• The cerebellum · Mar 2011

    Comparative Study

    Greater disruption to control of voluntary saccades in autistic disorder than Asperger's disorder: evidence for greater cerebellar involvement in autism?

    • Chloe Stanley-Cary, Nicole Rinehart, Bruce Tonge, Owen White, and Joanne Fielding.
    • Centre for Developmental Psychiatry and Psychology, School of Psychology and Psychiatry, Monash University, Notting Hill, Clayton, VIC, Australia. chloesc@gmail.com
    • Cerebellum. 2011 Mar 1;10(1):70-80.

    AbstractIt remains unclear whether autism and Asperger's disorder (AD) exist on a symptom continuum or are separate disorders with discrete neurobiological underpinnings. In addition to impairments in communication and social cognition, motor deficits constitute a significant clinical feature in both disorders. It has been suggested that motor deficits and in particular the integrity of cerebellar modulation of movement may differentiate these disorders. We used a simple volitional saccade task to comprehensively profile the integrity of voluntary ocular motor behaviour in individuals with high functioning autism (HFA) or AD, and included measures sensitive to cerebellar dysfunction. We tested three groups of age-matched young males with normal intelligence (full scale, verbal, and performance IQ estimates >70) aged between 11 and 19 years; nine with AD, eight with HFA, and ten normally developing males as the comparison group. Overall, the metrics and dynamics of the voluntary saccades produced in this task were preserved in the AD group. In contrast, the HFA group demonstrated relatively preserved mean measures of ocular motricity with cerebellar-like deficits demonstrated in increased variability on measures of response time, final eye position, and movement dynamics. These deficits were considered to be consistent with reduced cerebellar online adaptation of movement. The results support the notion that the integrity of cerebellar modulation of movement may be different in AD and HFA, suggesting potentially differential neurobiological substrates may underpin these complex disorders.

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