Wernicke's encephalopathy 526664 222855020 2008-07-01T13:06:12Z DOI bot 6652755 Citation maintenance. Formatted: title. You can [[WP:DOI|use this bot]] yourself! Please [[User:DOI_bot/bugs|report any bugs]]. {{Infobox_Disease | Name = Wernicke encephalopathy | Image = Thiamine-2D-skeletal.png | Caption = [[Thiamine]] | DiseasesDB = | ICD10 = {{ICD10|E|51|2|e|50}} | ICD9 = {{ICD9|265.1}} | ICDO = | OMIM = | MedlinePlus = | eMedicineSubj = emerg | eMedicineTopic = 642 | MeshID = }} '''Wernicke encephalopathy''' is a [[syndrome]] characterised by [[ataxia]], [[ophthalmoplegia]], confusion, and impairment of [[short-term memory]].<ref name="Aminoff">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</ref><ref name="Beers">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</ref> 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]])<ref name="Aminoff"/>, especially in conjunction with [[carbohydrate]] ingestion.<ref name="Aminoff"/> Its most common correlate is prolonged alcohol consumption resulting in thiamine deficiency. [[Alcoholism|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.<ref name="Kumar">Kumar, Vinay, Abbas, Abul K., Fausto, Nelson (2005), ''Pathologic Basis of Disease (7th ed.)'', page 1399, Elsevier Saunders. ISBN 0-8089-2302-1</ref><ref name="Sullivan">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.</ref> ==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.<ref name="Aminoff"/><ref name="Beers"/> 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]].) ==Treatment== Treatment begins with [[intravenous]] or [[intramuscular]] [[Injection (medicine)|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<ref>{{cite journal |author=Zimitat C, Nixon P, |title= Glucose loading precipitates encephalopathy in thiamine-deficient rats |journal= Metabolic Brain Disease |volume=14 |issue=1 |pages=1–10 |year=2000 |doi= 10.1023/A:1020653312697 }}</ref>; 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. == See also == * [[Karl Wernicke]] * [[ataxia]] * [[Beriberi]] * [[human brain]] * [[thiamine]] * [[Korsakoff's syndrome]] * [[Wernicke-Korsakoff syndrome]] == References == {{reflist}} == External links == *[http://www.merck.com/mrkshared/mmanual/section14/chapter169/169e.jsp The Merck Manual, Amnesias - Wernicke's encephalopathy] *[http://rad.usuhs.edu/medpix/medpix_cow.html?mode=quiz&pt_id=11885&quiz=no#top Images of Wernicke's encephalopathy] MR and Gross Brain Pictures {{Nutritional pathology}} [[Category:Neurological disorders]] [[de:Wernicke-Enzephalopathie]] [[es:Encefalopatía de Wernicke]] [[fr:Encéphalopathie de Wernicke]] [[ja:ウェルニッケ脳症]] [[pl:Encefalopatia Wernickego]] [[pt:Encefalopatia de Wernicke]] [[fi:Wernicken enkefalopatia]]