Journal articles: 'Alcoholic encephalopathy'

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Dr, Sumit Kumar Bochiwal, Vishakha Vinod Dr., Chetan Maniya Dr., and Deepak Shukla Dr. "Study of clinical profile of alcoholic hepatitis : A Case series of 100 cases." International Multispeciality Journal of Health 5, no. 5 (2019): 106–11. https://doi.org/10.5281/zenodo.3236817.

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Abstract— Alcohol consumption is associated with a wide range of adverse health and social consequences. Alcoholic Hepatitis is one of the consequence of alcoholism. So an observational study was designed over the period of one year to study clinical profile and effects of Alcoholic Hepatitis. The study was carried out in 100 consecutive patients admitted to tertiary care hospital with alcoholic hepatitis. Data entry and analysis was done in Microsoft excel through Descriptive statistic and chi-square tests. It was observed that most patients with Alcoholic Hepatitis drinks more than 100 g/d with 150-200 g per day being common. In the present study 92% of patients were heavy alcoholics i.e. more than 80gm/day. This suggests that alcoholic hepatitis mostly occurs in heavy drinkers. Present study suggests that Discriminate Factor score does not associate with complications like hepatic encephalopathy and ascites. SGOT, SGPT, serum bilirubin, prothrombin time and serum albumin didn’t associate well with amount of alcohol intake. This study also observed that patient with Glasgow Alcoholic Hepatitis Score of more than 9 have more chance of complications like hepatic encephalopathy and ascites. It can be concluded from this study that  most of the alcoholic hepatitis patients were young adults and middle age population, who were is active and productive mass of society. Early detection of alcoholic liver disease can decrease both morbidity and mortality due to alcoholic liver disease.

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Cotelli, Maria Sofia, Patrizia Civelli, and Marinella Turla. "Mild symptomatic Wernicke’s Encephalopathy: a case report." Journal of Health Sciences 8, no. 3 (2018): 197–200. http://dx.doi.org/10.17532/jhsci.2018.269.

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Wernicke’s encephalopathy (WE) is an acute, neuropsychiatric syndrome which results from a deficiency in vitamin B1 (thiamine), which in its biologically active form, thiamine pyrophosphate, is an essential coenzyme in several biochemical pathways in the brain, often due to alcohol abuse (alcoholic WE). Non-alcoholic WE variant manifests in many different clinical settings, such as gastrointestinal tumors, hyperemesis gravidarum, chemotherapy, acquired immunodeficiency syndrome, prolonged therapeutic fasting, protracted parenteral nutrition and bariatric surgery, anorexia nervosa and can even be secondary to socioeconomic factors. The classic triad of encephalopathy, oculomotor dysfunction, and gait ataxia is only seen in approximately one-third of patients and is more common in alcoholics; only some of these symptoms are usually present. Here we describe a case of an occasional neuroradiological finding of Wernicke Encephalopathy not related to symptoms or signs.

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

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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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Lyons, Daniel A., Luke L. Linscott, and Darcy A. Krueger. "Non-alcoholic Wernicke Encephalopathy." Pediatric Neurology 56 (March 2016): 94–95. http://dx.doi.org/10.1016/j.pediatrneurol.2015.12.007.

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Kladova, Ye A., and B. M. Doronin. "Neuropshycological recovery dynamics in patients with ischemic stroke and alcoholic encephalopathy." Bulletin of Siberian Medicine 9, no. 4 (2010): 70–72. http://dx.doi.org/10.20538/1682-0363-2010-4-70-72.

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Examination of recovery dynamics of cognitive impairments in patients with ischemic stroke and with or without alcoholic encephalopathy was conducted. It was shown that in patients with ischemic stroke and alcoholic encephalopathy dementia prevails, and positive dynamics is extremely rare.

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Pomier-Layrargues, Gilles, Ngoc Huu Nguyen, Claire Faucher, Jean-François Giguère, and Roger F. Butterworth. "Subclinical Hepatic Encephalopathy in Cirrhotic Patients: Prevalence and Relationship to Liver Function." Canadian Journal of Gastroenterology 5, no. 4 (1991): 121–25. http://dx.doi.org/10.1155/1991/680528.

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Neuropsychological tests were administered to 22 alcoholic cirrhotic patients, 20 nonalcoholic cirrhotic patients and 42 control subjects matched for age and educational background. Liver function estimated by Pugh score was identical in alcoholic and nonalcoholic cirrhotics. Thirty-two cirrhotic patients (76%) failed one or more psycho logical test. Performance was worse in cirrhotics than in controls in all but one test: the degree of neurological impairment was similar in alcoholics and nonalcoholics and correlation with the severity of Liver dysfunction was only marginal. A combination of the five more sensitive tests was able to identify 31 of 32 cirrhotic patients with subclinical encephalopathy; this ‘mini battery’ of tests can be performed within 10 mins. Suhclinical hepatic encephalopathy is frequent in cirrhotic patients and can adversely affect their psychosocial behaviour.

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Tatiana, Roshchupkina. "Cognitive violations of persons with alcoholic encephalopathy and paroxismal states." ScienceRise: Medical Science, no. 6(33) (November 29, 2019): 43–46. https://doi.org/10.15587/2519-4798.2019.185782.

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The article addresses the issues of cognitive impairment among persons with alcohol dependence, aggravated by alcoholic encephalopathy and paroxysmal conditions. The aim of the study was to identify the levels of impaired short-term memory, to identify cognitive impairment of patients with alcohol addiction with alcoholic encephalopathy and paroxysmal conditions. Materials and methods: 132 people from the contingent of alcohol addicts (AА) and from the contingent of healthy and 4 comparison groups have been identified and examined over the two years on the basis of KNP CHOR «Regional Clinical Narcological Hospital No. 3». The following techniques were used to assess psychosocial and cognitive impairment: “Jacobson Short-Term Memory Measurement Technique”; "The methodology for determining the index of short-term memory proposed by L. S. Muchnik and V. M. Smirnov (1968)". Result. According to the results of the researches, the cognitive and mnemonic sphere of persons with AА, AE and PS were expressed in the form of significant reduction of short-term memory and cognitive impairment. The presence of significantly "deeper" and "gross" degenerative-organic lesions of the central nervous system in chronic alcoholic lesions with the development of alcoholic encephalopathy and paroxysmal states of alcoholic genesis has been proved. Conclusions. Thus, the obtained research results only confirm the data of numerous world sources on the development of cognitive decline in individuals with alcohol dependence

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Victor, Maurice. "Alcoholic Dementia." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 21, no. 2 (1994): 88–99. http://dx.doi.org/10.1017/s031716710004899x.

