Wernicke's encephalopathy (WE) is the best known acute neurologic complication of vitamin B_1 (B_1) deficiency and often occurs in chronic alcoholism. The plausible causes of B_1 deficiency in alcoholics depend on the underlying mechanisms, such as a low dietary intake of B_1, inadequate absorption of B_1 from the intestine due to the gastrointestinal tract damage, and coexistent alcoholic liver disease altering the capacity of B_1 storage and the metabolism of biologically important nutrients. Because the use of the classic triad of WE may overlook a mild form of WE that can be detected as inactive WE pathology, Caine and colleagues have proposed the clinical criteria for diagnosis of WE in chronic alcoholics based on the clinical-neuropathological correction. The Caine criteria include dietary deficiency, oculomotor abnormalities, cerebellar dysfunction and either altered mental status or mild memory impairment, two of which are required for diagnosis of clinical WE. In our cohort, 13 alcoholic patients who fulfilled the Caine criteria were followed up and CSF-tau levels increased at the acute stage of the disease and then decreased at the chronic stage, suggesting that the patients have a transient neuronal damage. The Caine criteria enabled an immediate intravenous administration of B_1 and provided a favorable prognosis. For the therapy of WE, parenteral treatment with a high dose of B_1 is now recommended. A typical regimen is that 500 mg of B_1 is intravenously administered three times daily for two consecutive days and 500 mg of B_1 is intravenously administered once daily for additional five days, in combination with other B vitamins. After establishment of a sufficiently low threshold for parenteral B_1 treatment, the B_1 treatment should be conducted in all alcoholic patients with altered mental status, oculomotor disorders or ataxia.