree of coordination among activated brain areas in autism. Recent studies found that the brain activity was less synchronized across activated brain areas (i.e., there was reduced functional connectivity) in autism” (Just, Cherkassy, Keller, & Minshew, 2007) Neuroanatomical studies suggest that autism's mechanism includes alteration of brain development soon after conception. Just after birth, the brains of autistic children tend to grow faster than usual, followed by normal or relatively slower growth in childhood. It is not known whether the early overgrowth take place in all autistic children. It seems to be most prominent in brain areas underlying the development of higher cognitive specialization (Just et al., 2007). Suggestions for the bases of pathological early overgrowth include; an excess of neurons that causes local over connectivity in key brain regions and abnormal formation of synapses and dendritic spines (Courchesne, Pierce, Shumann, Redcay, Buckwalter, Kennedy& Morgan, 2007). Interactions between the immune system and the nervous system begin early during the embryonic stage of life, and successful neurodevelopment depends on a balanced immune response. It is possible that abnormal immune activity during critical periods of neurodevelopment is part of the mechanism of some forms of Autism (Ashwood, Wills, Van de Wood, 2006). Five MRI studies of individuals with autism at a wide range of ages have found the cerebellum to be enlarged compared to individuals without the disease (Amaral, Schumann, & Nordahl, 2008). Evidence has been found in functional neuroimaging studies on autistic individuals and by a brainwave study that suggested that adults with Autism have local over connectivity in the cortex and weak functional connections between the frontal lobe and the rest of the cortex. Other evidence suggests the under connectivity is mainly within each hemisphere of the cortex and that autism is a disorder of the association cortex .The amygdala in autism patients also show a difference compared to normal individuals. The amygdala in boys with autism appears to undergo an abnormal developmental time that includes a period of enlargement that persists through late childhood (Amaral et al., 2008). Other brain regions show affects of autism. There is also evidence, although somewhat inconsistent , for abnormalities within the hippocampus, both in volume and more recently in shape 68 S.R. Dager et al., Shape mapping of the hippocampus in young children with autism spectrum disorder, AJNR Am. J. Neuroradiol. 28 (2007), pp. 672–677. View Record in Scopus | Cited By in Scopus (11). In post-mortem studies, showed increased cell packing density and smaller neurons in the hippocampus in all autism cases examined (Amaral et al.,...