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Abstract:At least four distinct cerebral diseases — Wernicke-Korsakoff, Marchiafava-Bignami, pellagrous encephalopathy, and acquired hepatocerebral degeneration — have a close association with chronic alcoholism. Each is characterized by a distinctive pathologic change and a reasonably wellestablished pathogenesis; in each the role of alcohol in the causation is secondary. The question posed in this review is whether there is, in addition to the established types of dementia associated with alcoholism, a persistent dementia attributable to the direct toxic effects of alcohol on the brain — i.e., a primary alcoholic dementia. The clinical, psychologic, radiologic, and pathologic evidence bearing on this question is critically reviewed. None of the evidence permits the clear delineation of such an entity. The most serious flaw in the argument for a primary alcoholic dementia is that it lacks a distinctive, well-defined pathology, and it must remain ambiguous until such time as its morphologic basis is established.

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Abdaal, Maham, Zafeer-ul-Hassan Iqbal, Numan Ghafoor, Muhammad Usman, Saqib Hussain, and Mehi Naqvi. "Determine the Frequency of Factors Leading to Hepatic Encephalopathy in Patients with Liver Cirrhosis." Pakistan Journal of Medical and Health Sciences 16, no. 12 (2022): 197–99. http://dx.doi.org/10.53350/pjmhs20221612197.

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Aim: To determine the frequency of factors leading to hepatic encephalopathy in patients with liver cirrhosis. Study design: Retrospective study Place and duration of study: Department of Internal Medicine, Rawalpindi Medical Universityfrom 01-07-2021 to 30-06-2022 Methodology: One hundred patients were included and divided into two groups. One group was those which developed hepatic encephalopathy while the other group was of those which did not develop any hepatic encephalopathy. Various risk factors and their frequencies were measured through a modelled hepatic encephalopathy pharmacological, clinical as well as demographic data. Comparison on the frequency of the variable seen in hepatic encephalopathy patients with non-hepatic encephalopathy was conducted for better assessment of the frequency of risk factors. Results: Seventy patients did not develop hepatic encephalopathy while 30 patients did develop hepatic encephalopathy. Fifteen patients had developed alcoholic liver cirrhosis followed by hepatitis C and non-alcoholic cirrhosis. Age greater than 60 years had a percentage of 60% within cases of hepatic encephalopathy only. Prevalence of hepatitis C cirrhosis in 36.6%, diabetes in 49%, cardiovascular disease in 51%, hepatocellular carcinoma in 6.6%, use of proton pump inhibitor in 63.3% were presented and were higher than who did not develop hepatic encephalopathy. Benzodiazepines, gamma aminobutyric acid [GABA]ergics, opioids and proton pump inhibitors each of them was associated with increased chances of hepatic encephalopathy. Conclusion: Hepatic encephalopathy was more commonly observed in older patients (60%) and more specifically in male population. Higher frequency of comorbidities (hypertension, diabetes, cardiovascular disease, ascites, alcoholic cirrhosis), CCI score and pharmacological drugs were identifiable risk factors for hepatic encephalopathy. Key words: Neurotoxicity; Cirrhosis, Complications, Hepatitis C, Deteriorate

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Wadekar, Abhijit, Sanyukta Hepat, Anamika Giri, and Sourya Acharya. "Wernicke’s Encephalopathy with Normal Neuroimaging - Suspect and Treat - A Case Report." Journal of Evolution of Medical and Dental Sciences 10, no. 33 (2021): 2867–69. http://dx.doi.org/10.14260/jemds/2021/584.

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Wernicke’s encephalopathy (WE) is an unrecognized nutritional deficiency which often goes unnoticed. WE is clinically often composed of a triad including nystagmus, ophthalmoplegia and altered mental status. Although this triad practically is present only in a handful of cases1 it is also described as an acute neuropsychiatric presentation of thiamine deficiency. Early diagnosis and prompt treatment are of utmost importance here as it can prevent chronic brain damage which is often the end effect of thiamine deficiency. Wernicke’s encephalopathy is most commonly found in patients with chronic alcoholism, less frequent in non-alcoholic patients. In non-alcoholic patients, Wernicke’s encephalopathy might develop due to erosion of upper portion of gastrointestinal tract or secondary to intractable vomiting, inadequate dietary intake or malabsorption. Other causes include malignancies (gastric cancer, leukaemia, lymphoma), hyperemesis, anorexia, thyroid conditions.1,2 Wernicke’s encephalopathy is caused due to thiamine (B1) deficiency. B1 is a water-soluble vitamin which acts as a co-factor for carbohydrate metabolism. It is also important for neuronal cell function.2 This vitamin can’t be synthesised in the human body and thus dietary intake play a very important role. Symptoms of thiamine deficiency Include - Nystagmus, ataxia, encephalopathy, mental confusion. Early onset includes symptoms like: - headache, irritability, fatigue and abdominal discomfort. Prophylactic thiamine supplementation forms a major treatment for patients at risk for developing refeeding syndrome (RFS). RFS is an underdiagnosed condition which is characterised by potential shift in the fluid and electrolytes.

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Tóth, Adrián, Gabriella Aradi, György Várallyay, Zsuzsanna Arányi, Dániel Bereczki, and Ildikó Vastagh. "Wernicke’s encephalopathy induced by the use of diet pills and unbalanced diet." Orvosi Hetilap 155, no. 12 (2014): 469–74. http://dx.doi.org/10.1556/oh.2014.29847.

