Optokinetic nystagmus (OKN) was induced in six monkeys by rotation of a full field drum. After unilateral lesions of the inferior parietal lobule and prestriate cortex (IPL-PS lesion), three monkeys had diminished velocity of slow components when the drum rotated toward the side of the lesion. OKN slow components appeared normal when the drum rotated in the opposite direction, while fast components appeared normal in both directions. The severity of the slow component deficit was greater at higher rates of stimulus rotation than at lower ones. Recovery occurred within 7-10 days for two monkeys; no recovery was evident after 2 weeks for the third. Subsequent bilateral IPL-PS lesions in two of these monkeys reduced OKN slow phase velocity in both directions. Two monkeys with unilateral lesions limited to the inferior parietal lobule (IPL lesions) had only very mild and transient deficits lasting 1-3 days. Bilateral IPL lesions also produced only slight OKN deficits. One monkey had a lesion which destroyed most of the lateral striate cortex of one hemisphere and had no discernable OKN deficit. These results demonstrate that, in contrast to earlier reports, lesions of parieto-occipital cortex in monkeys produce deficits which are qualitatively similar to, although of shorter duration than, those OKN deficits which commonly are associated with posterior parietal damage in humans.