Thiamin plays a key role in a variety of enzymes and metabolic pathways, including involvement in transketolase and glucose metabolism within the central nervous system. Chronic thiamin deficiency depletes the body’s thiamin stores within 2-3 weeks. As blood thiamin levels decline, the thiamin-dependent enzyme systems involved in preventing cellular damage are impaired and metabolic demands increase, which can lead to the selective brain damage associated with Wernicke’s encephalopathy and Korsakoff’s syndrome. Thus, the development of thiamine deficiency and Korsakoff syndrome is particularly prevalent in malnourished patients, often due to a shift in diet from vitamin-rich foods to a high intake of carbohydrate-based alcohol, as is the case with chronic alcoholism. Wernicke’s encephalopathy is an acute neuropsychiatric disorder caused by vitamin B1 deficiency. first named for Carl Wernicke in 1881, the traditional signs and symptoms of the disease include altered mental status, ataxia, and ocular symptoms (including nystagmus and oculomotor palsy). The classic trinity of ocular signs, ataxia, and altered mental status is neither universal nor unique, but is more diagnostically indicative when used in conjunction with clinical imaging.MRI signal characteristics: reversible cytotoxic edema, represented by symmetric changes in the thalamus, papillae, and parietal plate. The differential diagnosis may include other encephalopathies, middle thalamic infarction, primary cerebral lymphoma, multiple sclerosis, Creutzfeldt-Jakob disease, and Leigh disease. Thiamine replacement has been identified as the primary treatment for Korsakoff’s syndrome to reverse mental status changes and prevent further disease progression. Parenteral thiamine is used in the acute treatment of Wernicke’s encephalopathy because the intestinal absorption of thiamine may be impaired, as in the case of alcoholics.