Abstract
Eye movements evoked by optokinetic and vestibular stimulation were measured by scleral search coil before and up to 8 weeks after unilateral cortical lesions in 11 cats. During both monocular and binocular viewing conditions, several deficits in the velocity-storage component of optokinetic nystagmus (OKN) were found. At low target velocities, the final steady-state slow-phase eye velocity and the peak value of optokinetic afternystagmus (OKAN) were reduced for slow phases towards the side of the lesion. At high target velocities OKN and OKAN were no longer elicited. The time constant of OKAN was also reduced for slow phases towards the side of the lesion. These deficits in OKN and OKAN were quantitatively similar in cats with large cortical (LC) lesions involving all known visual areas and in cats with suprasylvian (SS) lesions involving areas 21a, 21b, PMLS, and VLS. Ablation of areas 17 and 18 alone had no effect, but when combined with section of the corpus callosum (17/18+CC) resulted in a qualitatively similar but less severe deficit as the LC and SS lesions. By 3 weeks postoperatively, OKN recovered to near preoperative values in cats with SS lesions. Vestibular adaptive capabilities were impaired during the duration of the study in cats with LC, SS, and 17/18+CC lesions. Cats with these lesions could not normally increase VOR gain for slow phases directed ipsilateral to the lesion, and following vestibular adaptation most of these cats developed persistent asymmetries in VOR gain and VOR time constants. These results can be better conceptualized using a mathematical model of the vestibulo-ocular and optokinetic system adapted from Robinson (1977). This model contains a single positive- feedback velocity storage loop common to the VOR and OKN systems and a retinal-slip velocity nonlinearity. Our results suggest that SS cortex improves the retinal-slip nonlinearity feeding into the velocity- storage system by extending its range and increasing its gain. The SS cortex depends in part upon areas 17 and 18 either directly, or indirectly via the corpus callosum, for processing of high retinal-slip velocities. Cerebral cortex is also involved in increasing the gain of the velocity-storage loop during vestibular adaptation for ipsilaterally directed slow phases.