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OCULAR MOTOR DEFICITS IN PARKINSON'S DISEASE
II. CONTROL OF THE SACCADIC AND SMOOTH PURSUIT SYSTEMS

OWEN B. WHITE, JEAN A. SAINT-CYR, R. DAVID TOMLINSON, JAMES A. SHARPE
DOI: http://dx.doi.org/10.1093/brain/106.3.571 571-587 First published online: 1 September 1983

Summary

We quantified the horizontal pursuit and saccadic function of 14 parkinsonian patients and 10 normal subjects matched for age. Eight patients had mild, and 6 advanced disease. Ocular motor deficits were more marked in patients with advanced disease. Saccadic reaction times and postsaccadic refractory periods were prolonged. Peak saccadic velocities were significantly reduced. Slow saccades may be caused by inappropriate coactivation of opposing ocular muscles. Multiple step, hypometric saccades were abnormally frequent. Correct final eye position towards a brief target flash was attained without visual feedback. Brief corrective intervals occurred after hypometric saccades. They are attributed to internal (nonvisual) efference copy feedback of eye position errors. Frequent square wave jerks were also a feature of Parkinson's disease.

Smooth pursuit gain was lowered in all patients while tracking sinusoidal targets at frequencies from 0.25 to 1 Hz. Pursuit gain was uniformly reduced at all target velocities at each frequency. This decrease in gain indicates that dysfunction of the gain element, rather than abnormal drop acceleration saturation is responsible for impaired smooth pursuit.

The results indicate that Parkinson's disease damages structures involved in the regulation of the saccadic and pursuit systems. We infer that nigrostriatal pathways, known to be damaged in Parkinson's disease, control the latency, velocity and amplitude of saccades, and the gain element of smooth pursuit.

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