The role of cerebellar disease in the production of nystagmus continues to be controversial. The cerebellum receives projections from visual and ocular muscle receptor afferents, and cerebellar efferent fibers project to vestibular and oculomotor nuclei and to the pontine reticular formation. These connections provide ample basis for disturbances of oculomotor control in cerebellar disease.1,2 Some authors are reluctant to attribute spontaneous nystagmus to disturbances of the cerebellum itself. The probability of concurrent dysfunction of the brainstem produced either by pressure or by direct brainstem involvement has been emphasized.3,4
The observations of Gordon Holmes5 provide pertinent oculomotor guidelines. After acute cerebellar hemispheric injuries, Holmes described paralysis of ipsilateral gaze followed by gaze-paretic nystagmus on gaze toward the side of injury. The slow phase was directed to a "rest point" located 10° to 30° from midline on the unaffected side. On gaze to the other side of the rest
Sharpe JA. Rebound Nystagmus—A Cerebellar Sign? JAMA. 1974;227(6):648–649. doi:10.1001/jama.1974.03230190040012
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