Relevant bibliographies by topics / Alcoholic encephalopathy

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Academic literature on the topic 'Alcoholic encephalopathy'

Author: Grafiati

Published: 4 June 2025

Last updated: 23 June 2025

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Journal articles on the topic "Alcoholic encephalopathy"

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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Dissertations / Theses on the topic "Alcoholic encephalopathy"

García, Lezana Teresa. "Nuevos modelos experimentales para el estudio de mecanismos fisiopatológicos en enfermedad hepática crónica." Doctoral thesis, Universitat Autònoma de Barcelona, 2017. http://hdl.handle.net/10803/457870.

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La enfermedad hepática crónica (CLD) es un proceso de destrucción progresiva del parénquima hepático que desencadena fibrosis y cirrosis. El avance de la patología está frecuentemente asociado con la aparición de hipertensión portal, fallo hepático y el desarrollo de las complicaciones de la cirrosis. Mejorar el conocimiento de la fisiopatología de la CLD y las complicaciones asociadas, así como de los mecanismos subyacentes, es esencial para el desarrollo de nuevas técnicas diagnósticas y terapéuticas, y esto depende en gran medida del desarrollo de modelos animales sólidos y reproducibles. El objetivo de esta tesis doctoral es el desarrollo de dos nuevos modelos animales y su aplicación en la investigación de mecanismos fisiopatológicos asociados con la enfermedad hepática crónica. En el primer estudio se evalúa, mediante experimentos de trasplante fecal, el papel de la microbiota intestinal (IM) en el desarrollo de la hipertensión portal (PH) en el contexto de la esteatohepatitis no alcohólica (NASH). En él se muestra por primera vez como la IM tiene un papel clave en la patogénesis de la PH, independientemente de la fibrosis. Concretamente observamos que el trasplante de una IM sana en ratas con NASH e PH sin fibrosis (originada tras 8 semanas siguiendo una dieta rica en grasa con glucosa y fructosa) restablece la PH hasta niveles comparables a los controles. Esta reducción de la PH se asocia con una disminución de la resistencia vascular intrahepática probablemente mediada por una mejoría de la disfunción endotelial y la resistencia a la insulina intrahepática. En el segundo estudio exploramos el proceso neurodegenerativo consecuencia de la encefalopatía hepática (HE), una de las complicaciones de la cirrosis. Primero, desarrollamos un modelo animal de HE episódica en el que simulamos 10 episodios repetidos de HE, uno cada dos semanas, desencadenados por dos de los principales factores precipitantes: hiperamonemia y/o inflamación. Después, mediante análisis estereológicos, evidenciamos que estos episodios repetidos de HE desencadenan procesos, no reversibles, de degeneración y muerte de las neuronas de Purkinje en el cerebelo. La reducción del número de neuronas de Purkinje parece, además, estar mediada por la apoptosis de la glía de Bergman y por procesos de activación de astrocitos y microglía en el cerebelo. Estos dos nuevos modelos son herramientas que nos han permitido investigar factores y mecanismos poco explorados hasta el momento en CLD y que podrían convertirse en un futuro en nuevas dianas terapéuticas. Chronic liver disease (CLD) is a process of progressive destruction of liver parenchyma that triggers fibrosis and cirrhosis. The progression of the pathology is frequently associated with the occurrence of portal hypertension, hepatic failure and the development of cirrhosis complications. Improving the knowledge of the pathophysiology of CLD and associated complications, as well as the underlying mechanisms, is essential for the development of new diagnostic and therapeutic techniques. This depends to a great extent on the development of robust and reproducible animal models. The aim of this doctoral thesis is the development of two new animal models and their application in the investigation of pathophysiological mechanisms associated with chronic liver disease. In the first study we explored the role of the intestinal microbiota (IM) in the development of portal hypertension (PH) in the context of nonalcoholic steatohepatitis (NASH), evaluated by means of faecal transplantation experiments. It is showed for the first time that IM plays a key role in the pathogenesis of PH, regardless of fibrosis. Specifically, we observed that transplantation of a healthy IM in rats with NASH and PH without fibrosis (originated after 8 weeks following a high-fat glucose-fructose diet) restored PH to levels comparable to controls. This reduction of PH was associated with a decrease in intrahepatic vascular resistance probably mediated by an improvement of endothelial dysfunction and intrahepatic insulin resistance. In the second study we explored the neurodegenerative process consequence of hepatic encephalopathy (HE), one of the complications of cirrhosis. First, we developed an animal model of episodic HE in which we simulated 10 repeated episodes of HE, one every two weeks, triggered by two of the main precipitating factors: hyperammonemia and / or inflammation. Then, by means of stereological analysis, we showed that these repeated episodes of HE triggered irreversible processes of degeneration and death of Purkinje neurons in the cerebellum. Reduction in the number of Purkinje neurons appeared to be mediated by apoptosis of Bergman glia and activation of astrocytes and microglia in the cerebellum. These two new models are tools that have allowed us to investigate factors and mechanisms not very explored so far in CLD and that could become new therapeutic targets in a future.

