Wernicke encephalopathy (WE) is an acute, life-threatening neurological emergency caused by severe thiamine (vitamin B1) deficiency. Thiamine pyrophosphate (TPP) is the active coenzyme for pyruvate dehydrogenase, alpha-ketoglutarate dehydrogenase (citric acid cycle), and transketolase (pentose phosphate pathway). Without adequate thiamine, neurons cannot complete aerobic glucose metabolism, leading to intracellular ATP depletion, cytotoxic edema, lactate accumulation, and selective neuronal death in metabolically active brain regions. The most vulnerable structures include the mammillary bodies, medial thalamus, periventricular gray matter, periaqueductal gray, cerebellar vermis, and oculomotor/abducens nuclei. Damage to these regions produces the classic clinical triad: (1) encephalopathy/confusion from thalamic and cortical dysfunction, (2) oculomotor dysfunction including nystagmus, lateral rectus palsy (CN VI), and conjugate gaze palsy from brainstem nuclei involvement, and (3) cerebellar ataxia from vermian degeneration. However, the complete triad is present in only approximately 16-33% of cases. The most common cause is chronic alcohol use disorder (ethanol impairs intestinal thiamine absorption, hepatic storage, and TPP phosphorylation), but other etiologies include hyperemesis gravidarum, bariatric surgery (especially Roux-en-Y gastric bypass), prolonged vomiting, anorexia nervosa, refeeding syndrome, prolonged TPN without supplementation, and cancer-related malnutrition....