Ocular Motor Deficits in Parkinson's Disease

Eye-head coordination was measured in patients with Parkinson's disease as they made horizontal gaze shifts in response to predictable and unpredictable target steps and to targets moving smoothly with either constant or sinusoidally varying velocity. Patients preferred not to move their heads for both large and small amplitude gaze shifts. Both eye and head movement reaction times were prolonged. Saccades were hypometric and, frequently, slow. Head movements were also slow, hypometric, and varied in amplitude for target shifts of a given amplitude. Compensatory eye movements (CEMs) that normally stabilize gaze direction during head movement varied in gain from zero to greater than unity, and often drove the eyes off target. CEM abnormalities occurred most commonly in patients with abnormal vestibulo-ocular reflex (VOR) gain in darkness. We attribute these abnormalities of programming combined eye-head saccades to dysfunction of striatonigralcollicular circuits. Smooth gaze pursuit gain, the ratio of gaze velocity to target velocity, was lowered in patients while tracking sinusoidal targets at 0.3, 0.5 and 1.0 Hz. Some patients could track these targets with the head fixed but not with the head free. We attribute this to abnormal suppression of the vestibuloocular reflex. The results indicate that Parkinson's disease impairs motor programming of coordinated eye-head gaze saccades and disrupts normal interaction between head movement and the VOR.