Thrombosed Giant Aneurysm of the Basilar Artery that Developed from Dolichoectasia: A Case Report

H. Oyama, K. Hattori, A. Kito, Hideki Maki, Aichi Niwa
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Abstract

A 66-year-old male patient suffered a lacunar infarction 7 years previously and was treated with 100 mg/day of cilostazol. The fluid attenuated inversion recovery (FLAIR) image of a follow-up magnetic resonance imaging (MRI) scan revealed dolichoectasia of the basilar artery with a small luminal thrombus. Thirteen months later, a left cerebellar infarction occurred. The size of the aneurysm and luminal thrombus had increased. The dosage of cilostazol was increased to 200 mg/day. Three weeks later, he suffered a left pontine infarction and 100 mg/day of aspirin was added to the treatment regimen. Seventeen months after the cerebellar infarction, the aneurysm enlarged further. Surgical treatment was performed using a flow reduction method. After anastomoses of the right superficial temporal artery-superior cerebellar artery and left superficial temporal artery-posterior cerebral artery were performed, the bilateral vertebral arteries were embolized using a coil. The patient became comatose 12 hours after the last procedure. Three-dimensional computed tomography angiography revealed the complete occlusion of the basilar artery. Four days later, recanalization of the basilar artery was achieved by using an intravenous urokinase infusion. Nevertheless, marked infarction occurred in the bilateral cerebellar hemispheres and brain stem. He died and an autopsy was performed. The aneurysm was found embedded in the brain stem at autopsy. A microscopic examination showed fragmentation of the internal elastic lamina with atrophy of the muscle layer and adventitia. Neoangiogenesis within the thickened intima may have caused intramural hemorrhage and thrombus formation. Furthermore, a new sickle-shaped clot located between the arterial wall and the old thrombus may have caused the hemodynamic expansion of the aneurysm. Antiplatelet drugs were used to treat ischemic events caused by perforator or branch occlusion. However, use of these drugs should be carefully considered with regards to the risk of potentiating the compression of the brain stem due to aneurysmal enlargement.
基底动脉扩张形成的血栓性巨动脉瘤1例
66岁男性患者7年前发生腔隙性梗死,给予100mg /d西洛他唑治疗。后续磁共振成像(MRI)扫描的液体衰减反转恢复(FLAIR)图像显示基底动脉微缩扩张伴小腔血栓。13个月后,发生左侧小脑梗死。动脉瘤和腔内血栓增大。西洛他唑剂量增加至200mg /d。三周后,他患上了左脑桥梗死,治疗方案中加入了100毫克/天的阿司匹林。小脑梗塞17个月后,动脉瘤进一步扩大。手术治疗采用血流减少法。右颞浅动脉-小脑上动脉、左颞浅动脉-大脑后动脉吻合后,用线圈栓塞双侧椎动脉。病人在最后一次手术后12小时处于昏迷状态。三维计算机断层血管造影显示基底动脉完全闭塞。四天后,通过静脉输注尿激酶实现了基底动脉的再通。然而,在双侧小脑半球和脑干发生明显的梗死。他死了,并进行了尸检。尸检时发现动脉瘤嵌在脑干中。显微镜检查显示内部弹性板碎裂,肌层和外膜萎缩。增厚的内膜内新血管生成可能引起壁内出血和血栓形成。此外,位于动脉壁和旧血栓之间的新镰状血块可能导致动脉瘤的血流动力学扩张。抗血小板药物用于治疗穿支或支闭塞引起的缺血性事件。然而,使用这些药物应仔细考虑由于动脉瘤增大而加剧脑干压迫的风险。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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