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Wernicke encephalopathy in patients with depression: A systematic review.

ABSTRACT:

SUBMITTER: Oudman E

PROVIDER: S-EPMC7590192 | biostudies-literature | 2020 Oct

REPOSITORIES: biostudies-literature

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Wernicke encephalopathy in patients with depression: A systematic review.

Oudman Erik E

Psychiatry and clinical neurosciences 20200806 10

PMID: 32657502

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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.

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Gaze-evoked nystagmus in Wernicke encephalopathy.

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.

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Wernicke encephalopathy: MR findings at clinical presentation in twenty-six alcoholic and nonalcoholic patients.

Project description:Background and purposeWernicke encephalopathy is a severe neurologic disorder that results from a dietary vitamin B1 deficiency. It is characterized by changes in consciousness, ocular abnormalities, and ataxia. This study was undertaken to analyze and compare findings on MR imaging and neurologic symptoms at clinical presentations of patients with Wernicke encephalopathy with and without a history of alcohol abuse.Materials and methodsA multicenter study group retrospectively reviewed MR brain imaging findings, clinical histories, and presentations of 26 patients (14 female, 12 male) diagnosed between 1999 and 2006 with Wernicke encephalopathy. The age range was 6-81 years (mean age, 46 .6+/-19 years).ResultsFifty percent of the patients had a history of alcohol abuse, and 50% had no history of alcohol abuse. Eighty percent showed changes in consciousness, 77% had ocular symptoms, and 54% had ataxia. Only 38% of the patients showed the classic triad of the disease at clinical presentation. At MR examination, 85% of the patients showed symmetric lesions in the medial thalami and the periventricular region of the third ventricle, 65% in the periaqueductal area, 58% in the mamillary bodies, 38% in the tectal plate, and 8% in the dorsal medulla. Contrast enhancement of the mamillary bodies was statistically positively correlated with the alcohol abuse group.ConclusionsOur study confirms the usefulness of MR in reaching a prompt diagnosis of Wernicke encephalopathy to avoid irreversible damage to brain tissue. Contrast enhancement in the mamillary bodies is a typical finding of the disease in the alcoholic population.

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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.

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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.

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