archived papers - sensory

Brain Anatomy and Sensorimotor Gating in Asperger's Syndrome

M. Grainne and Mc Alonan et al., Brain (2002), 127, 1594 - 1606.

There are few studies on brain anatomy of Asperger's Syndrome, and no focal anatomical abnormality has been reliably reported from brain imaging studies of autism, although there is increasing evidence for differences in limbic circuits. These brain regions are important in sensorimotor gating, and impaired 'gating' may partly explain the failure of people with autistic with autistic disorders to inhibit repetitive thoughts and actions. Thus, we compared brain anatomy and sensorimotor gating in healthy people with Asperger's Syndrome and controls. We included 21 adults with Asperger's Syndrome and 24 controls. All had normal IQ and were aged 18 - 49 years. We studied brain anatomy using quantitative MRI, and sensorimotor gating using prepulse inhibition of startle in a subset of 12 individuals with Asperger's Syndrome and 14 controls. We found significant age-related differences in volume of cerebral hemispheres and caudate nuclei (controls, but not people with Asperger's Syndrome, had age-related reductions in volume). Also, people with Asperger's Syndrome had significantly less grey matter in fronto-striatal and cerebellar regions than controls, and widespread differences in white matter. Moreover, sensorimotor gating was significantly impaired in Asperger's Syndrome. People with Asperger's Syndrome most likely have generalised alterations in brain development, but this is associated with significant differences from controls in the anatomy and function of specific brain regions implicated in behaviours characterising the disorder. We hypothesize that Asperger's Syndrome is associated with abnormalities in fronto-striatal pathways resulting in defective sensorimotor gating, and consequently characteristic difficulties inhibiting repetitive thoughts, speech and actions.

We found that, compared with controls, people with Asperger's Syndrome have age-related differences in brain anatomy, structural abnormalities in fronto-striatal systems and the cerebellum, and impaired sensorimotor gating. We suggest that Asperger's Syndrome probably arises from a generalised abnormality in brain development (causing widespread white matter abnormalities). This neurodevelopmental abnormality may, in turn, be modulated by environmental factors such as social isolation. Some regions are more affected than others, ad our findings support the hypothesis that a proportion of autistic symptomatology may be explained by frontostriatal disorder.