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自发性夹层导致基底动脉闭塞患儿血管内治疗后完全功能恢复:1 例报告。

Complete functional recovery in a child after endovascular treatment of basilar artery occlusion caused by spontaneous dissection: a case report.

机构信息

Department of Surgical Sciences, Radiology, Uppsala University, Uppsala, Sweden.

Department of Pathology, Uppsala University, Uppsala, Sweden.

出版信息

Childs Nerv Syst. 2022 Aug;38(8):1605-1612. doi: 10.1007/s00381-021-05428-w. Epub 2021 Dec 10.

Abstract

Stroke caused by dissection of arteries of the vertebrobasilar system in children is still poorly investigated in terms of etiology, means of treatment, course of disease, and prognosis. The aim of this report was to describe the unusual course of a spontaneous dissection of the basilar artery (BA) in a child treated with endovascular techniques and to point out that the plasticity of the brain stem can fully compensate for structural damage caused by stroke. We report the case of a 15-year-old boy who suffered a wake-up stroke with BA occlusion caused by spontaneous dissection. A blood clot was aspirated from the false lumen and the true lumen re-opened, but the patient deteriorated a few hours later, and repeated angiography revealed that the intimal flap was detached, occluding the BA again. The lumen of BA was then reconstructed by a stent. Despite a large pons infarction, the patient was completely recovered 11 months after the onset. The case was analyzed with angiograms and magnetic resonance imaging, macroscopic and microscopic pathological analysis, computed tomographic angiography, magnetic resonance-based angiography, and diffusion tensor imaging. This case illustrates that applied endovascular techniques and intensive care measures can alter the course of potentially fatal brain stem infarction. Our multimodal analysis gives new insight into the anatomical basis for the plasticity mechanism of the brain stem.

摘要

儿童椎基底动脉系统动脉夹层引起的中风在病因、治疗方法、病程和预后方面的研究仍不够充分。本报告旨在描述一名儿童接受血管内治疗后基底动脉(BA)自发性夹层的不寻常病程,并指出脑干的可塑性可以完全代偿中风引起的结构损伤。我们报告了一例 15 岁男孩的病例,他因自发性夹层导致基底动脉闭塞而发生觉醒性中风。从假腔中抽吸血栓并重新开放真腔,但患者数小时后恶化,重复血管造影显示内膜瓣再次脱落,再次阻塞 BA。然后通过支架重建 BA 的管腔。尽管脑桥有大面积梗死,但患者在发病后 11 个月完全康复。通过血管造影、磁共振成像、宏观和微观病理分析、计算机断层血管造影、磁共振血管造影和扩散张量成像对该病例进行了分析。该病例表明,应用血管内技术和重症监护措施可以改变潜在致命性脑桥梗死的病程。我们的多模态分析为脑干可塑性机制的解剖学基础提供了新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ad2/9325841/a75530bb6b5e/381_2021_5428_Fig1_HTML.jpg

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