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Dennis, Claude Vincent. "The Role Of Cell Proliferation In Hepatic Encephalopathy." Thesis, The University of Sydney, 2017. http://hdl.handle.net/2123/17568.

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Chronic alcohol misuse or alcohol use disorder is a common problem worldwide. Excessive alcohol consumption can affect almost every organ in the body but neurological complications can occur due to acute intoxicating effects as well as longer term damage known as alcohol-related brain damage. The cognitive impairments associated with chronic alcohol misuse can be compounded by associated liver damage leading to an increase in circulating neurotoxic substances such as ammonia giving rise to a condition known as hepatic encephalopathy. The pathogenesis of hepatic encephalopathy is currently unknown however animal models of alcohol misuse suggest that aberrant cell proliferation attributed to neurogenesis may play a role. Neurogenesis occurs in the adult mammalian brain in two neurogenic niches the subventricular zone lining the lateral ventricles and the subgranular zone of the hippocampus and involves the proliferation of a neural stem cell and eventual integration of an immature neuron into the existing circuitry. Although this process has been widely proven in animals its existence in humans remains controversial. So, prior to addressing a role for neurogenesis in disease its existence needs to be proven in normal individuals. Here, cell proliferation and neurogenesis were simultaneously examined in the subventricular zone and subgranular zone of 23 individuals aged 0.2-59 years, using immunohistochemistry and immunofluorescence in combination with unbiased stereology. This demonstrated a marked decline in proliferating cells in both the subventricular zone and subgranular zone in early infancy such that the levels of proliferation were similar to the adjacent parenchyma by four and one years, respectively. Furthermore, the phenotype of proliferating cells changed with age such that in the adult subventricular zone and subgranular zone, and adjacent parenchyma, all proliferating cells co-localised with the microglial marker, Iba1. Taken together this suggests that adult neurogenesis is a residual process and that any potential disease-related alterations in proliferation in the adult brain are likely associated with microglia. Indeed, widespread proliferating cells that co-localised with the microglial marker Iba1 were found in a subset of chronic alcoholics with a pathological diagnosis of HE. In contrast cases without microglial proliferation displayed microglial dystrophy and associated neuronal loss in the prefrontal cortex. There were no obvious differences between these subsets from the clinical and pathological data available. To determine the cause and pathogenic significance of this microglial proliferation, a pilot study was conducted to develop an animal model of chronic hepatic encephalopathy using the hepatotoxin, thioacetamide and combinations of known risk factors for hepatic encephalopathy; chronic alcohol use and a high-fat diet. Animals receiving thioacetamide had macroscopic evidence of liver injury, elevations of transaminases and associated anxiety-like behaviour measured in an open-field test. There were however no associated microglial or astrocytic changes in these animals and combinations of alcohol and high-fat diet had no additional effects. In conclusion, this work has shown that the majority of the rare proliferative events in the adult human brain are microglia. Chronic alcoholism with a pathological diagnosis of hepatic encephalopathy results in shifts in microglial phenotype with one subset of patients demonstrating proliferation and another dystrophy. Future work is required to develop an animal model of chronic hepatic encephalopathy, where the role of microglial dysfunction in hepatic encephalopathy pathogenesis can be further elucidated.

