Effects of mesencephalic reticular formation lesions on optokinetic nystagmus

Optokinetic nystagmus (OKN) was studied in monkeys after lesions of the mesencephalic reticular formation (MRF). After the MRF was damaged, there was gaze preference and spontaneous nystagmus to the side of the lesion. Gaze palsy was not produced. Originally OKN could not be induced to the contralateral side. Later, contralateral OKN was evoked, but the beats were smaller and less frequent than beats of ipsilateral OKN, and the maximum velocity of the slow phases was low. In several animals, changes in contralateral OKN were permanent. Ipsilateral OKN and caloric nystagmus to either side were little affected by MRF lesions. It is inferred that an important part of the descending visual-oculomotor pathways responsible for optokinetic nystagmus in the horizontal plane lies in the MRF. It is postulated that the primary defect in OKN after MRF lesions was an inability to generate ipsilateral slow phases of adequate velocity. If so, activity carried in the MRF responsible for OKN may be more closely related to production of slow than quick phases of nystagmus.