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12 Jan L’encefalopatia di Wernicke colpisce più frequentemente soggetti etilisti cronici, ma può complicare molte condizioni di malnutrizione in. 30 Aug Wernicke-Korsakoff syndrome is the best known neurologic complication of thiamine (vitamin B1) deficiency [1]. The term refers to two different. Abstract. GRANDEZ-URBINA, J. Antonio et al. Wernicke Korsakoff disease in hyperemesis gravidarum: Case presentation at the Hospital Hipólito Unanue, Lima.

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There do not appear to be studies investigating or suggesting a genetic susceptibility of one racial group or sexual predisposition. Diagnosis of Wernicke encephalopathy or disease is made clinically. Infants breastfed by mothers with inadequate intake of thiamine [ 24 ].

Sign Up It’s Free! Thiamine-deficient formula [ 11 ]. Following this an immediate intravenous or intramuscular dose of thiamine should be administered [32] two or three times daily. Case Report and Review of the Literature”. Received salary from Medscape for employment. Average age at onset of WE is 50 years.

Wernicke encephalopathy

Thiamine is an essential vitamin critical to glucose metabolism. Despite its name, WE is not related to Wernicke’s area, a region of the brain associated with speech and language interpretation.


Alcohol abuse Malnutrition Central nervous system disorders Vitamin deficiencies Thiamine Medical triads. Memory disorder may be permanent. The patients, 2 males with alcoholism and a female with persistent vomiting following sulfuric acid ingestion, exhibited these findings, developed coma, and eventually died.

Patients who have undergone gastric bypass surgery are recommended to adhere to a balanced diet and continue vitamin supplementation. This website also contains material copyrighted by 3rd parties. Thiamine plays a vital role in the metabolism of carbohydrates. Acidosis affecting periventricular structures i. Monitoring of an acute case for twelve years. However, in actuality, only a small percentage of patients experience all three symptoms, [8] and the full triad occurs more frequently among those who have overused alcohol.

Pathophysiology Thiamine is absorbed from the duodenum.

Practice Essentials An important cause of acute or subacute delirium, Wernicke encephalopathy WE is a neurological disorder induced by thiamine, vitamin B1, deficiency. Pharmacokinetics of high-dose oral thiamine hydrochloride in healthy subjects. Rivastigmine in Wernicke-Korsakoff’s syndrome: Diverse MRI signal intensities with Wernicke encephalopathy. Need a Curbside Consult?

Wernicke-Korsakoff Syndrome: Background, Etiology, Pathophysiology

Articles Cases Courses Quiz. A placebo-controlled study of memantine Ebixa in dementia of Wernicke-Korsakoff syndrome. Visual disturbance after bariatric surgery. Rapid development of central pontine myelinolysis after recovery from Wernicke encephalopathy: Risk of thiamine deficiency and Wernicke’s encephalopathy after gastrointestinal surgery for cancer.


Without thiamine, glucose is metabolized through less efficient anaerobic pathways that produce lactic acid. These cases include patients with AIDS, individuals receiving hemodialysis, persons with hyperemesis gravidarum, and patients with malignancy with or without chemotherapy.

WE may develop in nonalcoholic conditions, such as prolonged starvation, hyperemesis gravidarum, and bariatric surgery. Elevated Lactate Secondary to Gastrointestinal Beriberi.

Early symptoms are nonspecific, [33] [34] and it has been stated that WE may present nonspecific findings. Herpesvirus-6 encephalitis complicated by Wernicke-Korsakoff syndrome in a encefaalopatia recipient of unrelated cord blood transplantation. Thiamine, also called B1, helps to break down glucose.

Wernicke’s encephalopathy in a patient with unresectable gastric carcinoma and literature review. Clin Lymphoma Myeloma Leuk. Support Radiopaedia and see fewer ads. Concurrent toxic effects of alcohol should also be considered.

What would you like to print? The natural history and pathophysiology of Wernicke’s Encephalopathy and Korsakoff’s Psychosis.

If cells with high metabolic requirements have inadequate stores of thiamine to draw from, energy production drops, and neuronal damage ensues.