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Wernicke’s encephalopathy is an acute, potentially life-threatening, neurological syndrome resulting from thiamine deficiency. The disorder is still greatly underdiagnosed and, without prompt treatment, the condition can lead to the chronic form of the disease, Korsakoff’s syndrome or even death. In developed countries Wernicke’s encephalopathy has been associated with alcoholism, but in recent years there has been an increasing number of non-alcoholic cases. Authors report the case of a 23-year-old woman who developed oculomotor dysfunction, encephalopathy and ataxia as a result of an extreme diet and use of diet pills. The diagnosis of Wernicke’s encephalopathy was supported by the resolution of neurological signs after parenteral thiamine replacement. This case is presented because of the rare etiology and diagnostic difficulty, and the latest diagnostic and therapic guidelines are also highlighted. Orv. Hetil., 2014, 155(12), 469–474.

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K. O. Gerasymenko. "Forensic medical diagnosis of alcoholic encephalopathy." Bukovinian Medical Herald 17, no. 3 (67) p.1 (2013): 40–41. http://dx.doi.org/10.24061/2413-0737.xvii.3.67.2013.123.

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Ikeda, Kojiro, Hiroyuki Yano, Tetsushi Higa, and Mitsuyo Kinjo. "Nystagmus in non-alcoholic Wernicke encephalopathy." BMJ Case Reports 14, no. 2 (2021): e241130. http://dx.doi.org/10.1136/bcr-2020-241130.

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Ostapchuk, Ostapchuk E. S., and Chikviladze S. S. Chikviladze. "Wernicke encephalopathy of non-alcoholic genesis." Therapy 5_2024 (July 18, 2024): 122–28. http://dx.doi.org/10.18565/therapy.2024.5.122-128.

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Rathakrishnan, Rahul, and Einar-Wilder Smith. "MRI in non-alcoholic Wernicke’s encephalopathy." Journal of Clinical Neuroscience 15, no. 4 (2008): 478–80. http://dx.doi.org/10.1016/j.jocn.2007.03.007.

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Okafor, Chukwudumebi, Manojna Nimmagadda, Sarthak Soin, and Lavanya Lanka. "Non-alcoholic Wernicke encephalopathy: great masquerader." BMJ Case Reports 11, no. 1 (2018): e227731. http://dx.doi.org/10.1136/bcr-2018-227731.

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Thiamine is an important coenzyme, which is essential for metabolism and maintaining cellular osmotic gradient. Thiamine deficiency can cause focal lactic acidosis, alteration of the blood–brain barrier and the production of free radicals through cell death by necrosis and apoptosis. Wernicke encephalopathy (WE) is a clinical diagnosis. Cytotoxic and vasogenic oedema are the most typical neuroimaging findings of WE, presenting as bilateral symmetrical hyperintense signals on T2-weighted MR images. MRI is not necessary for the diagnosis of WE, but it can be helpful in ruling out alternative diagnosis. We present the case of an 61-year-old man with the history of class II obesity presenting with diplopia, dysarthria and vertigo, confirmed to be non-alcoholic WE. We aim to highlight the occurrence of WE in patients with large bowel resection though. Delay in diagnosis, particularly in obese individuals due to lack of suspicion, can lead to grim prognosis.

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Theodoreson, Mark D., Ausrine Zykaite, Michael Haley, and Saroj Meena. "Case of non-alcoholic Wernicke’s encephalopathy." BMJ Case Reports 12, no. 11 (2019): e230763. http://dx.doi.org/10.1136/bcr-2019-230763.

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A 61-year-old obese man presented with 8-week history of nausea and occasional vomiting. He reported poor appetite and unintentional weight loss of more than 20 kg of his body mass. A week after admission, he developed double vision and unsteady gait. Neurological examination revealed isolated sixth cranial nerve palsy on the left side with horizontal nystagmus that progressed to bilateral lateral gaze palsy with normal vertical gaze. Brain MR revealed T2/fluid attenuation inversion recovery (FLAIR) high signal in mammillary bodies, tectum of the midbrain and the periaqueductal grey matter. He was diagnosed with Wernicke’s encephalopathy (WE). WE is a medical emergency that carries high mortality yet can be often under-diagnosed in the non-alcoholic patient. Varied presentation and absence of alcohol dependence lowers the degree of suspicion and this was true in this case. The patient was given intravenous thiamine and made a rapid and dramatic recovery.

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Maybogin, A. M., M. K. Nedzvedz, and N. V. Kornev. "Morphological changes in the brain in liver cirrhosis of alcoholic and viral etiology." Acta Biomedica Scientifica 7, no. 5-2 (2022): 122–30. http://dx.doi.org/10.29413/abs.2022-7.5-2.13.

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Background. Hepatic encephalopathy is an actual problem of modern medicine. However, its pathogenesis and histological picture are currently insufficiently studied. Less is known about the impact of the nature of primary liver disease on pathogenesis and histological picture of hepatic encephalopathy. This determines the relevance of further morphological studies of the brain in the late stages of liver cirrhosis of various etiologies.The aim. To establish and compare the morphological changes in the brain in alcoholic liver cirrhosis and viral (hepatitis C virus (HCV)) cirrhosis.Materials and methods. The morphological study of the brain of 40 deceased in outcome of HCV-associated cirrhosis and 23 patients died in outcome of chronic alcoholism was carried out. Histological changes in various parts of the brain were studied using survey and elective stains. The immunohistochemical study of HCV NS3 and CD68 expression in different brain regions was performed in cases of HCV-infection.Results. The changes of neurons, glial cells and cerebral microvessels underlie in the basis of morphological picture of brain damage in both studied groups underlie that corresponds to the “classical” model of hepatic encephalopathy pathogenesis. At the same time, a number of morphological features were observed. The most prominent differences concerned the manifestations of the glial reaction. The productive changes of macroglial cells with the appearance of multiple Alzheimer’s astrocytes type 2 as well as spongious changes in subcortical white matter dominated in the observations of alcoholic cirrhosis. In contrast, microglia cells reaction (microgliosis) in white matter was noticed in HCV-associated cirrhosis.Conclusions. The differences in histological signs of brain in the terminal stages of liver disease of viral and alcoholic etiology are shown. They broaden current idea of morphological picture of hepatic encephalopathy, and may be used to study its pathogenesis.

