Letteratura scientifica selezionata sul tema "Wernicke-Korsakoff Syndrome"

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

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

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

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

Doctor of Philosophy (PhD)
Proteomics is rapidly achieving recognition as a complimentary and perhaps superior approach to examine global changes in protein abundance in complex biological systems and the value of these techniques in neuropsychiatry is beginning to be acknowledged. Characterizing the brain’s regional proteomes provides a foundation for the detection of proteins that may be involved in disease-related processes. Firstly, optimal conditions were achieved for the application of two dimensional-gel electrophoresis (2D-GE)-based proteomics with postmortem human brain tissue. These optimized techniques were then applied to soluble fractions of adjacent grey and white matter of a single cytoarchitecturally defined area (Brodmann area 9; BA9) and of two adjacent regions of frontal white matter (BA9 and CC body) from healthy individuals. These normative proteomic comparisons highlighted the importance of correct tissue sampling, i.e. proper separation of regional white matter, as heterogeneity in the respective proteomes was demonstrated. Furthermore, they stressed the necessity for future molecular brain mapping studies. The main focus of this thesis however, was to examine the proteomes of brain regions specifically vulnerable to alcohol-induced damage underlying cognitive dysfunction. Alcoholic patients commonly experience mild to severe cognitive decline. It is postulated that cognitive dysfunction is caused by an alcohol-induced region selective brain damage, particularly to the prefrontal cortex. The cerebellum is increasingly recognized for its role in various aspects of cognition and alcohol–induced damage to the cerebellar vermis could indirectly affect neurocognitive functions attributed to the frontal lobe. We used a 2D-GE-based proteomics approach to compare protein abundance profiles of BA9 grey and white matter and the cerebellar vermis from human alcoholics (neurologically uncomplicated and alcoholics complicated with liver cirrhosis) and healthy control brains. Among the protein level changes observed are disturbances in the levels of a number of thiamine-dependent enzymes. A derangement in energy metabolism perhaps related to thiamine deficiency seems to be important in all regions analysed, even where there are no clinical or pathological findings of Wernicke-Korsakoff Syndrome. Evidence of oxidative changes was also seen in all regions and effects of liver dysfunction in the vermis found. However, overall, these results highlight the complexity of this disease process in that a number of different proteins from different cellular pathways appear to be affected. By identifying changes in protein abundance levels in the prefrontal grey and white matter and the cerebellar vermis, hypotheses may draw upon more mechanistic explanations as to how chronic ethanol consumption causes the structural and functional alterations associated with alcohol-related brain damage. Furthermore, by comparing these results, we may be able to isolate disturbances in molecular pathways specific to the brain damage caused by alcohol, severe liver dysfunction and thiamine deficiency.

