Wernicke’s Encephalopathy

Abstract

Wernicke’s encephalopathy (WE) is a potentially reversible metabolic brain dysfunction resulting from thiamine deficiency. It is generally characterized by ataxia, ophthalmoplegia and global confusion. Described in Berlin in 1881 by Carl Wernicke, it was initially known as polioencephalitis hemorrhagica superioris and considered a fatal syndrome. The first reported cases were three patients, two with alcoholism and one with persistent vomiting after the ingestion of sulfuric acid in a suicide attempt. The common feature shared by these cases upon post-mortem exam consisted of punctate hemorrhages in the grey matter of the walls of the third and fourth ventricles and mammillary bodies (Cirignotta et al., 2000; Truswell, 2000). In 1935, Strauss discovered that the cause of Wernicke’s findings was vitamin B1 (thiamine) deficiency (Chiossi et al., 2006). Bonhoeffer posited that Wernicke’s encephalopathy and the psychosis described by Korsakoff actually represented two phases of the same pathological process (Cirignotta et al., 2000). The observation that Wernicke’s encephalopathy and Korsakoff’s psychosis have identical neuropathology supported this belief (Charness, 1999). Thus Wernicke’s encephalopathy (WE) and Korsakoff’s psychosis (KP) are often used interchangeably as the Wernicke-Korsakoff Syndrome (WKS).