special subjects
Wernicke Encephalopathy
Introduction
Wernicke encephalopathy is characterized by acute onset of confusion, nystagmus, partial ophthalmoplegia, and ataxia due to Thiamin Deficiency . Diagnosis is primarily clinical. The disorder may remit with treatment, persist, or degenerate into Wernicke encephalopathy results from inadequate intake or absorption of thiamin plus continued carbohydrate ingestion. Severe Alcohol Toxicity and Withdrawal is a common underlying condition. Excessive alcohol intake interferes with thiamin absorption from the gastrointestinal tract and hepatic storage of thiamin; the poor nutrition associated with alcoholism often precludes adequate thiamin intake. Wernicke encephalopathy may also result from other conditions that cause prolonged undernutrition or vitamin deficiency (eg, recurrent dialysis, hyperemesis, starvation, gastric plication, cancer, AIDS). Giving a carbohydrate load to patients with thiamin deficiency (ie, refeeding after starvation or giving IVdextrose-containing solutions to high-risk patients) can trigger Wernicke encephalopathy. Not all people who misuse alcohol and are thiamin-deficient develop Wernicke encephalopathy, suggesting that other factors may be involved. Genetic abnormalities that result in a defective form of transketolase, an enzyme that processes thiamin, may be involved. Characteristically, central nervous system lesions are symmetrically distributed around the 3rd ventricle, aqueduct, and 4th ventricle. Changes in the mamillary bodies, dorsomedial thalamus, locus ceruleus, periaqueductal gray matter, ocular motor nuclei, and vestibular nuclei are common. 