Psychology Wiki
Don't have an account?
Register
Advertisement
Register
in: Pages with reference errors, Pages with incomplete PMID references, Pages using ISBN magic links,
and 5 more

Wernicke's encephalopathy

Revision as of 15:11, 7 November 2013 by Dr Joe Kiff (Message Wall | contribs) (→‎See also)
Sign in to edit
This article describes the neurological syndrome Wernicke encephalopathy. For other syndromes associated with the German physician Karl Wernicke, see Wernicke syndrome.
Wernicke's encephalopathy
Classification and external resources
ICD-10 E512
ICD-9 291.1

Wernicke's encephalopathy or now often Wernicke's disease refers to the presence of neurological symptoms caused by biochemical lesions of the central nervous system after exhaustion of B-vitamin reserves, in particular thiamine. The condition is part of a larger group of diseases related to vitamin B1 insufficiency, including beriberi in all its forms, and Korsakoff syndrome. When Wernicke's encephalopathy occurs simultaneously with Korsakoff syndrome it is known as Wernicke-Korsakoff syndrome.[1][2]

Classically, Wenicke's encephalopathy is characterised by the triad ophthalmoplegia, ataxia, and confusion. However, only 10% of patients exhibit all three features, and other symptoms may also be present.[3] While it is commonly regarded as a condition peculiar to malnourished people with alcohol misuse, a variety of diseases can lead to Wernicke's encephalopathy.[1][4] Wernicke's encephalopathy (WE) 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. Often other nutrients also need to be replaced, depending on the cause.

Wernicke encephalopathy may be present in the general population with a prevalence of around 2%, and is considered under diagnosed, probably many cases are patients do not have symptoms presumed to be associated with WE.[5]

File:Hypothalamus image.png

Hypothalamus.

Signs and symptoms

The classic triad of symptoms found in Wernicke's encephalopathy is:[6]

  • ophthalmoplegia (later expanded to other eye movement abnormalities, most commonly affecting the lateral rectus[6] or any eye sign).
  • ataxia (later expanded to imbalance or any cerebellar signs)
  • confusion (later expanded to other mental changes, including asthenia. Has 82% incidence in diagnosis cases)
  • the triad was also expanded to dietary deficiencies.

However, in actuality, only a small percentage of patients experience three of those four symptoms,[7] and occurs more frequently among those who have overused alcohol. Probably occurs in only 10% of patients (Harper1986).

Also a much more diverse range of symptoms has been found in patients with this condition, including:

Although hypothermia is usually diagnosed with a body temperature of 35 °C / 95° Fahrenheit, or less, incipient cooling caused by deregulation in the CNS, needs to be monitored because it can promote the development of an infection.[13] The patient may report feeling cold, followed by mild chills, cold skin, moderate pallor, tachycardia, hypertension, tremor or piloerection. External warming techniques are advised to prevent hypothermia.

  • Among the frequently altered autonomic functions are deregulation of the cardio circulatory system . There may be tachycardia, dyspnea, chest pain, orthostatic hypotension, changes in heart rate and blood pressure.[22] The lack of thiamine sometimes affects other major energy consumers, the myocardium, and patients may have developed cardiomegaly.[24] Heart failure with lactic acidosis syndrome has been observed.[25] Cardiac abnormalities are an aspect of the WE, which was not included in the traditional approach,[2][26] and can not be classified as a separate disease.

Infections have been pointed out as one of the most frequent triggers of death in WE.[26][27] Furthermore, infections are usually present in pediatric cases.[28][29]

In the last stage others symptoms may occur: hyperthermia, increased muscle tone, spastic paralysis, choreic dyskinesias and coma.

Because of the frequent involvement of heart, eyes and peripheral nervous system, several authors prefer to call it Wernicke disease rather than simply encephalopathy.[2][30]

Early symptoms are nonspecific,[31][32] and it has been stated that WE may present nonspecific findings.[33] In Wernicke Korsakoff’s syndrome some single symptoms are present in about one-third.[34]

File:Third ventricle small.gif

Ventricles.

