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. Experimental data show that loss of the neural integrator also abolishes slow conjugate eye movements, i.e. smooth pursuit eye movements and the vestibulo-ocular reflex (VOR). Since the smooth pursuit system has its own premotor circuits, a smooth pursuit deficit can be either the result 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 pursuit deficits were studied in detail. It was found that the majority (71%) had a combined smooth pursuit and gaze-holding deficit. Thirteen patients (25%) had a smooth pursuit deficit only. Only 2 patients (4%) had an isolated gaze-evoked nystagmus, which was comparatively weak. Thus a major finding is that each substantial gaze-evoked nystagmus is combined with a smooth pursuit deficit; the two deficits are well correlated (coefficient r = 0.81). In all patients with a smooth pursuit deficit, visual suppression of the VOR was similarly impaired, when comparing the groups with and without gaze-evoked nystagmus. It is argued here that, although gaze-holding and smooth pursuit deficits are well correlated, the gaze-holding deficits seen in patients are not severe enough to explain the smooth pursuit deficit solely as a consequence of the gaze-holding deficit. Rather it probably reflects the close anatomical vicinity of gaze-holding and smooth pursuit mechanisms in the floccular region, the vestibular nuclei/nucleus prepositus complex and its connecting pathways.