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Duve, Khrystyna, and Svitlana Shkrobot. "Neuroimaging aspects in encephalopathies of various genesis." Ukrains'kyi Visnyk Psykhonevrolohii, Volume 31, issue 3 (116), 2023 (September 18, 2023): 25–28. http://dx.doi.org/10.36927/2079-0325-v31-is3-2023-4.

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This article is devoted to the analysis of the neuroimaging picture of the most common types of encephalopathies. In particular, in 2021 and 2022, we examined 520 patients with post-traumatic encephalopathy (TE) (n = 145), vascular encephalopathy (VE) in case of chronic brain ischemia (n = 145), alcoholic encephalopathy (AE) (n = 102), and post-infectious encephalopathy (PIE) (n = 128). We studied the neuroimaging characteristics of each of these subtypes, their features and frequency. Thus, we established that the most frequent expansion of the ventricles was observed in patients with VE (53.79 %), which probably exceeded the similar indicator in patients with TE (by 26.89 %), with AE (by 15.55 %) and from PIE (by 37.38 %). Expansion of the subarachnoid spaces was equally common in the groups of patients with TE (38.62 %) and VE (40.00 %), with a probable difference in relation to the group with PIE (7.81 %). Patients with AE (60.78 %) had significantly more frequent manifestations of gliosis than patients with TE (47.59 %). The highest frequency of cystic changes was observed in the group with TE (45.05 %), which significantly exceeded the indicators of other groups. The correlations between neuroimaging changes and clinical syndromes were clarified. Key words: encephalopathy, post-traumatic encephalopathy, vascular encephalopathy in case of chronic brain ischemia, alcoholic encephalopathy, post-infectious encephalopathy

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Begum, Tahera, Shafiul Hasan, and M. Nazimuddin. "Wernicke’s Encephalopathy Due to Hyperemesis Graviderum : A Rare Presentation." Chattagram Maa-O-Shishu Hospital Medical College Journal 16, no. 1 (2017): 54–56. http://dx.doi.org/10.3329/cmoshmcj.v16i1.34988.

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Wernicke’s encephalopathy is a common and preventable acute neurological symptom due to deficiency of thiamine. Alcoholism also causes Thiamine deficiency. It can occur in non-alcoholic conditions such as prolonged starvation, hyperemesis graviderum, bariatric surgery, HIV, AIDS. The characteristics clinical triad of disease is ophthalmoplagia,ataxia & global confusion. Here a patient was studied who was diagnosed on M.R.I as Wernicke’s encephalopathy.Chatt Maa Shi Hosp Med Coll J; Vol.16 (1); Jan 2017; Page 54-56

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Swain, Sanjana Simansu, and Suhasin Ganta. "Korsakoff Syndrome: A Chronic Nutritional Deficiency Neuropsychiatric condition." YMER Digital 21, no. 05 (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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Pinchuk, V. A., G. Ya Silenko, M. Yu Delwa, A. M. Kryvchun, and І. І. Delwa. "WERNICKE’S NON-ALCOHOLIC ENCEPHALOPATHY: A CLINICAL OBSERVATION." Bulletin of Problems Biology and Medicine 2, no. 1 (2021): 123. http://dx.doi.org/10.29254/2077-4214-2021-2-160-123-126.

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Park, Seong Ho, Duk Lyul Na, Jae Hong Lee, et al. "Alcoholic pellagra encephalopathy combined with Wernicke disease." Journal of Korean Medical Science 6, no. 1 (1991): 87. http://dx.doi.org/10.3346/jkms.1991.6.1.87.

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Kuo, H. C. "Non-alcoholic Wernicke’s encephalopathy with cortical involvement." Journal of the Neurological Sciences 381 (October 2017): 500. http://dx.doi.org/10.1016/j.jns.2017.08.3616.

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Liss, Leopold. "P-171: Alzheimer disease and “alcoholic encephalopathy”." Alzheimer's & Dementia 3, no. 3S_Part_2 (2007): S153. http://dx.doi.org/10.1016/j.jalz.2007.04.134.

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Michowitz, Yoav, Laurian Copel, Eli Shiloach, Ilia Litovchik, and Micha Jehuda Rapoport. "Non-alcoholic Wernicke's encephalopathy — unusual clinical findings." European Journal of Internal Medicine 16, no. 6 (2005): 443–44. http://dx.doi.org/10.1016/j.ejim.2005.02.009.

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Liss, Leopold. "P3-274: Alzheimer's disease and Alcoholic Encephalopathy." Alzheimer's & Dementia 7 (July 2011): S604. http://dx.doi.org/10.1016/j.jalz.2011.05.1716.

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Khuvituguldur, Telmen, Munkhbaatar Dagvasumberel, and Delgerdalai Khashbat. "A Typical MRI Features of Wernicke’s Encephalopathy: A Case Report." Central Asian Journal of Medical Sciences 10, no. 4 (2024): 158–61. https://doi.org/10.24079/cajms.2024.04.004.

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Objective: This case report highlights the rare occurrence of Wernicke encephalopathy (WE) in a non-alcoholic patient with atypical imaging findings. Methods: Diagnosis is made based on clinical and imaging findings. Results: A 44-year-old man with a history of inability to walk, ataxia, and did not have a habit of alcoholism. Magnetic resonance imaging (MRI) showed symmetrical bilateral basal ganglia changes. Conclusion: We should always be included in the differential diagnosis for bilateral basal ganglia lesions. MRI has proven useful in diagnosing WE in patients with occasional neurological symptoms and atypical imaging findings.

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John, Elizabeth S., Ramy Sedhom, Ishita Dalal, and Ranita Sharma. "Posterior reversible encephalopathy syndrome in alcoholic hepatitis: Hepatic encephalopathy a common theme." World Journal of Gastroenterology 23, no. 2 (2017): 373. http://dx.doi.org/10.3748/wjg.v23.i2.373.

