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Articoli di riviste sul tema "Wernicke-Korsakoff Syndrome"

Autore: Grafiati

Pubblicato: 4 giugno 2021

Ultima modifica: 9 giugno 2025

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1

Mushtaq, Raheel, Sheikh Shoib, Tabindah Shah, Mudasir Bhat, Randhir Singh, and Sahil Mushtaq. "Unusual Presentation of Uncommon Disease: Anorexia Nervosa Presenting as Wernicke-Korsakoff Syndrome—A Case Report from Southeast Asia." Case Reports in Psychiatry 2014 (2014): 1–3. http://dx.doi.org/10.1155/2014/482136.

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Anorexia nervosa presenting as Wernicke-Korsakoff syndrome is rare. The causes of Wernicke-Korsakoff syndrome are multiple like alcohol abuse, thyrotoxicosis, haemodialysis, severe malnutrition because of gastric carcinoma and pyloric obstruction, hyperemesis gravidarum, and prolonged parenteral feeding. We report a case of anorexia nervosa, who presented with Wernicke's encephalopathy and progressed to Korsakoff's syndrome. Knowledge, awareness, and early intervention of anorexia nervosa by mental health professionals can prevent development of Wernicke-Korsakoff syndrome.

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Kotov, S. V., A. I. Lobakov, E. V. Isakova, G. A. Stashuk, and T. V. Volchenkova. "Wernicke–Korsakoff syndrome." Zhurnal nevrologii i psikhiatrii im. S.S. Korsakova 116, no. 7 (2016): 4. http://dx.doi.org/10.17116/jnevro2016116714-11.

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3

Schaefer, Sandra. "Wernicke?Korsakoff Syndrome." Journal of the American Academy of Nurse Practitioners 8, no. 9 (September 1996): 435–36. http://dx.doi.org/10.1111/j.1745-7599.1996.tb00692.x.

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4

Sivolap, Yu P., and I. V. Damulin. "Wernicke–Korsakoff syndrome." Neurology, Neuropsychiatry, Psychosomatics, no. 4 (December 10, 2014): 76. http://dx.doi.org/10.14412/2074-2711-2014-4-76-80.

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5

MCNAMARA, M. EILEEN, JOHN J. CAMPBELL, and PATRICIA RYAN RECUPERO. "Wernicke-Korsakoff Syndrome." Journal of Neuropsychiatry and Clinical Neurosciences 3, no. 2 (May 1991): 232. http://dx.doi.org/10.1176/jnp.3.2.232.

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6

Zubaran, C., J. G. Fernandes, and R. Rodnight. "Wernicke-Korsakoff syndrome." Postgraduate Medical Journal 73, no. 855 (January 1, 1997): 27–31. http://dx.doi.org/10.1136/pgmj.73.855.27.

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7

Brockington, I. "Wernicke-Korsakoff syndrome." Archives of Women's Mental Health 9, no. 1 (December 22, 2005): 58–59. http://dx.doi.org/10.1007/s00737-005-0112-x.

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Madeira, N., T. Santos, and J. L. Pio-Abreu. "Wernicke-Korsakoff Syndrome: A Common Yet Elusive Diagnosis." European Psychiatry 24, S1 (January 2009): 1. http://dx.doi.org/10.1016/s0924-9338(09)71095-8.

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In 1897, Murawieff proposed that a common cause was responsible for the two syndromes previously described by Carl Wernicke and Sergei Korsakoff. More than 100 years afterwards, the neuropsychiatric nosological entity known as Wernicke-Korsakoff syndrome remains one of the most significant, yet under-recognized, consequences of long-term alcohol abuse.Prompt recognition and treatment of Wernicke's encephalopathy with parenteral thiamine can prevent permanent cognitive impairment, involving severe short-term memory loss - Korsakoff's amnesic syndrome. Such condition has devastating consequences for patients, not infrequently demanding long-term institutionalization.Based on two clinical vignettes, the authors review some epidemiological, clinical and neuropathological features of Wernicke-Korsakoff syndrome, besides issues concerning differential diagnosis, treatment and prognosis.

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Pokale, Yogesh Jagannath, and Sunil G. Gupte. "A Case Report on Wernicke–Korsakoff Syndrome." MVP Journal of Medical Sciences 1, no. 1 (January 1, 2014): 44. http://dx.doi.org/10.18311/mvpjms/2014/v1/i1/835.

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<strong>Background:</strong> Alcohol use is one of the most serious problems in public health and the Wernicke-Korsakoff Syndrome is one of the gravest consequences of alcoholism. Post-mortem studies suggest that Wernicke-Korsakoff Syndrome occurs in 12.5% of dependent drinkers and in 2% of the general population. Korsakoff Syndrome is an amnestic disorder generally followed by untreated Wernicke's Encephalopathy. Wernicke-Korsakoff Syndrome is most commonly a post-mortem diagnosis. <strong>Aim and Objective:</strong> To report a case of Korsakoff Syndrome since the clinical presentation is often undiagnosed or misdiagnosed. <strong>Case description:</strong> 50 year old male, drinking heavily since 25 years presented with complaints of forgetfulness, talking irrelevantly since last 18 months. Patient developed symptoms of confusion, ataxia, and altered behaviour 2 years back, for which he was treated as a case of encephalitis and not treated with thiamine. He later progressed to show symptoms of amnesia. On examination, patient showed recent memory deficit with anterograde and variable retrograde amnesia with confabulations. Neurological examination revealed absent deep tendon reflexes and signs of peripheral neuropathy. MRI brain showed global cortical atrophy. The sequence of events in this case study demonstrates the possible effects of long term alcohol use, namely Wernicke-Korsakoff Syndrome. Highlights of the medical model of Wernicke-Korsakoff Syndrome will be subsequently presented. Lastly, suggestions for treatment and prevention of further damage will be discussed.

