Abstract

Cells in the vestibular nuclei may participate in or reflect neural events associated with nystagmus. There are several reasons for believing that the quick phases of nystagmus are not primarily generated in the vestibular nuclei: (1) Quick phases of optokinetic nystagmus (OKN) and of nystagmus induced by the vestibular system have similar characteristics, and along with saccadic eye movements probably has a common site of origin. (2) Unilateral destruction of almost every part of the vestibular nuclei in two recent studies did not abolish quick phases of nystagmus induced by the vestibular system. (3) After midline section, which interrupted commissural fibers among the vestibular nuclei in the monkey, synchronous beats of nystagmus were still induced in the two eyes by vestibular or optokinetic stimuli. If the decussation of the MLF was cut, there was paralysis of adduction in both eyes. However, the adductive paralysis was present during all types of eye movements, including saccades and OKN, and probably was because of the interruption of axons, which originate in the pontine reticular formation, not in the vestibular nuclei. (4) Neural activity in the pontine reticular formation precedes each rapid eye movement, and lesions of this region cause profound changes in horizontal saccades and quick phases of nystagmus to the ipsilateral side. Less is known of the supranuclear motor organization for production of rotatory eye movements.

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