17 June 2025
: Case report
[In Press] Distinguishing Wernicke Encephalopathy from Artery of Percheron Infarction in a 43-Year-Old Man: A Case Report
Unusual clinical course, Challenging differential diagnosis
Syed Raza1ABCDEF, Salma Mohamed23AB, Nazia Naz S. Khan23ABCDEFDOI: 10.12659/AJCR.948636
Am J Case Rep In Press; DOI: 10.12659/AJCR.948636
Available online: 2025-06-17, In Press, Corrected Proof
Publication in the "In-Press" formula aims at speeding up the public availability of the pending manuscript while waiting for the final publication. The assigned DOI number is active and citable. The availability of the article in the Medline, PubMed and PMC databases as well as Web of Science will be obtained after the final publication according to the journal schedule
Abstract
BACKGROUND
Wernicke’s encephalopathy (WE) and Artery of Percheron (AOP) infarction share overlapping presentations, including mental status changes, ocular-motor signs, and similar thalamic MRI findings; but require distinct time-sensitive treatment, making prompt differentiation critical. WE results from thiamine deficiency, often due to alcohol use, causing oxidative damage in highly metabolically active brain regions. In contrast, an AOP infarction results from thrombotic occlusion of a rare perforating artery. The aim of this case report is to delineate the similarities and differences between WE and AOP infarction and to underscore the importance of early empiric thiamine replacement.
CASE REPORT
A 43-year-old man presented with altered mental status, fever, and generalized weakness. Non-contrast head computed tomography (CT) showed cerebellar hypoattenuation, prompting activation of a code stroke. The lesion was later deemed artifactual, and he was admitted for further evaluation. The following morning, the patient’s condition acutely changed, with new oculomotor abnormalities and worsening right lower extremity weakness. An urgent brain MRI demonstrated symmetric hyperintensities in the medial thalami. Uncertain whether the lesions represented an AOP infarction or WE, the team ordered a serum thiamine analysis, which returned low. Intravenous thiamine was initiated, resulting in rapid clinical improvement, and confirming WE as the final diagnosis.
CONCLUSIONS
WE can closely mimic AOP infarction both on clinical presentation and on radiologic appearance. High-dose thiamine is a low-risk, potentially lifesaving intervention, particularly when initial CT imaging is nondiagnostic and further imaging is pending. Empiric thiamine administration is especially warranted if MRI shows bilateral thalamic lesions of uncertain etiology.
Keywords: Stroke; Thiamine Deficiency; Wernicke Encephalopathy; Cerebral Infarction; Magnetic Resonance Imaging; Case Reports
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