ENCEFALOPATIA DE WERNICKE KORSAKOFF PDF

NCBI Bookshelf. Sarayu Vasan ; Anil Kumar. Authors Sarayu Vasan 1 ; Anil Kumar 2. Wernicke encephalopathy WE is an acute neurological condition characterized by a clinical triad of ophthalmoparesis with nystagmus, ataxia, and confusion. This is a life-threatening illness caused by thiamine deficiency, which primarily affects the peripheral and central nervous systems. Korsakoff syndrome is a neuropsychiatric disorder associated with memory disturbances in which there are significant deficits in anterograde and retrograde memory.

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NCBI Bookshelf. Sarayu Vasan ; Anil Kumar. Authors Sarayu Vasan 1 ; Anil Kumar 2. Wernicke encephalopathy WE is an acute neurological condition characterized by a clinical triad of ophthalmoparesis with nystagmus, ataxia, and confusion. This is a life-threatening illness caused by thiamine deficiency, which primarily affects the peripheral and central nervous systems.

Korsakoff syndrome is a neuropsychiatric disorder associated with memory disturbances in which there are significant deficits in anterograde and retrograde memory. Immediate memory is maintained, but short-term memory is diminished with intact sensorium. The disorder is associated with patients fabricating stories in the setting of clear consciousness.

Confabulations can be spontaneous or provoked with provoked confabulation commonly seen in chronic Korsakoff syndrome and spontaneous confabulation usually noted in the acute Wernicke state. Thiamine deficiency is characteristically associated with severe alcohol use disorder. A common inciting event that precipitates WE is an acute infection. Other triggers include prolonged carbohydrate or glucose loading in the presence of thiamine deficiency.

In general, patients who receive glucose should also be administered thiamine at the same time. Several studies indicate that prevalence rates via analysis of clinical records are lower in comparison to necropsy studies as the diagnosis is easily overlooked or missed. This vitamin acts as a cofactor for several enzymes in the Krebs cycle and the pentose phosphate pathway, including alpha-keto-glutamic acid oxidation and pyruvate decarboxylation.

Thiamine-dependent enzymes function as a connection between glycolytic and citric acid cycles. Therefore, deficiency of thiamine will lead to decreased levels of alpha-keto-glutarate, acetate, citrate, acetylcholine and accumulation of lactate and pyruvate. This deficiency can cause metabolic imbalances leading to neurologic complications including neuronal cell death. Neuronal death in the mammillary bodies and thalamus were implicated in multiple cases of Wernicke encephalopathy studied.

The lesions are usually symmetrical in the midbrain, hypothalamus, and cerebellum. Other oculomotor symptoms include cranial nerve involvement of oculomotor, abducens, and vestibular nuclei causing conjugate gaze palsies.

Pupillary sluggishness, ptosis, and anisocoria are also common. Also, gait can worsen, and in many cases, patients are unable to walk. Physical examination may include a complete neurological exam with cerebellar testing.

Disorientation and altered sensorium characterize encephalopathy. Some other warning signs could include hyperthermia and hypotension.

The patient could also present with peripheral neuropathy and commonly includes the lower extremity, and an examination would reveal distal sensory loss. WE should be a consideration in a patient with long term malnutrition and episodes of confusion and altered mental status. Over the past few decades, bariatric surgery has been associated with WE and malnutrition; the key reason is that after surgery, there is limited intake of food and the stores of thiamine are rapidly depleted.

However, a complete blood count and the comprehensive metabolic panel can be completed to exclude other causes of central nervous system abnormalities. Caine et al. MRI may reveal hyperintense signaling in the periventricular thalamus, mammillary bodies and the periaqueductal gray matter. Erythrocyte transketolase levels can detect thiamine deficiency. Levels of lactate and pyruvate are often measured since thiamine is a cofactor for pyruvate dehydrogenase enzyme. The aim of treatment is prompt and quick correction of the thiamine deficiency in the brain.

Parenteral administration of thiamine is most effective and provides for rapid administration, however, in some cases, there are persistent neurological deficits, and the acute condition can progress to chronic Korsakoff syndrome. All malnourished patient may need higher doses of thiamine.