Location of the lesion

Depending of the location of the brain lesion different symptoms are more frequent

  • Brainstem tegmentum. - Ocular: pupillary changes. Extraocular muscle palsy; gaze palsy: nystagmus.
  • Hypothalamus. Medulla: dorsal nuc. of vagus. - Autonomic dysfunct.: temperature; cardiocirculatory; respiratory.
  • Medulla: vestibular region. Cerebellum. - Ataxia.
  • Dorsomedial nuc. of thalamus. Mammillary bodies. - Amnestic syndrome for recent memory.
  • Diffuse cerebral dysfunction.- Altered cognition: global confusional state.
  • Brainstem: periaqueductal gray.- Reduction of consciousness[35]
  • Hypothalamic lesions may also affect the immune system, which is known in alcohol abusers, causing dysplasias and infections.

Korsakoff's syndrome

Korsakoff's syndrome, characterised by memory impairment, confabulation, confusion and personality changes, has a strong and recognised link with WE.[1][36] A very high percentage of patients with Wernicke-Korsakoff syndrome also have peripheral neuropathy, and many alcoholics have this neuropathy without other neurologic signs or symptoms.[37] Korsakoff´s occurs much more frequently in WE due to chronic alcoholism.[36] It is uncommon among those who do not consume alcohol abusively. Up to 80% of WE patients who abuse alcohol develop Korsakoff's syndrome.[38] In Korsakoff's, is usually observed atrophy of the thalamus and the mammillary bodies, and frontal lobe involvement. [33] In a study half of Wernicke-Korsakoff cases had good recovery from the amnesic state which may take from 2 months to 10 years.

Risk factors

Wernicke's encephalopathy has classically been thought of as a disease solely of alcoholics, but it is also found in the chronically undernourished, and in recent years had been discovered post bariatric surgery .[6][38] Without being exhaustive, the documented causes of Wernicke's encephalopathy have included:

  • pancreatitis, liver dysfunction, chronic diarrhea, celiac disease, Crohn disease, uremia,[38] thyrotoxicosis[39]
  • vomiting,[4] hyperemesis gravidarum,[39] malabsorption, gastrointestinal surgery or diseases[4]
  • incomplete parenteral nutrition,[39] starvation/fasting[4]
  • chemotherapy,[38] renal dialysis,[39] diuretic therapy,[39] stem cell/marrow transplantation[4]
  • cancer, AIDS,[40] Creutzfeldt-Jacob disease,[6][41] febrile infections[4]
  • this disease may even occur in some people with normal, or even high blood thiamine levels.[6] Selected genetic mutations, including presence of the X-linked transketolase-like 1 gene, SLC19A2 thiamine transporter protein mutations, and the aldehyde dehydrogenase-2 gene, which may predispose to alcoholism.[38] The APOE e3 allele, involved in Alzheimer's disease, may increase the chance of developing neurological symptoms.[38]
File:Diencephalon small.gif

Diencephalon.

Pathophysiology

Thiamine deficiency and errors of thiamine metabolism, are believed to be the primary cause of Wernicke encephalopathy. Thiamine, also called B1, helps to breakdown glucose. Specifically, it acts as an essential coenzyme to the TCA cycle and the pentose phosphate shunt. Thiamine is first metabolised to its more active form, thiamine diphosphate (TDP), before it is used. The body only has 2–3 weeks of thiamine reserves, which are readily exhausted without intake, or if depletion occurs rapidly, such as in chronic inflammatory states or in diabetes.[6][38] Thiamine is involved in:[38][42]

  1. Metabolism of carbohydrates, creating energy.
  2. Production of neurotransmitters including glutamic acid and GABA.
  3. Lipid metabolism, necessary for myelin production.
  4. Amino acid modification.
  5. Neuromodulation.[43]

Neuropathy

The primary neurological-related injury caused by thiamine deficiency in WE is three-fold: oxidative damage, mitochondrial injury leading to apoptosis, and directly stimulating a pro-apoptotic pathway.[43] Thiamine deficiency affects both neurons and astrocytes, glial cells of the brain. Thiamine deficiency alters the glutamate uptake of astrocytes, through changes in the expression of astrocytic glutamate transporters EAAT1 and EAAT2, leading to excitotoxicity. Other changes include those to the GABA transporter subtype GAT-3, GFAP, glutamine synthetase, and the Aquaporin 4 channel.[44] Focal lactic acidosis also causes secondary oedema, oxidative stress, inflammation and white matter damage.[45]

Pathological anatomy

Despite its name, WE is not related to Wernicke's area, a region of the brain associated with speech and language interpretation.

