Abstract
The cortical control of horizontal optokinetic nystagmus (OKN) has been studied in 13 adult cats with unilateral lesions. OKN was induced by rotating the visual field around the animals in both binocular and monocular conditions. (1) No deficits of OKN appeared following unilateral ablations of visual cortex. (2) Lesions of different parts of suprasylvian cortex were made: the posterior and the middle suprasylvian cortex involving area 7 and the lateral suprasylvian area (LSA). Only the middle suprasylvian cortex damage produced an OKN asymmetry due to a decrease of the slow-phase velocity directed toward the side of the lesion. The deficits were compensated for within about 10 days. We conclude that the middle suprasylvian cortex and particularly LSA regulate the ipsilateral slow phases of OKN.
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