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Wernicke Encephalopathy

Practice Essentials

An important cause of acute or subacute delirium, Wernicke encephalopathy (WE) is a neurological disorder induced by thiamine, vitamin B1, deficiency. WE is the most important encephalopathy due to a single vitamin deficiency. WE presents with the classic triad of ocular findings, cerebellar dysfunction, and confusion.

Korsakoff amnestic syndrome is a late neuropsychiatric manifestation of WE with memory loss and confabulation; sometimes, the condition is referred to as Wernicke-Korsakoff syndrome (WKS) or Wernicke-Korsakoff psychosis.

Thiamine deficiency is characteristically associated with chronic alcoholism, because alcohol affects thiamine uptake and utilization. However, WE may develop in nonalcoholic conditions, such as prolonged starvation, hyperemesis gravidarum, bariatric surgery, and human immunodeficiency virus (HIV)/acquired immunodeficiency syndrome (AIDS), and can even develop in healthy infants given the thiamine deficient formulas.

Frequently unrecognized, WE is more prevalent than commonly supposed. Epidemics of WE can occur, as evidenced by a report of Israeli infants with infantile thiamine deficiency who were fed formula deficient in thiamine.

Signs and symptoms

In addition to the classical triad of symptoms—encephalopathy, ataxic gait, and oculomotor dysfunction—clinical signs of WE may include the following:

Acute confusion




Memory disturbance

Hypothermia with hypotension

Delirium tremens


The clinical diagnosis of WE in alcoholics requires two of the following four signs: (i) dietary deficiencies (ii) eye signs, (iii) cerebellar dysfunction, and (iv) either an altered mental state or mild memory impairment. 

Although WE remains a clinical diagnosis with no characteristic abnormalities in diagnostic studies, the use of laboratory and radiographic tests remains important to exclude alternate or coexisting medical conditions.


Rapid correction of brain thiamine deficiency is the goal of therapy.
Administration of thiamine improves the patient’s condition to some degree in almost all cases; however, persistent neurologic dysfunction is common.
Oral absorption is unreliable in patients at risk of Wernicke encephalopathy, which emphasizes the importance of parenteral treatment.

Although as little as 2 mg of thiamine may be enough to reverse symptoms, the dose of thiamine required to prevent or treat WE in most alcoholic patients may be as high as greater than 500 mg given once or, preferably, 2 or 3 times daily parenterally, intravenous is preferred to intramuscular administration. 

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