In most, early lesions completely reversed with immediate and adequate supplementation.

Lesions are usually symmetrical in the periventricular region, diencephalon, the midbrain, hypothalamus, and cerebellar vermis. Brainstem lesions may include cranical nerve III, IV, VI and VIII nuclei, the medial thalamic nuclei, and the dorsal nucleus of the vagus nerve. Oedema may be found in the regions surrounding the third ventricle, and fourth ventricle, also appearing petechiae and small hemorrhages.[46] Chronic cases can present the atrophy of the mammillary bodies.[47]

Endothelial proliferation, hyperplasia of capillaries, demyelination and neuronal loss can also occur.

An altered blood brain barrier may cause a perturbed response to certain drugs and foods.[48]

Diagnosis

Diagnosis of Wernicke's encephalopathy or disease is made clinically.[4][49] Caine et al. in 1997 established criteria that Wernicke's encephalopathy, can be diagnosed in any patient with just two or more of the main symptoms noted above.[50] The sensitivity of the diagnosis by the classic triad was 23% but increased to 85% taking two or more of the four classic features. All the cases he studied were alcoholics.

Some consider it sufficient to suspect the presence of the disease with only one of the principal symptoms.[51][52] Some British hospital protocols suspect WE with any one of these symptoms: confusion, decreased consciousness level (or unconsciousness, stupor or coma), memory loss, ataxia or unsteadiness, ophthalmoplegia or nystagmus, and unexplained hypotension with hypothermia. The presence of only one sign should be sufficient for treatment.[53]

File:Wernicke enceph MRIs.jpg

Brain MRIs in a WE patient. Arrows indicate hyperintense lesions in A, B and D. Arrow in C indicates enhancement of mammillary bodies.

As a much more diverse range of symptoms has been found frequently in patients it is necessary to search for new diagnostic criteria, however Wernicke's encephalopathy remains a clinically-diagnosed condition. Neither the MR, nor serum measurements related to thiamine are sufficient diagnostic markers in all cases. Non-recovery upon supplementation with thiamine is inconclusive.

The sensitivity of MR was 53% and the specificity was 93%. The reversible cytotoxic edema was considered the most characteristic lesion of WE. The location of the lesions were more frequently atypical among non-alcoholics, while typical contrast enhancement in the thalamus and the mammillary bodies was observed frequently associated with alcohol abuse.[47] These abnormalities may include:[6]

There appears to be little value for CT scans.[4]

Thiamine can be measured using an erythrocyte transketolase activity assay,[4] or by activation by measurement of in vitro thiamine diphosphate levels.[4] Normal thiamine levels do not necessarily rule out the presence of WE,[4] as this may be a patient with difficulties in intracellular transport.

Treatment

Most symptoms will improve quickly if deficiencies are treated early. Memory disorder may be permanent.[54]

In patients suspected of WE thiamine should be started immediately.[55] Blood should be immediately taken to test for thiamine, other vitamins and minerals levels. Following this an immediate intravenous or intramuscular dose of thiamine should be administered [30] two or three times daily. Thiamine administration is usually continued until clinical improvement ceases.

Considering the diversity of possible causes and several surprising symptomatologic presentations, and because there is low assumed risk of toxicity of thiamine, because the therapeutic response is often dramatic from the first day, some qualified authors indicate parenteral thiamine if WE is suspected, both as a resource for diagnosis and treatment.[4] The diagnosis is highly supported by the response to parenteral thiamine, but is not sufficient to be excluded by the lack of it.[56] Parenteral thiamine administration is associated with a very small risk of anaphylaxis.

