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Wernicke's encephalopathy is a severe syndrome characterised by loss of short-term memory. It is linked to damage to the mammillary bodies in the brain, and is the result of inadequate intake or absorption of thiamine (Vitamin B1) coupled with continued carbohydrate ingestion. The most common cause of an onset is severe alcoholism, though there are several other causes. Wernicke's encephalopathy onsets acutely, and usually presents with nystagmus, gaze palsies, ophthalmoplegia (especially of the abducens nerve, CN VI), gait ataxia, confusion, and short-term memory loss. The classic triad for this disease is encephalopathy, ophthalmoplegia and ataxia. Untreated, this condition may progress to coma. Despite its name, Wernicke's encephalopathy is not related to damage of the speech and language interpretation area named Wernicke's area (see Wernicke's aphasia). Instead the pathological changes in Wernicke's encephalopathy are concentrated in the mammillary bodies cranial nerve nuclei III, IV, VI and VIII, as well as the thalamus, hypothalamus, periaquiductal grey, cerebellar vermis and the dorsal nucleus of the vagus nerve. The ataxia and ophthalmoparesis relate to lesions in the oculomotor (ie IIIrd, IVth, and VIth nerves) and vestibular (ie VIIIth nerve) nuclei. Treatment includes an intravenous (IV) or intramuscular (IM) injection of thiamine, as well as the active exclusion of central nervous system (CNS) diseases or other metabolic disturbances. Patients are usually dehydrated, and so rehydration to restore blood volume should be started. If the condition is treated early, recovery may be rapid and complete.
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