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Sharma, Abhishek, Smiti N. Panchal, and Vidhi Thakkar. "UNUSUAL PRESENTATION- MY BRAIN IS WET WITHOUT ALCOHOL: A CASE REPORT OF NON ALCOHOLIC WERNICKES ENCEPHALOPATHY." International Journal of Advanced Research 10, no. 06 (2022): 1090–93. http://dx.doi.org/10.21474/ijar01/14988.

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Case of 72 years male with Nonalcoholic Wernickes encephalopathy (NWE) who was initially investigated managed as Stroke, Metabolic encephalopathy or Suspected Meningoencephalitis. Patient managed clinically, until MRI report and with clinical correlation patient was diagnosed with NWE. Thiamine deficiency is associated with chronic alcoholics which was not among the common differentials in this case and its emphasis in ED among the differentials to be ruled out. A male who is Non-alcoholic was brought to ED having Slurred Speech, confusion, weak memory and evaluated, investigated with multiple tests which turned out to be normal Until MRI showed a well defined area of hyper intensity on DWI in peri-ductal region possibility of WE. We recommend using criteria to diagnose and treat NWE as early as possible to avoid misdiagnosis and treatment delays. We should focus on patients with altered mental symptoms even in coma, administering parenteral thiamine.

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Rahman, AKM Ferdous, Mohiuddin Ahmed, Md Ashraful Haque, Zannatul Naiem, and Manos Kanti Mojumder. "Wernicke’s encephalopathy: A case report." Bangladesh Critical Care Journal 10, no. 2 (2022): 158–60. http://dx.doi.org/10.3329/bccj.v10i2.62212.

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We described a case of an alcoholic patient who presented with a history of Jaundice for 25 days, generalised weakness and loss of appetite for 20 days and altered level of consciousness for 2 days. On examination, patient was grossly icteric and there were no palpable lymphnode. Central nervous system examination revealed low GCS (E2V2M3), Pupil bilaterally pin point, Planter extensor bilaterally and abdominal examination showed mild hepatomegaly. MRI of Brain showed symmetrical hyperintense areas on T2W and FLAIR images seen in the Mamillary bodies, dorsomedial thalami, tectal plate, periaqueductal area and around the third ventricle. The lesions are hypointense on T1W images and showed diffusion restriction on DW images. These findings are compatible with Wernickes Encephalopathy. He was started on thiamine supplementation with which neurological signs improved. Patient had a history of RTA about 1 month prior to ICU admission. Then he underwent Spleenectomy operation. Again a laparotomy operation was done due to intra-abdominal collection and repair of the omental vessels done with thorough peritoneal collection. It is important to consider Wernickes encephalopathy in alcoholic patients with intra-abdominal surgery Bangladesh Crit Care J September 2022; 10(2): 158-160

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Kantariya, R. O., O. N. Vetchinnikova, A. V. Vatazin, and L. A. Sherman. "Non-alcoholic Wernicke’s encephalopathy in a kidney transplant recipient." Russian Journal of Transplantology and Artificial Organs 23, no. 2 (2021): 76–83. http://dx.doi.org/10.15825/1995-1191-2021-2-76-83.

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Background. Non-alcoholic Wernicke’s encephalopathy occurs in various somatic conditions with thiamine deficiency, excessive excretion of thiamine, or impaired thiamine metabolism. Very few cases of this pathology have been described in chronic kidney disease (CKD). We present a unique case of non-alcoholic Wernicke’s encephalopathy in a patient with a kidney transplant is presented.Past medical history. The patient underwent kidney transplantation in 2008. Outpatient follow-up by a nephrologist was irregular. Renal graft function remained relatively stable: blood creatinine 200–240 μmol/L, estimated glomerular filtration rate 40–30 mL/min, tacrolimus plasma concentrations tended to increase (5.7–7.6–8.4–10.4 ng/mL); repeated graft biopsy (in 2015 and in 2017) determined the chronic toxicity of calcineurin inhibitors. The patient’s condition worsened in late January 2020: body temperature increased to 38°C, nausea, vomiting, loose, watery stools for up to 5 times per day, 8 kg weight loss, decreased diuresis. A few days later, double vision, shaky gait and then immobility appeared. Biochemical examination results: potassium 3.8 mmol/L, sodium 139 mmol/L, alpha-amylase 159 units/L (norm 0–100 units/L), creatinine 242 mmol/L, urea 13.2 mmol/L; ultrasound signs of pancreatitis. Magnetic resonance imaging (MRI) of the brain: bilateral diffuse lesions of the midbrain, thalamus, and cerebellum. Based on the clinical picture and on brain MRI results, Wernicke’s encephalopathy was diagnosed. Parenteral administration of thiamine had a good effect.Conclusion. Possible mechanisms of the development of Wernicke’s encephalopathy in a patient were discussed. Vigilance is required regarding this disease when metabolic disorders occur in patients with CKD.

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Nelaturi, Prabhudas, Sangeetha P Kadamani, and Ravikumar Sambandam. "Alcoholism and Socioeconomic Status among Patients with Hepatic Encephalopathy in Association with Increased Mortality." Addiction and Health 16, no. 1 (2024): 1–5. http://dx.doi.org/10.34172/ahj.2024.1467.

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Background: Hepatic encephalopathy (HE) is a complex neuropsychiatric disorder indicated by a deterioration in the functioning of hepatocytes. Impaired brain function is observed in advanced alcoholic liver disease particularly manifesting as HE. The pathophysiology of alcohol-related HE remains unclear. Accordingly, this study aimed to assess alcoholism and socioeconomic status of patients with liver disease compared with stages of HE. Methods: This cross-sectional study was conducted on 62 alcoholic patients who have been consuming alcohol for more than 14 years. Patients were recruited based on the assessment of clinical symptoms and diagnosed according to the MELD and Child-Pugh scoring systems. Findings: Descriptive statistics including demographic details and clinical features of patients were classified based on alcoholism and socioeconomic status. Patients belonging to the lower- and middle-income classes were more in number with a mean age of 46.66±10.21 and 47.14±6.36 years, respectively compared to upper-middle- and upper-income classes. The amount of alcohol intake was 116.59±45.60 in the middle class and 110.0±62.45 in the upper class. Conclusion: Increased progression of HE leads to a rise in the mortality rate due to higher consumption of alcohol. HE is a severe complication in alcohol-related liver cirrhosis that contributes to impaired cognitive function in patients.