Alcohol abusers may have poor dietary intakes of several vitamins and impaired thiamine absorption, metabolism, and storage and require higher doses.[31]

If glucose is given, such as in hypoglycaemic alcoholics, thiamine must be given concurrently. If this is not done, the glucose will rapidly consume the remaining thiamine reserves, exacerbating this condition.[38]

The observation of edema in MR, and also the finding of inflation and macrophages in tissues necropsied,[46] has led successfully administer antiinflammatorys.[57][58]

Other nutritional abnormalities should also be looked for, as they may be exacerbating the disease.[27][59] In particular, magnesium, a cofactor of transketolase which may induce or aggravate the disease.[38]

Other supplements may also be needed, including: cobalamin, ascorbic acid, folic acid, nicotinamide, zinc,[60][61] phosphorus (dicalcium phosphate)[62] and in some cases taurine, especially suitable when there cardiocirculatory impairment.[63][64] Patient-guided nutrition is suggested. In patients with Wernicke-Korsakoff syndrome, even higher doses of parenteral thiamine are recommended. Concurrent toxic effects of alcohol should also be considered.[65][66][67]

There are some patients that may lead normal lives with extraordinary high levels of thiamine in serum.

When symptoms persist beyond several supplements and anti-inflammatorys, other forms of therapy may also be needed.[48] As hypertrophy may occur, as well as hyperplasia of the capillaries, ginkgo biloba has sometimes been used to improve irrigation, Coenzyme Q10 (ubiquinone) to improve mitochondrial functions, or fluoxetine to control thermal regulation. Additionally, sulbutiamine has been useful in controlling exacerbation of fatigue.[48]

As often happens in neurological diseases, this encephalopathy can be exacerbated by reduced body temperature, physical exertion, infections, or certain drugs. This neurological deterioration is potentially dangerous because it predisposes the patient to hypothermia and decreased immunity, facilitating superimposed infections which in turn further aggravate the disease.[26] To overcome this cycle, neurological treatment is proposed. Possible infection can cause cytokines to be continually released,which can cause new adverse events from affected areas of the brain. Successful treatment can only be effective if infection is controlled. Gabapentin, with its relation to the inhibitory neurotransmitter GABA, has been tried prophylactically three times a day in low doses to reduce the effects and number of disordered responses to adverse external stimuli.[48]

File:Thalamus small.gif

Thalamus.

Prevention

There are hospital protocols for prevention, supplementing with thiamine in the presence of: history of alcohol misuse or related seizures, requirement for IV glucose, signs of malnutrition, poor diet, recent diarrhoea or vomiting, peripheral neuropathy, intercurrent illness, delirium tremens or treatment for DTs, and others.[53][68] Some experts advise parenteral thiamine should be given to all at-risk patients in the Emergency Room.[4]

In the clinical diagnosis should be remembered that early symptoms are nonspecific,[31][32] and it has been stated that WE may present nonspecific findings.[33] There is consensus to provide water soluble vitamins and minerals after gastric operations.

In some countries certain foods have been supplemented with thiamine, and have declining WE cases. Improvement is difficult to quantify because they applied several joint actions.

Avoid alcohol and have adequate nutrition restricts one of the main risk factors for developing the Wernicke-Korsakoff syndrome.

Epidemiology

There are no conclusive statistical studies, all figures are based on partial studies, and because of the ethical problems in conducting controlled trials are unlikely to be obtained in the future.

Wernicke´s lesions were observed in 0.8 to 2.8% of the general population autopsies, and 12.5% ​​of alcoholics. This figure increases to 35% of alcoholics if including cerebellar damage due to lack of thiamine.[69]

Most autopsy cases were from alcoholics. Autopsy series were performed in hospitals on the material available which is unlikely to be representative of the entire population. Considering the slight affectations, previous to the generation of observable lesions at necropsy, the percentage should be higher. There is evidence to indicate that Wernicke's encephalopathy is underdiagnosed.[7][70] For example, in one 1986 study, 80% of cases were diagnosed postmortem.[7] Is estimated that only 5–14% of patients with WE are diagnosed in life.[71]

In a series of autopsy studies held in Recife, Brazil, it was found that only 7 out of 36 had had alcoholic habits, and only a small minority had malnutrition.[72] In a reviewed of 53 published case reports from 2001 to 2011, the relationship with alcohol was also about 20% (10 out of 53 cases).[6]

In this statistic fetal and infant damage with upcoming intellectual limitations should be included.[73] WE is more likely to occur in males than females.[38] Among the minority who are diagnosed, mortality can reach 17%.[2] The main factors triggering death are thought to be infections and liver dysfunctions.[2]

File:Cerebellum small.gif

Cerebellum.

