El síndrome de Wernicke-Korsakoff (SWK) es una enfermedad neurológica. La encefalopatía de Wernicke y la psicosis de Korsakoff son, respectivamente. El beriberi, la enfermedad causada por una deficiencia severa de tiamina, fue y psicosis de Korsakoff, especialmente en personas que abusan del alcohol. Presentación del síndrome de Wernicke-Korsakoff secundario a encefalitis en cadena en tiempo real en el diagnóstico de enfermedad por citomegalovirus en.

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Wernicke encephalopathy WEalso Wernicke’s encephalopathy [1] is the presence of neurological koesakoff caused by biochemical lesions of the central nervous system after exhaustion of B-vitamin reserves, in particular thiamine vitamin B1. The condition is part of a larger group of thiamine deficiency disorders, that includes beriberi in all enfsrmedad forms, and alcoholic Korsakoff syndrome.

When it occurs simultaneously with alcoholic Korsakoff syndrome it is known as Wernicke—Korsakoff syndrome. Classically, Wernicke encephalopathy is characterised by the triad — ophthalmoplegiaataxiaand confusion. The classic triad of symptoms found in Wernicke encephalopathy is: However, in actuality, only a small percentage of patients experience all three symptoms, [8] and the full triad occurs more frequently among those who have overused alcohol. Also a much more diverse range entermedad symptoms has been found in patients with this condition, including:.

External warming techniques are advised to prevent hypothermia. Among the frequently altered functions are the cardio circulatory. There may be tachycardia, dyspnea, chest pain, orthostatic hypotension, changes in heart rate and blood pressure. Infections have korwakoff pointed out as one of the most frequent triggers of death in WE.

In the last stage others symptoms may occur: Because of the frequent involvement of heart, eyes and peripheral nervous system, several authors prefer to call it Wernicke disease rather than simply encephalopathy.

Early symptoms are nonspecific, [33] [34] and it has been stated that WE may present nonspecific findings. Korsakoff’s syndromecharacterised by memory impairment, confabulation, confusion and personality changes, has a strong and recognised link with WE. Wernicke encephalopathy has classically been thought of as a enfermedav solely of alcoholics, but it is also found in the chronically undernourished, and in recent years had been discovered post bariatric surgery.

Thiamine deficiency and errors of thiamine metabolism are believed to be the primary cause of Wernicke encephalopathy. Thiamine, also called B1, helps to break down 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 TDPbefore it is used. The enfermeddad 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.

The primary neurological-related injury caused by thiamine deficiency in WE is three-fold: Thiamine deficiency alters the glutamate uptake of astrocytes, through changes in korsakorf expression of astrocytic glutamate transporters EAAT1 and EAAT2, leading to koorsakoff.


Despite its name, WE is not related to Wernicke’s area, a region of the brain associated with speech and language interpretation. Lesions are usually symmetrical in the periventricular region, diencephalonthe midbrainhypothalamus, and cerebellar vermis. Oedema may be found in the regions surrounding the third ventricleand fourth ventriclealso appearing petechiae and small hemorrhages.

Endothelial proliferation, hyperplasia of enfermedae, demyelination and neuronal loss can also occur. An altered blood—brain barrier may cause a perturbed response to certain drugs and foods.

Diagnosis of Wernicke encephalopathy or disease is made clinically. Enferkedad criteria is challenged because 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. The presence of koreakoff one sign should be sufficient for treatment. 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 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 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.

There appears to be very little value for CT scans. Thiamine can be measured using enfermedaad erythrocyte transketolase activity assay, [5] or by activation by measurement enfefmedad in vitro thiamine diphosphate levels. Most symptoms nefermedad improve quickly if deficiencies are treated early. Memory disorder may be permanent. In patients suspected of WE, thiamine treatment should be started immediately. Following this an immediate intravenous or intramuscular dose of thiamine should be administered [32] two fnfermedad three times daily.

Korsakoff syndrome

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. Alcohol abusers may have poor dietary intakes of several vitamins, and impaired thiamine absorption, metabolism, and storage; they may thus require higher doses.

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 kordakoff thiamine reserves, exacerbating this krosakoff.

SINDROME DE KORSAKOFF by Yanira Oria Rodríguez on Prezi

The observation of edema in MR, and also the finding of inflation and macrophages in necropsied tissues, [49] has led to successful administration of antiinflammatories. Other nutritional abnormalities should also be looked for, as they may be exacerbating the disease.

Other supplements may also be needed, including: In patients with Wernicke-Korsakoff syndrome, even higher doses of parenteral thiamine are recommended.


Concurrent toxic effects of alcohol should also be considered. There are hospital protocols for prevention, supplementing with thiamine in the presence of: In the clinical diagnosis should be remembered that early symptoms are nonspecific, [33] [34] and it has been stated that WE may present nonspecific findings.

In some countries certain foods have been supplemented with thiamine, and have reduced WE cases. Improvement is difficult to quantify because they applied several different actions. Avoiding alcohol and having adequate nutrition reduces one of the main risk factors in developing Wernicke-Korsakoff syndrome.

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. 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 encephalopathy is underdiagnosed. 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.

In this statistic fetal and infant damage with upcoming intellectual limitations should be included. WE was first identified in by the German neurologist Carl Wernickealthough the link with thiamine was not identified until the s. A similar presentation of this disease was described by the Russian psychiatrist Sergei Korsakoff in a series of articles published — From Wikipedia, the free encyclopedia.

European Journal of Neurology. Journal of Neurology, Neurosurgery, and Psychiatry. The Journal of the Association of Physicians of India. Unusual early signs of Wernicke encephalopathy”. Case Report and Review of the Literature”. Japanese Journal of Clinical Oncology. American Journal of Psychiatry. Revue neurologique in French. Color Atlas of Neurology. The Interface of Neurology and Internal Medicine. Brain and Nerve in Japanese. Harcourt Brace De Espana Sa. Cecil Medicine, Chapter, 23rd ed.

Síndrome de Korsakoff | Dallas Medical Specialists

The International Journal of Infectious Diseases. Case Reports in Oncology. Journal of the American College of Cardiology. American Journal of Roentgenology. Monitoring of wnfermedad acute case for twelve years.

Papadakis; associate editor, Michael W. The management of the alcohol withdrawal syndrome and Wernicke encephalopathy. Cecil Medicine, chapter23rd ed. An overview in health and disease” PDF.

Rinsho Shinkeigaku in Japanese.

Brain lesions in alcoholics. A neuropathological study with clinical correlations.

Wernicke encephalopathy

J Neurol Sci ; A neuropathological study of 51 cases”. Report of a case and literature review”. Zhonghua er ke koraakoff zhi. Pediatric Neurology Part I.