Wernicke’s encephalopathy is a serious neurological condition that results primarily from a deficiency of the nutrient thiamine which is also known as Vitamin B1. This condition is an inflammatory, hemorrhagic, degenerative condition of the brain. It is characterized by lesions in several parts of the brain, including the hypothalamus, mammillary bodies, and tissues surrounding the ventricles and aqueducts, double vision, ophthalmoplegia, involuntary and rapid movements of the eyes, lack of muscular coordination, and decreased mental function, which may be mild or severe. The disease is comprised of three main symptoms: mental confusion, lack of muscle coordination, and a paralysis of the muscles which control eye movements.
- The male-to-female ratio is 1.7:1, likely owing to alcoholism being 3-4 times more frequent in men than in women.
- Wernicke encephalopathy have placed the incidence between 0.8% and 2.8% of the general population
- The incidence can be as high as 12.5% in a population of alcoholics
- This disease is caused by a lack of thiamin (vitamin B1), which leads to problems with the normal functioning of the brain.
- Thiamine deficiency is characteristically associated with chronic alcoholism, because it affects thiamine uptake and utilization. Most cases of Wernicke’s encephalopathy are rooted in chronic alcohol abuse. Alcohol can, over time, severely impair the body’s ability to absorb thiamine, gradually leading to a deficiency of this nutrient. When someone who is known to abuse alcohol has symptoms such as confusion and gait ataxia, meaning lack of coordination in walking, Wernicke’s encephalopathy should be considered as a possible cause.
- Wernicke encephalopathy may develop in nonalcoholic conditions such as:
- prolonged starvation
- hyperemesis gravidarum (continuous nausea and vomiting during pregnancy)
- bariatric surgery and other gastric bypass surgeries
- healthy infants given the wrong formulas
- complication of GI tract disease
- Cancers that have spread throughout the body
- Heart failure (when treated with long-term diuretic therapy)
- Long periods of intravenous (IV) therapy without receiving thiamine supplements
- Long-term dialysis
- Very high thyroid hormone levels (thyrotoxicosis)
- Chronic renal failure
- Carbohydrate loading in the presence of marginal thiamine stores (feeding after starvation)
- Absence of thiamine from the diet (in the case of infants fed formula without the addition of thiamine)
- Congenital transketolase function abnormalities