Effects of Brainstem Lesions on Optokinetic Nystagmus in Monkeys

Publisher Website
Google Scholar
Abstract
The optokinetic responses of 57 monkeys were studied before and after electrolytic lesions were made throughout various regions of the brainstem. Only 1 lesion was produced in each animal. A small lesion made in the paramedian zone of the tegmentum of the brainstem, particularly at the level of the pons, causes an enduring paralysis of ipsilateral horizontal ocular deviation. Under certain experimental conditions, this is accompanied by a complete loss of optokinetic nystagmus. Lesions made in the more ventral portions of the paramedian zone near the basis pontis may result in transitory changes in the optokinetic nystagmus without concomitant paresis of ipsilateral horizontal eye movement. Lesions in the pretectal region may cause loss or impairment of optokinetic nystagmus on the side opposite the lesion. This may or may not be associated with paresis of contralateral horizontal conjugate gaze. The impulses for optokinetic nystagmus and for spontaneous deviation of eyes are mediated through a common or identical descending pathways through the brainstem. A defect in optokinetic response was found to always accompany a defect in conjugate ocular gaze.