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Slyvka, Nataliia Oleksyivna, O. V. Besedynska, V. O. Samsonyuk, and Igor Antonovych Plesh. "WERNICKE’S ENCEPHALOPATHY AS A CAUSE OF DEATH IN ALCOHOL ADDICTS: AUTOPSY STUDY." Thesis, Материалы научной конференции студентов-медиков с международным участием. - Актуальные проблемы современной медицинской науки. - Самарканд, 27 мая 2016 г, 2016. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/11619.

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Slyvka, N. O., O. V. Besedynska, V. O. Samsonyuk, and Igor Antonovych Plesh. "WERNICKE’S ENCEPHALOPATHY AS A CAUSE OF DEATH IN ALCOHOL ADDICTS: AUTOPSY STUDY." Thesis, Материалы научной конференции студентов-медиков с международным участием. - Актуальные проблемы современной медицинской науки. - Самарканд, 27 мая 2016 г, 2016. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/11717.

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Reid, Natasha Elizabeth. "Improving Outcomes for Children with Fetal Alcohol Spectrum Disorders: An Investigation of Self-Regulation as a Potential Mechanism of Change." Thesis, Griffith University, 2017. http://hdl.handle.net/10072/367266.

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Fetal alcohol spectrum disorder (FASD) is a term used to indicate the range of conditions that can arise from prenatal exposure to alcohol. The pattern of central nervous system (CNS) dysfunction is somewhat variable by individual, but often involves impairments in learning and memory, self-regulation (including executive functions), social communication, and adaptive skills. Additionally, children with FASD often experience significant behavioural difficulties that impact on their functioning at home, school, and in community settings. As a consequence, individuals with FASD are at a high-risk of experiencing secondary conditions, such as mental health problems, school disruption, and involvement with the criminal justice system, particularly as they enter adolescence. These neurocognitive difficulties, behaviour problems, and secondary conditions contribute to the high burden for families raising children with FASD. Therefore, caregivers of children with FASD often experience higher levels of stress and increased risk of parent-child relationship difficulties. Thesis (PhD Doctorate) Doctor of Philosophy in Clinical Psychology (PhD ClinPsych) School of Applied Psychology Griffith Health Full Text

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Books on the topic "Alcoholic encephalopathy"

1911-, Adams Raymond D., and Collins George H. 1927-, eds. The Wernicke-Korsakoff syndrome and related neurologic disorders due to alcoholism and malnutrition. 2nd ed. F.A. Davis Co., 1989.

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Book chapters on the topic "Alcoholic encephalopathy"

Henderson, George I., Jennifer Stewart, and Steven Schenker. "Alcohol, Neuron Apoptosis, and Oxidative Stress." In Metabolic Encephalopathy. Springer New York, 2008. http://dx.doi.org/10.1007/978-0-387-79112-8_13.

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Roberts, Roderick K., Anastacio M. Hoyumpa, George I. Henderson, and Steven Schenker. "Alcohol-Induced Encephalopathy." In Cerebral Energy Metabolism and Metabolic Encephalopathy. Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-1209-3_16.

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"Alcoholic Encephalopathy." In Diagnostic Imaging: Brain. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-323-37754-6.50263-3.

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"Alcoholic Encephalopathy." In Imaging in Neurology. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-323-44781-2.50177-7.

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Butterworth, Roger F. "Hepatic encephalopathy in alcoholic cirrhosis." In Handbook of Clinical Neurology. Elsevier, 2014. http://dx.doi.org/10.1016/b978-0-444-62619-6.00034-3.

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"Liver disease." In Oxford Handbook of Nutrition and Dietetics, edited by Joan Webster-Gandy, Angela Madden, and Michelle Holdsworth. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199585823.003.0028.

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Introduction and nutritional assessment 620 Hepatitis and cirrhosis 622 Ascites and oedema 624 Portal systemic encephalopathy 626 Steatorrhoea and oesophageal varices 627 Non-alcoholic fatty liver and non-alcoholic steatohepatitis 628 Liver transplantation 630 Nutrition-related functions of the liver include: • emulsification of dietary fat by bile prior to digestion;...

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Mann, Karl F., and Falk Kiefer. "Alcohol and psychiatric and physical disorders." In New Oxford Textbook of Psychiatry. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199696758.003.0058.

