GAZE-EVOKED NYSTAGMUS AND SMOOTH-PURSUIT DEFICITS - THEIR RELATIONSHIP STUDIED IN 52 PATIENTS

Gaze-evoked nystagmus occurs with cerebellar and brainstem lesions and reflects a deficiency of the so-called common neural integrator. Expe rimental data show that loss of the neural integrator also abolishes s low conjugate eye movements, i.e. smooth pursuit eye movements and the vestibulo-ocular reflex (VOR). Since the smooth pursuit system has it s own premotor circuits, a smooth pursuit deficit can be either the re sult of a premotor smooth pursuit lesion or the consequence of a gaze- holding deficit. To study this question DC eye movement recordings of 52 patients with horizontal gaze-evoked nystagmus and/or smooth pursui t deficits were studied in detail. It was found that the majority (71% ) had a combined smooth pursuit and gaze-holding deficit. Thirteen pat ients (25%) had a smooth pursuit deficit only. Only 2 patients (4%) ha d an isolated gaze-evoked nystagmus, which was comparatively weak. Thu s a major finding is that each substantial gaze-evoked nystag mus is c ombined with a smooth pursuit deficit; the two deficits are well corre lated (coefficient r=0.81). In all patients with a smooth pursuit defi cit, visual suppression of the VOR was similarly impaired, when compar ing the groups with and without gaze-evoked nystagmus. It is argued he re that, although gaze-holding and smooth pursuit deficits are well co rrelated, the gaze-holding deficits seen in patients are not severe en ough to explain the smooth pursuit deficit solely as a consequence of the gaze-holding deficit. Rather it probably reflects the close anatom ical vicinity of gaze-holding and smooth pursuit mechanisms in the flo ccular region, the vestibular nuclei/nucleus prepositus complex and it s connecting pathways.