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Wernicke's encephalopathy

Wernicke encephalopathy
Classification & external resources
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][2] 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.[3][4]



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][2] 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 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. [5]. If the patient is hypoglycemic (common in alcoholism), a thiamin injection should always precede the glucose infusion.

See also


  1. ^ a b c d Aminoff, Michael J, Greenberg, David A., Simon, Roger P. (2005) Clinical Neurology (6th ed.). page 113 Lange Medical Books/McGraw-Hill. ISBN 0-07-142360-5
  2. ^ a b Beers, Mark H. et al (2006), The Merck Manual of Diagnosis and Therapy (18th ed.), pages 1688-1689, Merk Research Laboratories 2006, ISBN 0911910-18-2
  3. ^ Kumar, Vinay, Abbas, Abul K., Fausto, Nelson (2005), Pathologic Basis of Disease (7th ed.), page 1399, Elsevier Saunders. ISBN 0-8089-2302-1
  4. ^ Sullivan, Joseph; Hamilton, Roy; Hurford, Matthew; Galetta, Steven L; Liu Grant T (2006), "Neuro-Opthalmic Findings in Wernicke's Encephalopathy after Gastric Bypass Surgery", Neuro-Ophthalmology, Jul/Aug2006, Vol. 30 Issue 4, p85-89
  5. ^ Zimitat C, Nixon P, (2000). "Glucose loading precipitates encephalopathy in thiamine-deficient rats.". Metabolic Brain Disease 14 (1): 1-10.
This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Wernicke's_encephalopathy". A list of authors is available in Wikipedia.
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