We propose to study smooth pursuit eye movements in a selected group of patients who have suffered unilateral cerebral infarction. The smooth pursuit system provides a quantifiable model of sensorimotor interaction that incorporates cortical mechanisms for visual motion processing, attention and ocular motor control. Patterns of defective smooth pursuit resulting from focal brain damage reflect the asymmetrical organization of cerebral hemispheric smooth pursuit pathways according to the retinal hemifield and direction of target motion and the gaze field in which eye motion takes place. We will measure horizontal and vertical eye movements with magnetic search coil oculography, using step-ramp and sinusoidal stimuli to identify retinotopic, directional and craniotopic asymmetries of smooth pursuit in patients. Our testing paradigms will explore the physiological bases of directional and craniotopic pursuit deficits. Mathematical modeling of results will be used to describe the operations taking place in cerebral cortex. Pursuit impairment in patients will be correlated with the anatomy of cerebral damage as demonstrated by neuroimaging procedures, to refine localization of cortical regions that participate in smooth pursuit control in humans. In monkeys, significant recovery of smooth pursuit impairment has been documented after cerebral cortical injury. Both local and remote neural plasticity probably facilitate this adaptation. We will compare results, of ocular motor testing done in patients within the first week after cerebral infarction to testing done after four to six months of recovery. This analysis will provide quantitative assessment of the dysfunction caused by focal neural damage in humans and of the degree to which the impairment can be compensated. Comparison of the nature and extent of recovery to the type of pursuit deficit and to the anatomy of the cerebral damage will help characterize the adaptive mechanisms used by the smooth pursuit system.
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