In 1881 Wernicke,1 on the basis of 3 patients studied during life and at the autopsy table, delineated a clinical syndrome characterized by clouding of consciousness, varying ophthalmoplegias and ataxia. The author did not indict alcohol as the causative agent, but suggested that various toxins, including alcohol, might produce the clinicopathologic picture of acute hemorrhagic polioencephalitis superior. The essential pathology was described by Wernicke and has been further elaborated by others.2 In general, the lesions are confined to the periventricular gray matter and are characterized by small foci of degeneration and varicose deformities of the blood vessels. There is subacute necrosis of the adjoining parenchyma, and small petechial hemorrhages are frequently, but not always, seen throughout the lesions. The areas most constantly involved are the paramedian and paraventricular nuclei of the thalamus and the hypothalamus, the mamillary bodies and the periaqueductal regions of the midbrain (nuclei of the
WORTIS H, BUEDING E, STEIN MH, JOLLIFFE N. PYRUVIC ACID STUDIES IN THE WERNICKE SYNDROME. Arch NeurPsych. 1942;47(2):215–222. doi:10.1001/archneurpsyc.1942.02290020031002
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