Wernicke's encephalopathy
From Wikipedia, the free encyclopedia
| Wernicke encephalopathy Classification and external resources |
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| Thiamine | |
| ICD-10 | E51.2 |
| ICD-9 | 265.1 |
| eMedicine | emerg/642 |
Wernicke encephalopathy is a syndrome characterised by ataxia, ophthalmoplegia, confusion, and impairment of short-term memory.[1][2] It is caused by lesions in the medial thalamic nuclei, mammillary bodies, periaqueductal and periventricular brainstem nuclei, and superior cerebellar vermis, often resulting from inadequate intake or absorption of thiamine (Vitamin B1)[1], especially in conjunction with carbohydrate ingestion.[1] Its most common correlate is prolonged alcohol consumption resulting in thiamine deficiency. Alcoholics are therefore particularly at risk, but it may also occur with thiamine deficiency states arising from other causes, particularly in patients with such gastric disorders as carcinoma, chronic gastritis, and repetitive vomiting.[3][4]
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[edit] Presentation
Wernicke encephalopathy begins abruptly, usually with eye movement disorders (nystagmus, gaze palsies, and ophthalmoplegia, especially of the lateral rectus muscles), gait ataxia, confusion, confabulation, and short-term memory loss.
The classic triad of the syndrome is encephalopathy (brain damage), ophthalmoplegia (eye paralysis), and ataxia (loss of coordination). Untreated, it may progress to Korsakoff's psychosis, coma, and death.[1][2] The pathological changes seen in Wernicke's encephalopathy are concentrated in the mammillary bodies, cranial nerve nuclei III, IV, VI and VIII, the thalamus, hypothalamus, periaqueductal grey, cerebellar vermis, and the dorsal nucleus of the vagus nerve. The ataxia and ophthalmoparesis are related to lesions in the oculomotor, trochlear, abducens, and vestibular (IIIrd, IVth, VIth, and VIIIth cranial) nerve nuclei.
Despite its name, Wernicke's encephalopathy is not related to Wernicke's area, a region of the brain associated with speech and language interpretation. (See Wernicke's aphasia.)
[edit] Treatment
Treatment begins with intravenous or intramuscular injection of thiamine, followed by assessment of central nervous system and metabolic conditions. In the presence of sub-clinical thiamine deficiency, a large dose of sugar (especially glucose) can precipitate the onset of overt encephalopathy[5]; therefore, correcting hypoglycemia should not be attempted before thiamine replenishment. Rehydration to restore blood volume should follow, as needed.
When treated early, recovery may be rapid and complete; though there are almost always some minor neurological signs that persist.
[edit] See also
[edit] References
- ^ 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
- ^ a b Beers, Mark H. et al (2006), The Merck Manual of Diagnosis and Therapy (18th ed.), pages 1688-1689. Merck Research Laboratories 2006, ISBN 0911910-18-2
- ^ Kumar, Vinay, Abbas, Abul K., Fausto, Nelson (2005), Pathologic Basis of Disease (7th ed.), page 1399, Elsevier Saunders. ISBN 0-8089-2302-1
- ^ Sullivan, Joseph; Hamilton, Roy; Hurford, Matthew; Galetta, Steven L.; Liu, Grant T. (2006), "Neuro-Ophthalmic Findings in Wernicke's Encephalopathy after Gastric Bypass Surgery," Neuro-Ophthalmology, Jul/Aug2006, Vol. 30 Issue 4, p85-89.
- ^ Zimitat C, Nixon P, (2000). "Glucose loading precipitates encephalopathy in thiamine-deficient rats.". Metabolic Brain Disease 14 (1): 1-10.
[edit] External links
- The Merck Manual, Amnesias - Wernicke's encephalopathy
- Images of Wernicke's encephalopathy MR and Gross Brain Pictures
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