Proteomics is rapidly achieving recognition as a complimentary and perhaps superior approach to examine global changes in protein abundance in complex biological systems and the value of these techniques in neuropsychiatry is beginning to be acknowledged. Characterizing the brain’s regional proteomes provides a foundation for the detection of proteins that may be involved in disease-related processes. Firstly, optimal conditions were achieved for the application of two dimensional-gel electrophoresis (2D-GE)-based proteomics with postmortem human brain tissue. These optimized techniques were then applied to soluble fractions of adjacent grey and white matter of a single cytoarchitecturally defined area (Brodmann area 9; BA9) and of two adjacent regions of frontal white matter (BA9 and CC body) from healthy individuals. These normative proteomic comparisons highlighted the importance of correct tissue sampling, i.e. proper separation of regional white matter, as heterogeneity in the respective proteomes was demonstrated. Furthermore, they stressed the necessity for future molecular brain mapping studies. The main focus of this thesis however, was to examine the proteomes of brain regions specifically vulnerable to alcohol-induced damage underlying cognitive dysfunction. Alcoholic patients commonly experience mild to severe cognitive decline. It is postulated that cognitive dysfunction is caused by an alcohol-induced region selective brain damage, particularly to the prefrontal cortex. The cerebellum is increasingly recognized for its role in various aspects of cognition and alcohol–induced damage to the cerebellar vermis could indirectly affect neurocognitive functions attributed to the frontal lobe. We used a 2D-GE-based proteomics approach to compare protein abundance profiles of BA9 grey and white matter and the cerebellar vermis from human alcoholics (neurologically uncomplicated and alcoholics complicated with liver cirrhosis) and healthy control brains. Among the protein level changes observed are disturbances in the levels of a number of thiamine-dependent enzymes. A derangement in energy metabolism perhaps related to thiamine deficiency seems to be important in all regions analysed, even where there are no clinical or pathological findings of Wernicke-Korsakoff Syndrome. Evidence of oxidative changes was also seen in all regions and effects of liver dysfunction in the vermis found. However, overall, these results highlight the complexity of this disease process in that a number of different proteins from different cellular pathways appear to be affected. By identifying changes in protein abundance levels in the prefrontal grey and white matter and the cerebellar vermis, hypotheses may draw upon more mechanistic explanations as to how chronic ethanol consumption causes the structural and functional alterations associated with alcohol-related brain damage. Furthermore, by comparing these results, we may be able to isolate disturbances in molecular pathways specific to the brain damage caused by alcohol, severe liver dysfunction and thiamine deficiency.

