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Wernicke's encephalopathy: causes, symptoms, diagnosis, treatment
Medical expert of the article
Last reviewed: 07.07.2025
Wernicke encephalopathy is characterized by acute onset, confusion, nystagmus, partial ophthalmoplegia, and ataxia due to thiamine deficiency. Diagnosis is primarily clinical. The disorder may improve with treatment, persist, or progress to Korsakoff's psychosis. Treatment consists of thiamine and general measures.
Wernicke encephalopathy results from inadequate intake and absorption of thiamine in combination with continued carbohydrate ingestion. Severe alcoholism is often an underlying condition. Excessive alcohol consumption interferes with thiamine absorption from the gastrointestinal tract and thiamine accumulation in the liver. Poor nutrition associated with alcoholism often prevents adequate thiamine intake. Wernicke encephalopathy may also result from other conditions that cause prolonged malnutrition or vitamin deficiency (eg, repetitive dialysis, persistent vomiting, fasting, gastric plication, cancer, AIDS). Carbohydrate loading of thiamine-deficient patients (ie, feeding after fasting or giving IV dextrose-containing solutions to high-risk patients) may precipitate Wernicke encephalopathy.
Not all patients with alcohol abuse and thiamine deficiency develop Wernicke's encephalopathy, suggesting that other factors may be involved. Genetic changes that result in abnormal forms of transketolase, an enzyme involved in thiamine metabolism, may be involved in the disease.
The lesion is characteristically distributed symmetrically around the 3rd ventricle, aqueduct, and 4th ventricle. Changes in the mammillary bodies, dorsomedial thalamus, blue spot, gray matter around the aqueduct, oculomotor and vestibular nuclei are often detected.
Symptoms of Wernicke's Encephalopathy
Clinical changes occur acutely. Oculomotor disturbances are common, including horizontal and vertical nystagmus, partial ophthalmoplegia (eg, gaze abduction palsy, conjugation palsy). Pupillary response may be abnormal, sluggish or asymmetrical.
Vestibular dysfunction without hearing loss is often observed, the oculovestibular reflex may be impaired. Ataxic gait may be the result of vestibular disorders or cerebellar dysfunction, the gait is wide, slow, with short steps.
General confusion characterized by gross disorientation, indifference, inattention, drowsiness, or stupor is often present. Peripheral nerve pain thresholds are often elevated, and many patients develop severe autonomic dysfunction characterized by sympathetic hyperactivity (eg, tremor, agitation) or hypoactivity (eg, hypothermia, postural hypotension, syncope). If untreated, stupor may progress to coma and then death.
Diagnosis, prognosis and treatment of Wernicke's encephalopathy
The diagnosis is clinical and depends on recognition of underlying malnutrition or vitamin deficiency. There are no characteristic changes in cerebrospinal fluid, evoked potentials, brain imaging, or EEG. However, these studies, as well as laboratory tests (eg, blood count, blood glucose, blood count, liver function tests, arterial blood gases, toxicology screening), are needed to exclude other etiologies.
The prognosis depends on the timeliness of diagnosis. Early treatment can correct all abnormalities. Eye symptoms begin to subside within 24 hours of early administration of thiamine. Ataxia and confusion may persist for days or months. If untreated, the disorder progresses; mortality reaches 10-20%. Korsakoff's psychosis develops in 80% of surviving patients (this combination is called Wernicke-Korsakoff syndrome).
Treatment consists of immediate administration of thiamine 100 mg intravenously or intramuscularly, then daily for at least 3-5 days. Magnesium is an essential cofactor in thiamine metabolism, and hypomagnesemia should be corrected with magnesium sulfate 1-2 g intramuscularly or intravenously every 6-8 hours or magnesium oxide 400-800 mg orally once daily. General treatment consists of rehydration, correction of electrolyte disturbances, and restoration of adequate nutrition, including multivitamins. Patients with advanced disorder require hospitalization. Alcohol cessation is mandatory.
Because Wernicke encephalopathy is preventable, all malnourished patients should be given thiamine (usually 100 mg IM, then 50 mg PO daily) plus vitamin B12 and folate (both 1 mg/day orally), especially if intravenous dextrose is necessary. It is prudent to give thiamine before any treatment in patients with altered consciousness. Malnourished patients should continue thiamine after hospital discharge.
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