Optokinetic nystagmus deficits following parieto-occipital cortex lesions in monkeys

Abstract

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.

Vestibulo-ocular and optokinetic impairments in left unilateral neglect

“…In N+, ocular compensation of leftward head rotation was not achieved through a reduction of the phase shift between eye and head velocities comparable to that found in N− (as indicated by the significant lower decrease of the intercept value in N+). 2 The pathological reduction of the velocity and frequency of the slow phases of the OKR directed ipsilesionally clearly points out the relevant contribution of higher neural mechanisms in OKR, confirming previous findings in animals and humans [21,39,45,47].…”

Visual Pathway for the Optokinetic Reflex in Infant Macaque Monkeys

“…Lesion studies in primates demonstrate the relevance of striate and extrastriate visual cortical areas for unperturbed slow eye movements and symmetric mhOKN (e.g., Ter Braak and Van Vliet, 1963;Lynch and McLaren, 1983;Zee et al, 1987;Dürsteler and Wurtz, 1988). As we failed to reveal a cortical input to the NOT-DTN at P9, binocularity in the NOT-DTN up to this age should indeed originate from the direct projections of retinal ganglion cells from both eyes (Ballas et al, 1981;Kourouyan and Horton, 1997;Telkes et al, 2000).…”

Projections from visual areas of the cerebral cortex to pretectal nuclear complex, terminal accessory optic nuclei, and superior colliculus in macaque monkey

“…Additionally, neurons in area 7a are responsive to vestibular stimuli, moving visual stimuli, and saccades (Kawano et al, 1984;Andersen et al, 1990). On the other hand, lesions of this area result in impaired OKN toward the side of the lesion, but only when combined with lesions of wider portions of the prestriate visual cortex, namely, portions of areas 18, 19, and 5 (Lynch and McLaren, 1983).…”