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Visual-vestibular interaction and cerebellar atrophy

University of California, Los Angeles, Department of Neurology (Dr. Baloh); Department of Surgery/Division of Head and Neck (Otolaryngology) (Drs. Jenkins, Honrubia, and Lau); and the Jules Stein Eye Institute, Department of Ophthalmology (Dr. Yee), UCLA School of Medicine, Los Angeles, California.

The vestibular and optokinetic ocular control systems were studied in 10 patients with cerebellar atrophy and in 10 normal subjects using (1) constant velocity optokinetic stimulation, (2) sinusoidal rotation in the dark, and (3) sinusoidal rotation in the light with a surrounding fixed optokinetic drum. The gain (maximum slow component velocity/maximum head or drum velocity) of induced nystagmus was calculated from electro-oculographic recordings. Optokinetic nystagmus was abnormal in seven patients and the average optokinetic gain in the patients was significantly (p < 0.01) less than that of the normal group. Three patients with "clinically pure" cerebellar atrophy had increased vestibular responses, and one patient with clinical signs of peripheral neuropathy had decreased responses, probably due to associated vestibular nerve disease. The average vestibulo-ocular reflex gain in patients did not differ significantly from controls (p > 0.05). Three patients had normal vestibular and optokinetic responses when tested independently, but had abnormal visual-vestibular interaction. These patients probably had selective disorders of the midline cerebellar pathways that mediate visual-vestibular interaction. By studying each system, both independently and during interaction, all patients were identified as abnormal, and a more precise anatomic localization of the atrophy was obtained.

Requests for reprints should be addressed to Dr. Baloh, Department of Neurology, Reed Neurological Research Center, Center for the Health Sciences, UCLA, Los Angeles, CA 90024.

This study was supported by NIH Grant No. NS 09823 and a grant from the Deafness Research Foundation.

Accepted for publication March 21, 1978.

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