Symmetrical Optokinetic After-Nystagmus Loss in Wallenberg's Syndrome and Multiple Sclerosis

Abstract

Horizontal optokinetic after-nystagmus (OKAN), first described by Ohm (1921), has been shown to be profoundly affected by unilateral or bilateral, partial or complete loss of labyrinthine function (Cohen et al., 1973; Ireland & Jell, 1982; Zee et al., 1976). Cohen et al. (1977) have postulated a velocity storage mechanism in the brain stem to explain the phenomenon of OKAN. This “integrator”, possibly shared by both optokinetic and vestibular systems, is apparently compromised by peripheral vestibular lesions resulting in severe modifications of ifs ability to drive the eyes. Evidence has also been obtained that, in monkeys, OKAN is permanently abolished by unilateral lesions in the brain stem in the region medial to the medial vestibular nucleus, the site of the nucleus prepositus hypo-glossi (Uemera & Cohen, 1973). We now present evidence that, in patients with unilateral brain stem disorders, OKAN may be lost with optokinetic stimulation in either direction while caloric responses, although qualitatively abnormal, are still present. This implies the ability to distinguish between loss of OKAN from peripheral causes and that due to brain stem pathology.