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Swain, Sanjana Simansu, and Suhasin Ganta. "Korsakoff Syndrome: A Chronic Nutritional Deficiency Neuropsychiatric condition." YMER Digital 21, no. 05 (May 27, 2022): 1217–33. http://dx.doi.org/10.37896/ymer21.05/d6.

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In this review we have focused on Korsakoff syndrome, which is an aftermath of Wernicke encephalopathy (WE). Wernicke-Encephalopathy is neuropathologically marked by thiamine or vitamin B1 deficiency, typically induced by excessive alcohol use over an extended period of time in alcoholic patients, while in Nonalcoholic patients, it may be due to impaired utilization or accelerated usage of thiamine. Wernicke-Korsakoff syndrome (WKS) affects the brain region such as the mammillary bodies, periaqueductal and periventricular grey matter, colliculi bodies, and thalamus. The classic triads of WE are ophthalmoplegia, Nystagmus, and ataxia. The brain is examined using MRI and shows damage to the nuclei or memory transit- papez circuit that connects mamillary bodies to the anterior thalamus using the mammillothalamic tract responsible for the recollective memory in the diencephalon. Patients can be treated by parenteral thiamine administration and by abstinence of alcohol within their lifestyle. Keywords: Korsakoff Syndrome, alcoholic, non-alcoholic, Alzheimer's, memory-loss Wernicke encephalopathy, Wernicke-Korsakoff syndrome

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Zdunek, Roksana, Karolina Strus, Magdalena Madera, Natalia Dąbrowska, Sylwia Mazur, Agata Mazur, Aleksy Bizan, Emilia Nagórska, Krzysztof Marcinkowski, and Aleksandra Kublińska. "Deficiency of thiamine and Wernicke-Korsakoff syndrome – review of pathophysiology, clinical presentation , diagnostics and treatment." Journal of Education, Health and Sport 72 (May 29, 2024): 51248. http://dx.doi.org/10.12775/jehs.2024.72.51248.

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Introduction and aim of the study: Thiamine is a water-soluble vitamine, which bioactive form is necessary for energy metabolism in all cells. Deficiency of thiamine may be caused by malnutrition, alcoholism and certain diseases and it leads to an acute neuropsychiatric disorder called Wernicke encephalopathy. Untreated patients can develop a residual syndrome called Korsakoff syndrome. The aim of our study is to present current knowledge of history, pathophysiology, causes, symptoms and treatment of vitamine B1 depletion and Wernicke-Korsakoff’s syndrome. Material and methods: Our review is based on the analysis of materials collected in „Pubmed”, „Google Scholar” and other scientific articles using keywords: „thiamine”, „thiamine deficiency”, „Wernicke encephalopathy”, „Korsakoff syndrome”. Conclusions: Despite numerous studies, Wernicke encephalopathy is still difficult to diagnose. Attention should be paid to the possibility of vitamin B1 deficiency in people who are at risk of it like alcoholics, malnourished or psychiatric patients. Wernicke encephalopathy is an acute neuropsychiatric disorder so the treatment should be started as soon as possible to reduce the risk of developing Korsakoff syndrome.

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Silva, A. F., R. M. Lopes, V. S. Melo, C. A. Rodrigues, P. M. Coelho, F. M. A. Santos, I. S. Fernandes, and L. P. Delgado. "From wernicke-korsakoff to central pontine myelinolysis: the potentially irreversible risks of alcohol use." European Psychiatry 67, S1 (April 2024): S400. http://dx.doi.org/10.1192/j.eurpsy.2024.820.

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Introduction Sustained alcohol intake, when combined with incomplete treatment, can result in chronic structural changes in the Central Nervous System, including generalized cortical and cerebellar atrophy, amnesic syndromes like Korsakoff’s syndrome, and white matter disorders such as Central Pontine Myelinolysis and Marchiafava-Bignami syndrome. It is crucial to prevent these complications due to their potential for irreversible and debilitating consequences. For Wernicke-Korsakoff syndrome, early recognition and thiamine administration for prevention are paramount, as it arises from thiamine deficiency due to malnutrition caused by persistent alcohol use. In the case of Central Pontine Myelinolysis, which is caused by abrupt fluctuations in serum osmolality, controlled sodium correction is essential.ObjectivesThrough a clinical case and a review of published literature, this study aims to reflect on the importance of preventing neurological injuries associated with chronic alcohol consumption, specifically Wernicke-Korsakoff Syndrome and Central Pontine Myelinolysis.Methods A literature review was conducted by searching for articles on PubMed using the terms “Alcohol Use Disorder,” “Wernicke-Korsakoff syndrome,” and “Central pontine myelinolysis.” A clinical case is presented, featuring a 50-year-old patient with alcohol use disorder who developed Wernicke-Korsakoff syndrome and Central Pontine Myelinolysis. Considering this case, we reflect on the primary approaches that could have been beneficial in preventing these complications and propose a straightforward method for doing so.Results A 50-year-old patient presented with poor general condition, characterized by low weight, significant loss of strength in the limbs and arms, and incoherent speech with anterograde amnesia and confabulation. This condition had progressed to a point where the patient could no longer walk, perform basic self-care tasks such as bathing, dressing, and eating independently, underscoring the severity of his condition. The diagnoses of Wernicke-Korsakoff syndrome and Central Pontine Myelinolysis were established based on clinical manifestations and the presence of hyperintense lesions observed in the central pons on T2/FLAIR axial MRI scans. This clinical case highlights the importance of proper and precocious prevention of complications in patients with alcohol use disorder. The foremost step in preventing these complications is to treat alcohol dependence effectively, even when faced with patient resistance. It’s vital to remain vigilant about potential complications and implement suitable prophylactic measures.ConclusionsThe devastating effects of complications arising from Alcohol Use Disorder, such as Wernicke-Korsakoff syndrome and Central Pontine Myelinolysis, underscore the importance of enhanced attention that clinicians should provide when approaching these patients at all clinical interactions.Disclosure of InterestNone Declared

