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Ocular motor findings in Wernicke’s encephalopathy (WE) include gaze evoked nystagmus (GEN), central positional nystagmus, weakness of abduction, internuclear ophthalmoplegia and horizontal or vertical gaze palsy to total ophthalmoplegia. Another feature of WE is vestibular paresis.1 2 Previous studies documented hypoactive vestibular responses to both caloric and rotational stimuli, and a short vestibulo-ocular reflex (VOR) time constant. To address differential susceptibility of individual semicircular canals (SCC) according to stimulation frequency, we measured high acceleration VOR of the individual SCC using head impulse manoeuvres, and the low frequency VOR using bithermal caloric and rotatory chair tests in two patients with WE.
Patient No 1
A 63-year-old woman had undergone Whipple’s operation because of carcinoma of the ampulla of Vater 1 month previously and had received total parenteral nutrition (TPN). Two weeks after initiation of TPN, she began to suffer from anorexia, vomiting and vertigo which progressed to psychomotor slowing, apathy, forgetfulness and ataxia. On examination, she was awake but not attentive. She was fluent, but comprehension was impaired. The pupils were normal. Horizontal saccades were slowed and limited, and the limited ocular motor range did not improve with oculocephalic stimulation of the VOR. Other findings included horizontal GEN, limb dysmetria and severe truncal ataxia. T2 weighted …
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