The ability to hold an eccentric position of gaze has been attributed to a brainstem network termed the ocular motor neural integrator. For this integrator to function properly, an intact cerebellum is necessary. This report describes a patient with cerebellar dysfunction who showed an unusual form of nystagmus: each slow phase had a waveform of increasing velocity. This contrasts with gaze paretic nystagmus, the more typical manifestation of cerebellar disorder, in which each slow phase has a waveform of decreasing velocity. Based on these observations and results from basic research, we propose that (1) the cerebellum controls neural integration in the brainstem by a positive feedback loop, and (2) pathological alterations in the strength of transmission (or gain) through the feedback loop cause the eyes to drift off target, with either an exponentially increasing (gain too high) or decreasing (gain too low) velocity.