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This chapter covers the clinical symptoms of alcohol intoxication, withdrawal (without complications and with perceptual disturbances, grand mal seizures, delirium tremens, and alcoholic hallucinosis), and psychiatric disorders, including alcohol-induced mood disorders and alcohol-induced anxiety disorders. The effects of alcohol on the brain are covered in detail, including Wernicke’s encephalopathy, Korsakoff’s syndrome, cerebellar degeneration, hepatocerebral degeneration, and foetal alcohol syndrome, as are the effects on the body, including malnutrition and vitamin deficiency, peripheral neuropathy, effects on the muscle, liver, pancreas, skin, and heart, and the relationship between alcohol and hypertension and cancer.

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"Gastroenterology." In Emergencies in Clinical Medicine, edited by Piers Page, Asif Shah, Greg Skinner, Alan Weir, and Natasha Eagles. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198779117.003.0006.

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This chapter explores a number of gastroenterological conditions, including hepatic encephalopathy, ascites, spontaneous bacterial peritonitis, hepatorenal syndrome, alcohol withdrawal, peptic ulcer disease, alcoholic hepatitis, inflammatory bowel disease, and upper gastrointestinal varices. Grading scales are used to assess the severity of presentation, after which the steps required for each condition’s immediate management are laid out, including the ABCDE assessment and various intravenous techniques. Finally, the condition’s further management and causes are explored, with further grading scales and up-to-date guidelines on pharmaceutical courses. Further reading is provided at the end of each topic.

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Ramrakha, Punit S., Kevin P. Moore, and Amir H. Sam. "Gastroenterological emergencies." In Oxford Handbook of Acute Medicine. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198797425.003.0003.

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This chapter describes gastroenterological emergencies, including acute upper gastrointestinal (GI) bleeding, peptic ulcer disease, erosive gastritis/oesophagitis, variceal haemorrhage, Mallory–Weiss tear, gastroenteritis (acute, bacterial, viral), Clostridium difficile, giardiasis, travellers’ diarrhoea, bloody diarrhoea, dysentery (bacterial, amoebic), inflammatory bowel disease (IBD), jaundice, hepatitis (viral, alcoholic, drug-induced, autoimmune), acholuric jaundice, sepsis, ischaemic hepatitis, obstructive jaundice, gallstone disease, acute cholecystitis, biliary obstruction, ascites, acute liver failure, ‘acute-on-chronic’ liver failure, hepatic encephalopathy, liver abscesses, and acute pancreatitis.

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Marjot, Thomas. "Liver disorders." In Best of Five MCQS for the European Specialty Examination in Gastroenterology and Hepatology. Oxford University Press, 2021. http://dx.doi.org/10.1093/oso/9780198834373.003.0008.

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This chapter covers core curriculum topics relating to liver disorders including the anatomy, physiology, and biochemistry of the liver as it relates to disease processes. There is a focus on the investigation and management of acute hepatitis including viral, drug- and toxin-induced, and the risk stratification of patients with acute liver failure. All major chronic liver diseases are discussed including non-alcoholic fatty liver disease, autoimmune liver disease, alcohol related liver disease and chronic viral hepatitis. There is also education on managing the complications of cirrhosis including renal dysfunction, hepatic encephalopathy, variceal haemorrhage, and spontaneous bacterial peritonitis. Additional important topics covered include nutrition in liver disease, hepatocellular carcinoma, liver transplantation indications and assessment, and complications following liver transplantation. Additional curriculum material regarding liver disorders will also be covered in the mock examination chapter.

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Conference papers on the topic "Alcoholic encephalopathy"

Li, Mengjiao, Haijing Guan, Cuicui Cui, and Ying Xing. "THE IMAGING CHARACTERISTICS OF ACUTE ALCOHOLIC ENCEPHALOPATHY: A CASE REPORT." In 2016 International Conference on Biotechnology and Medical Science. WORLD SCIENTIFIC, 2016. http://dx.doi.org/10.1142/9789813145870_0032.

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"PV-004 - THE COMPLEXITY OF DUAL PATHOLOGY: REGARDING A CASE REPORT OF SEIZURES." In 24 CONGRESO DE LA SOCIEDAD ESPAÑOLA DE PATOLOGÍA DUAL. SEPD, 2022. http://dx.doi.org/10.17579/abstractbooksepd2022.pv004.