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13

Wijnia, Jan. "A Clinician’s View of Wernicke-Korsakoff Syndrome." Journal of Clinical Medicine 11, no. 22 (November 15, 2022): 6755. http://dx.doi.org/10.3390/jcm11226755.

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The purpose of this article is to improve recognition and treatment of Wernicke-Korsakoff syndrome. It is well known that Korsakoff syndrome is a chronic amnesia resulting from unrecognized or undertreated Wernicke encephalopathy and is caused by thiamine (vitamin B1) deficiency. The clinical presentation of thiamine deficiency includes loss of appetite, dizziness, tachycardia, and urinary bladder retention. These symptoms can be attributed to anticholinergic autonomic dysfunction, as well as confusion or delirium, which is part of the classic triad of Wernicke encephalopathy. Severe concomitant infections including sepsis of unknown origin are common during the Wernicke phase. These infections can be prodromal signs of severe thiamine deficiency, as has been shown in select case descriptions which present infections and lactic acidosis. The clinical symptoms of Wernicke delirium commonly arise within a few days before or during hospitalization and may occur as part of a refeeding syndrome. Wernicke encephalopathy is mostly related to alcohol addiction, but can also occur in other conditions, such as bariatric surgery, hyperemesis gravidarum, and anorexia nervosa. Alcohol related Wernicke encephalopathy may be identified by the presence of a delirium in malnourished alcoholic patients who have trouble walking. The onset of non-alcohol-related Wernicke encephalopathy is often characterized by vomiting, weight loss, and symptoms such as visual complaints due to optic neuropathy in thiamine deficiency. Regarding thiamine therapy, patients with hypomagnesemia may fail to respond to thiamine. This may especially be the case in the context of alcohol withdrawal or in adverse side effects of proton pump inhibitors combined with diuretics. Clinician awareness of the clinical significance of Wernicke delirium, urinary bladder retention, comorbid infections, refeeding syndrome, and hypomagnesemia may contribute to the recognition and treatment of the Wernicke-Korsakoff syndrome.

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Shrestha, Priya, Chandan Chaudhary, and Suraj Nepal. "Cognitive impairment - goodness of fit: Case report on intricacies in diagnosis." Journal of Psychiatrists' Association of Nepal 13, no. 1 (July 29, 2024): 34–36. http://dx.doi.org/10.3126/jpan.v13i1.68184.

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Sporadic Creutzfeldt-Jakob disease (sCJD) is a rare neurodegenerative disorder characterized by rapid onset dementia and neurological symptoms, often challenging to differentiate from other neuropsychiatric conditions such as Wernicke-Korsakoff syndrome, especially in patients with alcohol dependence. We present a case of a 61-year-old female with a history of alcohol dependence, who initially presented with hallucinatory behaviour, memory impairment, and ataxic gait. Diagnostic evaluation revealed features reflecting Wernicke-Korsakoff syndrome on initial evaluation. However clinical profile, aided with MRI findings were suggestive of sCJD. The overlapping symptoms of sCJD and Wernicke-Korsakoff syndrome constitute a diagnostic dilemma, which gets further complicated with resource constraints for assessment. This case underscores the importance of enhancing our skills as clinicians in neurocognitive assessment to locate specific brain network dysfunction to conclude on a brain disorder, among cases presenting with neuropsychological symptoms.

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Sunitha, D., P. Anusri, and M. Sudhakar. "Wernicke-Korsakoff Syndrome: An Overview." Asian Journal of Pharmaceutical Research 9, no. 2 (2019): 104. http://dx.doi.org/10.5958/2231-5691.2019.00017.0.

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Kirk Phillips, B., M. Victoria Ingram, and Geoffrey G. Grammer. "Wernicke-Korsakoff Syndrome and Galantamine." Psychosomatics 45, no. 4 (July 2004): 366–68. http://dx.doi.org/10.1176/appi.psy.45.4.366.

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Sechi, GianPietro, Lucia Batzu, Luigi Agrò, and Chiara Fois. "Cancer-related Wernicke-Korsakoff syndrome." Lancet Oncology 17, no. 6 (June 2016): e221-e222. http://dx.doi.org/10.1016/s1470-2045(16)30109-7.

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Gomez, Osmanny, Sarthak Parikh, TY Davis, Abby Halpern, Felix Stanziola, and Arturo Corces. "Chronic Posterior Tibiofemoral Dislocation of a Cruciate Retaining Total Knee Arthroplasty in the Setting of Wernicke-Korsakoff Syndrome: A Case Report." Journal of Orthopaedic Case Reports 12, no. 7 (2022): 60–65. http://dx.doi.org/10.13107/jocr.2022.v12.i07.2918.