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Stepanova, Anastasia V., and Tatiana V. Shuteeva. "Features of the diagnosis of Wernicke’s encephalopathy: a clinical case." Человек и его здоровье 27, no. 1 (2024): 23–29. http://dx.doi.org/10.21626/vestnik/2024-1/03.

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Wernicke's encephalopathy (WE) is a rare neurological disorder caused by vitamin B1 (thiamine) deficiency and is associated with a significant risk of developing persistent neurological deficiency, chronification, disability and ultimately death if the aetiopathogenetic therapy with high doses of vitamin B1 is initiated late. Objective: to raise awareness among physicians about the characteristics of clinics, diagnostics and treatment of Wernicke's encephalopathy. Materials and methods. Retrospective analysis of the medical records of a patient with alcoholic Wernicke's encephalopathy. Results. This paper presents the own clinical observation of a patient with newly diagnosed alcoholic Wernicke's encephalopathy, clinical manifestations and MRI picture, describes the main features of aetiology and pathogenesis of this pathological process. Conclusion. An important role in the diagnosis of WE is played by the correct collection of anamnestic data and magnetic resonance imaging (MRI) of the brain, which has a sufficiently high specificity and is the only diagnostic method that allows this disease to be identified with high reliability. Thus, it is the thorough collection of anamnesis and the timely MRI examination that allow the doctor to point in the right direction of the diagnostic search in a timely manner.

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Gyan, Bhushan Raman, Baid Atul, and Kumari Vandana. "A Retrospective Study Evaluating Clinical Spectrum of the Patients with Acute Hepatic Encephalopathy." International Journal of Current Pharmaceutical Review and Research 16, no. 05 (2024): 508–11. https://doi.org/10.5281/zenodo.12788239.

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AbstractAim: The aim of the present study was to assess the clinical profile of the patients with acute hepaticencephalopathy in a tertiary health care center.Methods: The present study is a retrospective study carried on patients with acute hepatic encephalopathy patientsattending OPD and emergency in Department of Medicine, Mata Gujari Memorial Medical College, Kishanganj,Bihar, India from February 2019 to January 2020. Total 100 patients with inclusion criteria were studied.Results: Majority of the patients were in the age group of 41- 50 years (35%) followed by 31-40 years (24%).Patients were less in the age group below 20 years (4%). %). Out of total 100 patients 75 were male and 25 werefemales. In our study alcoholic liver disease was most common etiological factor (44%). Hepatitis B infectionwas seen in 32% and Hepatitis C infection in 13% patients. Six patients showed alcoholic liver disease withhepatitis B infection. Unknown etiology was observed in 6% patients. According to Child Pugh score, 58%patients were in group A followed by Group B (33%) and Group C (9%). Majority of the patients were in GradeIV (36%), followed by Grade III (32%). Grade I included 20% patients and Grade II included 12%. Our studyrevealed majority patients were of type C (80%) Hepatic encephalopathy followed by type A (19%).Conclusion: Factors affecting mortality in hepatic encephalopathy were Male sex, alcohol intake, Child-PughClass C, Grade III and IV hepatic encephalopathy

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Soutter, D. I., B. Langer, B. R. Taylor, and P. Greig. "Emergency Portasystemic Shunting in Cirrhotics With Bleeding Varices — A Comparison of Portacaval and Mesocaval Shunts." HPB Surgery 1, no. 2 (1989): 107–18. http://dx.doi.org/10.1155/1989/70865.

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Despite the best conservative measures available for the control of major variceal hemorrhage, some patients either continue to bleed, or rebleed early, and require emergency surgery. One hundred patients with cirrhosis and uncontrolled bleeding were treated with emergency portasystemic shunts between 1968 and 1983. Fifty eight patients had end-to-side portacaval shunts and 42 had Dacron interposition mesocaval shunts. Both groups were comparable with respect to age, sex and prevalence of alcoholism. There was an increased severity of liver disease as assessed by Child's class in the mesocaval group of patients.Overall in-hospital mortality was 31% with no significant difference demonstrated between the mesocaval group (28%) and the portacaval group (33%), nor between alcoholic cirrhotics (34%) and non-alcoholic cirrhotics (21%). Mortality rates based on severity of liver disease were: Child's A (1/6) 17%, Child's B (9/48) 19%, and Child’s C (21/46) 46%. There was a statistically significant difference between Child's A & B and Child's C (p < 0.01). Four patients were lost to follow-up. No significant differences were found in 5 year survival by life table analysis comparing portacaval (39%) vs. mesocaval (28%) groups or alcoholic cirrhotics (36%) vs. non-alcoholic cirrhotics (29%). Encephalopathy in survivors was absent in 46%, mild in 28% and severe in 26% of patients. There was no significant difference in encephalopathy rates following portacaval or mesocaval shunting.Neither operation was clearly superior and choice of operation can be made on the basis of technical and anatomical factors and surgeon experience. Emergency shunting remains a useful option for patients with variceal bleeding refractory to other more conservative therapy, and is associated with acceptable early mortality and long term survival rates.

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Simionescu, Oana, Laura Dumitrescu, Alexandra Oprisan, et al. "Update on Wernicke’s: considerations on epidemiology (II)." Romanian Journal of Neurology 10, no. 4 (2011): 172–78. http://dx.doi.org/10.37897/rjn.2011.4.2.

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Wernicke Encephalopathy (WE) is frequently missed out in clinical practice. The consequences of under diagnosing WE are deleterious. WE is caused by thiamine (vitamin B1) deficiency and may occur in alcoholic and non-alcoholic patients. A better knowledge on epidemiology may shed light on the real nature of this condition. In this short review we outline epidemiological factors associated with WE.