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Objectives: Wernicke's encephalopathy (WE) is a potentially reversible neuropsychiatric emergency caused by thiamine deficiency, whose classical triad consists of confusion, ataxia, and oculomotor dysfunction. The diagnosis is missed in 75-80% of cases and approximately 80% of untreated patients develop Korsakoff Syndrome, whereby recognition of nutritional deficiency or any portion of the triad should prompt treatment. We present a case of a 44-year-old Ukrainian man with suspected background of chronic alcohol abuse and psychiatric history of schizoaffective disorder, who presented with acute onset of confusion, psychomotor agitation, gait ataxia and nystagmus. Anamnesis was hampered by the language barrier and absence of past medical history and patient's alcoholic habits remained unclear. After suspicion of WE it was introduced thiamine and diazepam, with significant improvement. After discontinuation of diazepam, the patient presented with several episodes of tonic-clonic seizures. Starting from this case report, we pretend to discuss the differential diagnosis of seizures in dual pathology. Materials and methods: Clinical records and Pubmed search using the keywords: Wernicke’s Encephalopathy, Seizures, Alcohol, Benzodiazepines. Results and conclusions: Seizures are a common presentation of various conditions associated with alcohol use, whose differential diagnosis is difficult, especially in patients with dubious alcohol consumption. Alcohol abuse is a major precipitant of status epilepticus as seizure threshold is raised by alcohol drinking. Seizures may also occur during alcohol withdrawal for which treatment with benzodiazepines is recommended, however carefully, since both abrupt cessation and high-dose use are critical for the appearance of seizures. Although very rare, WE may also present with seizures, whereby overdiagnosis and overtreatment are preferred to prevent persistent neurocognitive impairments. At discharge the diagnostic discussion prevailed and the patient was medicated for seizures with clinical stabilization. The complexity of psychiatric diagnoses in dual pathology requires a longitudinal assessment for a better understanding of clinical conditions as illustrated here.

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Buttler, Laura, Anja Tiede, Marie Griemsmann, et al. "Impact of thiamine (vitamin B1) supplementation on hepatic encephalopathy and mortality in patients with decompensated alcoholic liver cirrhosis." In 40. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag, 2024. http://dx.doi.org/10.1055/s-0043-1777521.

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Salman, Dan Mohamed, Raphael Palomo Barreira, Marcelo Tognato Ximenes, et al. "Machiafava-Bigmami and Wernicke’s Encephalopathy: Association of two rare conditions." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.669.

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Introduction: Both Machiafava-Bigmami disease (MBD) and Wernicke’s encephalopathy (WE) result from hypovitaminosis mainly associated with chronic alcoholism. The former affects the corpus callosum while the latter affects mostly the mammillary bodies. There are two main clinical subtypes for MBD in Heinrich’s classification. In type A the entire corpus callosum is affected and is characterized by acute or subacute lowering of consciousness and pyramidal deficits. A poor outcome is expected even with initial, prompt therapy. Methods: Case study with medical record review. Case report: Female patient, 53 years old, with subacute monoparesis in the right lower limb, progressing to generalized paresis, altered mental status and communication impairment. She reported smoking and chronic alcohol addiction for 30 years. She was emaciated, dehydrated, drowsy, sometimes agitated; she had eye opening to speech, dysarthric, bradypsychic, hypoactive pupils, bilateral evoked horizontal nystagmus, proximal paresis with dystonic posture. Impaired coordination and gait, with no other positive findings. Head-CT showed hypodensity in the corpus callosum, more pronounced in the splenium. Head- MRI indicated signs of abnormal impregnation in the mammillary bodies, cerebellar atrophy in the anterior vermis, diffuse cytotoxic lesion in the corpus callosum compatible with toxic demyelination. Conclusion: Although rare, such conditions must be recognized and treated promptly in order to delay progress and improve prognosis.

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Ju, Wen-bo, Zhi-wei Qu, and Wei-gao Shen. "Protective effects of puerarin solution on alcohol encephalopathy hippocampus." In 2011 International Conference on Human Health and Biomedical Engineering (HHBE). IEEE, 2011. http://dx.doi.org/10.1109/hhbe.2011.6028385.