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Introduction: Knee dislocations are an uncommon complication following total knee arthroplasty (TKA). There are many causes of TKA dislocation; however, Wernicke-Korsakoff syndrome is one uncommon neurologic condition that increases the risk of TKA dislocation. Case Report: A 71-year-old male with presented to a local community hospital with knee pain due to advanced osteoarthritis of the knee and subsequently underwent an uncomplicated TKA with a cruciate retaining prosthesis. He eventually returned to the hospital due to infection, medical instability, chronic knee instability, and posterior tibiofemoral dislocation. A revision process was required. Throughout the course of management, the patient had altered mental status and was admitted to the intensive care unit. The first procedure involved removing the cruciate retaining prosthesis and replacing it with a static cement antibiotic spacer. This prosthesis was eventually dislocated through the tibia and a second procedure requiring the placement of an intercalary fusion was needed. The patient has not followed up after the hospital admission. Conclusion: Wernicke-Korsakoff Syndrome is an uncommon condition that affects lcoholics and complicates treatment with joint replacement surgery. Patients with Wernicke-Korsakoff syndrome provide a unique set of challenges that may require multiple surgeries and varying prostheses. Chronic posterior tibiofemoral dislocation is one specific complication that may affect the management of these patients. As orthopedic surgeons, it is important to consider alcohol use disorder and Wernicke-Korsakoff Syndrome when treating patients with total joint replacement.

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Galvão, Nathalia Dias, Isadora Munaretto Reolon, Marcela Barbosa Hércules, Armando Gabriel Machado Arruda, Maria Eugênia Caires Santos, Mariana Costa Teixeira, Graziely Marques Lima, and Mario de Souza Lima e. Silva. "Síndrome de Wernicke-Korsakoff associada ao álcool / Wernicke-Korsakoff syndrome associated with alcohol." Brazilian Journal of Health Review 3, no. 6 (2020): 18435–44. http://dx.doi.org/10.34119/bjhrv3n6-237.

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Galvão, Nathalia Dias, Isadora Munaretto Reolon, Marcela Barbosa Hércules, Armando Gabriel Machado Arruda, Maria Eugênia Caires Santos, Mariana Costa Teixeira, Graziely Marques Lima, and Mario de Souza Lima e. Silva. "Síndrome de Wernicke-Korsakoff associada ao álcool / Wernicke-Korsakoff syndrome associated with alcohol." Brazilian Journal of Health Review 3, no. 6 (2020): 18435–44. http://dx.doi.org/10.34119/bjhrv3n6-237.

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Donnelly, Alexander. "Wernicke-Korsakoff syndrome: recognition and treatment." Nursing Standard 31, no. 31 (March 29, 2017): 46–53. http://dx.doi.org/10.7748/ns.2017.e10440.

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Parkin, Alan J., J. Blunden, J. E. Rees, and Nicola M. Hunkin. "Wernicke-Korsakoff syndrome of nonalcoholic origin." Brain and Cognition 15, no. 1 (January 1991): 69–82. http://dx.doi.org/10.1016/0278-2626(91)90016-2.

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Sullivan, E. V., and A. Pfefferbaum. "Neuroimaging of the Wernicke-Korsakoff Syndrome." Alcohol and Alcoholism 44, no. 2 (January 16, 2009): 155–65. http://dx.doi.org/10.1093/alcalc/agn103.

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Jiménez Cabañas, M., F. Ruiz Guerrero, A. Bermejo Pastor, F. Mayor Sanabria, M. Fernández Fariña, and M. D. Saiz González. "Wernicke Encephalopathy: A case report." European Psychiatry 65, S1 (June 2022): S453. http://dx.doi.org/10.1192/j.eurpsy.2022.1149.

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Introduction We report a case of a 56-year old woman with a history of depressive disorder between 2012 and 2017 achieving full remission after treatment with antidepressants and anxiolytics. In the year 2021 was presented to the emergency department manifesting alteration of behavioral patterns, ataxia, mental confusion and horizontal nystagmus. A chronic alcohol abuse was also discovered while interviewing. She also exhibited low mood, anterograde amnesia and confabulations that improved rapidly after following treatment with thiamine. Objectives Reviewing clinical manifestations and treatment of Wernicke encephalopathy and the development of Korsakoff syndrome. Methods We systematically reviewed articles using PubMed. Results Wernicke encephalopathy is a well-known complication of thiamine deficiency, mostly associated with alcohol use disorder. Classically, the syndrome comprises changes in mental status, gait ataxia and ophthalmoplegia. However, the full triad has been described in only 10-17 % of cases, which in our the case is report. After the diagnosis was established and was treated with thiamine, a rapid improvement in the patient´s clinical status was observed. Cognitive impairment was later identified, taking into account the possibility of a Korsakoff syndrome characterized by irreversible brain damage and subsequent loss of anterograde memory. In our patient, this specific diagnosis was dismissed due to the clinical improvement after thiamine treatment. Conclusions It is relevant to emphasize the importance of a precise diagnosis and treatment of patients with Wernicke Encephalopathy to avoid the development of a Korsakoff syndrome. Disclosure No significant relationships.

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Gargot, T., and N. Bouaziz. "Évolution favorable d’un cas de syndrome de Wernicke et Korsakoff en secteur de psychiatrie." European Psychiatry 29, S3 (November 2014): 530. http://dx.doi.org/10.1016/j.eurpsy.2014.09.386.

