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Neurology 1999;52:917
© 1999 American Academy of Neurology


Articles

Oculomotor evidence for neocortical systems but not cerebellar dysfunction in autism

Nancy J. Minshew, MD, Beatriz Luna, PhD and John A. Sweeney, PhD

From the Departments of Psychiatry and Neurology, University of Pittsburgh School of Medicine, PA.

Address correspondence and reprint requests to Dr. Nancy J. Minshew, University of Pittsburgh School of Medicine, 3811 O’Hara Street, 430 Bellefield Towers, Pittsburgh, PA 15213.

OBJECTIVE: To investigate the functional integrity of cerebellar and frontal systems in autism using oculomotor paradigms.

BACKGROUND: Cerebellar and neocortical systems models of autism have been proposed. Courchesne and colleagues have argued that cognitive deficits such as shifting attention disturbances result from dysfunction of vermal lobules VI and VII. Such a vermal deficit should be associated with dysmetric saccadic eye movements because of the major role these areas play in guiding the motor precision of saccades. In contrast, neocortical models of autism predict intact saccade metrics, but impairments on tasks requiring the higher cognitive control of saccades.

METHODS: A total of 26 rigorously diagnosed nonmentally retarded autistic subjects and 26 matched healthy control subjects were assessed with a visually guided saccade task and two volitional saccade tasks, the oculomotor delayed-response task and the antisaccade task.

RESULTS: Metrics and dynamics of the visually guided saccades were normal in autistic subjects, documenting the absence of disturbances in cerebellar vermal lobules VI and VII and in automatic shifts of visual attention. Deficits were demonstrated on both volitional saccade tasks, indicating dysfunction in the circuitry of prefrontal cortex and its connections with the parietal cortex, and associated cognitive impairments in spatial working memory and in the ability to voluntarily suppress context-inappropriate responses.

CONCLUSIONS: These findings demonstrate intrinsic neocortical, not cerebellar, dysfunction in autism, and parallel deficits in higher order cognitive mechanisms and not in elementary attentional and sensorimotor systems in autism.




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