Horizontal optokinetic nystagmus in the cat: Recovery from cortical lesions

Abstract

We have examined recovery from the acute effects of unilateral and bilateral visual cortex lesions on horizontal optokinetic nystagmus (OKN) in the cat. A single bilateral cortical lesion virtually abolishes monocular OKN in response to temporalward stimulation, and severely reduces OKN in response to nasalward stimulation at higher drum velocities. A unilateral cortical lesion causes deficits in OKN toward the side of the lesion, but these changes are less substantial than those observed after a bilateral lesion. The nature of the acute changes in OKN caused by cortical lesions supports the notion that the visual cortex has two important roles in the OKN system of the cat: first, it mediates OKN in response to temporal ward motion of the visual environment during monocular viewing; second, it expands the response range of the OKN system to include higher stimulus velocities. Finally, the results from unilaterally lesioned cats suggest that a single hemisphere can mediate OKN in both directions, with an emphasis on the direction ipsilateral to that hemisphere. The patterns of recovery of OKN in lesioned cats follow two major trends: a small, gradual increase in the overall gain of OKN from its severely depressed level immediately after a large bilateral lesion, and a ‘balancing’ process that reduces the marked asymmetry between rightward and leftward OKN caused by a unilateral lesion. This balancing of the reflex is accomplished by an improvement in performance in one direction while performance in the opposite direction actually declines. Recovery is faster and more pronounced in lesioned cats with one cortical hemisphere intact, suggesting that the surviving visual cortex compensates for the effects of the lesion by modifying activity in subcortical pathways. These experiments indicate that the visual system of the cat has the capacity to recover at least partially from the deficits in OKN behavior caused by cortical lesions, and that this recovery is the outcome of an interaction between cortical and subcortical pathways mediating this important visuomotor reflex.