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Le syndrome de Wernicke est caractérisé par un syndrome confusionnel, une paralysie oculomotrice, une ataxie cérébelleuse. Il serait secondaire à une carence en vitamine B1 souvent liée à une carence d’origine alcoolique. Le syndrome de Korsakoff est une complication du syndrome de Wernicke auquel s’ajoutent des troubles de la mémoire antérograde, des fabulations, des fausses reconnaissances et une polyneuropathie. Classiquement, le syndrome de Korsakoff est considéré de mauvais pronostic. Qu’apporte une prise en charge bio-psychosociale de ces troubles en secteur de psychiatrie ? Nous rapportons le cas d’un patient hospitalisé pour une tentative de suicide sans alcoolo-dépendance connue. Quelques jours après son admission, il présente un syndrome confusionnel, une paralysie oculomotrice, une ataxie cérébelleuse, une amnésie antérograde, des fabulations, des fausses reconnaissances et une polyneuropathie des membres inférieurs. Un diagnostic de syndrome de Wernicke compliqué de syndrome de Korsakoff a été posé. Par ailleurs, apparaissent une humeur dépressive, une alcoolo-dépendance niée, un délire confuso-onirique, une décompensation d’hypertension artérielle, diabétique et une hyperexcitabilité auriculaire. Des dosages montrent des carences en 25-OH vitamine D et en vitamine B9. Le dosage de la vitamine B1 est normal. Il reçoit des benzodiazépines à l’admission. En phase aiguë, il reçoit des vitamines B1, B6, D et B9. Après amélioration, il est traité par de la fluoxétine et de l’acamprosate. L’imagerie cérébrale après rémission ne montre pas d’atteinte des corps mamillaires. Un suivi psychométrique par mini mental state examination, un test de l’horloge et un test des 5 mots de Dubois a montré une normalisation. Après rémission, nous avons utilisé une approche psychothérapeutique motivationnelle. Une lourde prise en charge sociale axée sur la réinsertion a été nécessaire. Le syndrome de Korsakoff pris à un stade précoce ne serait pas toujours de mauvais pronostic. Une vision bio-psycho-sociale semble pertinente dans ces pathologies.

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Cavalcante, Rafael Leituga de Carvalho, Enzzo Cavalcante Pereira, Guilherme Protázio Oliveira Pires de Sá, Rhaira Fernanda Ayoub Casalvara, Sophya Bezerra Silva Rocha, Julia Cordeiro Schneider Ferreira, Fernando Rodrigues Dias, Fillipe Eduardo Amorim Mesquita, and Thúlio Willen Siqueira Neder. "Avanços no diagnóstico e tratamento da Síndrome de Wernicke-Korsakoff: Uma análise integrativa da literatura." Research, Society and Development 13, no. 5 (May 26, 2024): e8913545878. http://dx.doi.org/10.33448/rsd-v13i5.45878.

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A Síndrome de Wernicke-Korsakoff (SWK) é uma condição neuropsiquiátrica debilitante, caracterizada por uma tríade clássica de sintomas: encefalopatia de Wernicke, que inclui confusão mental, ataxia e oftalmoplegia; e a síndrome de Korsakoff, que envolve déficits de memória anterógrada e retrograda, confabulação e alterações de humor. Esta síndrome é comumente associada ao consumo crônico de álcool e deficiência de tiamina, embora também possa ocorrer em casos de má nutrição, distúrbios gastrointestinais, cirurgia bariátrica, entre outros. Para iniciar o processo de revisão, foi realizada uma busca na base de dados eletrônica PubMed, com o intuito de identificar estudos publicados nos últimos 10 anos (2014 a 2024) que abordassem avanços no diagnóstico e tratamento da SWK. Os descritores MESH específicos utilizados foram “Wernicke-Korsakoff Syndrome”, “Diagnosis”, “Treatment”, “Therapeutics”. Esses termos foram selecionados para garantir a inclusão de estudos que abordassem diferentes aspectos relacionados ao diagnóstico e tratamento da SWK, desde novas técnicas diagnósticas até estratégias terapêuticas emergentes. Após a busca inicial, os resultados foram filtrados para incluir apenas estudos relevantes à temática da revisão. Os critérios de inclusão exigiam que os estudos abordassem especificamente avanços no diagnóstico e tratamento da Síndrome de Wernicke-Korsakoff e oferecessem insights sobre perspectivas atuais e futuras nessa área. Os estudos que não atendiam a esses critérios foram excluídos da revisão. A conclusão desta análise sobre o tratamento da Síndrome de Wernicke-Korsakoff destaca a importância de abordagens multidisciplinares e baseadas em evidências para o manejo eficaz dessa condição neuropsiquiátrica complexa. Os avanços recentes no diagnóstico precoce, terapia com tiamina e reabilitação cognitiva representam progressos significativos no tratamento da SWK, proporcionando melhorias na qualidade de vida dos pacientes afetados.

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McIntosh, Claire, Valerie Kippen, Fiona Hutcheson, and Andrew McIntosh. "Parenteral thiamine use in the prevention and treatment of Wernicke–Korsakoff syndrome." Psychiatric Bulletin 29, no. 3 (March 2005): 94–97. http://dx.doi.org/10.1192/pb.29.3.94.

