Abstract
Wernicke encephalopathy is a thiamine deficiency condition that has a wide range of somatic causes in addition to alcohol abuse. Most patients do not have the classical clinical triad — oculomotor dysfunction, ataxia and cognitive impairment at the onset of the disease, which makes timely diagnosis difficult. The disease may manifest as dizziness, unsteadiness, double vision, or cognitive impairment. Key clinical manifestations include symmetrical gaze-evoked nystagmus, truncal ataxia, bilateral abducens paresis, internuclear ophthalmoplegia, bilateral vestibular-ocular reflex reduction, and anterograde amnesia. To make a diagnosis, the presence of a condition leading to thiamine deficiency is required. The diagnosis is confirmed by MRI, but even with clinical suspicion of Wernicke encephalopathy, it is necessary to initiate parenteral therapy with thiamine in an adequate dose. With timely treatment, the disease has a good prognosis.
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