Le syndrome de Wernicke-Korsakoff (SWK) est un désordre neuropsychiatrique causé par la déficience en thiamine (DT). Dans la DT expérimentale comme dans le SWK, on observe une mort neuronale et des hémorragies dans certaines régions précises du diencéphale et du tronc cérébral. Les lésions diencéphaliques du SWK sont particulièrement sévères et entraînent souvent des séquelles amnésiques permanentes. Le lien entre la dysfonction métabolique induite par la DT et la mort neuronale n’est pas connu. Des rapports précédents ont démontré que la perméabilité de la barrière hémato-encéphalique (BHE) était altérée et ce, précédant l’apparition du dommage neuronal, suggérant un rôle critique de la dysfonction vasculaire. Les jonctions serrées (JS) interendothéliales, la base anatomique de la BHE, constituent un réseau moléculaire incluant l’occludin et les zonula occludens (ZOs). Cette thèse démontre une perte d’expression et une altération de la morphologie de ces protéines en relation avec la dysfonction de la BHE dans le thalamus de souris déficientes en thiamine, fournissant une explication pour la présence d’hémorragies. Le stress oxydatif peut entraîner des dommages directs aux protéines des JS et interférer avec leurs mécanismes de régulation. De plus, l’oxyde nitrique (NO) peut induire la métalloprotéinase matricielle-9 (MMP-9) impliquée dans la dégradation de ces protéines. L’endothélium vasculaire cérébral (EVC) semble être une source importante de NO dans la DT, l’expression de l’oxyde nitrique synthase endothéliale (eNOS) étant sélectivement induite dans les régions vulnérables. Le NO peut réagir avec les espèces réactives oxygénées et former du peroxynitrite, entraînant un stress oxydatif/nitrosatif endothélial. Les résultats présentés démontrent que la délétion du gène de eNOS prévient le stress oxydatif/nitrosatif cérébrovasculaire, l’extravasation des immunoglobulins G (IgGs) et l’altération de l’occludin et des ZOs dans le thalamus de souris déficientes en thiamine. De plus, cette délétion prévient l’induction de l’expression de MMP-9 dans l’EVC. Des résultats similaires ont été obtenus avec l’antioxydant N-acétylcystéine (NAC). Les mécanismes précis par lesquels les espèces réactives altèrent les protéines des JS sont inconnus. Caveolin-1, une composante majeure du caveolæ de l’EVC, est impliquée dans la régulation de l’expression des protéines des JS, et celle-ci est modulée par le stress oxydatif/nitrosatif; l’altération de l’expression de caveolin-1 a été récemment associée à la rupture de la BHE. Les résultats présentés démontrent que l’expression de caveolin-1 est sélectivement altérée dans l’EVC du thalamus de souris déficientes en thiamine, coïcidant avec la rupture de la BHE, et démontrent que la normalisation de l’expression de caveolin-1 par le NAC est associée avec l’atténuation du dommage à la BHE. Pris ensemble, ces résultats démontrent un rôle central du stress oxydatif/nitrosatif cérébrovasculaire, particulièrement celui provenant de eNOS, dans l’altération des JS de la BHE via des dommages directs et via l’induction de MMP-9 et de caveolin-1. Cette rupture de la BHE contribue par conséquent à la mort neuronale dans le thalamus, puisque la prévention des altérations cérébrovasculaires par la délétion du gène de eNOS et le NAC atténue significativement la mort neuronale. L’administration précoce d’antioxydants en combinaison avec la thiamine devrait donc être une considération importante pour le traitement du SWK.
Wernicke-Korsakoff syndrome (WKS) is a neuropsychiatric disorder caused by thiamine deficiency (TD). In experimental TD as in WKS, neuronal cell death and hemorrhages are observed in specific diencephalic and brainstem areas. Diencephalic lesions in WKS are especially severe and often lead to permanent amnesic symptoms. The link between TD-induced metabolic dysfunction and neuronal cell death is unknown. Previous reports have shown that blood-brain barrier (BBB) permeability was impaired and that this occurred prior to the onset of neuronal damage, suggesting a critical role for vascular dysfunction. Interendothelial tight junctions (TJs), the anatomical basis of the BBB, constitute a molecular network comprising occludin and zonula occludens (ZOs). This thesis shows a loss of expression and alterations in the morphology of these proteins in relation to BBB dysfunction in the thalamus of thiamine-deficient mice, providing an explanation for the presence of hemorrhages. Oxidative stress can lead to direct oxidative damage to TJ proteins and interfere with their regulation mechanisms. Also, nitric oxide (NO) can induce matrix metalloproteinase-9 (MMP-9) involved in the degradation of these proteins. Cerebral vascular endothelium (CVE) seems to be an important source of NO in TD, since endothelial nitric oxide synthase (eNOS) expression is selectively induced in vulnerable areas. NO can react with reactive oxygen species and form peroxynitrite, leading to endothelial oxidative/nitrosative stress. Results have show that eNOS gene deletion prevents cerebrovascular oxidative/nitrosative stress, immunoglobulins G (IgGs) extravasation and occludin and ZOs alterations in the thalamus of thiamine-deficient mice. Also, eNOS gene deletion prevents the induction of MMP-9 in CVE. Similar results have been obtained with the antioxidant N-acetylcysteine (NAC). Precise mechanisms by which reactive species alter TJ proteins are unknown. Caveolin-1, a major component of CVE caveolæ, is involved in the regulation of TJ protein expression, and is modulated by oxidative/nitrosative stress; alteration in caveolin-1 expression has been recently associated with BBB breakdown. The present results show that caveolin-1 expression is selectively altered in CVE of the thalamus of thiamine-deficient mice, and show that normalization of caveolin-1 expression by NAC is associated with the attenuation of BBB damage. Taken together, these results demonstrate a central role for cerebrovascular oxidative/nitrosative stress, especially coming from eNOS, in BBB TJ protein alterations via direct damage and via induction of MMP-9 and caveolin-1. As a result, BBB breakdown contributes to neuronal cell death in the thalamus, since prevention of cerebrovascular alterations by eNOS gene deletion and NAC significantly attenuates neuronal cell death. Early administration of antioxidants combined with thiamine should therefore be an important consideration for the treatment of WKS.