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Trussell, Alex S. "3132 Wernicke’s encephalopathy in the absence of alcohol use caused by profound dietary restriction." In ANZAN Annual Scientific Meeting 2024 Abstracts. BMJ Publishing Group Ltd, 2024. http://dx.doi.org/10.1136/bmjno-2024-anzan.117.

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Demoner, Caroline Colnago, Lucas Grobério Moulim de Moraes, Giselle Alves de Oliveira, Paula Zago Melo Dias, and Marcelo Ramos Muniz. "Wernicke encephalopathy in a patient with uncontrollable vomiting. A case report." In XIV Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2023. http://dx.doi.org/10.5327/1516-3180.141s1.528.

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Wernicke encephalopathy is a neurological disorder caused by lack of thiamine. The main symptoms include ophthalmoplegia, ataxia, and confusion. We described a case of an elderly woman who presented with suddenonset vertigo, uncontrollable vomiting and blurred vision on the left eye. On the following days, she evolved with gait imbalance with a tendency to fall to the left side, fluctuating drowsiness and bilateral ophthalmoplegia. She had a previous history of systemic arterial hypertension, depressive disorder, gastritis and gastric cancer 15 years ago, treated with chemotherapy and radiotherapy. No history of tobacco or alcohol abuse. Neurological examination showed disorientation in time and space, drowsiness, gait ataxia and positive Romberg test. Furthermore, she had Babinski sign on the right toe. In addition, she had bilateral ophthalmoplegia, visual acuity in the right eye 20/40 and left eye 20/50. Serum tests were normal, including thyroid function, ions/metabolics, and viral serologies. Cerebrospinal fluid analysis showed six leukocytes (100% mononuclear) and 51 mg/dL of protein. A brain nuclear resonance imaging showed hypersignal on T2 and FLAIR (Fluid-Attenuated Inversion Recovery) sequences located in the medial portions of the thalamus, symmetrically and bilaterally, in the periaqueductal gray matter, around the fourth ventricle and in the cortico-subcortical transition of the post-central gyri, which in the context suggested Wernicke’s encephalopathy. The treatment was performed with thiamine (300 mg/ day), with significant neurological deficit recovery.

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"CHRONIC EFFECTS OF ALCOHOL. A CASE REPORT." In 23° Congreso de la Sociedad Española de Patología Dual (SEPD) 2021. SEPD, 2021. http://dx.doi.org/10.17579/sepd2021p021s.

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OBJECTIVES: The alcohol dependence is a chronic disease and Wernicke-Korsakoff syndrome is one of the best known neurologic complication. Through a clinical case seen in the Emergency department, we will explain the importance of a good anamnesis and physical examination to obtain the diagnosis and prevent chronic defects. MATERIAL AND METHODS: A 55-year-old male patient who came to the Emergency department of our Hospital that was transferred by the ambulance of Emergency after being found at home on the ground without being able to get up. The patient presents generalized tremor, lack of strength in the lower extremities and visual hallucinations of dead relatives. The patient refers to being treated with alprazolam, lorazepam and trazodone due to anxiety, under follow-up by his family doctor.He has normally been drinking 5 glasses of brandy a day for 15 years and smoking 2 joints a day.The last time he drank alcohol was yesterday. The patient comments that for a year he has been out in a wheelchair. A blood and urine analysis is requested in addition to blood ethanol levels and an intramuscular injection of vitamin B1 is prescribed, followed by glucosaline serum and intravenous diazepam. On the general physical examination, she presented telangiectasia and bilateral palmar erythema. In the neurological examination, he presented hyporeflexia in the lower extremities, predominantly right cerebellar tremor, bilateral dysmetria in the heel-knee test, and gait ataxia with loss of strength in both legs. RESULTS AND CONCLUSIONS: This syndrome was classically described as a clinical triad consisting of altered mental status, nystagmus or ophthalmoplegia, and ataxia. However, less than a third of patients present with this complete triad. Gait abnormalities of Korsakoff syndrome are often irreversible if Wernicke encephalopathy is not treated adequately.

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