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Vidya, Bulla Sri. "NON-ALCOHOLIC WERNICKE ENCEPHALOPATHY COMPLICATING WITH HYPEREMESIS GRAVIDUM." Journal of Medical Pharmaceutical And Allied Sciences 9, no. 2 (2020): 2506–8. http://dx.doi.org/10.22270/jmpas.v9i2.947.

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Yang, Xian-Xin, Qi-Hua Wu, Li-Ling Chen, Shan-Zhu Mo, and De-Fang Chen. "Nutritional status in non alcoholic subclinical portosystemic encephalopathy." World Journal of Gastroenterology 4, no. 2 (1998): 52. http://dx.doi.org/10.3748/wjg.v4.isuppl2.52.

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Sohn, Min Kyun, Pil Soon Choi, Sung Kyum Kim, Sung Ju Jee, and Tae Sung Lee. "Hypoglycemic Encephalopathy in an Alcoholic: A case report." Brain & Neurorehabilitation 1, no. 2 (2008): 197. http://dx.doi.org/10.12786/bn.2008.1.2.197.

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Santos Andrade, C., L. Tavares Lucato, M. da Graça Morais Martin, et al. "Non-alcoholic Wernicke's encephalopathy: broadening the clinicoradiological spectrum." British Journal of Radiology 83, no. 989 (2010): 437–46. http://dx.doi.org/10.1259/bjr/27226205.

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Matikas, G., D. Tzanetakos, C. Papastergios, I. Markakis, and G. Gekas. "Diffusion-weighted imaging in non-alcoholic Wernicke's encephalopathy." Journal of the Neurological Sciences 333 (October 2013): e722. http://dx.doi.org/10.1016/j.jns.2013.07.2491.

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P, Bapat. "Aluminium Leukoencephalopathy in an Alcoholic Patient." Vaccines & Vaccination Open Access 8, no. 1 (2023): 1–3. http://dx.doi.org/10.23880/vvoa-16000159.

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Potentially toxic elements have a wide range of use for human mankind. But with those applications, they also have a darker side with its impact on human health. The affection of potentially toxic elements in humans causing neurological symptoms is also well known. Out of those potentially toxic elements, aluminium is known to cause dialysis encephalopathy in chronic kidney disease patients in the past. Aluminium leukoencephalopathy resulting from other causes is not commonly reported. To the best of our knowledge only seven cases have been reported in the literature till date. We present aluminium intoxication in a patient consuming country liquor causing leukoencephalopathy.

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Choi, Evan Y., William A. Gomes, Missak Haigentz, and Jerome J. Graber. "Association between malignancy and non-alcoholic Wernicke's encephalopathy: a case report and literature review." Neuro-Oncology Practice 3, no. 3 (2015): 196–207. http://dx.doi.org/10.1093/nop/npv036.

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Abstract Background Wernicke's encephalopathy is a serious medical condition associated with high morbidity and mortality caused by deficiency of thiamine. This disease is classically associated with alcoholism, but is underappreciated in the nonalcoholic population. There is growing acknowledgement of the development of Wernicke's encephalopathy in patients with malignancies. Methods We conducted a literature review in PubMed for cases of Wernicke's encephalopathy occurring in patients with malignancy. We also present the case of a 47-year-old woman with recurrent laryngeal cancer and multiple hospital admissions for malnutrition. Neurological examination was notable for pendular nystagmus, severe gait ataxia, confusion, and poor memory consolidation. MRI of the brain was significant for T2-weighted fluid-attenuated inversion recovery hyperintensities in periaqueductal regions, medial thalami, and the tectal plate, typical for Wernicke's encephalopathy. She was treated with thiamine repletion, and had marked improvement in her mental status and some improvement in her vision problems and ataxia, although some nystagmus and significant short-term memory impairment persisted. Results The literature review yielded dozens of case reports of Wernicke's encephalopathy in patients with malignancy, dominated by cases of patients with malignancies of the gastrointestinal system, followed by those with hematologic malignancies. Conclusions Malignancy is an important risk factor for the development of Wernicke's encephalopathy. This diagnosis is underappreciated and difficult for the clinician to discern from multifactorial delirium. Clinicians should be aware to treat at-risk patients with thiamine immediately, especially if multiple risk factors are present.

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Amine, Mnaili Mohamed, Toufgua Zakaria, El Kharras Abdennasser, and Bourazza Ahmed. "Wernicke Syndrome with Cerebellar Involvement on MRI: An Atypical Presentation." Journal of Cerebrovascular Sciences 12, no. 1 (2024): 18–20. https://doi.org/10.4103/jcvs.jcvs_21_23.

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Gayet–Wernicke encephalopathy is a neuropsychiatric emergency due to thiamine deficiency (Vitamin B1), secondary to several factors. This represents a prototype of metabolic encephalopathies. This is a consequence of malnutrition with Vitamin B1 deficiency. The diagnostic is mainly clinical and the treatment must be started as soon as possible using parenteral thiamine. We report a case of Gayet–Wernicke encephalopathy in a 29-year-old woman who did not consume alcoholic beverages, presenting with balance disorder after uncontrollable vomiting during pregnancy. The classic triad of symptoms and magnetic resonance imaging played an important role, in particular, in the diagnosis of Gayet–Wernicke encephalopathy. Our case illustrates that Wernicke’s encephalopathy may have atypical imaging manifestations.

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Nisrine, Dr Benaouicha, Dr Mouiman F. Z, Dr Louzali F. Z, et al. "Gayet-Wernicke Encephalopathy Complicating a Pregnancy of 17 Weeks of Amenorrhea: A Case Report." Scholars International Journal of Obstetrics and Gynecology 5, no. 4 (2022): 184–86. http://dx.doi.org/10.36348/sijog.2022.v05i04.008.

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Gayet-Wernicke encephalopathy is a neuropsychiatric emergency due to thiamine (vitamin B1) deficiency, secondary to several factors, it is a disorder characterized by confusion of acute onset, nystagmus, partial ophthalmoplegia and ataxia. The diagnosis is mainly clinical. The disorder may resolve with treatment, persist, or degenerate into Korsakoff's psychosis. We report a case of Gayet-Wernicke encephalopathy in a 39 year old non-ethylic patient, pregnant at 17 weeks of age who presented with consciousness disorders with paresthesia of the 4 limbs and dyspnea. Clinical and magnetic resonance imaging (MRI) have an important place, especially in the diagnosis of non-alcoholic Wernicke's encephalopathy.

