Abstract

Carl Wernicke, a German neurologist, published the formal description of the encephalopathy for whom it is named 131 years ago. The clinical symptoms included lethargy, ophthalmoplegia, ataxia, andmental compromise.Within the same decade but unaware of Wernicke’s description, Sergei Korsakoff, a Russian psychiatrist, presented his doctoral dissertation, “Alcoholic Paralysis,” on the circumscribed amnesia occurring in certain cases of chronic alcoholism. More than half a century lapsed before the common etiology of thiamine deficiencywas discovered as the cause of the signs, symptoms, and link between these conditions (for historical reviews, see Charness, et al. 1989; Victor, et al. 1989). We now acknowledge the temporal linkage of Wernicke’s Encephalopathy (WE) and Korsakoff’s Syndrome (KS), depicted in Fig. 1 (cover image): 1) the acute phase of the encephalopathy, which results in bilateral lesions of periventricular nuclei, thalami, and structures of Papez’s circuit, notably the mammillary bodies; and 2) the chronic phase of the syndrome, which resolves into relatively permanent bilateral lesions and enduring global amnesia. In recognition of this linkage, the resulting condition is often referred to as the Wernicke-Korsakoff Syndrome (WKS). The profound amnesia provided a compelling link to neuropsychology and set the stage for dissecting memory’s component processes and identifying its dissociable neural substrates. Why is Study of WE and KS Still important?

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