Wernicke's Encephalopathy Mimicking Acute Onset Stroke Diagnosed by CT Perfusion

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Abstract

Background. Metabolic syndromes such as Wernicke's encephalopathy may present with a sudden neurological deficit, thus mimicking acute onset stroke. Due to current emphasis on rapid admission and treatment of acute stroke patients, there is a significant risk that these stroke mimics may end up being treated with thrombolysis. Rigorous clinical and radiological skills are necessary to correctly identify such metabolic stroke mimics, in order to avoid doing any harm to these patients due to the unnecessary use of thrombolysis. Patient. A 51-year-old Caucasian male was admitted to our hospital with suspicion of an acute stroke due to sudden onset dysarthria and unilateral facial nerve paresis. Clinical examination revealed confusion and dysconjugate gaze. Computed tomography (CT) including a CT perfusion (CTP) scan revealed bilateral thalamic hyperperfusion. The use of both clinical and radiological findings led to correctly diagnosing Wernicke's encephalopathy. Conclusion. The application of CTP as a standard diagnostic tool in acute stroke patients can improve the detection of stroke mimics caused by metabolic syndromes as shown in our case report.

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Most cited references 10

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Clinical signs in the Wernicke-Korsakoff complex: a retrospective analysis of 131 cases diagnosed at necropsy.

Keith M Giles, Eric R Finlay, Joyce Harper (1986)

A recent necropsy study has shown that 80% of patients with the Wernicke-Korsakoff syndrome were not diagnosed as such during life. Review of the clinical signs of these cases revealed that only 16% had the classical clinical triad and 19% had no documented clinical signs. The incidence of clinical signs in this and other retrospective pathological studies is very different from that of prospective clinical studies. This discrepancy may relate to "missed" clinical signs but the magnitude of the difference suggests that at least some cases of the Wernicke-Korsakoff syndrome may be the end result of repeated subclinical episodes of vitamin B1 deficiency. In order to make the diagnosis, clinicians must maintain a high index of suspicion in the "at risk" group of patients, particularly alcoholics. Investigations of thiamine status may be helpful and if the diagnosis is suspected, parenteral thiamine should be given.

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Distinguishing between stroke and mimic at the bedside: the brain attack study.

Richard Lindley, D. Hand, Elizabeth S. Dennis … (2006)

The bedside clinical assessment of the patient with suspected stroke has not been well studied. Improving clinical skills may accelerate patient progress through the emergency department. We aimed to determine the frequency and nature of stroke mimics and to identify the key clinical features that distinguish between stroke and mimic at the bedside. Consecutive presentations to an urban teaching hospital with suspected stroke were recruited. A standard bedside clinical assessment was performed. The final diagnosis was determined by an expert panel, which had access to clinical features, brain imaging, and other tests. Univariate and multivariate analyses determined the bedside features that distinguished stroke from mimic. There were 350 presentations by 336 patients. The final diagnosis was stroke in 241 of 350 (69%) and mimic in 109 (31%). The mimics included 44 events labeled "possible stroke or TIA." Eight items independently predicted the diagnosis in patients presenting with brain attack: cognitive impairment and abnormal signs in other systems suggested a mimic, an exact time of onset, definite focal symptoms, abnormal vascular findings, presence of neurological signs, being able to lateralize the signs to the left or right side of the brain, and being able to determine a clinical stroke subclassification suggested a stroke. The bedside clinical assessment can be streamlined substantially. This has important implications for teaching less experienced clinicians how to assess the patient with suspected stroke.

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Update of cell damage mechanisms in thiamine deficiency: focus on oxidative stress, excitotoxicity and inflammation.

Alan Hazell, Roger Butterworth (2016)

Thiamine deficiency (TD) is a well-established model of Wernicke's encephalopathy. Although the neurologic dysfunction and brain damage resulting from the biochemical consequences of TD is well characterized, the mechanism(s) that lead to the selective histological lesions characteristic of this disorder remain a mystery. Over the course of many years, various structural and functional changes have been identified that could lead to cell death in this disorder. However, despite a concerted effort to explain the consequences of TD in terms of these changes, our understanding of the pathophysiology of this disorder remains unclear. This review will focus on three of these processes, i.e. oxidative stress, glutamate-mediated excitotoxicity and inflammation and their role in selective vulnerability in TD. Since TD inhibits oxidative metabolism, a feature of many neurodegenerative disease states, it represents a model system with which to explore pathological mechanisms inherent in such maladies, with the potential to yield new insights into their possible treatment and prevention.

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Author and article information

Journal

Journal ID (nlm-ta): Case Rep Neurol Med

Journal ID (iso-abbrev): Case Rep Neurol Med

Journal ID (publisher-id): CRINM

Title: Case Reports in Neurological Medicine

Publisher: Hindawi Publishing Corporation

ISSN (Print): 2090-6668

ISSN (Electronic): 2090-6676

Publication date (Print): 2014

Publication date (Electronic): 23 February 2014

Volume: 2014

Electronic Location Identifier: 673230

Affiliations

¹Department of Neurology, Stavanger University Hospital, 4068 Stavanger, Norway

²Neuroscience Research Group, Stavanger University Hospital, 4068 Stavanger, Norway

³Department of Radiology, Stavanger University Hospital, 4068 Stavanger, Norway

Author notes

*Martin W. Kurz: kurzmartin@ 123456gmx.net

Academic Editors: P. Berlit and K. Wessel

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Alok Bhan http://orcid.org/0000-0002-6711-4083

Elisabeth Farbu http://orcid.org/0000-0001-9710-6589

Article

DOI: 10.1155/2014/673230

PMC ID: 3970369

PubMed ID: 24716022

SO-VID: 12f46e72-357e-4777-bbc3-fe081faa385f

License:

This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Wernicke's Encephalopathy Mimicking Acute Onset Stroke Diagnosed by CT Perfusion

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Abstract

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Stroke MRI

Most cited references 10

Clinical signs in the Wernicke-Korsakoff complex: a retrospective analysis of 131 cases diagnosed at necropsy.

Distinguishing between stroke and mimic at the bedside: the brain attack study.

Update of cell damage mechanisms in thiamine deficiency: focus on oxidative stress, excitotoxicity and inflammation.

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