L’excitotoxicité est un mécanisme physiopathologique majeur impliqué dans la pathogenèse de la déficience en thiamine (DT). Dans les régions cérébrales vulnérables à la DT, on observe une mort cellulaire induite par excitotoxicité dont l’origine semble être la conséquence d’une perturbation du métabolisme énergétique mitochondrial, d’une dépolarisation membranaire soutenue et d’une diminution de l’absorption du glutamate par les astrocytes suite à la diminution de l’expression des transporteurs EAAT1 et EAAT2. Il est clairement établi que le glutamate joue un rôle central dans l’excitotoxicité lors de la DT. Ainsi, la mise en évidence des mécanismes impliqués dans la diminution de l’expression des transporteurs du glutamate est essentielle à la compréhension de la physiopathologie de la DT. L’objectif de cette thèse consiste en l’étude de la régulation des transporteurs astrocytaires du glutamate et la mise au point de stratégies thérapeutiques ciblant la pathogenèse de l’excitotoxicité lors de l’encéphalopathie consécutive à la DT. Les principaux résultats de cette thèse démontrent des perturbations des transporteurs du glutamate à la fois dans des modèles animaux de DT et dans des astrocytes en culture soumis à une DT. La DT se caractérise par la perte du variant d’épissage GLT-1b codant pour un transporteur du glutamate dans le thalamus et le colliculus inférieur, les régions cérébrales affectées lors d’une DT, en l’absence de modification des niveaux d’ARNm. Ces résultats suggèrent une régulation post-transcriptionnelle de l’expression des transporteurs du glutamate en condition de DT. Les études basées sur l’utilisation d’inhibiteurs spécifiques des facteurs de transcription NFkB et de l’enzyme nucléaire poly(ADP)ribose polymérase-1 (PARP-1) démontrent que la régulation de l’expression du transporteur GLT-1 est sous le contrôle de voies de signalisation NFkB dépendantes de PARP-1. Cette étude démontre une augmentation de l’activation de PARP-1 et de NFkB dans les régions vulnérables chez le rat soumis à une DT et en culture d’astrocytes DT. L’inhibition pharmacologique du facteur de transcription NFkB par le PDTC induit une augmentation des niveaux d’expression de GLT-1, tandis que l’inhibition de PARP-1 par le DPQ conduit à l’inhibition de l’hyperactivation de NFkB observée lors de DT. L’ensemble de ces résultats met en évidence un nouveau mécanisme de régulation des transporteurs du glutamate par l’activation de PARP-1. L’accumulation de lactate est une caractéristique de la DT. Un traitement avec le milieu de culture d’astrocytes en condition de DT sur des cultures d’astrocytes naïfs induit une diminution de l’expression de GLT-1 ainsi qu’une inhibition de la capacité d’absorption du glutamate par les astrocytes naïfs. En revanche, l’administration de lactate exogène ne modifie pas le niveau d’expression protéique de GLT-1. Ainsi, des facteurs solubles autres que le lactate sont sécrétés par des astrocytes en condition de perturbation métabolique et peuvent potentiellement réguler l’activité des transporteurs du glutamate et contribuer à la pathogenèse du syncytium astroglial. En outre, la ceftriaxone, un antibiotique de la famille des β-lactamines, augmente de façon différentielle l’expression du variant-d’épissage GLT-1 dans le colliculus inférieur chez le rat DT et en culture d’astrocytes DT. Ces résultats suggèrent que la ceftriaxone peut constituer une avenue thérapeutique dans la régulation de l’activité des transporteurs du glutamate lors de DT. Pour conclure, la mort cellulaire d’origine excitotoxique lors de DT survient en conséquence d’une dysfonction mitochondriale associée à une perturbation du métabolisme énergétique cérébral. La modification de l’expression des transporteurs du gluatamate est sous le contrôle des voies de signalisation NFkB dépendantes du facteur PARP-1. De plus, l’inhibition métabolique et l’augmentation des sécrétions de lactate observées lors de DT peuvent également constituer un autre mécanisme physiopathologique expliquant la diminution d’expression des transporteurs de glutamate. Enfin, la ceftriaxone pourrait représenter une stratégie thérapeutique potentielle dans le traitement de la régulation de l’expression des transporteurs du glutamate et de la perte neuronale associés à l’excitotoxicité observée lors de DT.
