脑动静脉畸形多学科诊疗专家共识
国家神经疾病医学中心
中国医师协会神经介入专业委员会
世界华人神经外科医师协会放射神经外科专家委员会
通信作者：
洪韬，首都医科大学宣武医院神经外科，北京 100053，Email：Hongtao.edu@gmail.com；
朱巍，复旦大学附属华山医院神经外科，上海 200040，Email：drzhuwei@fudan.edu.cn；
孙时斌，首都医科大学附属北京天坛医院立体定向放射外科，北京 100070，Email：gksssb@163.com；
陈光忠，南方医科大学附属广东省人民医院（广东省医学科学院）神经外科，广州 510080，Email：chengz5413@126.com
DOI:
10.3760/cma.j.cn112137-20240109-00061
【摘要】脑动静脉畸形（BAVM）是一类基因突变导致的难治性脑血管结构异常疾病，目前的治疗措施包括手术切除、介入栓塞以及立体定向放射治疗。三种治疗方式针对不同的病变血管结构各具优势，但受限于病变复杂的血管构筑及其与脑组织密切的解剖关系，任何单一治疗措施都无法安全有效的治疗所有BAVM病例。为了更好地规范和指导我国脑动静脉畸形患者的临床诊疗，国家神经疾病医学中心、中国医师协会神经介入专业委员会以及世界华人神经外科医师协会放射神经外科专家委员会经共同讨论，制定了本专家共识。经过深入分析国内外循证医学证据，专家组结合我国的具体情况，给出针对脑动静脉畸形出血预测因素、妊娠期临床风险、影像学诊断措施、临床治疗策略等具体临床诊疗问题的33条推荐意见，以期为全国范围内脑动静脉畸形诊疗提供指导。
【关键词】脑动静脉畸形；脑出血；手术；介入栓塞；立体定向放射外科
脑动静脉畸形（brain arteriovenous malformation，BAVM）是一类复杂难治的脑血管结构异常疾病，其病灶由供血动脉、畸形血管团（nidus）以及引流静脉组成。由于毛细血管网缺失，大量血液由动脉经畸形血管直接进入静脉系统，使病变血管流量显著增大，并最终因破裂出血或盗血导致患者神经功能障碍，甚至死亡［1-3］。
BAVM被认为是脑血管病诊疗中最具挑战的疾病。目前成熟的治疗措施包括手术切除、介入栓塞以及立体定向放射治疗。受限于复杂的血管构筑及其与脑组织密切的解剖关系，任何单一治疗措施都无法安全有效的治疗所有BAVM病例［4-7］。在实际BAVM治疗策略制定的过程中，术者需要根据个体化的病变解剖和血管构筑特点匹配恰当的治疗方法。对于复杂的病变往往需要组合多种疗法以取得理想的预后。但BAVM在血管构筑和解剖特点上具有极高的异质性。而显微手术、血管内介入和立体定向放射等治疗方法分属不同学科，这为BAVM治疗策略的制定带来了一定的困难和挑战。
第一部分 共识制定方法学
本共识邀请国内神经外科、神经介入以及放射医学等学科的专家学者组成专家组，针对脑动静脉畸形诊疗现状的学术论文、行业报告及相关政策文件进行了充分检索，在国内外医学数据库（Pubmed、Web of Science、PsychoInfo、Cochrane library、Embase、万方医学网和中国知网）中，通过以下关键词进行检索：“brain arteriovenous malformation、brain vascular malformation、intracranial arteriovenous malformations、cerebrovascular disorders、central nervous system vascular malformations、central nervous system vascular malformations、cerebral arteriovenous malformation、cerebral vascular malformation、arteriovenous fistula、intracranial hemorrhage、cerebral hemorrhage、operation、embolization、Gamma Knife radiosurgery、stereotactic radiation、linear accelerator radiosurgery、steraotactic radiation therapies、脑动静脉畸形、脑血管畸形、颅内动静脉畸形、脑血管病、中枢神经系统血管畸形、中枢神经系统动静脉畸形、脑动静脉瘘、脑出血、外科手术、介入栓塞、伽马刀、立体定向放射外科治疗、直线加速器”。纳入的文献类型包括临床实践指南、专家共识、综述、荟萃分析和原始临床研究。撰写小组成员广泛检索文献，并按照美国心脏协会评分系统［8］对所纳入的文献进行证据质量分级，然后在此基础上进行推荐强度分级，形成初稿。其中，证据等级分为ABC三个级别，推荐等级分为I、IIa、IIb、III，形成最终的推荐意见。缺乏文献证据的意见由专家委员会成员根据临床经验进行判断，组织专家讨论后达成共识，初稿完成后，由所有专家组成员对草拟的共识意见进行匿名投票，当意见达到70%的“同意”或“强烈同意”时将其纳入专家共识，低于70%同意率的意见经过修改，重新提交下一轮，最多进行三轮投票，最终形成共识意见。
第二部分 流行病学
BAVM好发于中青年人群。一项纳入1 289例患者的队列研究显示，BAVM平均确诊年龄为31岁（95%CI：30~32岁），约50%的患者在20~40岁之间确诊［9］。该病男女患者比例约为5∶4［4］。
虽然有关BAVM发病率和患病率的研究相对较少，但已有研究结论较为统一。既往大宗的尸检研究显示BAVM检出率为（1~1.8）/10万人［3，10］，6项分别基于Northern California、Olmsted County Minnesota、New York Islands、Scotland、Netherlands Antilles以及Sweden地区人口的流行病学研究显示BAVM的年发病率（incidence）为（1.1~1.4）/10万人［11-16］。随着磁共振的普及，无症状BAVM的检出率逐渐提高［12，14，16-17］。一项纳入15 000余例头颅MR结果的荟萃分析显示无症状BAVM的检出率可高达1/2 000［18］。
第三部分 病因和病理生理机制
一、病因
脑动静脉畸形的发病机制研究在近10年取得了重要进展，现已明确多数BAVM的病因为血管内皮细胞基因突变。根据突变模式的不同，BAVM病例可分为家族遗传性动静脉畸形和散发性动静脉畸形两种，其中散发性动静脉畸形约占95%［19-22］。
（一）家族遗传性脑动静脉畸形
目前研究发现，部分家族遗传性疾病的致病基因与调控血管发育的通路密切相关，导致患者罹患脑BAVM的风险显著升高。其中最常见的是遗传性出血性毛细血管扩张症（hereditary hemorrhagic telangiectasia，HHT）和毛细血管畸形-动静脉畸形（capillary malformation-arteriovenous malformation，CM-AVM）综合征。
HHT也称为Osler-Weber-Rendu综合征，是一种常染色体显性遗传病，患病率为1/5 000~1/8 000［23］。HHT患者特征性病变是皮肤黏膜表面的毛细血管扩张和内脏器官（肝脏、肺和中枢神经系统）的动静脉畸形［24］。HHT患者最常见的表现是鼻出血，在临床中有10%~20%的HHT患者合并BAVM，根据血管构筑特点可进一步划分为软脑膜动静脉瘘、团块性动静脉畸形和毛细血管畸形［25-26］。在致病机制上，目前至少有4种基因与HHT发生相关，包括ENG基因（编码Endoglin蛋白，是TGF-β的内皮辅助受体，突变后可以导致1型HHT）、ALK1基因（编码ACVRL1蛋白，是跨膜丝氨酸/苏氨酸激酶受体，可以影响内皮细胞的增殖和迁移，突变后导致2型HHT）、SMAD4基因和GDF2基因［27-28］。在小鼠模型中，Eng和Alk1基因的纯合性缺失会导致小鼠胚胎期致死，但是杂合性突变的小鼠在受到血管内皮生长因子（vascular endothelial growth factor，VEGF）刺激后可以形成动静脉畸形［29-31］。
CM-AVM是常染色体显性遗传病［32］。此病外显率高，97%的患者可以出现面部或四肢的毛细血管畸形（capillary malformation，CM），常表现为皮肤表面多发，圆形或椭圆形、红色至紫色的非典型斑片，多平坦，直径为1~2 cm，带有苍白晕环。大约有1/3的患者可以合并有高流量血管畸形，病变结构以软膜动静脉瘘为主，有文献报道部分CM-AVM患者还可以合并有淋巴管畸形［33-34］。CM-AVM的致病基因为RASA1（编码Ras-GTPase激活蛋白，突变后导致CM-AVM1型）或EPHB4（编码EphB4蛋白，是跨膜Eph受体酪氨酸激酶，突变后导致CM-AVM2型）［35］。
此外，可导致动静脉畸形发病率升高的家族遗传性疾病还有1型神经纤维瘤病（NF1失活突变）以及Cowden综合征（PTEN失活突变），但两者多发生颅外AVM（如肌肉AVM和椎旁AVM），暂未见合并BAVM的病例报道［36-37］。
（二）散发性脑动静脉畸形
近年来，散发BAVM的遗传学机制研究取得了一系列重要突破。2018年初，Nikolaev等［38］在《新英格兰医学杂志》报道了利用深度全外显子测序（平均序列深度，339±64×），在63%（45/72）的BAVM血管内皮细胞中发现功能获得性KRAS体细胞突变（c.35G➝T，p.Gly12Val；c.35G➝A，p.Gly12Asp；c.183A➝T，p.Gln61His），并经过微滴数字式聚合酶链式反应（droplet digital polymerase chain reaction，ddPCR）获得验证，丰度为2.4%~4%；而在匹配的患者血样中没有检测到相应突变，证明动静脉畸形组织中存在体细胞突变。同期，我国学者利用422个肿瘤基因靶向测序（Panel）对脑-脊髓AVM患者手术切除标本进行超深度外显子测序（平均测序深度1 077±298×），并通过ddPCR验证；在31例（21例BAVM，10例SAVM）标本中，发现27例携带KRAS/BRAF体细胞突变，比例高达87.1%。此外，该研究也证实了脑动静脉畸形与脊髓动静脉畸形在遗传上具有高度同质性［39］。随后的动物实验通过诱导脑血管内皮细胞KRAS突变，成功构建了小鼠BAVM模型，证实脑血管内皮细胞KRAS激活突变是散发BAVM的病因［40-41］。
二、病理生理机制
1.出血：出血是BAVM最主要的病理生理机制，畸形血管直径较大且缺少血管周细胞/平滑肌细胞的保护，高速动脉血流持续冲击畸形团和引流静脉将导致血管壁物理损伤。同时，畸形血管壁的慢性炎性反应也可能持续破坏血管壁稳定性。因此动静脉畸形病灶具有较高的出血风险。
2.盗血：由于动静脉畸形的血流阻力远低于毛细血管网，因此大量动脉血经BAVM直接回流至静脉系统，导致其供血动脉远端的血流不足形成“盗血”，引起相关脑组织灌注不足。长时间的缺氧微环境导致病灶周围胶质增生，还可能诱导病灶周围毛细血管扩张和血管新生。血流异常和血管盗血现象被认为是造成局灶性神经功能障碍以及癫痫的原因，但目前缺少客观评价工具［42］。
3.静脉高压：BAVM患者脑静脉系统承接了大量动脉血流。静脉窦在持续性高速血流的冲击下可能逐渐狭窄，导致脑静脉系统压力升高，进而影响正常脑组织的静脉回流。静脉高压可能与患者认知能力下降、癫痫发作和神经功能障碍有关［1，43］。
4.脑积水：脑室出血、畸形团的引流静脉扩张挤压中脑导水管或第四脑室、静脉高压导致脑脊液吸收障碍均可引起脑积水，严重时需要行脑室外引流［42-44］。
第四部分 临床表现和自然病史
一、临床表现
BAVM发病年龄通常为10~40岁，两个发病高峰年龄段为儿童期和30~50岁。BAVM的临床表现受年龄，病灶大小、位置和血管结构影响，通常包括以下5类：
