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Smooth pursuit dysfunction in Alzheimer's disease

From the Neuro-ophthalmology Unit, Division of Neurology and Playfair Neuroscience Unit, The Toronto Hospital, Departments of Medicine and Ophthalmology, University of Toronto, Ontario, Canada.

Smooth ocular pursuit was measured by magnetic search coil oculography in 13 patients with Alzheimer's disease and compared with control subjects. Smooth eye movement gain was uniformly reduced in Alzheimer's disease at all target velocities for several frequencies of sinusoidal target motion, signifying impairment of steady-state gain. Normal phase relationships between the target and eyes indicated an intact predictor mechanism for smooth pursuit. When peak target velocity was held constant, pursuit gain decreased markedly in response to small increments of target acceleration, indicating involvement of an acceleration saturating nonlinear element that limits smooth pursuit. Large-amplitude saccadic intrusions, in the direction of target motion, often disrupted pursuit; smooth eye movements continued in response to target velocity despite large position errors of the fovea from its target. These disorders of smooth eye movement control can quantify motor dysfunction in Alzheimer's disease.

Address correspondence and reprint requests to Dr. Sharpe, Division of Neurology, The Toronto Hospital, 399 Bathurst Street, Toronto, Ontario, M5T 2S8, Canada.

Supported by Medical Research Council of Canada Grants ME5409 and MT5404 (Dr. Sharpe) and by the Alberta Heritage Foundation for Medical Research. Dr. Fletcher was an Alberta Heritage Research Fellow in Neuro-ophthalmology at the University of Toronto, and is now with the Foothills Hospital, University of Calgary, Alberta.

Received March 5, 1987. Accepted for publication in final form May 6, 1987.

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