History

WE was first identified in 1881 by the German neurologist Carl Wernicke, although the link with thiamine was not identified until the 1930s. A similar presentation of this disease was described by the Russian psychiatrist Sergei Korsakoff in a series of articles published 1887-1891.[6]

Children

  • Infants and children. No one present clinical triad  : infections, heart diseases, etc.[28]
  • In children. infection on 22/36 cases, etc.[74]
  • Difficulties in diagnosing, pediatric statistics.[74]
  • Secondary microcephaly: poor transport of thiamine pyrophosphate.[75]

See also

References

  1. ↑ 1.0 1.1 1.2 Template:MEDRSSullivan, Edith V., Fama, Rosemary (2012). Wernicke's Encephalopathy and Korsakoff's Syndrome Revisited. Neuropsychology Review 22 (2): 69–71.
  2. ↑ 2.0 2.1 2.2 2.3 2.4 Ropper A, Brown R. Princ. of Neurology, Adams & Victor. 8º ed. McGraw Hill 2007.
  3. ↑ Cook CC (2000). Prevention and treatment of Wernicke-Korsakoff syndrome. Alcohol Alcohol Suppl 35 (1): 19–20.
  4. ↑ 4.00 4.01 4.02 4.03 4.04 4.05 4.06 4.07 4.08 4.09 4.10 4.11 4.12 Galvin R, Bråthen G, Ivashynka A, Hillbom M, Tanasescu R, Leone MA (December 2010). EFNS guidelines for diagnosis, therapy and prevention of Wernicke encephalopathy. Eur. J. Neurol. 17 (12): 1408–18.
  5. ↑ Isenberg-Grzeda E, Kutner HE, Nicolson SE (2012). Wernicke-Korsakoff-syndrome: under-recognized and under-treated. Psychosomatics 53 (6): 507–16.
  6. ↑ 6.0 6.1 6.2 6.3 6.4 6.5 6.6 6.7 6.8 6.9 Lough, Mary E. (2012). Wernicke's Encephalopathy: Expanding the Diagnostic Toolbox. Neuropsychology Review 22 (2): 181–194.
  7. ↑ 7.0 7.1 7.2 7.3 Harper, CG, Giles, M; Finlay-Jones, R (1986 Apr). Clinical signs in the Wernicke-Korsakoff complex: a retrospective analysis of 131 cases diagnosed at necropsy. Journal of neurology, neurosurgery, and psychiatry 49 (4): 341–5.
  8. ↑ PMID 2608577 (PMID 2608577)
    Citation will be completed automatically in a few minutes. Jump the queue or expand by hand
  9. ↑ Chitra, S, Lath, KV (2012 May). Wernicke's encephalopathy with visual loss in a patient with hyperemesis gravidarum. The Journal of the Association of Physicians of India 60: 53–6.
  10. ↑ 10.0 10.1 Truswell, AS (2000 Jun). Australian experience with the Wernicke-Korsakoff syndrome. Addiction (Abingdon, England) 95 (6): 829–32.
  11. ↑ Flabeau, O, Foubert-Samier, A; Meissner, W; Tison, F (2008 Aug 26). Hearing and seeing: Unusual early signs of Wernicke encephalopathy. Neurology 71 (9).
  12. ↑ Jethava, A, Dasanu, CA (2012 Nov-Dec). Acute Wernicke encephalopathy and sensorineural hearing loss complicating bariatric surgery. Connecticut medicine 76 (10): 603–5.
  13. ↑ 13.0 13.1 13.2 Tratado de Neurología, Codina Puiggros, pág. 823 y 824. ed.1994.
  14. ↑ Meierkord H, Boon P, Engelsen B, et al. (March 2010). EFNS guideline on the management of status epilepticus in adults. Eur. J. Neurol. 17 (3): 348–55.
  15. ↑ Kondo, K, Fujiwara, M; Murase, M; Kodera, Y; Akiyama, S; Ito, K; Takagi, H (1996 Aug). Severe acute metabolic acidosis and Wernicke's encephalopathy following chemotherapy with 5-fluorouracil and cisplatin: case report and review of the literature. Japanese journal of clinical oncology 26 (4): 234–6.
