Presentation
Wernicke's encephalopathy begins abruptly, usually with eye movement disorders (nystagmus, gaze palsies, and ophthalmoplegia, especially of the lateral rectus muscles), gait ataxia, confusion, confabulation, and short-term memory loss.
The classic triad of the syndrome is confusion, ophthalmoplegia (eye paralysis), and ataxia (loss of coordination), though these are only seen in combination in 10% of cases. Untreated it may progress to Korsakoff's psychosis, coma and death. The pathological changes seen in Wernicke's encephalopathy are concentrated in the mammillary bodies, cranial nerve nuclei III, IV, VI and VIII, the thalamus, hypothalamus, periaqueductal grey, cerebellar vermis, and the dorsal nucleus of the vagus nerve. The ataxia and ophthalmoparesis are related to lesions in the oculomotor, trochlear, abducens, and vestibular (IIIrd, IVth, VIth, and VIIIth cranial) nerve nuclei.
Despite its name, Wernicke's encephalopathy is not related to Wernicke's area, a region of the brain associated with speech and language interpretation. (See Wernicke's aphasia.) Rather, both are named for the 19th century neurologist Carl Wernicke.
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