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Wernicke encephalopathy has classically been thought of as a disease solely of people who drink excessive amounts of alcohol, but it is also found in the chronically undernourished, and in recent years has been discovered post bariatric surgery. [11] [39] Without being exhaustive, the documented causes of Wernicke encephalopathy have included:
Wernicke-Korsakoff syndrome (WKS) is the combined presence of Wernicke encephalopathy (WE) and alcoholic Korsakoff syndrome (AKS [clarification needed]). Due to the close relationship between these two disorders, people with either are usually diagnosed with WKS as a single syndrome.
Korsakoff syndrome (KS) [1] is a disorder of the central nervous system characterized by amnesia, deficits in explicit memory, and confabulation.This neurological disorder is caused by a deficiency of thiamine (vitamin B 1) in the brain, and it is typically associated with and exacerbated by the prolonged, excessive ingestion of alcohol. [2]
Risk factors include a diet of mostly white rice, alcoholism, dialysis, chronic diarrhea, and taking high doses of diuretics. [1] [6] In rare cases, it may be due to a genetic condition that results in difficulties absorbing thiamine found in food. [1] Wernicke encephalopathy and Korsakoff syndrome are forms of dry beriberi. [6]
The typical treatment of alcohol withdrawal is with benzodiazepines such as chlordiazepoxide or diazepam. [2] Often the amounts given are based on a person's symptoms. [2] Thiamine is recommended routinely. [2] Electrolyte problems and low blood sugar should also be treated. [2] Early treatment improves outcomes. [2]
Wernicke syndrome is an ambiguous term. It may refer to: Wernicke aphasia: the eponymous term for receptive or sensory aphasia.; Wernicke encephalopathy: an acute neurological syndrome of ophthalmoparesis, ataxia, and encephalopathy brought on by thiamine deficiency.
Rarer mimics of encephalopathy are meningitis, encephalitis, Wernicke's encephalopathy and Wilson's disease; these may be suspected on clinical grounds and confirmed with investigations. [9] [16] The diagnosis of hepatic encephalopathy is a clinical one, once other causes for confusion or coma have been excluded; no test fully diagnoses or ...
Treatment includes administration of intravenous saline to rehydrate and 5% dextrose to turn off gluconeogenesis. Electrolyte imbalances, specifically hypokalaemia, should be corrected. Thiamine supplementation is often included to prevent Wernicke encephalopathy. Insulin is generally not used due to risk of hypoglycemia. [5]