We studied horizontal visual tracking in 20 patients with unilateral cerebral lesions and in 10 age-matched control subjects. Five patients, all with posterior lesions, showed impaired smooth pursuit of predictable targets moving toward the side of the cerebral lesion. Using nonpredictable step-ramp stimuli, we identified two distinct deficits of visual tracking. The first was a unidirectional deficit of smooth pursuit, for targets moving toward the side of the lesion, in response to stimuli presented into either visual hemifield. The second deficit, identified in a sixth patient who did not show pursuit asymmetry to predictable targets, was a bidirectional inability to estimate the speed of a moving target in the visual hemifield contralateral to the side of the lesion; this caused inaccurate saccades to moving (but not stationary) targets and impaired smooth pursuit initiation. These visual tracking deficits were independent of homonymous hemianopia or hemispatial neglect. These two tracking deficits are similar to those described in rhesus monkeys with lesions of the medial superior temporal and middle temporal visual areas.

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We studied a patient with stereotyped focal seizures characterized by leftward conjugate eye- and head-turning followed by nystagmus. Eye deviation was associated with the appearance of seizure activity, recorded over the right temporo-occipital scalp, that did not spread frontally. The initial eye deviation consisted of a staircase of small saccades. The subsequent nystagmus showed rightward decreasing-velocity exponential slow phases and normal leftward quick phases. Saccadic eye movements due to seizures may occur via projections from posterior cortical areas as well as from the frontal eye fields.

We studied a patient with a cerebellar degeneration and hyperactive vestibulo-ocular reflex (VOR). He complained of oscillopsia and blurred vision with head movement. A twofold increase in VOR gain (peak eye velocity/peak head velocity) at high frequencies was associated with a VOR time constant of 6 seconds (low normal). Visual cancellation ("suppression") of the VOR and smooth pursuit were also abnormal. We hypothesized that his high VOR gain was due to dysfunction of olivocerebellar projections. Physostigmine reduced his VOR gain, consistent with the hypothesis that these projections are cholinergic.

We studied the effects of variable amounts of artificial retinal image stabilization (RIS) upon oscillopsia and visual acuity in eight patients with acquired nystagmus due to neurologic disease. We measured horizontal and vertical eye movements with the magnetic search coil technique and used these electronic signals to control the position of a visual stimulus on a screen in front of the patient. We also used an optical device to stabilize images of the real world upon the retina. During electronic stabilization, RIS was progressively increased until oscillopsia was abolished; this was achieved in all eight patients and corresponded to retinal image drift of 5 degrees/sec or less. In five patients with downbeat nystagmus, further increases in RIS caused the oscillopsia to reappear, but in the opposite direction. Electronic stabilization also improved visual acuity in four of five patients; the limitation of improvement could be related to coexistent visual system defects. Using electronic feedback, we could measure the range of RIS that any individual required to abolish oscillopsia; from this measurement, the components of the optical device that were best suited to provide a stable field of vision could be calculated.