  16. ↑ Becker, JT, Furman, JM; Panisset, M; Smith, C (1990). Characteristics of the memory loss of a patient with Wernicke-Korsakoff's syndrome without alcoholism. Neuropsychologia 28 (2): 171–9.
  17. ↑ Zhang, G, Ding, H; Chen, H; Ye, X; Li, H; Lin, X; Ke, Z (2013 Jan). Thiamine nutritional status and depressive symptoms are inversely associated among older Chinese adults. The Journal of nutrition 143 (1): 53–8.
  18. ↑ Worden, RW, Allen, HM (2006 Mar-Apr). Wernicke's encephalopathy after gastric bypass that masqueraded as acute psychosis: a case report. Current surgery 63 (2): 114–6.
  19. ↑ Jiang, W, Gagliardi, JP; Raj, YP; Silvertooth, EJ; Christopher, EJ; Krishnan, KR (2006 Jan). Acute psychotic disorder after gastric bypass surgery: differential diagnosis and treatment. The American journal of psychiatry 163 (1): 15–9.
  20. ↑ Lindberg, MC, Oyler, RA (1990 Apr). Wernicke's encephalopathy. American family physician 41 (4): 1205–9.
  21. ↑ Mann, MW, Degos, JD (1987). in Wernicke's encephalopathy. Revue neurologique 143 (10): 684–6.
  22. ↑ 22.0 22.1 Rohkamm, Color Atlas of Neurology, page 148 , 2004 Thieme ISBN 3-13-130931
  23. ↑ Biller José. The Interface of Neurology and Internal Medicine. 2008. Lippincott Williams & Wilkins Ed.
  24. ↑ Ishiko T, Taguchi T, Takeguchi M, Saito H, Nanri K. Case of Wernicke's encephalopathy and subacute combined degeneration of the spinal cord due to vitamin deficiency showing changes in the bilateral corpus striatum and cardiac arrest due to beriberi heart disease.Brain Nerve. 2009 Sep;61(9):1069-73.ABSTRACT PMID 19803406
  25. ↑ Harper C, Fornes P, Duyckaerts C, Lecomte D, Hauw JJ. An international perspective on the prevalence of the WernickeKorsakoff syndrome. Metab Brain Dis 1995; 10: 17–24
  26. ↑ 26.0 26.1 26.2 Zarranz, Juan J. (2007). Neurologia. (4a ed. ed.). Madrid, España: Harcourt Brace De Espana Sa. pp. 821 (Spanish.). ISBN 8480862289.
  27. ↑ 27.0 27.1 Brown, Allan H. Ropper, Robert H. (2007). Principios de neurología de Adams y Victor, 8a, 1132 (Spanish.), México: McGraw-Hill.
  28. ↑ 28.0 28.1 PMID 10328278 (PMID 10328278)
    Citation will be completed automatically in a few minutes. Jump the queue or expand by hand
  29. ↑ PMID 15687431 (PMID 15687431)
    Citation will be completed automatically in a few minutes. Jump the queue or expand by hand
  30. ↑ 30.0 30.1 Harrison’s Neurology in Clinical Medicine, 2º Edition, ISBN 978-0-07-174123-1
  31. ↑ 31.0 31.1 31.2 Mc.Phee & Papadakis. Current Medical Diagnosis & Treatment 2009, Forty-Eighth Edition.Lange.The McGraw-Hill Companies, Inc
  32. ↑ 32.0 32.1 Merk Manuals.http://www.merckmanuals.com/professional/nutritional_disorders/vitamin_deficiency_dependency_and_toxicity/thiamin.html?qt=wernicke%20encephalopathy&alt=sh
  33. ↑ 33.0 33.1 33.2 G Sechi MD, A Serra MD. Wernicke Encephalopathy. Lancet Neurol 2007; 6: 442-55
  34. ↑ Wernicke Korsakoff’s syndrome. Page 48.http://www.alcohol.gov.au/internet/alcohol/publishing.nsf/Content/2C3FC9166082567DCA257260007F81F8/$File/alcprobguide.pdf
  35. ↑ Haberland, Catherine. Clinical neuropathology : text and color atlas / 2007 by Demos Medical Publishing/ page 200 / ISBN 978-1-888799-97-2
  36. ↑ 36.0 36.1 Thomson, A. D., Guerrini, Irene; Marshall, E. Jane (2012). The Evolution and Treatment of Korsakoff's Syndrome. Neuropsychology Review 22 (2): 81–92.
