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Wernicke's encephalopathy

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Thiamine-2D-skeletal.png|
Wernicke encephalopathy
ICD-10 E512
ICD-9 265.1
OMIM [1]
DiseasesDB [2]
MedlinePlus [3]
eMedicine emerg/642
MeSH {{{MeshNumber}}}


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, and is the result of inadequate intake or absorption of thiamine (Vitamin B1) coupled with continued carbohydrate ingestion.[1] The most common cause of an onset is severe alcoholism, but it may 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]

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][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

Treatment includes an intravenous (IV) or intramuscular (IM) injection of thiamine, as well as the active exclusion of 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.

If the patient is hypoglycaemic (common in alcoholism), a glucose infusion should always be preceded with thiamine infusion. Glucose depletes thiamine stores in the brain, acutely worsening Wernicke's encephalopathy.

See also

References

1. ^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. ^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


External links


{enWP|Wernicke's encephalopathy}}

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