Wernicke's encephalopathy (WE) is a neurological disorder caused by thiamine (vitamin B1) deficiency. Thiamine is essential for the metabolism of carbohydrates; and deficiency results in lactic acid accumulation secondary to altered glucose metabolization. This gives rise to neurotoxic edema and oxidative stress that affects multiple brain structures.

Thiamine cannot be synthesized in the human body; and is only available via oral ingestion. However, thiamine is present in sufficient quantifies most “normal” diets. Where deficiency does occur, this should be viewed as an imbalance between availability and consumption.

Conditions that lead to diminished availability include malabsorption (e.g., due to inflammatory bowel disease) and malnutrition (e.g., due to chronic alcohol abuse or eating disorders). Conditions that give rise to increased consumption include increased metabolism (e.g., sepsis or malignancy), or increased carbohydrate intake in in predisposed individuals (e.g., IV dextrose administration to an already thiamine-deficient patient).

Diplopia is a classic symptom. This may be due to lesions of cranial nerves III, IV, or VI; or gaze palsies such as internuclear ophthalmoplegia.

WE is more frequent in alcoholic patients, in whom it often presents as a subclinical syndrome.