  37. ↑ Goldman: Cecil Medicine, Chapter 443, 2007, 23rd ed. Saunders, Elsevier.
  38. ↑ 38.00 38.01 38.02 38.03 38.04 38.05 38.06 38.07 38.08 38.09 38.10 Serra, A, Sechi, G; Singh, S; Kumar, A (2007 Aug 7). Wernicke encephalopathy after obesity surgery: a systematic review. Neurology 69 (6): 615; author reply 615–6. Cite error: Invalid <ref> tag; name "SECHI2007" defined multiple times with different content
  39. ↑ 39.0 39.1 39.2 39.3 39.4 http://www.nlm.nih.gov/medlineplus/ency/article/000771.htm
  40. ↑ L Ng, Kv, Nguyễn, LT (2013 Apr). The role of thiamine in HIV infection. International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases 17 (4): e221–7.
  41. ↑ Rosen, A, van Kuilenburg, A; Assmann, B; Kuhlen, M; Borkhardt, A (2011 May). Severe encephalopathy, lactic acidosis, vegetative instability and neuropathy with 5-Fluorouracil treatment - pyrimidine degradation defect or beriberi?. Case reports in oncology 4 (2): 371–6.
  42. ↑ Martin, PR, Singleton, CK; Hiller-Sturmhöfel, S (2003). The role of thiamine deficiency in alcoholic brain disease. Alcohol research & health : the journal of the National Institute on Alcohol Abuse and Alcoholism 27 (2): 134–42.
  43. ↑ 43.0 43.1 Hirsch, JA, Parrott, J (2012). New considerations on the neuromodulatory role of thiamine. Pharmacology 89 (1–2): 111–6.
  44. ↑ Hazell, AS (2009 Jul-Aug). Astrocytes are a major target in thiamine deficiency and Wernicke's encephalopathy. Neurochemistry international 55 (1–3): 129–35.
  45. ↑ Hazell, AS, Todd, KG; Butterworth, RF (1998 Jun). Mechanisms of neuronal cell death in Wernicke's encephalopathy. Metabolic brain disease 13 (2): 97–122.
  46. ↑ 46.0 46.1 James S. Nelson , Hernando Mena & S. Schochet, Principles and Practice of Neuropathology , page 193, edited University of Hawaii,
  47. ↑ 47.0 47.1 Zuccoli G, Pipitone N. Neuroimaging findings in acute. Wernicke s encephalopathy: review of the literature.AJR. Am J Roentgeno l2009;192:501–508.
  48. ↑ 48.0 48.1 48.2 48.3 Cernicchiaro, Luis. Enfermedad de Wernicke. Monitoring of an acute case for ten years. Enfermedad-de-Wernicke.weebly.com
  49. ↑ Rabow, edited by Stephen J. McPhee, Maxine A. Papadakis; associate editor, Michael W.. Current medical diagnosis & treatment 2012, 51st, New York: McGraw-Hill Medical.
  50. ↑ Caine, D, Halliday, G M; Kril, J J; Harper, C G (1 January 1997). Operational criteria for the classification of chronic alcoholics: identification of Wernicke's encephalopathy. Journal of Neurology, Neurosurgery & Psychiatry 62 (1): 51–60.
  51. ↑ Chick J. Hospital Pharmacist 2000; 7: 251-254
  52. ↑ Cook CCH. Alcohol & Alcoholism 2000; 35 (Suppl 1): 19-20
  53. ↑ 53.0 53.1 EAST KENT HOSPITALS NHS. TRUST PROTOCOL For: The management of the alcohol withdrawal syndrome and Wernicke’s encephalopathy.
  54. ↑ Goldman: Cecil Medicine, chapter 443, 23rd ed. 2007. Saunders, Elsevier.
  55. ↑ G Sechi MD, A Serra MD. Wernicke´s encephalopathy. Lancet Neurol 2007; 6: 442-55
  56. ↑ Thomson, Cook et al. 2008
  57. ↑ Beneficial effect of steroid pulse therapy PMID 7955722
  58. ↑ Corticotherapy of the severe forms of the Gayet-Wernicke encephalopathy.PMID 14005025
  59. ↑ Zarranz, Juan J. (2007). Neurologia., 4a, 821 (Spanish.), Madrid, España: Harcourt Brace De Espana Sa.
