2 0 0 0 MLDシステム表現に基づく平常時における群集挙動の解析
- 著者
- 宮田 悠 中原 一郎 太田 剛史 松本 省二 定政 信猛 石橋 良太 五味 正憲 坂 真人 岡田 卓也 西 秀久 園田 和隆 高下 純平 渡邉 定克 永田 泉
- 出版者
- 一般社団法人 日本脳卒中の外科学会
- 雑誌
- 脳卒中の外科 (ISSN:09145508)
- 巻号頁・発行日
- vol.44, no.2, pp.145-150, 2016 (Released:2016-06-07)
- 参考文献数
- 13
- 被引用文献数
- 11 10
We report a case of repeated cerebral infarction caused by internal carotid artery (ICA) dissection triggered by an elongated styloid process, a form of Eagle syndrome. A 41-year-old man presented with sudden, mild left hemidysesthesia. Magnetic resonance imaging (MRI) revealed a small acute cerebral infarction in the right parietal cortex and insular cortex. Magnetic resonance angiography and digital subtraction angiography (DSA) revealed a right-sided ICA dissection distal to the carotid bifurcation. Idiopathic carotid artery dissection was suspected, and the patient was prescribed aspirin and observed. However, 5 months after the initial cerebral infarction, he had a second episode of left hemiparesis and confusion accompanied by occlusion of the right ICA. Because the area of impaired perfusion in the right hemisphere was greater than that suggested by the diffusion-weighted images of head MRI and clinical status was worse than expected, we performed acute revascularization with aspiration of the thrombus and stenting to treat the carotid dissection. Recanalization with thrombolysis of cerebral infarction (TICI)-grade IIB was achieved. Computed tomographic (CT) angiography combined with analysis of bony structures revealed close proximity of the right ICA and an elongated styloid process with its tip directed toward the dissection. In an angiographic suite, a dynamic cone beam CT was performed with the head of the patient variedly rotated and tilted; the carotid artery dissection appeared to be triggered by the elongated styloid process. Resection of this process was performed to prevent recurrence of the cerebral infarction. Under the guidance of a navigation system, the elongated styloid process, which was located ventral to the anterior belly of the digastric muscle, was cut 3 cm from the tip. The patient was discharged on postoperative day 8 without medical problems, and no recurrence was observed for 12 months after the surgery.
1 0 0 0 OA 細胞外基質の産生分解から見た脳動脈瘤増大機構の解析と治療への展望
- 著者
- 青木 友浩 西村 真樹 片岡 大治 石橋 良太 森下 竜一 野崎 和彦 橋本 信夫 宮本 享
- 出版者
- 一般社団法人 日本脳卒中学会
- 雑誌
- 脳卒中 (ISSN:09120726)
- 巻号頁・発行日
- vol.32, no.6, pp.538-543, 2010-11-26 (Released:2010-12-03)
- 参考文献数
- 20
Cerebral aneurysm (CA) is a main cause of a lethal subarachnoid hemorrhage. Given the high incidence of CA in general population, the mechanisms of CA formation should be unlabelled and novel medical therapy for CA before rupture should be developed. The typical pathological feature of CA walls is the decrease of extracellular matrix (ECM). Decreased ECM results in the weakness of CA walls leading the enlargement and rupture of CA. In this article, we have reviewed the recent findings about the mechanisms of decreased ECM in CA walls mainly revealed by experiments using rodent CA models. ECM is the dynamic structure with the continuous synthesis and degeneration of matrix protein. In CA walls, the induced expressions of proteinases by chronic inflammation in arterial bifurcation are present and actively participated in the pathogenesis of CA. Further the synthesis of collagen is suppressed in CA wall through inflammatory stimulus in arterial walls. These results combined together indicate that both decreased synthesis and increased degeneration of ECM by chronic inflammation in CA walls contributes to CA formation. Further these results demonstrate the therapeutic potential of anti-inflammatory drugs for CA.