{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,10]],"date-time":"2026-01-10T21:35:59Z","timestamp":1768080959346,"version":"3.49.0"},"reference-count":29,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2004,10,8]],"date-time":"2004-10-08T00:00:00Z","timestamp":1097193600000},"content-version":"vor","delay-in-days":5455,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Annals of Neurology"],"published-print":{"date-parts":[[1989,11]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Two patients with Wernicke's encephalopathy were evaluated with quantitative vestibulo\u2010ocular reflex and ocular motor testing. Vestibulo\u2010ocular reflex testing included caloric irrigation, earth vertical axis rotational sinusoids, and rotational impulses. Both patients demonstrated hypoactive vestibular responses to both caloric and rotational stimuli at the time of presentation. One patient had upbeating nystagmus that diminished with upgaze, downgaze, or convergence. Following treatment with thiamine, both patients' vestibular responses improved but remained abnormal, with a short vestibulo\u2010ocular reflex time constant and increased low\u2010frequency rotational phase lead. Impairment of the velocity storage element attributable to damage to the vestibular nucleus and nucleus prepositus hypoglossi may account for this permanent effect on the vestibulo\u2010ocular reflex.<\/jats:p>","DOI":"10.1002\/ana.410260513","type":"journal-article","created":{"date-parts":[[2005,1,1]],"date-time":"2005-01-01T14:15:53Z","timestamp":1104588953000},"page":"669-674","source":"Crossref","is-referenced-by-count":29,"title":["Vestibular responses in wernicke's encephalopathy"],"prefix":"10.1002","volume":"26","author":[{"given":"Joseph M. 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