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Brain, Vol. 106, No. 3, 555-570, 1983
© 1983 Guarantors of Brain

research-article

OCULAR MOTOR DEFICITS IN PARKINSON'S DISEASE

I. THE HORIZONTAL VESTIBULO-OCULAR REFLEX AND ITS REGULATION

OWEN B. WHITE, JEAN A. SAINT-CYR and JAMES A. SHARPE

From the Neuro-ophthalmology Unit, Division of Neurology, the Playfair Neuroscience Unit, Toronto Western Hospital 399 Bathurst Street, Toronto M5T 2S8 Departments of Medicine, Ophthalmology and Anatomy, University of Toronto Canada

Correspondence to: Reprint requests to Dr J. A. Sharpe, Toronto Western Hospital, 399 Bathurst St., Toronto, Ontario M5T 2S8, Canada.

Horizontal vestibulo-ocular reflex (VOR) function was quantified in 14 parkinsonian patients and compared with that of 10 age-matched normals. Eight patients had mild and 6 had advanced rigidity and akinesia. In advanced disease VOR gains were subnormal in darkness during sinusoidal whole-body rotation at frequencies from 0.3 to 3.0 Hz. When fixating a stationary target, patients enhanced VOR gains to near unity, but gains of patients with advanced disease were significantly lower than controls. Visual suppression of the VOR by fixating a target moving with the head was defective in all stages of the disease. Advanced patients also exhibited defective voluntary control of the reflex in darkness: both voluntary enhancement, by imagining a stationary target, and voluntary suppression, by imagining a target moving with the head, were abnormal. This disordered voluntary control of the VOR was independent of defective visually mediated smooth pursuit.

Attempted visual and voluntary suppression of the reflex produced a rise in VOR gain, above the hypoactive values recorded in darkness in advanced disease. This inappropriate activation of the VOR implied structural integrity of brainstem smooth eye movement pathways, despite vestibulo-ocular hyporeflexia. Unrecognized degeneration in brainstem VOR circuits, or defective cerebral hemisphere control of the reflex caused by the nigrostriatal or cerebral cortical dysfunction of Parkinson's disease, may explain subnormal ocular responses to passive head motion. We attribute the abnormal visual and voluntary modulation of smooth eye movements to disordered long-loop cerebral control of the VOR and suggest that it is analogous to the defective long-loop cerebral regulation of spinal reflexes that occurs in Parkinson's disease.

Received July 7, 1982. Revised November 23, 1982.
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A. M. F. Wong, D. Tweed, and J. A. Sharpe
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