Excitotoxicity has been implicated as a major pathophysiological mechanism in the pathogenesis of thiamine deficiency (TD). Excitotoxic-mediated cell death is localized in areas of focal vulnerability in TD and may occur as a consequence of impairment in mitochondrial energy metabolism, sustained cell membrane depolarization and decreased uptake of glutamate by astrocytes due to the loss of excitatory amino acid transporters, (EAAT1 and EAAT2). Over the years, a number of studies have identified glutamate as being a major contributor to excitotoxicity in the pathophysiology of TD. Thus, downregulation of astrocytic glutamate transporters resulting in excitotoxicity is a key feature of TD and understanding the regulation of these transporters is essential to understanding the pathophysiology of the disorder. The objective of the present thesis project was to examine the underlying basis of astrocytic glutamate transporter regulation during TD encephalopathy. Major findings of the studies presented in this thesis project provide evidence for glutamate transporter abnormalities in TD animal models and astrocyte cultures exposed to TD. TD results in the loss of the glutamate transporter splice variant-1b (GLT-1b) in vulnerable areas of brain, i.e. thalamus and inferior colliculus, with no significant alteration in the mRNA levels of the transporters, suggesting that glutamate transporter regulation under conditions of TD is a posttranscriptional event. Studies using a specific inhibitor of the transcription factor, Nuclear factor-kappa B (NF-κB) and a nuclear enzyme poly (ADP)ribose polymerase-1 (PARP-1) provided evidence for the regulation of GLT-1 by PARP-1 dependent NF-κB signalling pathways. The major findings of this study suggested an increase in the activation of PARP-1 and NF-κB molecule in the vulnerable areas of TD rat brain and TD astrocyte cultures. Pharmacological inhibition of NF-κB showed an increase in the levels of GLT-1, while inhibition of PARP-1 using a specific PARP-1 inhibitor, DPQ inhibited the increased activation of NF-κB that was observed during TD. Overall results of this finding provided evidence for a mechanism involving PARP-1 activation in the regulation of glutamate transporters. Given the increased lactate accumulation as a classical feature of TD, we studied the effect of soluble factors produced by astrocytes on glutamate transporter function. Treatment of naïve astrocyte cultures with TD conditioned media resulted in decreased levels of GLT-1 and inhibition of glutamate uptake capacity concomitant with a loss of mitochondrial membrane potential. Administration of exogenous lactic acid produced a similar reduction in glutamate uptake to that resulting from conditioned media. However, lactic acid treatment did not result in a change in GLT-1 protein levels. In addition, the pro-inflammatory cytokine TNF-α was shown to be increased in astrocytes treated with TD along with elevated levels of the phospho-IκB fragment, indicative of increased activation of NFκB. Inhibition of NFκB led to an amelioration of the decrease in GLT-1 that occurs in TD, along with recovery of glutamate uptake. Thus, soluble factors released from astrocytes under conditions of metabolic impairment such as lactate and TNF-α impairment appear to exert a regulatory influence on glutamate transporter function. Ceftriaxone, a β-lactam antibiotic, has the ability to differentially stimulate GLT-1b (splice-variant) expression in the inferior colliculus in TD rats and under in vitro conditions with TD astrocyte cultures. Thus, ceftriaxone may be a potential therapeutic strategy in the regulation of glutamate transporter function during TD. In summary, excitotoxic cell death in TD occurs as a consequence of mitochondrial dysfunction associated with cerebral energy impairment and abnormal glutamate transporter status. A major underlying mechanism for glutamate transporter abnormalities is mediated by PARP-1 dependent NF-κB signaling pathways. In addition, metabolic inhibition with substantial production of lactate and TNF-α may be perhaps another mechanism responsible for glutamate transporter downregulation in TD.