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Aims and MethodA pre-/post-intervention audit of 163 case notes was conducted to assess the efficacy of printing information about the identification and treatment of the Wernicke–Korsakoff syndrome on the hospital alcohol detoxification sheet.ResultsParenteral thiamine was indicated in 42 of 163 patients; 26 had symptoms suggestive of Wernicke's encephalopathy and 16 were at risk. The intervention increased the chance of appropriate parenteral treatment by an odds ratio of 5.9 (95% CI 1.3–27.8). Admission to a specialist alcohol unit increased the chance of appropriate treatment by an odds ratio of 7.0 (95% CI 1.52–32.25). The mean number of doses rose from 3.08 to 4.62.Clinical ImplicationsA simple intervention may lead to improved treatment of patients with Wernicke–Korsakoff syndrome.

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28

Leyfman, Yan. "CONFABULATIONS IN A CHRONIC ALCOHOLIC- A SUBTLE PRESENTATION OF KORSAKOFF SYNDROME." International Journal of Research -GRANTHAALAYAH 7, no. 7 (July 31, 2019): 58–60. http://dx.doi.org/10.29121/granthaalayah.v7.i7.2019.716.

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Abstract (sommario):

Wernicke Encephalopathy is an acute neuropsychiatric condition, characterized by confusion, nystagmus, ataxia, and ophthalmoplegia, resulting from thiamine (Vitamin B1) deficiency, typically secondary to alcohol abuse. Failure to properly diagnose, which occurs in 80% of the time, can result in gradual progression to irreversible Korsakoff Syndrome, characterized by irreversible personality changes, and anterograde and retrograde amnesia. The present case report seeks to highlight this patient’s chronology to Korsakoff Syndrome and our attempted interventions.

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29

Yan, Leyfman. "CONFABULATIONS IN A CHRONIC ALCOHOLIC- A SUBTLE PRESENTATION OF KORSAKOFF SYNDROME." International Journal of Research - Granthaalayah 7, no. 7 (July 31, 2019): 58–60. https://doi.org/10.5281/zenodo.3354279.

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Abstract (sommario):

Wernicke Encephalopathy is an acute neuropsychiatric condition, characterized by confusion, nystagmus, ataxia, and ophthalmoplegia, resulting from thiamine (Vitamin B1) deficiency, typically secondary to alcohol abuse. Failure to properly diagnose, which occurs in 80% of the time, can result in gradual progression to irreversible Korsakoff Syndrome, characterized by irreversible personality changes, and anterograde and retrograde amnesia. The present case report seeks to highlight this patient’s chronology to Korsakoff Syndrome and our attempted interventions

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30

Alves Pereira de Carvalho Saraiva, Rodrigo, Maria Gonçalves, Carolina Sereijo, Tiago Mendes, Rita Barandas Kamyar, Manuela Abreu, and Ricardo Coentre. "Nonalcoholic Wernicke-Korsakoff Syndrome Resulting From Psychosis." Journal of Nervous & Mental Disease 209, no. 3 (March 2021): 229–31. http://dx.doi.org/10.1097/nmd.0000000000001287.

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31

Pokale, Yogesh Jagannath, and Sunil Govind Gupte. "A Case Report on Wernicke–Korsakoff Syndrome." MVP Journal of Medical Science 1, no. 1 (January 5, 2014): 44. http://dx.doi.org/10.15306/mvpjms/2014/v1i1/46891.

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32

Yoon, Chang-Kyoon, Moo-Hwan Chang, and Dong-Cho Lee. "Wernicke-Korsakoff Syndrome Associated with Hyperemesis Gravidarum." Korean Journal of Ophthalmology 19, no. 3 (2005): 239. http://dx.doi.org/10.3341/kjo.2005.19.3.239.

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33

Deb, Shoumitro, Richard Law-Min, and David Fearnley. "Wernicke-Korsakoff Syndrome following Small Bowel Obstruction." Behavioural Neurology 13, no. 3-4 (2002): 89–94. http://dx.doi.org/10.1155/2002/702526.

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We report a case of a 64-year-old lady who developed clinical features of Wernicke-Korsakoff syndrome following a laparotomy for small bowel obstruction. Following the operation she developed paralytic ileus and required total parenteral nutrition for one month. A suspected history of average 40 units of weekly alcohol consumption prior to the operation could not be confirmed and the patient did not show any sign of alcohol dependence. Within a few months of treatment with a daily oral dose of thiamine 200 mgs supplemented by multivitamins the patient showed subjective evidence of improvement in confusion, confabulation, and anterograde amnesia, although objective tests showed residual deficits in many areas of cognitive functioning, including immediate and delayed recall of verbal and non-verbal materials, planning and switching of attention.

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34

Truswell, A. Stewart. "Australian experience with the Wernicke-Korsakoff syndrome." Addiction 95, no. 6 (June 2000): 829–32. http://dx.doi.org/10.1046/j.1360-0443.2000.9568291.x.

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35

Jimoh, Idris Janos, Barbara Sebe, Peter Balicza, Mariann Fedor, Ilona Pataky, Gabor Rudas, Aniko Gal, Gabriella Inczedy-Farkas, Gyorgy Nemeth, and Maria Judit Molnar. "Wernicke–Korsakoff syndrome associated with mtDNA disease." Therapeutic Advances in Neurological Disorders 13 (January 2020): 175628642093897. http://dx.doi.org/10.1177/1756286420938972.

