Contribution of the nucleus of the optic tract to optokinetic nystagmus and optokinetic afternystagmus in the monkey: clinical implications.

1. The role of the pretectal NOT and the DTN in producing horizontal OKN and OKAN were studied using electrical stimulation and lesions. Positive stimulation sites lay in NOT, DTN, and in a fiber bundle in the pulvinar that is presumably a cortical input to NOT. 2. When the region of NOT was electrically stimulated in darkness, horizontal nystagmus was evoked with ipsilateral slow phases. Eye velocity rose slowly to a steady-state level and was followed by afternystagmus at the end of stimulation. The time constant of rise of stimulus-induced nystagmus was similar to the slow rise of slow-phase eye velocity during OKN. The saturation velocity of the induced nystagmus and the falling time constant of the stimulus afternystagmus were the same as those of OKAN. This suggests that electrical stimulation of NOT and DTN had elicited the slow component of OKN, i.e., that component produced by the velocity storage mechanism in the vestibular system. 3. Consistent with this postulate, activity induced by NOT stimulation could enhance, prolong, or block the slow component of OKN and OKAN depending on whether slow phases were to the same or opposite side. Stimulus-induced activity also interacted with vestibular nystagmus as would OKN and OKAN. 4. Unilateral lesions of NOT and DTN caused a loss of OKAN and the slow rise in OKN to the ipsilateral side. Steady-state velocities of OKN were reduced. The initial jump of OKN slow-phase velocity was the same or somewhat less after lesions but was not lost. 5. Partial lesions of a fiber bundle in the lateral pulvinar caused a transient change in OKN and OKAN, consistent with the idea that it carries activity for the slow component from the cortex to NOT. A lesion of the MRF, just rostral to the superior colliculus, caused a transient loss of the rapid component of OKN. This region appears to carry activity responsible for the initial jump in slow-phase velocity at the onset of stimulation. 6. We conclude that: (a) NOT and probably DTN lie in the indirect pathway that produces the slow component of horizontal OKN and OKAN to the ipsilateral side in the rhesus monkey. This pathway activates the velocity storage mechanism in the vestibular nuclei. (b) At the level of NOT, the pathway responsible for the slow component of OKN and OKAN is anatomically distinct from the pathway responsible for rapid changes in eye velocity at the onset of OKN.(ABSTRACT TRUNCATED AT 400 WORDS)