Wernicke Encephalopathy

Thiamine, or vitamin B1, is required for pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase. These enzymes allow cells to use glucose efficiently for energy. When thiamine is deficient, cerebral glucose metabolism falters, lactate accumulates, and energy-starved neurons become injured. The brain has a high and continuous energy demand, so neurological changes may appear before the cause is obvious. Chronic alcohol use is a well-known risk factor, but Wernicke encephalopathy can also occur with severe malnutrition, prolonged poor intake or vomiting, and after bariatric surgery. A patient does not need to look emaciated or have a documented alcohol history for the diagnosis to be possible. This is a time-sensitive neurological emergency. The injury may become permanent if treatment is delayed, and the classic three-part presentation is absent in many patients. The practical question is not, “Does this patient have every textbook sign?” It is, “Does this nutritionally vulnerable patient have enough of the characteristic findings to justify immediate thiamine?”