1.颅内出血（40%~60%）：BAVM的颅内出血可表现为脑实质出血、脑室内出血或蛛网膜下腔出血，具体取决于病变的位置。蛛网膜下腔出血在表浅AVM中较常见。回顾性数据显示，儿童初始表现为出血的比例高于成年人（56%比43%）［45］。
2.癫痫发作（10%~30%）：BAVM的癫痫发作通常以局灶性发作为起始，但随着病情进展可发展为全面性发作。癫痫发作类型和临床表现受BAVM病灶位置和血管构筑影响。位于皮质、大型、多发、表浅引流的BAVM更易出现癫痫［45］。
3.局灶神经功能障碍：BAVM患者出现局灶性神经功能障碍的原因可能是出血所致占位效应，或是癫痫发作后的残留症状［46］。有学者认为盗血是一部分局灶性神经功能障碍的原因，但目前缺少客观评价工具。
4.头痛：伴发于BAVM的头痛没有特异性表现，多数病例很可能为BAVM与其他原因导致的头痛偶然同时出现。一项研究发现，神经系统检查正常的头痛患者中有0.2%患有BAVM［47］。
5.偶然发现（10%~20%）：随着MR设备的普及，因其他原因接受脑MRI或CT检查而确诊的无症状BAVM患者比例呈上升趋势［48］。
二、自然病史
颅内出血是BAVM最常见且最具危害的发病方式，是制定治疗决策的关键因素。因此，既往BAVM的自然病程研究主要针对其出血风险开展。一项纳入3 923例患者随访18 423病人年的荟萃分析显示BAVM患者总体年出血率为3%［49］。另一项纳入了4项研究，共2 525例患者、随访6 074病人年，年汇总分析显示BAVM颅内出血的总体年发生率为2.3%（95%CI：2.0%~2.7%）［50］。ARUBA试验的观察组中，年出血率约为2%［5］。此外，有大样本量观察性研究显示BAVM的年出血风险可能会随着观察时间延长而下降［51］。
现已知多种因素可能影响BAVM的出血风险。在未经治疗的BAVM病例中，出血病史是后续出血事件的最强预测指标。既往荟萃分析表明，未破裂BAVM的年出血率为1.3%~2.2%，而破裂BAVM的年出血率为4.5%~4.8%［49-50］。有研究表明神经影像检查发现的无症状出血同样是再出血的危险因素［52］。高龄被发现可能是出血事件的危险因素。每增长10岁，BAVM的出血风险大约增加30%（HR=1.34，95%CI：1.17~1.53）［50］。BAVM的解剖和血管特征也影响出血事件的发生，包括：仅有深静脉引流（HR=2.4，95%CI：1.1~3.8），病灶位于脑深部（HR=2.4，95%CI：1.4~3.4）以及动脉瘤结构（HR=1.8，95%CI：1.6~2.0）。许多研究显示病变的大小与出血风险无关［49，51，53-54］。虽然一些回顾性研究发现体积较小的BAVM具有更高的出血比例，但不能排除这一结论存在选择偏倚。
临床工作中需综合考虑出血危险因素以预测BAVM的出血风险［55］。一项来自哥伦比亚数据库的研究将“出血为首发症状、深静脉引流和病灶位于脑深部”三项危险因素进行组合，发现各类情况的平均年出血率为：没有危险因素（1%），1项危险因素（5%），2项危险因素（10%~15%），3项危险因素（>30%）。我国学者通过对3 900余例前瞻性BAVM队列的血管构筑特点进行严格的统计分析，提出了基于中国人群的VALE评分系统。该评分纳入了3个危险因素：累及脑室（2分）、深部位置（1分）、单一深静脉引流（2分）及1个保护因素：静脉瘤（-4分）。VALE评分系统总跨度为10分（-4至5分），其中低风险组为-4至-3分，中风险组为-2至1分，高风险组为2至5分，能有效区分BAVM破裂高危患者［56］。此外，BAVM的破裂风险与异常血流动力学密切相关，研究发现病变引流静脉引流受阻或可提示病变存在较高出血风险［57-58］。
尽管多项研究显示BAVM出血的预后优于自发性脑出血，但其出血后12个月的病死率仍高达12%。高龄和初始血肿体积较大是不良预后的独立预测因素［59-60］。但Abla等［61］发现与幕上位置相比，后颅窝AVM出血即使血肿量较小也会导致更差的结果。
癫痫发作是第二常见的BAVM临床表现。既往研究提示在偶然发现的BAVM人群中，5年内首次癫痫发作风险为8%［62］。相比之下，有自发性脑出血或局灶性神经功能障碍病史人群的5年首次癫痫发作风险为23%。癫痫发作的其他危险因素包括年龄较小、病灶位于颞叶、皮质受累和病灶直径>3 cm［46］。无颅内出血或局灶性神经功能障碍病史的患者中，首次癫痫发作后的5年癫痫再发风险为58%［46］。
推荐意见1：明确BAVM的出血风险有助于制定合理的治疗策略，出血病史是BAVM出血事件的最强预测因素。此外还需考虑血管构筑等相关危险因素，综合判断患者的临床风险。（B级证据，Ⅰ级推荐）
三、妊娠期和产褥期风险
BAVM女性患者在妊娠期及产褥期的出血风险可能更高［63-68］。虽然尚有争议［64］，但近年来发表的大样本量研究多为阳性结果。2017年，Porras等［66］纳入270例女性BAVM患者并将患者整个观察期分为暴露期（妊娠期+产褥期）和非暴露期（整个观察期-暴露期），最终发现BAVM患者在暴露期内的出血风险为5.7%/年，显著高于非暴露期1.3%/年（P<0.001）。Gross等［65］在对54例女性患者的临床随访中也发现BAVM在妊娠期内破裂出血风险高于非妊娠期（8.1%/年比1.1%/年，HR=7.91，P<0.001）。一篇纳入9项研究超过60 000余例患者的系统回顾也提示妊娠和产褥期将增加BAVM的出血风险［69］。
妊娠期内BAVM破裂出血的治疗是棘手的临床问题，目前已有研究均为小样本临床队列。一项纳入27例妊娠期破裂但未行外科干预的BAVM患者的研究中，有7例患者在同一次妊娠过程中再出血，再出血率为26%［70］，远高于非妊娠期再出血风险［71-73］。Gross等［65］也指出大约有1/4的孕期BAVM出血患者在怀孕过程中再次出血。妊娠期内出血的BAVM可考虑采取积极的干预措施。然而，外科干预可能会对妊娠和胎儿带来的额外风险，因此需在妇产科、新生儿科及麻醉科等相关专科的共同参与下权衡两者的风险程度，个体化的制定治疗方案［74］。
BAVM患者的分娩方式尚存争议，2017年我国学者的研究结果提示阴道分娩并不会增加脑动静脉畸形妊娠出血的风险［75］，但是也有学者建议近期有颅内出血或新发神经功能障碍的患者应首选剖宫产［76］。
推荐意见2：对于患有BAVM的备孕患者需告知妊娠及产褥期的相关临床风险。（B级证据，Ⅱa级推荐）
推荐意见3：妊娠期及产褥期出现新发局灶性神经功能障碍、剧烈头痛或癫痫的患者，需行头颅MR检查。（C级证据，Ⅱa级推荐）
推荐意见4：妊娠及产褥期患者的BAVM外科干预需在神经外科、妇产科、新生儿科及麻醉科等相关专科的共同参与下权衡病变本身临床风险以及治疗措施对孕妇及胎儿的影响，个体化的制定治疗方案。（C级证据，Ⅱa级推荐）
第五部分 诊断
一、影像诊断
BAVM的影像学检查在其诊断、治疗策略制定以及随访中均发挥重要作用。常用影像工具包括CT、MR以及DSA，三者通常需要联合使用以提供更多的信息［77］。
（一）CT
对疑似颅内出血的患者进行CT扫描。CT平扫对急性蛛网膜下腔出血和脑实质内出血的灵敏度超过90%［78］。虽然CT在检测BAVM或其他病因方面的价值有限，但还是能发现血管异常的一些潜在征象，例如扩张或钙化的血管，并且畸形血管团的密度略高于正常脑组织［79］。脑实质内出血位置也有助于区分原发性与继发性出血［80-81］，年轻的脑叶或后颅窝出血患者发现BAVM或其他脑血管病的比例较高［81］。CT灌注图像可间接提示BAVM对颅内血流动力学造成的影响［82］。目前BAVM相关的血流动力学异常可主要归纳为三种模式。第一种是功能性盗血，指动静脉畸形从供血动脉近端盗血，导致其远端脑组织供血不足，此时CT灌注成像可见脑血流量、脑血容量和平均通过时间减少，有学者认为功能性盗血与癫痫发作相关。第二种模式称为缺血性盗血，指动静脉畸形从邻近脑组织的软膜侧支血管盗血，此时CT灌注成像可见脑血流量和血容量减少但在脑实质中的平均通过时间增加，该机制被认为与局灶性神经功能障碍相关。第三种血流模式为异常是静脉高压，CT灌注成像可见脑血容量和远隔部位大脑的平均通过时间增加。这些患者表现为进行性神经功能障碍。上述三种模式很少独立存在，BAVM患者脑血流动力学异常是多种模式共同作用的结果。
CTA的优势在于成像时间短，当CT平扫图像发现可疑脑血管病迹象时可直接通过CTA快速诊断［83］。CTA还具有良好的空间分辨率，与DSA相比，CTA在检测脑实质出血患者的血管异常方面具有理想的灵敏度（83.6%~100%）和特异度（77.2%~100%）［79，84-86］。Josephson等［84］对526例接受CTA检查的脑出血（intracerebral haemorrhage，ICH）患者资料进行了汇总分析，其CTA对于诊断潜在血管病因的特异度和灵敏度分别为0.95（95%CI：0.90~0.97）和0.99（95%CI：0.95~1.00）。CTA的局限性在于易受到金属制品及颅骨的影响而产生伪影。并且由于4D CTA技术尚未普及［87］，CTA在区分畸形团血管构筑方面相对DSA处于劣势。
（二）MRI
MRI具有理想的空间分辨率并且能提供更多脑组织信息，因此在筛查BAVM方面较CT更具优势，病灶在T2加权像上表现为典型的扩张血管流空信号，是目前筛查BAVM的首选成像方式［84］。大多数BAVM几乎对周围脑组织没有体积压迫效应，除非有大的静脉湖压迫邻近的脑实质和脑脊液引流通路。在未破裂BAVM患者中，畸形团周围脑水肿的存在是一个重要信号，通常与部分引流静脉血栓形成有关，导致进行性神经功能障碍、头痛和（或）癫痫发作。
磁敏感加权成像（SWI）识别既往的微出血灶。Guo等［52］对975例BAVM患者进行了一项回顾性研究，利用SWI在6.5%的患者中发现了陈旧性出血的证据，并与ICH病史（OR=3.97；P<0. 001）以及随访中新发 ICH（OR=3.53；P<0.010）均存在相关性。MR和CT在观察畸形团，脑组织和颅骨方面所能提供的影像信息各具优势，因此不能互相替代。通过影像融合技术可以将各类影像数据融合，有助于复杂病例治疗计划的制定［88］。
目前已普及的MRA空间分辨率略低于CTA。无论是时间飞跃法还是对比增强法，MRA在检测更小的血管（直径<1 mm）、动脉瘤［89］、畸形血管团（<10 mm）［90］，和引流静脉解剖［91-92］方面还存在一些局限性。但其无创、无辐射的特点使其在BAVM患者复查以及特殊人群（如儿童、孕妇）筛查中更具优势。
（三）DSA
DSA是诊断BAVM的金标准，具有目前最理想的时间和空间分辨率，能够提供准确的BAVM血管构筑和血流动力学信息［73，93-95］。然而，DSA属于有创操作，存在较高的并发症风险，如动脉夹层、血栓/斑块脱落等［96］。此外，BAVM的DSA检查通常需要高帧率和多次造影，可能导致患者辐射暴露剂量较高［97］。术者需在充分理解BAVM的DSA原理和成像过程的前提下评估以下信息，以便合理制定治疗策略：
（1）供血动脉：明确供血动脉的供血模式，包括“终末型”以及“过路型”两类。终末型供血动脉完全进入畸形团，不再向其他脑组织供血。终末型供血动脉通常是皮质动脉的远端以及小的穿支血管。过路型供血动脉本质上是较大的动脉血管发出多个细小分支进入畸形团，但该动脉血管的远端向正常脑组织供血。
（2）动脉瘤结构：动脉瘤结构是BAVM出血的重要危险结构，可发生在供血动脉，畸形团以及引流静脉近端。累及供血动脉的动脉瘤多与血流动力学异常相关，这些病变可以通过弹簧圈或NBCA胶进行栓塞，文献报道部分体积较小的血流相关动脉瘤在BAVM闭塞后可自愈。畸形团内的动脉瘤结构是病灶的薄弱点，可能是血流动力学以及局部炎性反应共同作用于畸形血管壁的结果，需要积极干预，通常使用液体栓塞剂进行填塞。
（3）畸形血管团：畸形血管团是BAVM的核心结构，本质上是大量动静脉瘘的集合。畸形团内若存在流量较高的瘘口应优先予以栓塞，可降低后续临床风险并为其他治疗方式创造条件。畸形血管团的弥散程度对多种外科治疗方式的有效性均有显著影响，但目前缺少可靠的量化工具对畸形团弥散程度进行评价。
（4）引流静脉：在DSA过程中需要明确是否存在流出道狭窄和静脉湖，深静脉是否参与引流以及引流静脉的数量。这些引流静脉参数对病变进展方向和治疗决策的制定都具有重要影响。
由于血肿可能对畸形血管造成压迫，一些体积较小的BAVM在出血急性期行DSA检查可能呈现阴性结果，待血肿吸收后，畸形团可能重新显影。因此，对于非典型部位的脑出血患者，建议在出血后4周复查血管造影。
DSA不仅可以相对完整的显示畸形血管团的结构细节，通过捕捉造影剂的流体力学特征还可以获得动静脉畸形的血流动力学参数，有学者通过彩色编码的定量DSA技术（color-cording quantitative，DSA）对BAVM进行了详细的血流动力学分析，发现“停滞指数”“畸形团血流通过相对速率”等一些血流动力学参数或与畸形团出血风险相关，是具有临床参考价值的影像工具［57，98］。
推荐意见5：对于可疑的脑出血患者进行脑血管影像检查（CTA、MRA或DSA）是合理的。（B级证据，Ⅱa级推荐）
推荐意见6：对于无明确病因反复头疼、癫痫发作或局灶性神经功能障碍的患者建议采用MRI筛查。（C级证据，Ⅱa级推荐）
推荐意见7：DSA是BAVM诊断的金标准，对于其他影像确诊或可疑的病例应行DSA检查。（B级证据，Ⅰ级推荐）
推荐意见8：非典型部位脑出血患者急性期DSA阴性患者建议血肿吸收后复查DSA或其他脑血管影像。（C级证据，Ⅱa级推荐）
二、基因诊断
现已明确几乎所有BAVM的发生均与基因突变有关，因此对BAVM患者及亲属进行基因筛查的必要性是目前需要关注的问题。
研究数据表明接近90%的散发BAVM病例的病因为KRAS或BRAF体细胞激活突变［38-39］。目前尚未发现散发BAVM的基因型与表型之间存在明确的相关性，且关于BAVM患者使用MAPK通路相关靶向药物的有效性尚无定论。此外，目前尚无手术切除之外的安全获得BAVM组织样本的活检方式。而对于可以手术切除的BAVM患者，其治愈率超过95%。
对于家族遗传性BAVM而言，患者面临较高的脑或脊髓AVM复发风险，同时还需考虑疾病的遗传风险。因此，建议对可疑的家族遗传性BAVM患者及亲属进行基因检测。以下临床特征提示家族性BAVM可能性大：
（1）多发AVM病变，包括颅内存在多个独立的AVM病变患者，以及除BAVM之外还合并其他内脏AVM（如脊髓、肺以及肝等器官存在AVM）的患者。注意头面部体节性动静脉畸形综合征（cerebrofacial arteriovenous metameric syndromes，CAMS）［99］的病因为体节性体细胞突变，因此不属家族遗传性BAVM病例范畴。
（2）存在血缘关系的亲属确诊脑或其他动静脉畸形。
（3）患者合并多发皮肤红斑及（或）黏膜（口咽鼻）毛细血管扩张病灶。
（4）患者及存在血缘关系的亲属均存在反复鼻出血和（或）消化道出血病史。
由于家族遗传性BAVM的致病基因均为种系突变（germline mutation），通常使用外周血白细胞DNA进行测序筛查。可选用的测序技术包括全外显子测序以及血管畸形相关基因Panel测序。全外显子测序的优势在于高通量，因此不容易遗漏罕见的致病基因突变；后者的优势在于测序成本较低，并且由于测序深度高可用于检测体细胞突变的低丰度突变，但检测基因均为已知致病基因。
推荐意见9：可疑的家族性BAVM患者应考虑进行基因检测。（C级证据，Ⅱa级推荐）
第六部分 治疗
目前尚无药物被证实具有闭塞或稳定BAVM的治疗效果。该疾病的治疗仍主要依赖外科技术，包括显微手术、介入栓塞以及立体定向放射治疗。这三种治疗方式的策略和目标有所区别：显微手术要求完全切除病灶，旨在快速并永久性消除BAVM后续的临床风险；立体定向放射治疗损伤较小，其首要目标同样是完全闭塞畸形团，但需要相对较长的过程。对于体积较大的病变只能达到部分闭塞的效果，为了达到理想的治疗结果可能需要配合显微手术或介入治疗；介入栓塞多数情况不以完全闭塞畸形团为首要目标，而是通过闭塞危险结构或降低病变流量的方式实现对临床风险的控制，或为手术及放射治疗创造有利条件。
现阶段BAVM的治疗结果并不理想。该疾病目前规模最大的系统回顾（142个队列，共13 698例BAVM患者）显示BAVM的整体治愈率仅为46%，治疗相关的永久性神经功能障碍发生率为6%［4］。此外，ARUBA研究显示未破裂BAVM的有创治疗预后劣于保守治疗［5］。这表明目前的三种治疗方式都存在一定局限性，难以适用于所有BAVM病例。
一、显微手术
外科手术治疗BAVM最早可追溯至19世纪中期［100］。1927年，Moniz首次将脑血管造影应用于BAVM的诊断［100］，使临床医生逐渐了解BAVM的血管结构，为BAVM的成功切除奠定了基础。1928年Dandy系统地开展了BAVM的手术治疗［101］。1969年Yasargil［102］首次将显微镜用于BAVM切除，标志着BAVM显微手术治疗的新纪元。随后，各类神经外科显微手术技术及相应辅助设备逐渐发展。目前，显微手术成为治疗BAVM治愈率最高的方式，其治愈率达95%~99%［103］。BAVM切除的常规手术步骤包括：
（1）开颅显露病变：BAVM手术通常要求骨窗范围应充分暴露畸形团，供血动脉以及引流静脉；
（2）辨别并阻断供血动脉：充分暴露病变后，对应DSA/CTA辨认病灶供血动脉，供血动脉通常较同级别的正常动脉血管扩张增粗有助于初步识别。明确供血动脉后应依次分离并电凝切断，注意流量较高的血管在电凝前应以AVM夹或迷你动脉瘤夹阻断其近端，可有效避免在电凝过程中血管破裂出血。
（3）切除畸形血管团：围绕畸形团，将畸形血管与周边脑组织环状剥离。因来自畸形团深部的供血无法完全在手术前半程离断，因此在剥离畸形团的过程中要保护引流静脉。
（4）切断引流静脉：主引流静脉的切断是手术的最后一步，必须在完全游离供血动脉和畸形团后才可进行。特别粗大的引流静脉需要缝扎或使用AVM夹夹闭。
（5）缝合伤口。
（一）适应证
显微手术的优势在于迅速并永久性的解除BAVM临床风险，但手术的有创性决定了显微手术需要设立严格的适应证来保障治疗安全性。目前已设立有多个评分系统用于评估BAVM显微手术的安全性，包括Spetzler-Martin（SM）分级、史氏分级、以及在SM分级基础上的改良SM分级和Lawton-Young分级，其中应用最为广泛的是Spetzler-Martin分级系统［104］。
SM分级根据畸形团的大小、畸形团部位是否累及功能区以及是否存在深静脉引流将BAVM划分为5级。此外，对于一些特殊的病灶，如位于功能区体积较大且弥散的畸形团或位置较深且极度弥散的畸形团，虽然未能在评分中获得较高分级，但因几乎不可避免的手术风险被划分为Ⅵ级，或直接划分为“不可手术”［104］。SM分级的优势在于易于评价，同时对于手术的安全性具有很好的分辨度。Spetzler和Ponce［105］在一项纳入1 476例手术BAVM患者的汇总分析中指出SM Ⅰ~Ⅴ级患者预后不良的比例分别为4%、10%、18%、31%以及37%。Spetzler等据此将SM Ⅰ~Ⅱ级，SM Ⅲ级以及SM Ⅳ~Ⅴ级的病例分别划分为三个等级，提出了更加简洁的Spetzler-Ponce分级（SPC）。该分级对BAVM手术难度的划分准确性得到了后续大样本量队列的验证［106-107］。在一项纳入641例手术治疗的BAVM队列中，SPC A级、B级、C级的不良预后［改良Rankin量表评分（modified Rankin Scale，mRS）升高>1分］比例分别为1.4%、19%以及39%［106］。
目前认为SM Ⅰ~Ⅱ级病例是合理的手术治疗适应证；SM Ⅳ~Ⅴ级病例手术风险较高，手术切除应慎重进行；SM Ⅲ级病例则需要综合患者具体临床特点和血管结构进行判断。
由于SM Ⅲ级的病例涵盖范围较广，因此后续Lawton等［108］对SM Ⅲ级的病例进行了更为细致的分析，发现小体积，功能区以及深部引流的病例（S1V1E1）手术风险与SM Ⅰ~Ⅱ级病例相似，建议手术治疗；中型体积，功能区以及表浅引流的病例（S2V0E1）具有较高的手术风险；中型体积，非功能区以及深部引流的病例（S2V1E0）的手术风险介于上述二者之间，仍需根据具体临床情况进行判断。（注：S3V0E0的病例数较少，因此暂无有效数据进行评价）
（二）术前栓塞
BAVM手术过程中的困难主要在于来自畸形团深面的供血动脉，以及畸形团内较高流量的动静脉瘘结构。这些因素会导致术中畸形团内血流量难以控制，从而增加手术中的出血风险。因此，有针对性的对上述结构进行术前栓塞的治疗策略应运而生，并在处理复杂BAVM病例中得到广泛应用。既往队列研究显示术前栓塞可有效降低术中出血量并缩短手术时间［109-111］。对于血流量较大的畸形团，术前栓塞也被认为具有预防术后灌注压突破的作用［112-113］。同时，若病灶内存在明确的动脉瘤等危险结构，术前靶向栓塞或可降低病变在围手术期的出血风险。此外，部分BAVM会接受来自硬膜的动脉供血，这些血管在开颅过程中可能会造成大量出血，也可通过术前栓塞将这部分血管闭塞降低相关风险。
目前常用的栓塞材料包括PVA颗粒以及液体栓塞剂（NBCA以及Onyx）。PVA颗粒多在病变供血动脉走行迂曲的病例中使用。颗粒往往堵塞在畸形团内各个瘘口的供血动脉远端，但随着时间的推移会逐渐被冲入引流静脉。因此PVA颗粒更适用于复合手术的术中栓塞。在应用液体栓塞剂闭塞供血动脉后也应在术后早期进行手术治疗。因为随着时间的延长，动静脉畸形较低的血流阻力会导致来自脑内、软膜以及硬脑膜的侧支血管向病变供血并逐渐扩张，有可能增加手术的难度［114］。
理论上通过术前栓塞有效降低畸形团血流量便可达到降低手术难度的目的。但在术前通过部分栓塞畸形团以降低SM分级是否有利于手术尚无结论。栓塞目标应由介入和手术医师根据病变个体化的血管构筑共同决策。
（三）手术辅助技术及复合手术室的应用
围绕BAVM手术的各类辅助技术以影像技术为主，其主要目标是降低手术并发症以及提高治愈率。功能磁共振以及基于DTI的纤维束成像对畸形血管团周围脑组织功能判断更加准确，可以清晰显示畸形团、功能区以及传导束的关系，避免了因脑功能重塑带来的手术风险，有助于复杂病例手术适应证的判断［115-116］。神经导航在融合CT及MR影像的基础上使术前畸形团定位更加精准，特别是对于深部BAVM具有显著优势［117-118］。术中血管显影技术是另一类重要的辅助技术，包括术中DSA以及术中吲哚菁绿荧光造影。术中DSA需要在复合手术室进行，而后者需要荧光激发设备的手术显微镜即可（但只能显示暴露在显微镜下的脑表面血管）。术中血管显影技术的主要作用包括辨别畸形团血管构筑（荧光造影）以及发现残留AVM病灶（术中DSA）［119-122］。BAVM术中残留病变是术后短期内再出血的重要危险因素，对于畸形团结构相对弥散的病灶应特别警惕。因此建议此类病例的手术应在复合手术室进行，可有效降低病变不全切除的发生率。
目前复合手术室已在各中心逐步推广，复合手术室内BAVM切除的主要操作流程包括：
（1）全麻后穿刺股动脉置鞘：可选用长鞘以便于术中铺设无菌单，穿刺侧别以手术体位下便于导管操作为准，置鞘后需保持鞘内滴注通畅。
（2）术前定位：必要时可在置鞘后于头皮表面安置金属定位点，此后行术前DSA以精确定位病灶，切口设计需充分暴露供血动脉、畸形血管团以及引流静脉近端。建议造影后撤出造影导管以免形成血栓。
（3）术中DSA：术中需明确病灶血管构筑、定位残余病灶时可行术中DSA，为提高定位的准确性可在术野关键部位或可疑血管旁放置迷你动脉瘤夹或AVM夹作为参照物。
（4）术中栓塞：若病变存在较多来自畸形团深面的供血可使用微导管超选目标供血动脉进行栓塞，建议在显微手术开始前进行栓塞。
推荐意见10：SM I-Ⅱ级患者可通过显微手术治疗。（A级证据，Ⅱa级推荐）
推荐意见11：SM Ⅲ级患者异质性较高，其中评分为S1V1E1的病例更适合手术治疗。（B级证据，Ⅱa级推荐）
推荐意见12：术前栓塞的目标是来自畸形团深方的供血、高流量的动静脉瘘、动脉瘤样结构以及来自硬膜的供血动脉，借此降低术中及围术期的出血风险。术前是否部分栓塞畸形团需根据个体化的血管构筑以及术者经验综合判断。（C级证据，Ⅱa级推荐）
推荐意见13：高级别BAVM手术治疗需慎重，术前行功能磁共振以及DTI扫描，并在术前栓塞和伽玛刀后进行。（C级证据，Ⅱa级推荐）
推荐意见14：复合手术室有助于复杂BAVM的手术治疗。（C级证据，Ⅱa级推荐）
二、立体定向放射外科治疗
20世纪60年代末期，在使用标准的分割放射治疗BAVM无效之后，人们开始考虑使用立体定向放射外科来治疗BAVM。上世纪70年代至80年代早期，Barker等［123］尝试使用质子设备低剂量多次治疗近1 000例BAVM患者，最后闭塞率只有20%左右。
与此同时，Lars Leksell和Ladislau Steiner［124］在瑞典于1970年使用第一代Leksell伽玛刀装置治疗了一例小体积的深部BAVM患者，采用双平面血管造影确定靶区，给予中心剂量50 Gy的单次立体定向放射外科治疗，术后2年血管造影证实其完全闭塞。1987年到2021年美国匹兹堡医学中心在Lunsford的领导下共治疗1 302例BAVM［125］，中位随访时间3年，78%的患者实现了BAVM的完全闭塞，21%的患者实现了近全闭塞。
此外，直线加速器技术［126-127］、射波刀［128］也可用于治疗BAVM。两种技术均基于分次的立体定向放疗理念，无需框架固定，但目前两者治疗BAVM的临床研究相对较少。文献报道射波刀治疗BAVM的2~3年的治愈率在57%~81%［128-129］。Niwa等［130］报道了使用射波刀治疗38例高级别BAVM的随访结果，其术后3年、5年的闭塞率为15.2%、16.7%。文献报道射波刀放射治疗后的年出血率在1.3%~4.9%［131-132］。
（一）适应证
伽玛刀放射外科适用于中、小体积的BAVM，尤其是位于深部（脑干、丘脑和基底节）或功能区（如运动感觉区、语言区、视觉皮质等）的病例；外科手术后或血管内栓塞治疗后残留的BAVM；无法进行其他治疗的、有症状的大型BAVM的挽救治疗。
其中，文献报道SM分级Ⅲ级的患者是放射外科良好的适应证［77］。这些病变具有深静脉引流和（或）位于功能区。特别是对于体积较大、存在深静脉引流和位于功能区的病灶，显微外科手术和介入栓塞可能面临较高治疗风险的病例，立体定向放射外科可通过精准图像引导、传输高剂量放射线至病灶区域，使BAVM逐渐闭塞，且不受位置限制。尤其对于有过出血史的患者，出血后的软化灶可减少正常脑组织受到高能射线的照射，减少放射不良反应（adverse radiation effects，ARE）的发生［133］。对于一些选择性的高级别BAVM，无法通过显微手术或者采用其他治疗手段具有严重并发症或高死亡率的患者，放射外科治疗也可获得确切的疗效。
需要注意的是，放射外科治疗后BAVM一般在治疗后2~4年才发生延迟闭塞，患者在此期间仍然具有出血的风险，并有伴发因放射靶区周围的结构被射线损伤所致的迟发性放射反应的可能。
（二）放射外科病理生理机制
1. 放射外科闭塞BAVM：高能射线照射畸形团，损伤血管内皮，诱导平滑肌细胞增殖和细胞外胶原积累形成，导致内膜逐渐增厚，被照射血管逐渐形成血栓，最终导致管腔闭塞［134］。
2. 射线诱导的不良反应（radiation-induced changes，RIC）：目前导致RIC的机制尚不完全清楚。RIC的典型放射学表现是在随访MR上表现为T2高信号，可能是BAVM间质内及其周围的正常脑组织被射线照射后，血脑屏障被破坏从而出现水肿［134-135］。
（三）治疗策略
1.单次治疗：单次治疗一般适用于中小体积的BAVM。一般单次治疗的周边处方剂量为16~22 Gy，等剂量曲线一般为50%。一项包含1 212例儿童动静脉畸形的研究显示，接受单次立体定向放射外科治疗（stereotactic radiosurgery，SRS）是安全有效的，其闭塞率可达65.9%，整体术后并发症发生率为8.0%（包含新发出血、新的神经功能障碍、死亡）［136］。
体积小于4 cm3的BAVM是接受SRS治疗预后良好的因素之一。一项包含1 012例患者接受伽玛刀治疗的研究发现，年龄≤65岁、体积4 cm3、非功能区、既往无出血史是预后良好的主要因素。基于此研究结果，形成了能够预测BAVM接受SRS治疗预后的弗吉尼亚BAVM放射外科评分（Virginia radiosurgery AVM scale，VRAS），其预测伽玛刀治疗BAVM预后的准确度高于SM分级［137］。
2.分期治疗：较大体积（体积>10 cm3）、位于或毗邻重要神经功能区、脑干、丘脑等部位的血管畸形，多采取分期治疗的方案。分期治疗策略主要分为体积分期和剂量分期2种方式［138-139］。
分期治疗的主要目的是提高获益/风险比，主要出于以下2种考虑：体积分期主要是降低照射体积，从而减少ARE的发生；剂量分期主要针对位于重要神经结构或功能区的畸形，如脑干、视神经、丘脑、内囊等部位，需要考虑不同神经结构对于射线的最大耐受量而相应降低剂量。
体积分期，是指将较大体积的畸形团分成若干部分，相对独立分期治疗，以达到提高畸形团闭塞率的同时降低放射并发症相当的临床疗效。一般间隔时间在3~6个月［140-142］。一般体积≥10 cm3的BAVM建议采取体积分期治疗。这样做的目的是在保持安全的前提下提高最终的闭塞率。在制订治疗计划期间，一般将BAVM分成数块比例大致相同的体积。这种策略增加了大脑的修复能力，从而减少了ARE的发生。而对于体积大于20 cm3的病变，一般采用多体积分期的策略。在治疗剂量足够高时，一般每次照射的体积尽量不超过8 cm3。体积分期通常以不同供血动脉区域作为划分原则，主引流区域最后处理。体积分期推荐的周边处方剂量多为15~17 Gy，3年的闭塞率能接近70%。实际临床工作中因诸多因素的限制，周边处方剂量的推荐尚无统一意见。Seymour等［143］报道了体积分期治疗31例BAVM（最大直径3 cm）的结果，随访4.8年后显示：体积分期2~4期（2期71%；3期26%；4期3%），每次治疗的体积为6.8 cm3，周边处方剂量17 Gy，总体闭塞率为42%，并发症发生率为13%。并发现周边剂量为17 Gy能显著提高闭塞率。Pollock等［144］报道了34例大型BAVM（平均体积22.2 cm3）采用体积分期治疗的研究：分为2期（间隔6个月），周边剂量16 Gy，平均随访8.2年，达到71%的闭塞率和6%ARE发生率，1例患者在间隔期内出血，但18%的患者在闭塞后仍发生了出血。
剂量分期一般指对整个畸形团进行全覆盖、分期重复的放射治疗，以达到提高畸形团闭塞率同时降低放射并发症的临床疗效。剂量分期的间隔时间尚无定论，国内多数的伽玛刀中心的一般间隔时间需要根据动态的影像随访结果判断，直到畸形不再继续缩小并无明显的放射性水肿后再进行补充治疗，间隔时间多在2~4年之间。整体而言，大型BAVM采用剂量分期闭塞率在0~70%，ARE发生率0~20%。Foote等［145］报道，大型BAVM采用低剂量放射外科方案（平均边缘剂量12.5 Gy），66%畸形团缩小。补救性放射外科（平均边缘剂量15 Gy，平均间隔41个月）二期治疗后60%的闭塞率，1.9%辐射相关并发症。Park等［146］治疗了37例大型BAVM（平均体积20.42 cm3），采用2阶段的剂量分期治疗，随访3.1年后，闭塞率达到62.5%且没有放射性坏死。在第一期治疗时平均边缘剂量为13 Gy，体积达到19.6 cm3，二期治疗时平均体积为6.9 cm3，边缘剂量17 Gy（间隔39个月）。
目前，体积分期和剂量分期的最终结果仍然存在争议，大型BAVM的放射外科治疗方案尚无统一定论。根据系统综述的结果，大部分研究支持体积分期的预后优于剂量分期，而推荐的剂量和最优的间隔时间尚在探索中。
（三）影像定位
BAVM伽玛刀治疗的影像定位主要通过DSA和MRI。DSA检查能够精准显示BAVM血管构筑，包括供血动脉、引流静脉、畸形血管团；并且能够发现是否存在出血的高危结构：如高流量瘘、动脉瘤样结构等；此外，对于既往栓塞的BAVM，亦能清楚的区分栓塞材料与残余畸形团的位置关系，有助于精准定位。MRI的扫描序列建议使用T1、T2、增强T1和3D TOF，建议采用轴位、无间隔、薄层扫描（一般要求≤1.5 mm）。提倡DSA/MR的联合定位。
（四）靶区勾画
立体定向放射外科照射的靶区是畸形血管团，一般不包括供血动脉及引流静脉。
（五）影像随访
规律的影像随访非常重要，提倡每半年至一年进行一次薄层MR检查，包括T1、T2、增强T1和3D TOF序列，尽量保持与伽玛刀治疗时的参数一致。当MRI上显示血管畸形团完全消失/放射外科治疗后3年，应行脑血管造影（DSA）检查予以确认。采取分期治疗策略时二次治疗前，推荐行脑血管造影（DSA）检查，以明确血管构筑的具体变化。
（六）SRS术前栓塞
伽玛刀术前栓塞的目的主要包括：
（1）靶向栓塞动脉瘤以及高流量动静脉瘘结构。由于畸形团在伽玛刀术后闭塞所需的中位时间达2~3年，在此期间患者仍面临病灶破裂出血的风险，因此靶向闭塞病灶内的危险结构可有效降低伽玛刀术后的出血风险。
（2）部分栓塞畸形团，将病变直径缩减至3 cm以下。伽玛刀术后的闭塞率与病变体积负相关，以往研究显示，当畸形团体积<10 cm³或最大径<3 cm时，伽玛刀治疗具有更显著的有效性和安全性［147-149］。
既往部分队列研究显示术前栓塞与BAVM伽玛刀的闭塞率呈负相关［140，150-152］。虽然机制尚未明确，但可能的原因包括：
（1）术前姑息性栓塞主要经动脉途径进行，主要的动脉被阻塞而较小的血管未被栓塞，进而引起的缺血导致新的血管生成，从而削弱了放射外科治疗的获益；
（2）栓塞材料在畸形团内不均匀分布，血管被液体栓塞剂部分填塞后在DSA/MR上不显影或显影模糊，未被涵盖在伽玛刀治疗靶区；
（3）液体栓塞剂在体积较大的畸形团内弥散具有一定随机性，导致畸形团被分割成若干区域，导致靶区勾画困难；
（4）栓塞材料可能对射线具有吸收或分散作用，导致畸形团的总体放射剂量减少。
然而，在非选择队列中，接受术前栓塞的病灶往往更加复杂。而既往相关研究在多数情况下是使用栓塞后残留的病灶的血管构筑特点作为基线进行分析的，这样的分析策略可能存在选择偏倚。近年来，一些学者对上述假设进行了更为详尽的分析。研究结果显示，在以术前栓塞后的血管构筑作为基线时，术前栓塞与BAVM伽玛刀术后的闭塞率负相关；而以栓塞前的血管构筑作为基线时，术前栓塞不降低伽玛刀术后闭塞率（也未能提高伽玛刀的闭塞率）［153-154］，但发现术前栓塞的患者在术后5年内具有相对更低的出血风险［154］。
上述研究结果提示，术前靶向栓塞可能降低BAVM在伽玛刀术后的出血风险。因此，对于存在明确危险结构的高出血风险病例，如包含动脉瘤结构的破裂BAVM，可考虑进行伽玛刀术前或术后即刻靶向栓塞，以消除出血的高危因素。对于是否通过术前栓塞明显减少BAVM体积的病例，提倡在介入与立体定向放射外科医师的共同参与下制定术前栓塞策略。
（七）分级
在过去的几十年，BAVM治疗决策主要沿用的是SM手术5层分级系统［104］。De Oliveira等［155］报道了改良的SM标准，将SM-Ⅲ级分为Ⅲ-A（直径大于6 cm）和Ⅲ-B（存在深静脉引流和/或位于重要功能区）。根据临床结果，I/Ⅱ的病灶应选择显微外科手术切除，Ⅲ级的病灶选用显微外科手术（IIIA）或者放射外科手术（IIIB），Ⅳ/Ⅴ级的病灶则需要个体化、综合性的治疗方法。
但是SM是针对显微手术技术进行设计的，未能考虑不同部位病灶及脑组织对射线的反应性差异。Karlsson等［156］和Schwarts等［157］分别开发了根据BAVM大小和边缘剂量来预测BAVMs的闭塞的指标。目前放射外科常用于预测患者预后的评分系统有以下几种［158-159］：
（1）Pollock-Flickinger AVM评分：Pollock-Flickinger AVM评分=0.1×（体积，ml）+0.02×（年龄，岁）+0.5×（位置）。（位置：大脑半球/胼胝体/小脑半球=0；基底节/丘脑/脑干=1）。
（2）基于放射外科治疗的AVM分级系统（radiosurgery-based AVM grading system，RBGS）：RBGS分级=0.1×（体积，ml）+0.02×（年龄，岁）+0.3×（位置）。（位置：额叶/颞叶=1；顶叶/枕叶/脑室内/胼胝体=1；基底节/丘脑/脑干=2）。
（3）Sheehan根据患者和AVM特点提出了VRAS，对于预测SRS治疗预后明显优于SM分级、RBGS分级（表1）。
（八）预后
BAVM立体定向放射外科治疗后3~5年的畸形团闭塞率一般在60%~90%之间。BAVM闭塞的影响因素包括：SM分级、VRAS评分、RBGS评分、畸形团的大小和位置［160-162］。除了闭塞的有利预测因子外，Sun等［161］报道了预先栓塞畸形团是闭塞的不利因素。此外，SRS能够有效减轻BAVM相关的头痛，有文献报道，约43.6%患者头痛程度减轻，53.4%患者头痛的频率降低，平均头痛减轻时间在治疗后6.5个月［163］。同时，接受立体定向放射外科的BAVM患者有较好的癫痫控制率，文献报道在55%~80%左右［164］。
Pollock等［165］对220例BAVM病人畸形团闭塞且没有新的神经功能障碍的比例与BAVM评分之间的关系进行了研究。研究结果表明，当BAVM采用Pollock-Flickinger评分为≤1、>1且≤1.5、>1.5且≤2以及>2分时，BAVM发生闭塞且没有功能障碍的比例分别为89%、70%、64%、46%（P<0.01）。
匹兹堡中心对351例BAVM患者使用（中位）20 Gy的周边处方剂量治疗，术后影像随访3~11年发现73%患者经DSA证实BAVM闭塞，86%患者MRI检查显示BAVM闭塞［161］，MRI显示闭塞的准确率大约在90%［162］。
（九）ARE
治疗早期的不良反应相对较少，包括安装头架带来的头部疼痛、清醒镇静药物带来的恶心，以及皮质下脑叶BAVM患者癫痫发作的风险［165-166］。周边剂量的高低与闭塞率正相关，但也要考虑高剂量ARE的发生概率。早期且最常见的并发症就是放射诱导改变（radiosurgery-induced changes，RIC），如脑水肿。其典型表现为磁共振T2序列上畸形团内及周围的高信号改变，常发生于治疗后6~24个月，发生率高达30%~40%，症状性RIC发生率为8.1%~11.8%。与RIC发生相关的主要因素有边缘剂量、BAVM体积、BAVM位置、BAVM静脉引流方式和V12（即12 Gy照射的脑组织体积）［167］。
放射外科的迟发ARE较少见。匹兹堡中心一项422例病例对照研究发现，8.29%出现永久性的症状性并发症［168］。此外，BAVM位置和受照≥12 Gy的正常脑组织体积与发生ARE风险密切相关。与脑叶位置相比，丘脑、中脑和脑干位置的患者出现ARE的风险明显增加。BAVM放射外科的其他并发症非常少见，包括闭塞后出血的风险（终生风险1%）、迟发囊肿形成或发展为慢性包裹性扩张性血肿（chronic encapsulated expanding hematoma，CEEH）［169-170］。Izawa等［171］报道了BAVM伽玛刀治疗后，3.4%出现迟发性囊肿形成。
ARE需要进行个体化治疗。皮质类固醇对放射外科治疗后并发症有较好的症状缓解作用，34%的患者症状完全缓解，49%的患者症状部分改善。此外，高压氧的早期干预也报道对ARE有改善作用。
推荐意见15：伽玛刀适用于中、小体积的BAVM，尤其适合位于深部的或功能区的BAVM。（B级证据，Ⅱa级推荐）
推荐意见16：外科手术后或血管内栓塞治疗后残留的BAVM也可进行伽玛刀治疗。（B级证据，Ⅱa级推荐）
推荐意见17：BAVM接受伽玛刀治疗后至完全闭塞有一段较长的等待期，一般为2~3年甚至更长时间，期间仍有出血风险。（B级证据，Ⅰ级推荐）
推荐意见18：对于大体积的BAVM需要分期治疗，可以选择体积分期或剂量分期，具体的治疗策略需要根据畸形团位置、体积、出血史及患者症状等情况个体化实施。（B级证据，Ⅱa级推荐）
推荐意见19：伽玛刀治疗后需要规律的临床及影像学随访，每半年至一年进行一次薄层MR检查，包括T1、T2、增强T1和3D TOF序列，及时评价近远期畸形团的变化以及ARE的发生。当MRI上显示血管畸形团完全消失以及放射外科治疗后3年时，应行DSA；采取分期治疗策略时二次治疗前，推荐行DSA检查，以明确血管构筑的具体变化。（B级证据，Ⅱa级推荐）
三、介入治疗
最早的BAVM介入治疗是Luessenhop在1959年开展的，术者通过暴露颈动脉分叉将甲基丙烯酸甲酯颗粒（3~4.2 mm）注入颈内动脉进行颅内AVM的栓塞治疗［172］。此后随着介入材料和理念的进步，BAVM的介入治疗得到快速的发展。1971年Doppman［173］提出使用硅胶导管选择AVM的供血动脉进行栓塞治疗。Kerber［174］在1976年首次使用球囊微导管将黏附型液体栓塞剂IBCA用于BAVM的治疗。1990年Taki［175］发明了非黏附性栓塞剂，将BAVM治愈性栓塞的成功率显著提高。时至今日，介入治疗已成为BAVM多学科治疗不可或缺的工具。BAVM的介入治疗策略包括以下五类：
（1）治愈性栓塞；
（2）靶向栓塞；
（3）姑息性栓塞；
（4）外科手术术前栓塞；
（5）立体定向放射治疗前栓塞。
（一）治愈性栓塞
BAVM行治愈性栓塞的策略适用于高度选择的病例，因为既往文献报道非选择性BAVM队列的介入治愈率不足20%［4，176］。Onyx由于具有更好的通过性，其治愈率高于传统的NBCA栓塞剂，文献报道对于高度选择性队列其治愈率可高达50%~90%［177-178］。
根据大样本量队列的研究结果，直径≤3 cm，位置浅表，单支供血动脉，单支引流静脉的BAVM具有更高的治愈栓塞比例［179-180］。因此栓塞治疗对于位置较深（如基底节、丘脑、中脑等）且血管构筑简单的病灶具有优势。治愈性栓塞的复发率高于显微手术［181］，可能的原因之一是非黏附性栓塞剂附着在管壁并向前推进，导致部分畸形团和引流静脉虽然血流明显下降但未完全闭塞。
经静脉入路治愈性栓塞近年来逐渐受到重视［182］。该技术的优势在于通过静脉端使Onyx胶在畸形团内逆行铸型，可有效闭塞病灶的畸形团、供血动脉和引流静脉。近年来的文献报道显示该技术的治愈率约为90%［182-185］。经静脉入路栓塞对于深部、体积较小、单支引流静脉但供血动脉走行迂曲或安全距离较小（如过路型供血、穿支供血等）的BAVM尤为适用［186］。目前已有针对静脉入路BAVM栓塞的RCT研究开展。
需要注意的是，经静脉栓塞治疗必然导致引流静脉完全闭塞。因此，若不能同时将病变供血动脉和瘘口完全闭塞将面临较高的出血风险。一些单中心队列研究表明经静脉入路栓塞的出血风险为8%-~20%［182，187］。这也是目前普遍建议将经静脉入路栓塞的适应证限制于破裂BAVM的原因［186］。此外，一些介入技术细节需要被强调和重视。控制性降压被经验性的应用于经静脉栓塞的手术中。在进行静脉入路栓塞的同时需要使用微导管经动脉入路超选畸形团进行辅助。动脉端微导管不仅可以反复造影明确畸形团血管构筑，也可以通过临时或永久的栓塞材料阻断病灶的流入血流，为静脉端栓塞提供条件并降低出血风险。此外若术中发生畸形团破裂，动脉端导管也将发挥重要保护作用［188］。“高压锅”技术是另一种有效提高静脉入路栓塞成功率的技术，该技术首先需要在畸形团动脉端控制供血动脉血流并在引流静脉近心端放置弹簧圈，随后在弹簧圈的远心端通过微导管进行Onyx推注，此时弹簧圈将为Onyx提供支撑，有助于栓塞剂向动脉端弥散［189-190］。最后，在微导管撤出的时候需要避免牵拉静脉系统，静脉系统一旦破裂将造成灾难性后果［191］，因此建议采用头端可解脱的微导管进行注胶［192］。
（二）靶向栓塞
靶向栓塞特指针对BAVM畸形的薄弱部位进行栓塞治疗以达到降低出血风险的治疗策略。这些薄弱部位包括动脉瘤结构以及高流量的动静脉瘘结构。既往有研究认为去除上述结构可有效降低病灶的出血风险［53，193-195］。因此，一旦在DSA中发现危险结构，在动脉通路条件允许的前提下可予以栓塞。目前暂缺少靶向栓塞后长期随访的可靠数据。但考虑到病变内造成的动脉瘤结构的病理生理机制（如高速血流冲击、局部血管壁炎性反应等）并未去除，有理由怀疑患者通过靶向栓塞的获益是暂时的。因此，靶向栓塞不应是BAVM的治疗终点，尤其是针对有出血史的病例，在有效去除危险结构后应考虑配合立体定向放射治疗或显微手术，以提高治愈病变的可能性［196-197］。但对于老年患者需要综合权衡出血风险和治疗风险，在靶向栓塞后进行长期观察也是合理的。
（三）姑息性栓塞
姑息性栓塞特指对无法治愈的BAVM畸形血管团进行部分栓塞。但姑息性栓塞治疗的有效性和安全性目前尚存在争议。这一问题需要根据治疗的目标分别讨论。从降低出血风险的角度考虑，目前的证据多不支持在靶向栓塞之外进行更多的畸形团栓塞，一些研究显示姑息性栓塞并不能有效降低患者的出血风险［198］。同时，有学者提出姑息性栓塞可能导致畸形团内血流重分配，一些原本薄弱区域的血流增加甚至可能提高出血风险［199］。对于一些因盗血或静脉高压等异常血流动力学引发神经功能障碍或持续性头痛的病例，姑息性栓塞或可以通过缓解异常血流而改善临床症状［200-201］。对于高流量病变进行姑息性栓塞需要避免灌注压突破，建议分次治疗以降低相关并发症风险。但随着侧支血管的加入，病变的血流量也将重新升高，因此患者的获益可能是暂时的。此外考虑到血流再分配增加出血风险的隐患，姑息性栓塞应谨慎进行，对于未破裂的复杂病例可考虑保守治疗作为一线治疗方式。
（四）介入治疗评分
虽然SM分级对BAVM的介入治疗结果具有一定的区分度，但鉴于介入治疗与显微手术存在明显技术差异，一些学者提出了针对介入治疗的BAVM评分系统，包括Puerto Rico评分［202］，Buffalo评分［203］以及AVM embocure评分［204］。
2011年Feliciano等［202］回顾了750篇相关文献，根据既往研究中明确的介入治疗并发症危险因素提出了BAVM介入治疗评分（Puerto Rico评分）。和SM分级类似，该分级根据供血动脉数量（<3为1分；3~5为2分；≥6为3分），是否位于功能区（否，0分；是，1分）以及是否存在动静脉瘘（否，0分；是，1分）将病变分为5级。Bell等［205］回顾分析了126例连续病例的治疗结果对上述评分进行了验证，发现Puerto Rico评分与SM评分具有显著的Spearman相关性（ρ=0.5，P<0.01），并且该分级与介入治疗并发症风险具有相关性，研究结果提示Feliciano评分≤2分具有较高的介入栓塞治愈率，而≤3时病变可通过多学科治疗得到较高的治愈率。
2015年Dumont等［203］提出了用于评估介入手术风险的Buffalo评分，该评分根据供血动脉数量（<3个为1分；3~4个为2分；≥4个为3分），供血动脉直径（>1 mm，0分；≤1 mm，1分）以及是否位于功能区（否，0分；是，1分）将病变分为五级。同时，作者在研究中分别使用SM分级和Buffalo评分对50例介入治疗的患者进行评估，发现Buffalo评分对介入治疗风险预估的准确性优于SM分级。
2016年Lopes等［204］分析了通过Onyx尝试治愈性栓塞时与治愈率相关的影响因素，提出了AVM embocure score。该评分较Puerto Rico评分和Buffalo评分更为全面，包括病变直径（<3 cm为1分；3~6 cm为2分；>6 cm为3分），供血动脉数量（≤3个为1分；4~6个为2分，>6个为3分），引流静脉数量（1个为1分；4~6个为2分；>6个为3分）以及是否位于功能区（否，0分；是，1分）。作者回顾了39例使用Onyx尝试治愈性栓塞的病例对评分进行了验证，发现3分的患者治愈率100%，且无并发症发生；4分患者治愈率75%，并发症发生率8%，5分患者治愈率78%，并发症发生率11%；评分>5分患者治愈率20%，并发症发生率高达30%。
上述评分的准确性目前尚有争议。2017年我国学者回顾了国内4家中心共270例病例，对Buffalo评分，Puerto Rico评分，AVM embocure 评分以及SM评分分别进行了验证，结果提示Puerto Rico评分对治愈率以及治疗风险的预测最为准确［206］。2020年，Benjamin等［207］回顾了104例介入治疗的BAVM连续病例，采用类似的分析方法，结果提示Buffalo评分对介入手术风险评估的准确性优于其他评分系统，而Buffalo评分、Puerto Rico评分、AVM embocure 评分对畸形团大部分栓塞（>85%）的预测准确性均优于SM分级。
（五）介入材料
目前，液体栓塞剂是BAVM介入治疗使用最广泛的材料，包括黏附性和非黏附性两类。黏附性栓塞剂主要是NBCA胶（N-butyl-2-cyanoacrylate，a-氰基丙烯酸正丁醋，Glubran），目前大范围使用的是其第二代产品，Glubran-2胶（NBCA metacryloxysulfolane，NBCA-MS）较第一代NBCA胶的优势在于相对更长的聚合时间（60~90 s 比15~40 s），有助于栓塞剂在畸形团内推注［208］。高浓度的NBCA类栓塞剂在接触血液的瞬间就会聚合凝固，因此在实际使用时需要与一定比例的碘油，目的在于延长栓塞剂凝固时间同时使栓塞剂能够在射线下显影，提高治疗的有效性和安全性。常用的浓度为20%~50%［209］，浓度越高聚合时间越短，需要术者根据畸形团血管结构及血流量进行综合判断［210］。
另一类广泛使用的是非黏附型栓塞剂（Onyx，Squid等），由乙烯醇共聚物（EVOH）、钽粉（X线显影）和二甲基亚砜（DMSO）组成。DMSO在接触血液后会快速从聚合物内脱离，使EVOH和钽粉混合物在血管内沉淀。由于不与血管壁黏合并且聚合时间较长，Onyx相对NBCA在畸形团的通过性上具有明显的优势且栓塞后黏管风险较低。Onyx在使用时需要在导管头端反流1~1.5 cm形成栓子，之后继续推注Onyx向畸形团远端流动。由于DMSO具有血管毒性，推注速度不宜过快，推荐控制在0.3 ml/min以下［210］。
弹簧圈和PVA颗粒在BAVM的介入治疗中也有应用。弹簧圈主要用于动脉瘤结构的靶向栓塞，或作为“塞子”辅助Onyx栓塞时使用［211］。PVA颗粒只能临时降低畸形团血流量，多在复合手术室术中栓塞中使用，目的是降低畸形团血流量辅助显微手术。
（六）介入治疗并发症
BAVM介入治疗的并发症包括出血性并发症和缺血性并发症［212］。出血性并发症发生的主要原因可概括为操作直接相关以及血流动力学改变相关［213-214］。操作相关原因包括导丝及导管对血管造成的物理性损伤以及使用液体栓塞剂后微导管回撤对血管的牵拉，上述因素均可通过谨慎操作避免。血流动力学相关原因包括灌注压突破，姑息性栓塞后血流重分配以及部分引流静脉栓塞导致的畸形团内压力升高。出血性并发症一旦发生需要迅速做出决策，若在术中发生应尽可能通过闭塞供血动脉降低病灶血流量并中和肝素；若在术后发生可采取适当降压、镇静等对症支持治疗。若脑室积血可进行侧脑室穿刺引流，若形成体积较大的脑内血肿应急诊进行血肿清除手术，术中是否一期切除畸形团需根据病灶的具体血管结构决定。
缺血性并发症的发生多因操作不慎导致栓塞剂闭塞了向正常脑组织供血的动脉所致，如Onyx向近心端反流过程中闭塞正常血管，或“过路型”供血动脉微导管到位不理想导致栓塞剂飘向远端。此外，反复微导管操作导致的血管痉挛，以及微导管无法撤出导致的血栓形成也可导致缺血性并发症的发生。发生缺血事件后应早期使用尼莫地平抗血管痉挛，同时适当升血压并扩容。必要时应复查DSA明确缺血病因。
推荐意见20：SM Ⅰ~Ⅱ级BAVM病变在通路理想情况下进行治愈性栓塞是合理的。（B级证据，IIa级推荐）
推荐意见21：对于拟行治愈性栓塞的病例，小体积者可通过1次治疗完全栓塞，体积较大者可分次进行。（C级证据，Ⅱa级推荐）
推荐意见22：单支引流且供血动脉走行迂曲或安全距离较小的BAVM可尝试经静脉入路栓塞。（C级证据，Ⅱa级推荐）
推荐意见23：非黏附性栓塞剂具有更高的畸形血管团通过性，是治愈性栓塞理想的栓塞剂。（C级证据，Ⅱa级推荐）
推荐意见24：具有明确危险结构的病例进行靶向栓塞是合理的。（C级证据，Ⅱa级推荐）
推荐意见25：对于因异常血流动力学导致临床症状的BAVM病例进行姑息性部分栓塞是可行的。（C级证据，Ⅱa级推荐）
四、治疗方式的选择
如前所述，显微手术、立体定向放射治疗和介入治疗三种治疗技术各自具有独立优势，但并非完全互补的关系。对于结构简单、位置较浅的病例（例如SM Ⅰ~Ⅱ级），三者均可取得相对理想的治疗效果。然而，对于体积较大，畸形团结构弥散的病例，无论采用何种方法，都面临较大的挑战。因此，对于相对复杂的BAVM病例，需要术者在充分理解各类治疗技术的前提下根据病变具体的血管结构合理的选择或组合各类治疗方法，以获得理想的治疗结果。SM评分虽然是针对显微手术的困难程度而设立的，但该评分对其他治疗方式也具有准确的指导价值［77］。
（一）SM Ⅰ~Ⅱ级病例
SM Ⅰ~Ⅱ级的BAVM病例通过三种治疗方式均可在相对安全的前提下获得理想的治愈率。既往临床数据显示，显微手术的治愈率高达98%，而永久性并发症发生率平均约为2.2%［215］；立体定向放射治疗后的治愈率随时间延长而提高，一项纳入1 102例的荟萃分析显示SM Ⅰ~Ⅱ级病变术后3年的平均治愈率为80%［216］，术后永久性神经功能障碍发生率为2%~3%［217］。Gami等［218］对比了Johns Hopkins中心在过去27年内收治的113例显微手术与同期的120例立体定向放射治疗的低级别BAVM患者的治疗数据，结果显示，在平均随访5年后，显微手术的治愈率显著高于立体定向放射治疗（96%比57%），且在控制治疗后出血风险方面更具优势。另一项对比显微手术与立体定向放射治疗的荟萃分析也得到了相似的结果（治愈率97.4%比64.4%，OR=16.94，95%CI：7.71~37.21）［219］。
随着Onyx的广泛应用以及对经静脉入路的探索，近年报道的低级别BAVM单纯介入治疗的治愈率提高至75%~98%，但出血性并发症发生率约为3%~10%［220-223］。虽然暂缺少直接对比低级别BAVM显微手术与介入治疗的临床研究，但已发表的数据间接提示介入治疗的治愈率和安全性略低于显微手术［223］。综上，SM Ⅰ~Ⅱ级的BAVM通过三种治疗方式进行治疗都是可行的，应结合个体化的临床特点，血管构筑以及术者的治疗经验综合判断。
（二）SM Ⅲ级病例
SM Ⅲ级的病例具有较高的手术风险，术后新发功能障碍的比例为20%［224］，但考虑到SM Ⅲ是SM各级中异质性最大的一组［225］，Lawton等［108］对SM Ⅲ级BAVM进行了进一步分型，认为小体积（<3 cm），功能区，具有深部引流的病变（S1V1E1）手术风险接近低级别病变（约3%）因此适合手术治疗，而中型体积（3~6 cm），功能区，浅表引流的病变（S2V0E1）不适合显微手术治疗。文献数据显示SM Ⅲ级BAVM队列介入治疗的治愈率为42%~47%，而治疗相关的并发症约30%［226-227］，亚组分析提示未破裂BAVM患者的严重并发症发生率显著高于破裂BAVM［226］。因此，介入治疗并不适合作为SM Ⅲ级BAVM的一线治疗方式，对于有明显危险结构的病例可进行靶向栓塞。
立体定向放射治疗是目前值得关注的SM Ⅲ级BAVM治疗方式。文献数据显示其术后5年治愈率为50%~70%，术后10年治愈率为80%，术后年出血风险0.8%~1.2%，术后平均8年中新发神经功能障碍发生率（包括死亡患者）约9.4%［140，228］。一项纳入近900例立体定向放射治疗SM Ⅲ级BAVM的国际多中心队列研究显示未破病例的治疗结果优于破裂病例［140］。
（三）SM Ⅳ~Ⅴ级病例
SM Ⅳ~Ⅴ级BAVM的治疗极具挑战，目前三种治疗方法的治疗结果均不理想。如前所述，高级别BAVM手术治疗导致的新发神经功能障碍发生率超过30%，有研究发现高级别BAVM手术不良预后的危险因素包括穿支血管供血，累及皮质脊髓束以及畸形团结构弥散［229］。因此进行手术治疗时应完善功能磁共振及DTI检查，复合手术室有助于术中判断病灶的切除状态，提高治愈率。高级别BAVM的介入治疗不追求治愈性栓塞，多数情况下是作为显微手术或立体定向放射治疗的术前辅助治疗 ［230］，但结论尚存争议［154，231-232］。
大样本量SM Ⅳ~Ⅴ级BAVM立体定向放射治疗后3年和10年的治愈率仅分别为10%~15%及20%~37%，治疗后年出血风险约3%。但术后新发神经功能障碍（包括死亡）发生率约10%~17%，低于显微手术数据［151，233］。从治疗安全性的角度考虑立体定向放射治疗似乎是高级别BAVM更好的选择，但低闭塞率可能意味着后续较高的累计出血风险。由于畸形团在接受放射治疗后体积可能出现显著缩小并导致BAVM降级，一些学者提出在立体定向放射治疗后进行手术切除的治疗策略，回顾性研究数据显示BAVM在伽玛刀术后进行显微手术治疗可有效提高手术的安全性［234］。
（四）深部BAVM病例
深部BAVM（deep-seated BAVM）特指位于基底节、丘脑及脑干的动静脉畸形，这些病变相对少见但具有较高的出血风险［235］，同时，由于病变位置较深，其SM分级相对较高（Ⅲ~Ⅳ级为主）［236-237］，部分体积更大或者结构弥散的病例会被归类为SM Ⅵ级或“不可手术”的病变［104］。只有少数体积较小，畸形团致密且位置相对表浅的病例会接受显微手术治疗［238］。由于多数深部BAVM均有来自穿支血管的供血，导致其单纯介入治疗的难度较高，文献报道介入治愈率约为20%［237］。但是部分体积较小且单支引流的深部BAVM可尝试经静脉入路栓塞。深部BAVM的伽玛刀治疗结果相对理想，一项荟萃分析显示放射治疗约5年后，脑干和丘脑/基底节AVM的闭塞率分别为60%（95%CI：54%~66%）和67%（95%CI：60%~73%），但值得注意的是脑干和丘脑/基底节AVM在立体定向治疗后的年出血风险依然高达7%和9%［239］，因此对病变的危险结构应予以靶向栓塞。
推荐意见26：BAVM需根据个体化的血管构筑和临床特点合理选择治疗方式。对于低级别病例应制定以治愈为目标的整体治疗策略；对于复杂的高级别病变目前各治疗方法均不理想，未破裂病例可采取保守观察的治疗策略，破裂病例需多学科联合治疗尽可能争取治愈。（C级证据，Ⅱa级推荐）
五、BAVM出血急性期的治疗
BAVM出血急性期的综合管理主要参考美国心脏和卒中协会脑出血指南［8，240-241］。理想情况下，BAVM出血急性期患者需要在具有持续监测一般生命体征及颅内压的重症监护病房进行治疗。对于有癫痫症状或位于脑叶的破裂BAVM应予抗癫痫药物治疗。有研究认为发热及高血糖可能加重脑损伤，因此需积极对症干预。虽然缺少直接临床证据，但血压管理或可降低急性期再出血风险［240，242-243］。
总体而言，目前针对BAVM出血急性期的手术治疗的临床研究结果偏向保守［77，242-244］。既往研究认为出血后脑组织肿胀将增加BAVM切除手术风险［244］，并且由于血肿的压迫，部分畸形团在急性期血管造影时可能不显影导致手术风险被低估，有研究显示40%的畸形团的血管构筑在出血急性期后会发生改变［244-245］。对于出血量较大或合并脑疝的患者需行急诊手术，对于脑室内积血或合并脑积水的患者需行脑室穿刺引流，但基于上述原因可保留BAVM病灶择期治疗。近期发表的一项前瞻性队列研究也显示破裂BAVM的早期和延迟切除具有相似的长期功能预后。延迟切除可带来更高的治愈率，但应警惕等待期间病变再破裂的风险［246］。
目前有研究数据支持对于位置浅表的SM Ⅰ~Ⅱ级BAVM在出血急性期进行显微手术治疗，认为早期手术切除有助于缩短住院时间并改善预后［242-243］。对于可取得治愈性栓塞且血肿体积相对较小的病例可在急性期行介入治疗。对于高级别的破裂BAVM，鉴于靶向栓塞可降低其出血风险，可在急性期靶向栓塞动脉瘤及高流量动静脉瘘等危险结构为后续手术治疗或立体定向放射治疗创造条件。此外，出血吸收后的脑软化灶可能提高立体定向放射治疗的安全性，有助于适当提高靶区的照射剂量进而提高病变的闭塞率。但立体定向放射外科治疗后不能立刻降低BAVM的出血风险，可在放射治疗前行靶向栓塞以降低出血风险［247］。
推荐意见27：BAVM出血急性期可单纯针对血肿进行治疗，畸形团可在血肿吸收后再行外科干预。（C级证据，Ⅱa级推荐）
推荐意见28：SM Ⅰ~Ⅱ级且位置表浅的BAVM可在出血急性期行BAVM切除术。术前需充分进行血管构筑评估，在复合手术室进行治疗有助于避免病灶残余。（C级证据，Ⅱa级推荐）
推荐意见29：有机会取得治愈性栓塞且血肿体积较小的BAVM可急诊行栓塞治疗。（C级证据，Ⅱa级推荐）
推荐意见30：高级别BAVM可在急性期针对危险结构行靶向栓塞为后续显微手术或立体定向放射外科治疗创造条件。（C级证据，Ⅱa级推荐）
六、BAVM癫痫的治疗
临床队列研究显示完全闭塞畸形团可有效控制癫痫发作。Englot等［248］发表了一项纳入440例手术治疗BAVM的前瞻性队列，其中130例（30%）术前有癫痫发作史。在显微手术治疗后平均20.7个月的随访中，80%的患者无癫痫发作，16%的患者仅在术后发作1次。有统计分析显示术后癫痫发作与深部穿支血管供血显著相关而与术前癫痫病史无显著相关性。立体定向放射外科治疗后的癫痫发作风险与治愈率显著相关，一项纳入129例立体的放射治疗BAVM的研究显示完全闭塞组和部分闭塞组的癫痫控制率分别为70%和55%［249］。Chen等［250］系统回顾了997例立体定向放射外科治疗的BAVM病例，结果显示术后44%的病例癫痫得到完全控制，其中病变治愈组的癫痫控制率显著高于部分闭塞组（82%比41%，OR=6.13；95%CI：2.16~17.44；P=0.0007）。
Baranoski等［251］回顾了20年内发表的24个队列研究共1 157例BAVM患者，显示显微手术后癫痫控制率为78.3%，立体定向放射外科术后为62.8%，而介入治疗术后为49.3%，其中经立体定向放射外科治愈的患者取得了最高的癫痫控制率（85%）。另一项荟萃分析也得到了相似的结果，在中位时间为6年的随访期内显微手术，立体定向放射外科以及介入栓塞三组患者的癫痫控制率分别为78%，66%以及50%，其中手术组达到癫痫完全控制所需的中位时间为1.1个月，显著优于立体定向放射外科组（20.5个月）以及介入栓塞组（8.1个月）［252］。目前暂无高质量临床试验评估术前脑电图以及术中皮质脑电监测对于BAVM相关癫痫患者的有效性，但有队列研究显示术前脑电图及术中皮质脑电监测会提高BAVM相关药物难治性癫痫患者接受海马切除以及畸形团以外的皮质癫痫病灶切除比例（约30%），并且相对接受常规畸形团切除术患者也获得了较高的癫痫控制率（75%比 52.9%）［253］。因此术前脑电图以及术中皮质脑电监测被认为有可能提高术后癫痫控制率，尤其适用于药物难治性癫痫患者［254-255］。
对于未破裂BAVM，ARUBA数据显示外科干预在癫痫控制方面并不优于单纯药物治疗［252］。同一时期的苏格兰未破裂BAVM前瞻性队列（SAIVMs）也得到了相似的结果，对于有癫痫发作病史的患者，其数据显示外科干预组和药物治疗组在5年随访中对癫痫症状的控制率相当［5］。关于抗癫痫药物的选择目前暂无有效临床数据参考，但现阶段单一药物可能难以有效控制BAVM相关癫痫，文献中约50%以上的病例需多种抗癫痫药物联合治疗以获得理想的癫痫控制率［255-257］。
推荐意见31：将病变完全闭塞可有效控制BAVM相关癫痫。（B级证据，Ⅰ级推荐）
推荐意见32：对于药物难治性癫痫患者行术前脑电图及术中皮质脑电监测是合理的选择。（C级证据，Ⅱa级推荐）
推荐意见33：对于未破裂难治性的BAVM癫痫患者可选择单纯抗癫痫药物治疗。（B级证据，Ⅱa级推荐）
第七部分 展望
一、药物治疗
由于BAVM现阶段的外科治疗结果并不理想，深入研究其破裂出血的机制，探索有效降低出血风险的药物疗法是迫切的临床需求。目前针对BAVM的药物治疗研究主要集中于血管生成、炎症、管壁完整性以及丝裂原活化蛋白激酶-细胞外受体激酶（MAPK/ERK）信号通路。贝伐珠单抗、米诺环素、多西环素、沙利度胺和曲美替尼等药物已在一系列BAVM小规模临床研究中进行验证。
1.抗血管生成药物的研究：虽然BAVM的形成和发展机制未被充分阐明，但有研究表明其发生发展与血管生成密切相关［1，258］。血管生成的过程受促血管生成因子和抗血管生成因子调控，二者比例的变化将刺激或抑制血管生成［259-260］。其中VEGF是一种重要的促血管生成分子，能刺激和调节血管生成。既往研究表明，BAVM患者血浆中VEGF水平和VEGF受体表达显著升高；一些动物研究也显示VEGF的升高是AVM形成的先决条件［261-263］。因此VEGF信号通路有望成为BAVM药物治疗的靶点。贝伐珠单抗是一种VEGF抗体，通过其抗血管生成作用已经被用于治疗几种实体癌症［264-265］。接受贝伐珠单抗治疗的HHT患者的初步临床结果似乎有效［266-269］。然而，在最近贝伐珠单抗治疗BAVM的概念验证研究未能发现该药具有治疗BAVM的效果［270］。值得注意的是，贝伐珠单抗对血管内皮细胞具有毒性，有学者认为它可能会增加BAVM的出血风险增加。该药其他的副作用也很显著：如血栓形成、严重高血压和心力衰竭等［271］。
2.炎症相关研究：大量研究表明炎症反应在BAVM进展中发挥重要作用［272］，在BAVM样本中能观察到一系列炎症因子的表达上调以及单核细胞和粒细胞的浸润。最近发表的BAVM单细胞转录组测序结果也进一步说明炎性反应可能导致脑动静脉畸形破裂出血［272］。然而日本学者早在2005年进行了BAVM和炎症相关药物的临床研究，通过多西环素降低了基质金属蛋白酶-9（MMP-9）表达［273］，但系列临床研究结果未能提示BAVM患者受益［274-275］。
3.血管壁稳定性研究：BAVM血管壁结构发育不良，表现为血管周细胞缺失［276-278］。招募血管平滑肌/周细胞从而稳定血管壁结构并预防畸形破裂出血可能是治疗BAVM的一种有效策略［276-278］。沙利度胺被证实具有上调血小板衍生生长因子-B/血小板衍生生长因子受体（PDGF-B/PDGF-R）通路的作用，而该通路恰好是新生血管募集血管周细胞的重要途径［279］。一系列临床研究证实，口服沙利度胺可显著预防HHT引起的鼻出血和胃肠道出血［280-281］。但沙利度胺具有较多不良反应，如致畸和周围神经病等［282］。
4.丝裂原活化蛋白激酶（MAPK）通路突变研究：目前已证实绝大多数散发AVM病例的病因是KRAS、BRAF或其下游基因MAP2K1体细胞激活突变，这一发现为该通路的靶向药物治疗奠定了理论基础［38-39，283］。文献中已有4例曲美替尼（MAP2K1抑制剂）治疗颅外AVM患者的病例报道，且均提示治疗有效［284-287］。此外，有研究发现曲美替尼可以在动物模型中限制BAVM的发生发展［40］。但目前暂无曲美替尼治疗BAVM患者的临床数据发表。
二、液体和血管内活检
现有研究已经阐明了大部分的BAVM的遗传基础。家族性BAVM可以通过检测外周血细胞等手段较为简单地获取突变信息［288］，但散发性BAVM在检测上存在一定困难。对于接受手术治疗的患者，其病理、遗传信息是可以准确获取的，而对于选择了保守观察、介入、伽玛刀等治疗策略的患者，病理标本和突变信息则难以获得，这也为未来潜在的药物精准治疗造成了阻碍。解决上述问题亟需开发新的检测方法，以实现通过显微手术之外的手段对这类患者进行基因检测。有研究尝试开发基于外周血脱落细胞或游离DNA（cfDNA）的液体活检技术，并尝试了包括BEAMing技术［289］和高通量测序技术等在内的一系列检测手段［290］。虽然一些研究指出外周血可能无法通过常规手段检出散发BAVM的体细胞突变［39，291］，但已有研究者成功在外周血和引流静脉中收集cfDNA检出KRAS突变［292］。另一种发展中的技术路线是依赖于血管内介入取样，即使用导丝、弹簧圈、支架等介入器材与血管内膜接触，收集脱落并黏附于器材上的细胞用于检测［293-295］。这一技术手段可获取的细胞数量在数十至数百不等，并被成功应用于流式细胞学和转录组检测［294-295］，未来有望用于动静脉畸形体细胞基因突变的直接检测。当前液体活检、血管内活检在可行性、稳定性等方面尚存在诸多不足，未来仍有一定改进空间，如能稳定地做到对非开放手术患者进行稳定可靠的突变检测，将为BAVM未来的药物治疗奠定基础。
总之，本共识的制订参考了脑动静脉畸形临床诊疗的最新研究进展，经过委员会45位专家研讨和反馈，多次修改后定稿。然而，脑动静脉畸形血管构筑复杂，病变异质性强，其临床诊疗策略仍有诸多关键点值得探讨。本共识仅代表撰写专家组的观点，不具备法律效力。未来，随着对中枢神经系统血管畸形相关临床研究的不断增加，将为本共识后续的完善提供更高价值的临床证据和指导。
本共识专家组成员：
执笔者：
于嘉兴（首都医科大学宣武医院神经外科）；
朱巍（复旦大学附属华山医院神经外科）；
孙时斌（首都医科大学附属北京天坛医院立体定向放射外科）；
陈光忠（南方医科大学附属广东省人民医院（广东省医学科学院）神经外科）；
洪韬（首都医科大学宣武医院神经外科）
参加本共识讨论、制定的专家（以姓氏汉语拼音为序）：
白卫星（河南省人民医院神经外科）；
陈风华（湘雅医院神经外科）；
陈光忠（南方医科大学附属广东省人民医院（广东省医学科学院）神经外科）；
陈骅（江苏省人民医院神经外科）；
陈劲草（武汉大学中南医院神经外科）；
陈晓霖（首都医科大学附属北京天坛医院神经外科）；
陈左权（上海市第十人民医院神经外科）；
邓剑平（空军军医大学唐都医院神经外科）；
段传志（南方医科大学珠江医院神经外科）；
方兵（浙江大学附属第二医院神经外科）；
冯文峰（南方医科大学南方医院神经外科）；
高歌（安徽省立医院神经外科）；
谷震（云南大学附属医院神经外科）；
郭庚（山西医科大学附属第一医院神经外科）；
郭宗铎（重庆医科大学附属第一医院神经外科）；
杭春华（南京鼓楼医院神经外科）；
何旭英（广东省第二人民医院神经医学中心）；
洪韬（首都医科大学宣武医院神经外科）；
黄清海（海军军医大学长海医院脑血管病中心）；
李聪慧（河北医科大学第一医院神经外科）；
李强（海军军医大学长海医院脑血管病中心）；
林元相（福建医科大学附属第一医院神经外科）；
刘翼（四川大学华西医院神经外科）；
路华（江苏省人民医院神经外科）；
买买提力（新疆医科大学附属第一医院神经外科）；
潘力（华山医院射波刀中心、上海伽玛医院伽玛刀中心）；
任军（兰州医科大学第二医院神经外科）；
史怀璋（哈尔滨医科大学附属第一医院神经外科）；
孙时斌（首都医科大学附属北京天坛医院立体定向放射外科）；
王大明（北京医院神经外科）；
王东海（山东大学齐鲁医院神经外科）；
王君（解放军总医院神经内科）；
许侃（吉林大学第一医院神经外科）；
杨华（贵州中医药大学第一附属医院神经外科）；
叶明（首都医科大学宣武医院神经外科）；
于嘉（西安交通大学第一附属医院神经内科）；
于嘉兴（首都医科大学宣武医院神经外科）；
喻博（中国医科大学盛京医院神经外科）；
张东（北京医院神经外科）；
张鸿祺（首都医科大学宣武医院神经外科）；
张华楸（华中科技大学附属同济医院神经外科）；
张鹏（首都医科大学宣武医院神经外科）；
赵元立（北京协和医院神经外科）；
钟书（中山大学附属第一医院广西医院神经外科）；
朱巍（复旦大学附属华山医院神经外科）
[1]LawtonMT, RutledgeWC, KimH, et al. Brain arteriovenous malformations[J]. Nat Rev Dis Primers, 2015, 1:15008. DOI: 10.1038/nrdp.2015.8.