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Chebli, S., M. Besbes, R. Felhi, G. Hamdi, and B. Paindaveine. "Neuropsychiatric presentation of Wernicke’s Encephalopathy occurs to a pregnant Woman: A case report." European Psychiatry 66, S1 (2023): S299—S300. http://dx.doi.org/10.1192/j.eurpsy.2023.668.

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IntroductionWernicke’s encephalopathy (WE) is a severe neuropsychiatric syndrome resulting from thiamine deficiency (vit B1) wich is often associated with chronic alcoholism. The classical presentation is characterized by ophtalmoplegia, ataxia and confusion.Unfortunately, WE is still underdiagnosed because it may not always show up with a classical presentation in one hand, and could also be seen in other non alcoholic condition in an other hand which delay diagnosis and managment of early proper treatementObjectivesThis case highlights the importance of considering atypical presentations of Wernicke’s encephalopathy, it’s medical etiologies and the importance of improving diagnosis to manage early treatementMethodsWe reported a case of a pregnant women who consulted for alterated mental status , asthenia and occurs to have Wernicke’s encephalopathy due to hyperemesis gravidarumResultsMrs X is a 35-year-old pregnant women with a past medical history of a cesarian, an hospitalisation in third month of this pregnancy for vomits, no known psychiatric illness or history of substance abuse. She was brought to the gynecology emergency department for asthenia and altered mental status. MRS X, was lethargic, had not eaten for several days, vomiting for more than a month. On the medical evaluation she appeared confused, disoriented, and unresponsive to verbal or manual redirection and prompting. She had also ataxia and gait incoordination. Laboratory testing was remarkable for lactic acidosis (blood lactate concentration lipasemia and normal electrolyte levels, cerebrospinal fluid (CSF) culture was unremarkable.A brain MRI was done and showed FLAIR signal abnormalities around the third ventricle and periaqueductal, suggesting Gayet-Wernicke encephalopathy. Thiamine (vit B1) 500mg thrice a day was administrated for the next days in associtation with vitamin B6.ConclusionsWernicke encephalopathy (WE) is an acute reaction to thiamine deficiency which usually presents with a classical triad. However, Clinicians tend to ignore WE in other non-alcoholic clinical settings and the diagnosis becomes even more difficult when thiamine deficiency presents with unusual neuropsychiatric signs and symptoms like catatonia. This case highlights the importance of considering atypical presentations of WE, it’s medical etiologies and the necessity of a complete medical evaluation and appropriate investigations to make prompt diagnosis and early management.Disclosure of InterestNone Declared

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Gupta, Rohit. "Altered sensorium in a chronic alcoholic: pancreatic encephalopathy, Wernicke’s encephalopathy or Marchiafava Biganami disease?" Tropical Gastroenterology 36, no. 4 (2015): 266–68. http://dx.doi.org/10.7869/tg.303.

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Ma, Jun, Xiao Mei Mu, Zhi Qiang Wang, Yan Wang, and Fan Li Kong. "The Role of ¹H-MRS in Diagnosis of Elderly Chronic Alcoholic Toxic Encephalopathy." Advanced Materials Research 641-642 (January 2013): 838–40. http://dx.doi.org/10.4028/www.scientific.net/amr.641-642.838.

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Objective: This study was undertaken to study the effect of MR imaging on patients with elderly chronic alcoholic toxic encephalopathy. Methods: 20 patients with chronic alcoholic toxic encephalopathy (CATE) and 18 patients cerebral infarction diagnosed were collected to analyze conventional imaging material and spectral spectrum line shape variation peak by magnetic resonance imaging (MRI). Results: Cerebral and cerebellar vermis atrophy and abnormal signal in the deep part of the cerebral hemispheres, basal ganglia, pons asymmetric small pieces long T1 and long T2 were detected in CATE patients. And 1H-MRS also showed that the concentrations of NAA and Cho in cerebellar vermis were significantly reduced. In cerebral infarction patients declined NAA and elevated Lac were found. Conclusion: Our study suggests that 1H-MRS play a positive role in CATE diagnosis, which keeps from further damage to the brain tissue.

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Hata, Takashi, John Stirling Meyer, Norio Tanahashi, et al. "Three-Dimensional Mapping of Local Cerebral Perfusion in Alcoholic Encephalopathy with and without Wernicke-Korsakoff Syndrome." Journal of Cerebral Blood Flow & Metabolism 7, no. 1 (1987): 35–44. http://dx.doi.org/10.1038/jcbfm.1987.6.

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Seventeen severe chronic alcoholic patients with and without Wernicke-Korsakoff syndrome (WKS) were examined prospectively after being treated by withdrawal from alcohol. The WKS patients also received thiamine supplements. Three-dimensional measurements of local cerebral blood flow (LCBF) and local partition coefficients (LΛ) were made utilizing xenon contrast computed tomography (Xe CT-CBF). Results were displayed as color-coded brain maps before and after treatment and these were correlated with neurological and cognitive examinations. Before treatment chronic alcoholics without WKS (n = 10) showed diffuse reductions of LCBF values throughout all gray matter including hypothalamus, vicinity of nucleus basalis of Meynert, thalamus, and basal ganglia. Similar, but more severe, reductions were seen in patients with WKS (n = 7), however, white matter perfusion was also reduced. In WKS, most prominent reductions of LCBF were also seen in hypothalamus and basal forebrain nuclei but thalamus, basal ganglia, and limbic systems were severely reduced. After treatment, both groups with alcoholic encephalopathy showed marked clinical improvement and cerebral perfusion was restored toward normal. Chronic alcohol abuse, in the absence of thiamine deficiency, reduces CBF by direct neurotoxic effects. If thiamine deficiency is also present, more severe and localized hemodynamic reductions are superimposed.

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Journal articles on the topic 'Alcoholic encephalopathy'

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