Nutritional disorders are often encountered in hospital neurology practice, especially deficiencies of vitamins B1 and B12. Medical conditions can predispose to nutritional disorders. This chapter discusses the presentation, diagnosis, and management of B12 deficiency, B1 deficiency, protein-energy malnutrition, folate deficiency especially in the context of pregnancy, B6 deficiency, B6 toxicity, copper deficiency, and vitamin D deficiency. Wernicke encephalopathy and Korsakoff syndrome are also discussed.

Introduction: The Wernicke-Korsakoff syndrome is a condition caused by thiamine (vitamin B1) deficiency in the brain, being a debilitating and potentially fatal factor. It is characterized by a classic triad: delirium, ophthalmoparesis and ataxia. Objectives: Analyze the possible effectiveness of using thiamine in the prognostic change of patients with the syndrome, as well as the ideal dose and identification of possible secondary outcomes of the use of thiamine. Methods: A systematic review made in March 2021, included studies published between 2011-2021. The descriptors selected according to the MeSH platform, were inserted in the SCIELO, Lilacs and PubMed databases, resulting in a total of 323 studies, of which only 8 were selected. Results: Among the 8 evaluated articles, 5 reinforce the effectiveness of thiamine therapy, with prognostic changes in those patients, and only 4 of these studies describe their clinical evolution, showing mostly a gradual regression of the ocular manifestations and ataxia, while neurological symptoms tend to develop later. Thus 62,5% of the articles show improvement of patients with these therapeutics. Other studies do not refer to the prognosis after the institution of the treatment. About the dose, it was observed that the therapeutic effectiveness was related to higher doses of thiamine. Conclusion: Most of the analyzed studies were favorable to the hypothesis of the early use of thiamine in regression of the symptoms. Regarding the most effective dose, the topic still needs studies with high scientific evidence, as it hasn’t yet been thoroughly discussed in the literature.

Introduction: The homeless population has a high prevalence of alcoholism and consumption of other drugs, which also means that they are at greater risk of developing all complications resulting from alcohol abuse. (MILER et al, 2021). The medical attention for homeless population is a device of the Unified Health System that claims social, health policies and the guarantee of fundamental rights (BRASIL, 2009). Methods: Evaluation of protocols and referral flows for the treatment of patients with ‘mental disorders and due to alcohol use’, of the medical attention for homeless population in the city of Petrópolis (Rio de Janeiro), between April / 2020 and April 2021, data from e-SUS, and literature review. Results: The city of Petrópolis (Rio de Janeiro) registered 259 people without home, 84.8% are men, all people are adults between 20-74 years old, 98% are born Brazilians, 92% reported alcohol consumption, and alcohol with other drugs 61% (cocaine, crack, marijuana, solvent, tobacco). There was 3 patients with diagnose of Wernicke-Korsakoff syndrome: 2 men and 1 woman (aged 60-65 years) in the period from April 2020 - April 2021 (BRAZIL, 2021 The medical attention for homeless population approach to alcoholism includes the CAGE and AUDIT tests, symptomatic treatment and brief psychological interventions. aimed at weaning, and the Clinical Institute Withdrawal Assessment of Alcohol Scale Revised scale to quantify the degree of abstinence. However, the majority of users do not want total cessation, generally they choose to reduce consumption (secondary prevention), and later recovery and reintegration into society, highlighting that self-help groups and social assistance have a prominent role (tertiary prevention) (MARSCHARLL; GREGANTI, 2002; LONGO, et al., 2013). Conclusion: Despite confounding / aggravating factors such as social determinants in health, and the difficulties of the health network, the medical attention for homeless population is fundamental in the secondary and tertiary prevention of neurological diseases due to chronic alcohol consumption; complex cases require complex interventions, that is, individualization, adaptation and flexibility.

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.