Wernicke's encephalopathy
You don't need to be Editor-In-Chief to add or edit content to WikiDoc. You can begin to add to or edit text on this WikiDoc page by clicking on the edit button at the top of this page. Next enter or edit the information that you would like to appear here. Once you are done editing, scroll down and click the Save page button at the bottom of the page.
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Phone:617-525-6884
Please Take Over This Page and Apply to be Editor-In-Chief for this topic: There can be one or more than one Editor-In-Chief. You may also apply to be an Associate Editor-In-Chief of one of the subtopics below. Please mail us [2] to indicate your interest in serving either as an Editor-In-Chief of the entire topic or as an Associate Editor-In-Chief for a subtopic. Please be sure to attach your CV and or biographical sketch.
Overview
| Wernicke encephalopathy Classification and external resources | |
| Thiamine | |
| ICD-10 | E51.2 |
| ICD-9 | 265.1 |
| eMedicine | emerg/642 |
Wernicke encephalopathy is a severe syndrome characterised by ataxia, ophthalmoplegia, confusion and loss of short-term memory.[1][1] It is linked to damage to the medial thalamic nuclei, mammillary bodies, periaqueductal, and periventricular brainstem nuclei , and superior cerebellar vermis. In the brain, it is the result of inadequate intake or absorption of thiamine (Vitamin B)[1] coupled with continued carbohydrate ingestion.[1] The most common cause of an onset is prolonged alcohol consumption that is sufficient enough to cause a thiamine deficiency. Alcoholics are therefore particularly at risk, but it may also occur due to other causes of malnutrition. Other causes of thiamine deficiency may be found in patients with carcinoma, chronic gastritis, or continuous vomiting.[1][1]
Presentation
Wernicke encephalopathy onsets acutely, and usually presents with nystagmus, gaze palsies, ophthalmoplegia (especially of the abducens nerve, CN VI), gait ataxia, confusion, and short-term memory loss.
The classic triad for this disease is encephalopathy, ophthalmoplegia, and ataxia. Untreated, this condition may progress to Korsakoff's psychosis or coma.[1][1] Despite its name, Wernicke's encephalopathy is not related to damage of the speech and language interpretation area named Wernicke's area (see Wernicke's aphasia). Instead the pathological changes in Wernicke's encephalopathy are concentrated in the mammillary bodies, cranial nerve nuclei III, IV, VI and VIII, as well as the thalamus, hypothalamus, periaquiductal grey, cerebellar vermis and the dorsal nucleus of the vagus nerve. The ataxia and ophthalmoparesis relate to lesions in the oculomotor (ie IIIrd, IVth, and VIth nerves) and vestibular (ie VIIIth nerve) nuclei.
Treatment
Treatment includes an intravenous (IV) or intramuscular (IM) injection of thiamine, prior to the assessment of other central nervous system (CNS) diseases or other metabolic disturbances. Patients are usually dehydrated, and so rehydration to restore blood volume should be started. If the condition is treated early, recovery may be rapid and complete.
In individuals with sub-clinical thiamine deficiency, a large dose of glucose (either as sweet food etc or glucose infusion), can precipitate the onset of overt encephalopathy. Glucose loading results in metabolic disturbances in the brain that exacerbate the signs and symptoms of encephalopathy, and may trigger cellular processes leading to brain damage. [1]. If the patient is hypoglycemic (common in alcoholism), a thiamin injection should always precede the glucose infusion.
See also
References
External links
Nutritional pathology (E40-68, 260-269) | |
|---|---|
| Malnutrition | Kwashiorkor - Marasmus - Catabolysis |
| Avitaminosis | B vitamins: B1: Beriberi/Wernicke's encephalopathy, B2: Ariboflavinosis, B3: Pellagra, B6: Pyridoxine deficiency, B7: Biotin deficiency, B9: Folate deficiency, B12: Vitamin B12 deficiency other vitamins: A: Vitamin A deficiency/Bitot's spots, C: Scurvy, D: Rickets/Osteomalacia |
| Mineral deficiency | Zinc deficiency - Iron deficiency - Magnesium deficiency - Chromium deficiency |
| Hyperalimentation | Obesity - Vitamin poisoning (Hypervitaminosis A, Hypervitaminosis D, Hypervitaminosis E) |
ja:ウェルニッケ脳症fi:Wernicken enkefalopatia
Acknowledgement and Attribution Regarding Sources of Content
Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .

