硬脑膜动静脉瘘的介入诊断及治疗 .pptxVIP

硬脑膜动静脉瘘的介入诊断及治疗硬脑膜动静脉瘘(DAVF)发生于硬脑膜及其附属结构如静脉窦、大脑镰、小脑幕上的异常动静脉分流约占颅内动静脉畸形的10%-15%可见于任何年龄,成人多见硬脑膜动静脉瘘(DAVF)硬脑膜窦畸形伴动静脉瘘新生儿或婴儿,常为巨大囊袋或硬膜湖,与其它窦或大脑静脉以缓流交通,多累及上矢状窦,常伴栓塞、闭锁或一侧颈内静脉球发育低下婴儿型DAVF高流速,高流量,多灶性,表现为大的窦及多发的局部动静脉瘘和大的供血血管,常继发引起皮层－软膜分流,直窦常缺如;静脉出口闭塞可引起颅压增高,脑室积水成人型DAVF婴儿型DAVF多支供血动脉静脉窦瘤样扩张梗塞性脑积水直窦缺如骨皮质改变女,10岁 进行性脑神经缺失(婴儿型DAVF)CT强化: 上矢状窦扩张,脑皮质钙化,白质变薄MR T1WI:上矢状窦及窦汇巨大流空影,小脑扁桃体下移成人型DAVF硬脑膜动脉前颅窝脑膜中动脉前支筛前、后动脉脑膜返动脉蝶腭动脉中颅窝脑膜中/副动脉颈内动脉下外侧干咽升动脉脑膜支后颅窝椎动脉脑膜支脑膜垂体干枕动脉脑膜支脑膜中动脉后支咽升动脉脑膜支大脑后动脉分支小脑上动脉分支小脑下后动脉分支发病机制DAVF与手术、头外伤、感染、硬脑膜窦血栓形成、雌激素等因素有关,但确切发病机制不明两种假说“生理性动静脉交通”开放:硬脑膜动静脉之间存“生理性动静脉交通”(dormant channels)或“裂隙样血管”(crack-like vessels),某些病理状态使其开放,形成DAVF新生血管:某些血管生长因子异常释放促使硬脑膜新生血管形成,致使DAVF形成分型按静脉引流方向分型:与临床表现及预后紧密相关按DAVF部位分型:与血供来源及治疗途径紧密相关静脉引流方向与病变部位相结合分型按静脉引流方向分型Borden classification1 Venous drainage directly into dural venous sinus or meningeal vein2 Venous drainage into dural venous sinus with CVR3 Venous drainage directly into subarachnoid veins(CVR only)Cognard classificationI Venous drainage into dural venous sinus with antegrade flowIIa Venous drainage into dural venous sinus with retrograde flowIIb Venous drainage into dural venous sinus with antegrade flow and CVRIIa+b Venous drainage into dural venous sinus with retrograde flow and CVRIII Venous drainage directly into subarachnoid veins (CVR only)IV Type III with venous ectasias of the draining subarachnoid veinsV Venous drainage into the perimedullary plexusCVR=cortical venous reflux(估计与静脉窦闭塞有关)按DAVF部位分型海绵窦DAVF横窦－乙状窦DAVF小脑幕DAVF上矢状窦DAVF前颅窝DAVF边缘窦DAVF岩上/下窦DAVF舌下神经管DAVF临床表现良性DAVF搏动性杂音眼眶充血颅神经麻痹慢性头痛无症状侵袭性DAVF颅内出血颅内高压非出血局部神经缺失血管性痴呆死亡Borden type 1Cognard typeI/ⅡaBorden type 2/3Cognard type IIb-Ⅴ皮层静脉返流(CVR)或深静脉引流是预后不良的重要因素头痛颅内出血中枢神经缺失,痴呆颅内出血头痛搏动性突眼球结膜水肿　和充血眶周杂音进行性视力　下降颅神经麻痹杂音,耳鸣颅内出血中枢神经缺失杂音,耳鸣,头痛眼部症状颅内出血(少见)诊断经颅多普勒:可探测血流动力学改变,特异性较低CT与MRI:对良性DAVF敏感性较低;对侵袭性DAVF,可显示异常血管,颅内出血,局部占位效应,脑水肿,脑积水,静脉窦血栓形成及颅骨骨质异常等征象CTA与MRA:可清楚显示异常增粗的供血动脉和扩张的引流静脉及静脉窦,对瘘口位置及“危险吻合”显示欠佳诊断DSA供血动脉瘘口位置引流静脉静脉窦扩张与闭塞脑循环异常L-ICA Male,62 tentorial DAVF(