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Introduction: Wernicke encephalopathy (WE) and Wernicke–Korsakoff syndrome (WKS) are well-known disorders caused by thiamine deficiency. In addition to the classical concept of these diseases, some literature data suggest a connection between mitochondrial dysfunction and WE/WKS. Psychotic disorders and WKS seem to run in families, as the deficiency of the oxidative phosphorylation can be a trigger factor in psychotic events and WE/WKS as well. We present a patient harbouring the m.A3243G mtDNA mutation with the clinical and magnetic resonance imaging (MRI) findings of WKS who developed schizophrenia with predominantly negative symptoms some years later. Case presentation: A 27-year-old woman was referred to our clinic with severe weight loss after severe vomiting episodes, memory dysfunction and gait ataxia. Family history, as well as clinical, imaging and laboratory findings suggested a mitochondrial aetiology of her symptoms. Brain MRI detected bilateral mild thalamic lesions and loss of corpus mammillae, indicating Wernicke encephalopathy. Genetic testing detected an m.A3243G mtDNA mutation, which has been frequently associated with mitochondrial encephalopathy with lactic acidosis and stroke-like episodes. High-dose vitamin B1 supplementation with supportive antioxidant therapy improved the patient’s memory and learning disturbance; however, some months later she developed psychosis with predominantly negative symptoms and her cognitive functions deteriorated again. Both cognitive and negative symptoms responded well to cariprazine monotherapy. Discussion: Mitochondrial disease due to mtDNA alteration can be a rare cause of WE. In addition to vitamin B1 supplementation, cariprazine with significant dopamine D3 receptor binding can be useful to treat the predominantly negative symptoms and cognitive dysfunction in patients with mitochondrial dysfunction. Conclusion: We assume that patients with a mitochondrial disorder might be prone to develop WE/WKS and therefore need tailored supportive therapy during metabolic crisis as well as symptom-based personalized antipsychotic treatment.

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36

Kim, Ki Hyang. "Wernicke-Korsakoff Syndrome in Primary Peritoneal Cancer." Case Reports in Oncology 6, no. 3 (December 11, 2013): 593–97. http://dx.doi.org/10.1159/000357519.

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37

Mariani, Francesca, Andrés Damian, Thalía Arias, Rodolfo Ferrando, and Sergio Dansilio. "Wernicke-Korsakoff syndrome in a young adult." Journal of Neurology & Stroke 13, no. 4 (August 4, 2023): 97–98. http://dx.doi.org/10.15406/jnsk.2023.13.00551.

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Abstract (sommario):

Introduction: Wernicke-Korsakoff Syndrome (WKS) presents a high underdiagnosis, and great clinical variability, mainly in brief alcohol consumption histories, being important to consider environmental and genetic factors that contribute to its early presentation. Clinical case: 35-year-old patient with SWK of alcoholic etiology assessed by neuropsychological study, magnetic resonance imaging studies and brain SPECT. He presented cognitive findings compatible with SWK. The MRI was normal and the SPECT was compatible with the SWK.

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38

ENGEL, PETER A., MARGARET GRUNNET, and BARRY JACOBS. "Wernicke-Korsakoff Syndrome Complicating T-Cell Lymphoma." Southern Medical Journal 84, no. 2 (February 1991): 253–56. http://dx.doi.org/10.1097/00007611-199102000-00026.

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39

Delin, Catherine R., and Terry H. Lee. "Wine, thiamine and the Wernicke‐Korsakoff syndrome." Journal of Wine Research 2, no. 1 (January 1991): 21–29. http://dx.doi.org/10.1080/09571269108717887.

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40

Moriyama,, Yasushi, Taro Muramatsu,, Motoichiro Kato, and Haruo Kashima. "Repeated clinical episodes of Wernicke-Korsakoff syndrome." Australian and New Zealand Journal of Psychiatry 38, no. 8 (August 2004): 653. http://dx.doi.org/10.1111/j.1440-1614.2004.01432.x.

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41

Arya, Dinesh K. "Wernicke-Korsakoff syndrome following self-induced starvation." Irish Journal of Psychological Medicine 12, no. 2 (June 1995): 66–67. http://dx.doi.org/10.1017/s0790966700004249.

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AbstractA non-alcoholic patient is reported who as a result of self-induced starvation was found to have nystagmus, gait ataxia and severe deficits in recent and remote memory and new learning, with intact immediate recall, abstraction and judgement capabilities. This pattern of cognitive deficit with nystagmus and ataxia suggests the diagnosis of Wernicke-Korsakoff syndrome.

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42

Cook, C. C. H. "Prevention and Treatment of Wernicke-Korsakoff Syndrome." Alcohol and Alcoholism 35, Supplement_1 (May 1, 2000): 19–20. http://dx.doi.org/10.1093/alcalc/35.supplement_1.19.

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43

Kopelman, Michael D. "Observations on the Clinical Features of the Wernicke–Korsakoff Syndrome." Journal of Clinical Medicine 12, no. 19 (September 30, 2023): 6310. http://dx.doi.org/10.3390/jcm12196310.

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Abstract (sommario):

This paper begins with a short case report of florid, spontaneous confabulation in a 61-year-old man with an alcohol-induced Wernicke-Korsakoff syndrome. His confabulation extended across episodic and personal semantic memory, as well as orientation in time and place, as measured on Dalla Barba’s Confabulation Battery. Five other brief case summaries will then be presented, followed by a summary of the clinical, neurological, and background neuropsychological findings in three earlier series of Korsakoff patients. These observations will be considered in light of Wijnia’s recent and my own, earlier reviews of the Korsakoff syndrome. Taken together, they indicate the need for a multi-faceted approach (clinical, neurological, neuropsychological, and neuroimaging) to the assessment and diagnosis of the disorder.

