脳底動脈のｄｏｌｉｃｈｏｅｃｔａｓｉａが巨大血栓化脳動脈瘤に移行した１例

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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.