Oral dosing is not reliable and not recommended. WE is a serious life-threatening disorder with enormous disability. While thiamine can induce partial improvement, the neuropsychological deficits persist in many cases. The confusional state usually improves when IV thiamine is administered by the learning and memory deficits only improve partially. A small number of patients fail to have any improvement and may develop Korsakoff psychosis, which often requires institutionalization.

Very few individuals recover at this point. Because the disorder can present with various manifestations, the patient is best managed by a neurologist and an intensivist.

Other specialists may be required according to organ involvement. The role of the nurse, dietitian, social worker, and pharmacist cannot be overemphasized. These patients are sick, frail and malnourished. A dietary consult should be done to assess the calorie needs and determine how to provide the food as well as thiamine.

Since many WE patients are managed as outpatients, the pharmacist should encourage abstinence from alcohol. Since the cornerstone of therapy is thiamine, the importance of compliance is vital. At the same time, the electrolyte deficiencies should be corrected.

Finally, the family should be educated about the prognosis of these individuals and make preparations for long-term care, in case the patient develops korsakoff syndrome. Close communication between members of the team is vital to ensure that the patient is receiving the current standard of care treatment. WE is a serious medical disorder which carries enormous morbidity and mortality. However, survivors of WE may develop korsakoff psychosis and require long-term institutionalization.

To access free multiple choice questions on this topic, click here. This book is distributed under the terms of the Creative Commons Attribution 4. Turn recording back on.

National Center for Biotechnology Information , U. StatPearls [Internet]. Search term. Introduction Wernicke encephalopathy WE is an acute neurological condition characterized by a clinical triad of ophthalmoparesis with nystagmus, ataxia, and confusion.

Etiology Thiamine deficiency is characteristically associated with severe alcohol use disorder. The clinical diagnosis of WE is present if the patient has two of the following features: Eye signs. Differential Diagnosis Differential diagnoses include: Hepatic encephalopathy. Staging Current Guidelines on Managing WE Clinical diagnosis of WE should be considered in alcoholics if the individual has a dietary deficiency, cerebellar dysfunction, eye signs, and altered mental status.

After bariatric surgery, follow thiamine levels and supplement with thiamine for at least 6 months. Prognosis WE is a serious life-threatening disorder with enormous disability. Complications Neurological injury. Consultations Internist.

Questions To access free multiple choice questions on this topic, click here. References 1. Missing the early signs of thiamine deficiency. A case associated with a liquid-only diet. Nutr Neurosci. Preventing Wernicke's encephalopathy in anorexia nervosa: A systematic review. Psychiatry Clin. Convergence Spasm in Wernicke Encephalopathy. Prevalence and predictors of postoperative thiamine deficiency after vertical sleeve gastrectomy. Surg Obes Relat Dis.

Korsakoff's syndrome: a critical review. Neuropsychiatr Dis Treat. Korean J Ophthalmol. Wernicke's encephalopathy in crack-cocaine addiction. Jan K. Wernicke encephalopathy: MRI picture worth a thousand words. Oxf Med Case Reports.

Diagnosis makes a difference: Perceptions of older persons with dementia symptoms. Exp Aging Res. Subclinical thiamine deficiency identified by preoperative evaluation in an ovarian cancer patient: Diagnosis and the need for preoperative thiamine measurement.

Palliat Support Care. Johnson JM, Fox V. Obes Surg. The alcohol withdrawal syndrome. Donnelly A. Wernicke-Korsakoff syndrome: recognition and treatment. Nurs Stand. Alcohol Alcohol. Clinical and pathological features of alcohol-related brain damage.

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Wernicke–Korsakoff syndrome

The Scientific Journal of the Spanish Society of Neurological Nursing publishes papers on topics of interest for nursing or health professionals in general, in any of their areas of activity, that help generate knowledge and are useful for the development of neurological nursing care. Preferably those that may have greater impact in clinical practice. The aim of Scientific Journal of the Spanish Society of Neurological Nursing is the research, study, dissemination and development of neurology at nursing level, as well as the development of neurological patient care, their family and environment. CiteScore measures average citations received per document published. Read more. SRJ is a prestige metric based on the idea that not all citations are the same.

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Wernicke encephalopathy

NCBI Bookshelf. Newton 3. Wernicke-Korsakoff syndrome is a common complication of a thiamine deficiency that is primarily seen with alcoholics. However, less than a third of patients present with this complete triad. Wernicke encephalopathy is characterized by an acute confusional state with clinical features that are often reversible.

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