Wernicke encephalopathy

Not to be confused with Wernicke aphasia.

Wernicke encephalopathy
Other namesWernicke's disease
Hypothalamus
SpecialtyNeurology Edit this on Wikidata
SymptomsAtaxia, ophthalmoplegia, confusion
CausesThiamine deficency
Risk factorsAlcohol use disorder, malnutrition

Wernicke encephalopathy (WE), also Wernicke's encephalopathy,[1] or wet brain is the presence of neurological symptoms caused by biochemical lesions of the central nervous system after exhaustion of B-vitamin reserves, in particular thiamine (vitamin B1).[2] The condition is part of a larger group of thiamine deficiency disorders that includes beriberi, in all its forms, and alcoholic Korsakoff syndrome. When it occurs simultaneously with alcoholic Korsakoff syndrome it is known as Wernicke–Korsakoff syndrome.[3][4]

Classically, Wernicke encephalopathy is characterised by a triad of symptoms: ophthalmoplegia, ataxia, and confusion. Around 10% of patients exhibit all three features, and other symptoms may also be present.[5] While it is commonly regarded as a condition particular to malnourished people with alcohol misuse, it can be caused by a variety of diseases.[3][6] It is treated with thiamine supplementation, which can lead to improvement of the symptoms and often complete resolution, particularly in those where alcohol misuse is not the underlying cause.[7] Often other nutrients also need to be replaced, depending on the cause. Medical literature notes how managing the condition in a timely fashion can avoid worsening symptoms.[6][8][9]

Wernicke encephalopathy may be present in the general population with a prevalence of around 2%, and is considered underdiagnosed; probably, many cases are in patients who do not have commonly-associated symptoms.[10]

  1. ^ "Wernicke Encephalopathy". MeSH Browser. U.S. National Library of Medicine.
  2. ^ Oudman E, Oey MJ, Batjes D, van Dam M, van Dorp M, Postma A, Wijnia JW (December 2022). "Wernicke-Korsakoff syndrome diagnostics and rehabilitation in the post-acute phase". Addiction Neuroscience. 4: 100043. doi:10.1016/j.addicn.2022.100043. ISSN 2772-3925. S2CID 253296206.
  3. ^ a b [unreliable medical source?]Sullivan EV, Fama R (June 2012). "Wernicke's encephalopathy and Korsakoff's syndrome revisited". Neuropsychology Review. 22 (2): 69–71. doi:10.1007/s11065-012-9205-2. PMC 4723427. PMID 22588370.
  4. ^ Ropper A, Brown R. Princ. of Neurology, Adams & Victor. 8º ed. McGraw Hill 2007.
  5. ^ Cook CC (2000). "Prevention and treatment of Wernicke-Korsakoff syndrome". Alcohol and Alcoholism. 35 (1): 19–20. doi:10.1093/alcalc/35.Supplement_1.19. PMID 11304070. S2CID 45726575.
  6. ^ a b Galvin R, Bråthen G, Ivashynka A, Hillbom M, Tanasescu R, Leone MA (December 2010). "EFNS guidelines for diagnosis, therapy and prevention of Wernicke encephalopathy". European Journal of Neurology. 17 (12): 1408–1418. doi:10.1111/j.1468-1331.2010.03153.x. PMID 20642790. S2CID 8167574.
  7. ^ Sechi G, Serra A (May 2007). "Wernicke's encephalopathy: new clinical settings and recent advances in diagnosis and management". The Lancet. Neurology. 6 (5): 442–455. doi:10.1016/s1474-4422(07)70104-7. PMID 17434099. S2CID 15523083.
  8. ^ Arts NJ, Pitel AL, Kessels RP (1 January 2021), Swaab DF, Kreier F, Lucassen PJ, Salehi A (eds.), "Chapter 29 - The contribution of mamillary body damage to Wernicke's encephalopathy and Korsakoff's syndrome", Handbook of Clinical Neurology, The Human Hypothalamus, 180, Elsevier: 455–475, doi:10.1016/b978-0-12-820107-7.00029-x, ISBN 9780128201077, PMID 34225949, S2CID 235746125, retrieved 18 November 2022
  9. ^ Oudman E, Wijnia JW, Oey MJ, van Dam M, Postma A (July 2021). "Wernicke-Korsakoff syndrome despite no alcohol abuse: A summary of systematic reports". Journal of the Neurological Sciences. 426: 117482. doi:10.1016/j.jns.2021.117482. PMID 34000679. S2CID 234769882.
  10. ^ Isenberg-Grzeda E, Kutner HE, Nicolson SE (2012). "Wernicke-Korsakoff-syndrome: under-recognized and under-treated". Psychosomatics. 53 (6): 507–516. doi:10.1016/j.psym.2012.04.008. PMID 23157990.