Wernicke Encephalopathy

Wernicke encephalopathy (WE) is an acute neuropsychiatric emergency caused by inadequate thiamine, or vitamin B1. Thiamine is required for enzymes that convert glucose into usable cellular energy, including pyruvate dehydrogenase, alpha-ketoglutarate dehydrogenase, and transketolase. When thiamine is deficient, the brain cannot process glucose efficiently. High-metabolic-demand structures become especially vulnerable, including the thalami, hypothalamus, mammillary bodies, and periaqueductal gray matter. The body stores only a small amount of thiamine. Depletion can occur within roughly 2–3 weeks of inadequate intake or absorption, sometimes sooner when vomiting, malabsorption, or increased metabolic demand is severe. Alcohol use disorder is a major risk factor, but it is not required. Other risks include hyperemesis gravidarum, prolonged vomiting or fasting, bariatric surgery, malabsorption, eating disorders, malignancy or chemotherapy, and prolonged parenteral nutrition without vitamin supplementation. Carbohydrate administration increases the demand for thiamine-dependent metabolism. In a thiamine-deficient patient, a sustained carbohydrate load can precipitate or worsen neurologic injury. This is why prompt thiamine is paired with nutritional or glucose therapy, but it does not justify withholding life-saving glucose from a patient with hypoglycemia.