Raza Syed, Mohamed Salma, Khan Nazia Naz S
College of Human Medicine, Michigan State University, East Lansing, MI, USA.
Department of Medicine, College of Human Medicine, Michigan State University, East Lansing, MI, USA.
Am J Case Rep. 2025 Jul 25;26:e948636. doi: 10.12659/AJCR.948636.
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.
背景 韦尼克脑病（WE）与大脑后动脉丘脑穿通支梗死（AOP）表现重叠，包括精神状态改变、眼球运动体征以及类似的丘脑磁共振成像（MRI）表现；但需要不同的时效性治疗，因此迅速鉴别至关重要。WE 由硫胺素缺乏引起，通常与饮酒有关，在高代谢活跃的脑区造成氧化损伤。相比之下，AOP 梗死是由一条罕见的穿通动脉血栓形成闭塞所致。本病例报告的目的是阐明 WE 与 AOP 梗死之间的异同，并强调早期经验性补充硫胺素的重要性。病例报告 一名 43 岁男性出现精神状态改变、发热和全身无力。头部非增强计算机断层扫描（CT）显示小脑低密度影，触发了卒中代码激活。该病变后来被认为是伪影，患者入院进一步评估。次日早晨，患者病情急剧变化，出现新的眼球运动异常，右下肢无力加重。紧急脑部 MRI 显示双侧丘脑内侧对称性高信号。由于不确定这些病变代表 AOP 梗死还是 WE，团队进行了血清硫胺素分析，结果偏低。开始静脉注射硫胺素，患者临床症状迅速改善，最终确诊为 WE。结论 WE 在临床表现和影像学表现上都可能与 AOP 梗死极为相似。大剂量硫胺素是一种低风险、可能挽救生命的干预措施，尤其是在初始 CT 成像无法诊断且进一步成像尚未完成时。如果 MRI 显示双侧丘脑病变且病因不明，经验性使用硫胺素尤其必要。