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44

Laureno, Robert. "Paul Yakovlev Remembered: An Interview with Maurice Victor." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 36, no. 03 (May 2009): 311–14. http://dx.doi.org/10.1017/s0317167100007034.

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Maurice Victor, the great Canadian neurologist, was an expert on the neurology of alcoholism including the Wernicke-Korsakoff syndrome. In Boston, Massachusetts he encountered the leading neuroanatomist, Paul Yakovlev, an immigrant from Russia. Together Victor and Yakovlev collaborated on translating the work of S.S. Korsakoff from Russian to English. This interview of Victor about Yakovlev is informative about both of these great figures in North American Neurology.

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45

De Reuck, Jacques. "The Wernicke-Korsakoff encephalopathy: An updated review." Journal of Neurology & Stroke 12, no. 3 (July 5, 2022): 79–82. http://dx.doi.org/10.15406/jnsk.2022.12.00505.

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Abstract (sommario):

Wernicke's encephalopathy is responsible for an acute neuropsychiatric syndrome that is associated with significant morbidity and mortality. It is most frequently due to alcoholism but can also be the result of chronic diseases, mainly systemic tumours, leading to thiamine deficiency. In the non-thiamine treated patients Korsakoff’s syndrome is the residual complication of the encephalopathy. The clinical diagnosis of Wernicke encephalopathy in alcoholics requires two of the following four signs: dietary deficiencies, eye signs, cerebellar dysfunction, and either disturbed mental state or mild memory impairment. These symptoms are less specific in the non-alcoholic patients. Korsakoff's syndrome is the residual condition in none thiamine treated patients. It is predominantly characterized by global amnesia, and in the more severe cases also by cognitive and behavioral dysfunction. Magnetic resonance imaging of the brain can detect the specific lesions and be helpful for the diagnosis. Treatment with 2500 mg thiamine intravenously is recommended as soon as possible.

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46

Zi-Jian, Cai. "Amnesic Pathologies in Regulation of Dopamine as Supplement to Wernicke-Korsakoff Syndrome: A Limbic-Reticular Coupling View." European Journal of Medical and Health Research 2, no. 4 (July 1, 2024): 111–17. https://doi.org/10.59324/ejmhr.2024.2(4).15.

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Abstract (sommario):

Background: It was suggested by the limbic-reticular coupling theory that the hippocampus and amygdala regulate such descending limbic structures as the mammillary bodies, septum, hypothalamus and habenula, and in turn regulate the ascending noradrenergic, serotonergic, dopaminergic and cholinergic systems to consolidate and recall declarative memory, while the anterior and mediodorsal thalamic nuclei of Wernicke-Korsakoff syndrome beyond limbic-reticular coupling be related else to familiarity. Aim: It was aimed to highlight a portion of limbic-reticular coupling structures in alcoholic Korsakoff’s syndrome, including the dopaminergic system, habenula, mammillary bodies, etc. Methods: It was searched the papers from Pubmed and Baidu. Results and Discussions: It is highlighted that, (a) the mesolimbic dopamine, liable to be affected by alcohol, induces the hippocampal theta rhythm via septum, helping encode and consolidate new memories, such as dopaminergic enhancement of motivational declarative memory in young human adults; (b) dopamine can activate cortical gamma wave and help recall; (c) joint damage of habenula and mammillary bodies, both sending efferents to ventral tegmental area(VTA) rich in dopaminergic neurons, is sufficient to cause Korsakoff’s amnesia; (d) the loop of hippocampal CA3 to lateral septum(LS) to VTA(CA3-LS-VTA) activates dopamine for contextual memory in animals, consistent with dopaminergic antagonist impairing declarative memory recall in humans; (e) whereas thiamine deficiency, the major nutritional deficit causing Wernicke-Korsakoff syndrome, impairs noradrenergic but spares dopaminergic system. Conclusion: It is supplemented the integrative dysfunctions in regulation of such neglected dopaminergic system, including the habenula, mammillary bodies and VTA dopamine, as partial contribution to memory impairments in Korsakoff’s syndrome.

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47

Victor, M. "MR in the diagnosis of Wernicke-Korsakoff syndrome." American Journal of Roentgenology 155, no. 6 (December 1990): 1315–16. http://dx.doi.org/10.2214/ajr.155.6.2122686.

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48

GIANNINI, A. JAMES, CYNTHIA SENG, and WILLIAM A. PRICE. "Wernicke-Korsakoff Syndrome Associated with Chronic Benzodiazepine Abuse." Journal of Clinical Psychopharmacology 5, no. 3 (June 1985): 185. http://dx.doi.org/10.1097/00004714-198506000-00026.

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49

Sandyk, Reuven, and Paul Iacono Robert. "Wernicke-Korsakoff??s Syndrome and the Opioid System." Journal of Clinical Psychopharmacology 7, no. 1 (February 1987): 49. http://dx.doi.org/10.1097/00004714-198702000-00023.

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50

Uehara, Takanori, Masatomi Ikusaka, Yoshiyuki Ohira, Kazutaka Noda, Shingo Suzuki, Kiyoshi Shikino, Takeshi Kondo, Hideki Kajiwara, Akiko Ikegami, and Yusuke Hirota. "Olmesartan-induced Enteropathy Manifesting as Wernicke-Korsakoff Syndrome." Internal Medicine 55, no. 24 (2016): 3675–78. http://dx.doi.org/10.2169/internalmedicine.55.7388.

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