  60. ↑ Harrison , Medicina Interna, pág. 2462 ed.2002
  61. ↑ Kelley, Medicina Interna, pág. 621, 974 ed.1990
  62. ↑ Allan D. Thomson, et al., Alcohol & Alcoholism Vol. 37, No. 6, pp. 513–521, 2002 The Royal College of Physicians Report on Alcohol: Guidelines for Managing Wernicke's Encephalopathy, http://alcalc.oxfordjournals.org/content/37/6/513.full.pdf+html
  63. ↑ Nutrición hospitalaria. pdf http://www.nutricionhospitalaria.com/pdf/3337.pdf
  64. ↑ http://www.ncbi.nlm.nih.gov/pubmed/7955722?dopt=Abstract
  65. ↑ Thomson, A. D., Guerrini, Irene; Marshall, E. Jane (NaN undefined NaN). The Evolution and Treatment of Korsakoff's Syndrome. Neuropsychology Review 22 (2): 81–92.
  66. ↑ Alcohol & Alcoholism Vol. 37, No. 6, pp. 513–521, 2002
  67. ↑ Royal College Of Physicians, AD, Cook, CC; Touquet, R; Henry, JA; Royal College of Physicians,, London (2002 Nov-Dec). The Royal College of Physicians report on alcohol: guidelines for managing Wernicke's encephalopathy in the accident and Emergency Department. Alcohol and alcoholism (Oxford, Oxfordshire) 37 (6): 513–21.
  68. ↑ Guy´s and St. Thomas Hospitals http://www.guysandstthomas.nhs.uk/resources/our-services/acute-medicine-gi-surgery/elderly-care/alcohol-withdrawal-syndrome.pdf Doncaster and Bassetlaw Hospitals http://www.alcohollearningcentre.org.uk/_library/17__Doncaster_Guidelines_For_The_Management_Of_Patients_with_Alcohol_Misuse_In_The_Acute_General_Hospital_Setting.pdf
  69. ↑ Torvik A, Lindboe CF, Rodge S. Brain lesions in alcoholics. A neuropathological study with clinical correlations. J Neurol Sci 1982; 56: 233-48.
  70. ↑ Harper, C (1979 Mar). Wernicke's encephalopathy: a more common disease than realised. A neuropathological study of 51 cases. Journal of neurology, neurosurgery, and psychiatry 42 (3): 226–31.
  71. ↑ Torviket al., 1982; Blansjaar and Van Dijk, 1992
  72. ↑ (1992). Coma and death in unrecognized Wernicke's encephalopathy. An autopsy study. Arq Neuropsiquiatr 50 (3): 329–33.
  73. ↑ (2013). The connection between maternal thiamine shortcoming and offspring cognitive damage and poverty perpetuation in underprivileged communities across the world. Medical Hypotheses 80 (1): 13–16.
  74. ↑ 74.0 74.1 PMID 22093426 (PMID 22093426)
    Citation will be completed automatically in a few minutes. Jump the queue or expand by hand
  75. ↑ PMID 23622158 (PMID 23622158)
    Citation will be completed automatically in a few minutes. Jump the queue or expand by hand

Further reading

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


v·d·e
Nutritional pathology (E40-68, 260-269)
Malnutrition

Kwashiorkor - Marasmus

Other underconsumption

B vitamins: B1: Beriberi/Wernicke's encephalopathy, B2: Ariboflavinosis, B3: Pellagra, B7: Biotin deficiency, B9: Folate deficiency, B12: Vitamin B12 deficiency

other vitamins: A: Vitamin A deficiency/Bitot's spots, C: Scurvy, D: Rickets/Osteomalacia

mineral: Zinc deficiency - Iron deficiency, Magnesium deficiency - Chromium deficiency

Hyperalimentation

Obesity - Hypervitaminosis A - Hypervitaminosis D


{enWP|Wernicke's encephalopathy}}

Community content is available under CC-BY-SA unless otherwise noted.
Advertisement

Fan Feed

More Psychology Wiki