Project description:Wernicke encephalopathy is caused by vitamin B1 deficiency. It presents as a triad consisting of altered mental status, oculomotor dysfunction, and gait ataxia. Early vitamin B1 administration alleviates symptoms. We present a video of gaze-evoked nystagmus in an elderly patient with Wernicke encephalopathy.

| S-EPMC8931301 | biostudies-literature

Wernicke encephalopathy in patients with depression: A systematic review.

Project description: Not available

| S-EPMC7590192 | biostudies-literature

Downbeat Nystagmus Is Abolished by Alcohol in Nonalcoholic Wernicke Encephalopathy.

Project description:Background and objectivesLesions of the cerebellar flocculus cause enduring downbeat nystagmus (DBN) with unrelenting oscillopsia. Unlike most patients with DBN, the flocculus is structurally spared in nonalcoholic Wernicke encephalopathy (nWE) with chronic DBN. The objective was to study the effects of alcohol in nWE.MethodsWe recorded eye movements of a unique patient with nWE under controlled alcohol consumption who said his oscillopsia disappeared with a few drinks of alcohol.ResultsHis DBN was markedly diminished by alcohol (by 77.4%), although he remained alert with normal saccades.DiscussionThis striking observation may be caused by the differential effect of alcohol on the perihypoglossal complex and the paramedian tract neurons, which control the level of activity in the flocculus, with opposite (inhibition and excitation, respectively) effects. The finding suggests new ideas about the treatment and pathophysiology of DBN with a structurally intact cerebellum.

| S-EPMC9647809 | biostudies-literature

An Atypical Long-Term Thiamine Treatment Regimen for Wernicke Encephalopathy

Project description:A patient with rapidly changing mental status responded to treatment with intramuscular or IV thiamine but not oral dosages, suggesting that presentation of thiamine deficiency can be highly variable, which can complicate the correct diagnosis and treatment.

| S-EPMC7535953 | biostudies-literature

Complex ophthalmoplaegia denoting Wernicke encephalopathy in a non-alcoholic individual.

Project description: Not available

| S-EPMC4386433 | biostudies-literature

Posterior reversible encephalopathy syndrome and Wernicke encephalopathy in patient with acute graft-versus-host disease.

Project description:Graft-versus-host disease (GVHD) is an immune triggered process leading to severe immune dysregulation and organ dysfunction until death and it is one of the worst medical complications after a transplant. Patients with GVHD may have several neurological alterations: during this acute severe phase there is coexistence of various and nonspecific neurological symptoms. We are reporting a case of a 53 year old woman with severe GVHD after bone marrow transplant with acute neurological signs and symptoms. MRI study showed findings consistent with Posterior reversible encephalopathy syndrome and Wernicke encephalopathy.

| S-EPMC6545363 | biostudies-literature

Wernicke encephalopathy in a patient with medullary infarctions: a case report.

Project description:Wernicke encephalopathy (WE) is an acute life-threatening neurological condition caused by thiamine (vitamin B1) deficiency. Patients with WE often present with a triad of symptoms consisting of ophthalmoplegia, gait ataxia, and mental confusion. If WE is not treated in a timely manner, it can lead to serious complications such as confusion, coma, or death. Although alcohol abuse is the most commonly reported cause of WE, nonalcoholic causes-although rare-do exist. Herein, we present the case of a nonalcoholic woman with medullary infarctions who presented with intractable vomiting. Her clinical state subsequently progressed to include ophthalmoplegia and gait ataxia. A diagnosis of WE was suspected based on her clinical presentation; this was confirmed by brain magnetic resonance imaging (MRI) and the finding of decreased serum thiamine levels. Brain magnetic resonance imaging demonstrated the complete resolution of abnormal hyperintensities during a follow-up visit, 6 months after treatment.

| S-EPMC11375649 | biostudies-literature

Wernicke Encephalopathy Presenting with Dysphagia: A Case Report and Systematic Literature Review.

Project description:Wernicke encephalopathy (WE) is a well-known neurological condition caused by thiamine (vitamin B1) deficiency that occurs in both alcoholic and non-alcoholic populations. We aimed to report a case of a patient with WE who presented with dysphagia and dysphonia and later developed typical symptoms of thiamine deficiency and to conduct a systematic review of the literature on this rare presentation of WE. We searched two databases (PubMed and Scopus) and included publications up to November 2022. We found 12 cases of WE and dysphagia, aged between 12 and 81 years; swallowing problems presented at the onset in nine patients (including the current case report). Our findings suggest that thiamine deficiency should be suspected in patients with dysphagia of unknown cause, even in the absence of alcohol abuse. In contrast to most WE patients, the majority of patients included in this review presented with dysphagia at the onset of their disease, even in the absence of the classic triad of cognitive impairment, ataxia, and oculomotor abnormalities, indicating that there could be varying susceptibilities to clinical manifestations of thiamine deficiency in different brain regions.

| S-EPMC9788281 | biostudies-literature

Wernicke Encephalopathy Related to Hyperemesis Gravidarum: A Retrospective Study of 12 Cases.

Project description:Objective: Wernicke encephalopathy (WE) related to hyperemesis gravidarum (HG) is a devastating neuropsychiatric syndrome that remains frequently undiagnosed in pregnant women. Although many cases have been published, more studies are required to establish guidelines for the early detection and treatment of this condition. Material and Methods: We conducted a retrospective study to analyze the available data concerning 12 cases of WE complicating HG in the Mother and Child Hospital's Obstetric Intensive Care Unit, belonging to Mohamed VI University Hospital of Marrakesh. Results: Twelve out of 76 HG admitted cases developed WE. Pregnant WE patients became depleted after 11 weeks of vomiting at median gestational weeks of 16.2. They had a severe weight loss of more than 5% of their body and had all presented prodromal signs of WE before the actual onset of the clinical triad. WE diagnosis was clinically made based on Caine's operational criteria as they allow early identification of the disease. A good tool that could also aid diagnosis is an encephalic MRI; however, it should not delay treatment with prompt administration of high doses of thiamin of > 500 mg/day. Chronic sequelae in this study occurred in 45.5% and death in one case. Conclusion: In HG, thiamin rapidly depletes which can lead to WE with adverse outcomes for the mother and fetus. Therefore, physicians must be vigilant in detecting early signs of WE to promptly provide a high dose of thiamin with targeted multimodal therapies as this could be lifesaving.

| S-EPMC11824303 | biostudies-literature

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