Autism is a severe developmental disorder of communication. reciprocal social interaction and repetitive, odd behaviors. Asperger syndrome (AS) shares many features with autism, and may therefore have a largely overlapping, but nevertheless distinguishable pathophysiology. While evidence for a biological basis for autism is substantial little is known about the neural mechanisms underlying the behavioral abnormalities seen in this disorder. Neuropathology and neuroimaging studies have demonstrated clear CNS abnormalities seen in patients with autism. Results from neuroirnaging studies in autism and related disorders, however, have often been difficult to interpret because of clinical heterogeneity of the samples studied. confounding effects of mental retardation. lack of neuropsychological evaluations and hypotheses, and lack of appropriate controls. These factors are even more problematic in the case of AS, given its current uncertain nosological status. necessitating, therefore, careful and comprehensive characterization. The proposed investigation attempts to address these limitations by correlating morphometric studies of the brain with neuropsychological, social-emotional and family genetics data to elucidate the pathophysiological basis of these disorders.
Specific Aims Collect Neuroimaging data in a large sample of high-functioning autism (HFA), Aspergers (AS) and control subjects. 1. Perform comprehensive morphmetic assessments using structural MRI data to test the following hypotheses: A. The volume of the amygdala is reduced in HFA compared to matched unaffected controls. B. The volume of select frontal lobe regions is reduced in HFA. C. Brain size is significantly larger in HFA. D. Individuals with HFA have a greater frequency of neurodevelopmental abnormalities (e.g. abnormally thickened cortex). E. The cross-sectional area of posterior regions of the corpus callosum are reduced in HFA F. The neocerebellar vermis is reduced in size in HFA. 2. Stratify the HFA and AS patients using structural MRI data to identify more homogenous diagnostic subtypes. 3. Examine structure -function relationships to test hypotheses that deficits in social-emotional processing and executive functioning correlate with structural MRI findings in the amygdala and frontal cortices.
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