Last updated on:August 21st, 2021
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).
Altered mentation is the most frequent symptom. This can manifest as: cognitive impairment, including impairment of memory and an inability to concentrate; delirium; spatial disorientation; dizziness; drowsiness; apathy; coma; or, death. Altered mentation is believed to occur due to lesions affecting the dorsomedial thalamus, mammillary bodies, and cerebral cortex.
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.
Patients should be asked about their diet, and if they have any conditions that might impact nutrition, including: alcoholism, malignancies, gastrointestinal disease, gastrointestinal surgery.
WE is more frequent in alcoholic patients, in whom it often presents as a subclinical syndrome.
Loss of balance
Patients may present with loss of balance and falls. This is due to ataxia.