[2]Al-ShahiR, WarlowC. A systematic review of the frequency and prognosis of arteriovenous malformations of the brain in adults[J]. Brain, 2001, 124(Pt 10):1900-1926. DOI: 10.1093/brain/124.10.1900.
[3]Arteriovenous Malformation Study Group.Arteriovenous malformations of the brain in adults[J]. N Engl J Med, 1999, 340(23):1812-1818. DOI: 10.1056/NEJM199906103402307.
[4]van BeijnumJ, van der WorpHB, BuisDR, et al. Treatment of brain arteriovenous malformations: a systematic review and meta-analysis[J]. JAMA, 2011, 306(18):2011-2019. DOI: 10.1001/jama.2011.1632.
[5]MohrJP, ParidesMK, StapfC, et al. Medical management with or without interventional therapy for unruptured brain arteriovenous malformations (ARUBA): a multicentre, non-blinded, randomised trial[J]. Lancet, 2014, 383(9917):614-621. DOI: 10.1016/S0140-6736(13)62302-8.
[6]Al-Shahi SalmanR, WhitePM, CounsellCE, et al. Outcome after conservative management or intervention for unruptured brain arteriovenous malformations[J]. JAMA, 2014, 311(16):1661-1669. DOI: 10.1001/jama.2014.3200.
[7]MohrJP, OverbeyJR, HartmannA, et al. Medical management with interventional therapy versus medical management alone for unruptured brain arteriovenous malformations (ARUBA): final follow-up of a multicentre, non-blinded, randomised controlled trial[J]. Lancet Neurol, 2020, 19(7):573-581. DOI: 10.1016/S1474-4422(20)30181-2.
[8]HemphillJC, GreenbergSM, AndersonCS, et al. Guidelines for the management of spontaneous intracerebral hemorrhage: a guideline for healthcare professionals from the American Heart Association/American Stroke Association[J]. Stroke, 2015, 46(7):2032-2060. DOI: 10.1161/STR.0000000000000069.
[9]HofmeisterC, StapfC, HartmannA, et al. Demographic, morphological, and clinical characteristics of 1289 patients with brain arteriovenous malformation[J]. Stroke, 2000, 31(6):1307-1310. DOI: 10.1161/01.str.31.6.1307.
[10]Al-ShahiR, FangJS, LewisSC, et al. Prevalence of adults with brain arteriovenous malformations: a community based study in Scotland using capture-recapture analysis[J]. J Neurol Neurosurg Psychiatry, 2002, 73(5):547-551. DOI: 10.1136/jnnp.73.5.547.
[11]BrownRD, WiebersDO, TornerJC, et al. Incidence and prevalence of intracranial vascular malformations in Olmsted County, Minnesota, 1965 to 1992[J]. Neurology, 1996, 46(4):949-952. DOI: 10.1212/wnl.46.4.949.
[12]StapfC, MastH, SciaccaRR, et al. The New York Islands AVM Study: design, study progress, and initial results[J]. Stroke, 2003, 34(5):e29-33. DOI: 10.1161/01.STR.0000068784.36838.19.
[13]HillmanJ. Population-based analysis of arteriovenous malformation treatment[J]. J Neurosurg, 2001, 95(4):633-637. DOI: 10.3171/jns.2001.95.4.0633.
[14]Al-ShahiR, BhattacharyaJJ, CurrieDG, et al. Prospective, population-based detection of intracranial vascular malformations in adults: the Scottish Intracranial Vascular Malformation Study (SIVMS)[J]. Stroke, 2003, 34(5):1163-1169. DOI: 10.1161/01.STR.0000069018.90456.C9.
[15]JessurunGA, KamphuisDJ, van der ZandeFH, et al. Cerebral arteriovenous malformations in The Netherlands Antilles. High prevalence of hereditary hemorrhagic telangiectasia-related single and multiple cerebral arteriovenous malformations[J]. Clin Neurol Neurosurg, 1993, 95(3):193-198. DOI: 10.1016/0303-8467(93)90123-x.
[16]GabrielRA, KimH, SidneyS, et al. Ten-year detection rate of brain arteriovenous malformations in a large, multiethnic, defined population[J]. Stroke, 2010, 41(1):21-26. DOI: 10.1161/STROKEAHA.109.566018.
[17]StapfC, LabovitzDL, SciaccaRR, et al. Incidence of adult brain arteriovenous malformation hemorrhage in a prospective population-based stroke survey[J]. Cerebrovasc Dis, 2002, 13(1):43-46. DOI: 10.1159/000047745.
[18]MorrisZ, WhiteleyWN, LongstrethWT, et al. Incidental findings on brain magnetic resonance imaging: systematic review and meta-analysis[J]. BMJ, 2009, 339:b3016. DOI: 10.1136/bmj.b3016.
[19]WillinskyRA, LasjauniasP, TerbruggeK, et al. Multiple cerebral arteriovenous malformations (AVMs). review of our experience from 203 patients with cerebral vascular lesions[J]. Neuroradiology, 1990, 32(3):207-210. DOI: 10.1007/BF00589113.
[20]PanP, WeinsheimerS, CookeD, et al. Review of treatment and therapeutic targets in brain arteriovenous malformation[J]. J Cereb Blood Flow Metab, 2021, 41(12):3141-3156. DOI: 10.1177/0271678X211026771.
[21]Barbosa Do PradoL, HanC, OhSP, et al. Recent advances in basic research for brain arteriovenous malformation[J]. Int J Mol Sci, 2019, 20(21):5324. DOI: 10.3390/ijms20215324.
[22]ChenW, ChoiEJ, McDougallCM, et al. Brain arteriovenous malformation modeling, pathogenesis, and novel therapeutic targets[J]. Transl Stroke Res, 2014, 5(3):316-329. DOI: 10.1007/s12975-014-0343-0.
[23]KühnelT, WirschingK, WohlgemuthW, et al. Hereditary hemorrhagic telangiectasia[J]. Otolaryngol Clin North Am, 2018, 51(1):237-254. DOI: 10.1016/j.otc.2017.09.017.
[24]FaughnanME, PaldaVA, Garcia-TsaoG, et al. International guidelines for the diagnosis and management of hereditary haemorrhagic telangiectasia[J]. J Med Genet, 2011, 48(2):73-87. DOI: 10.1136/jmg.2009.069013.
[25]GuttmacherAE, MarchukDA, WhiteRI. Hereditary hemorrhagic telangiectasia[J]. N Engl J Med, 1995, 333(14):918-924. DOI: 10.1056/NEJM199510053331407.
[26]KringsT, KimH, PowerS, et al. Neurovascular manifestations in hereditary hemorrhagic telangiectasia: imaging features and genotype-phenotype correlations[J]. AJNR Am J Neuroradiol, 2015, 36(5):863-870. DOI: 10.3174/ajnr.A4210.
[27]SabbàC, PasculliG, LenatoGM, et al. Hereditary hemorrhagic telangiectasia: clinical features in ENG and ALK1 mutation carriers[J]. J Thromb Haemost, 2007, 5(6):1149-1157. DOI: 10.1111/j.1538-7836.2007.02531.x.
[28]GallioneC, AylsworthAS, BeisJ, et al. Overlapping spectra of SMAD4 mutations in juvenile polyposis (JP) and JP-HHT syndrome[J]. Am J Med Genet A, 2010, 152A(2):333-339. DOI: 10.1002/ajmg.a.33206.
[29]SorensenLK, BrookeBS, LiDY, et al. Loss of distinct arterial and venous boundaries in mice lacking endoglin, a vascular-specific TGFbeta coreceptor[J]. Dev Biol, 2003, 261(1):235-250. DOI: 10.1016/s0012-1606(03)00158-1.
[30]UrnessLD, SorensenLK, LiDY. Arteriovenous malformations in mice lacking activin receptor-like kinase-1[J]. Nat Genet, 2000, 26(3):328-331. DOI: 10.1038/81634.
[31]ParkSO, WankhedeM, LeeYJ, et al. Real-time imaging of de novo arteriovenous malformation in a mouse model of hereditary hemorrhagic telangiectasia[J]. J Clin Invest, 2009, 119(11):3487-3496. DOI: 10.1172/JCI39482.
[32]Bayrak-ToydemirP, StevensonDA. Capillary Malformation-Arteriovenous Malformation Syndrome [M]//ADAM MP, FELDMAN J, MIRZAA GM, et al. GeneReviews(®). Seattle (WA); University of Washington, Seattle Copyright © 1993-2023, University of Washington, Seattle. GeneReviews is a registered trademark of the University of Washington, Seattle. All rights reserved. 1993.
[33]LapinskiPE, LubeckBA, ChenD, et al. RASA1 regulates the function of lymphatic vessel valves in mice[J]. J Clin Invest, 2017, 127(7):2569-2585. DOI: 10.1172/JCI89607.
[34]BurrowsPE, Gonzalez-GarayML, RasmussenJC, et al. Lymphatic abnormalities are associated with RASA1 gene mutations in mouse and man[J]. Proc Natl Acad Sci U S A, 2013, 110(21):8621-8626. DOI: 10.1073/pnas.1222722110.
[35]AmyereM, RevencuN, HelaersR, et al. Germline loss-of-function mutations in EPHB4 cause a second form of capillary malformation-arteriovenous malformation (CM-AVM2) deregulating RAS-MAPK signaling[J]. Circulation, 2017, 136(11):1037-1048. DOI: 10.1161/CIRCULATIONAHA.116.026886.
[36]HigaG, PacanowskiJP, JeckDT, et al. Vertebral artery aneurysms and cervical arteriovenous fistulae in patients with neurofibromatosis 1[J]. Vascular, 2010, 18(3):166-177. DOI: 10.2310/6670.2010.00032.
[37]TurnbullMM, HumeniukV, SteinB, et al. Arteriovenous malformations in Cowden syndrome[J]. J Med Genet, 2005, 42(8):e50. DOI: 10.1136/jmg.2004.030569.
[38]NikolaevSI, VetiskaS, BonillaX, et al. Somatic activating KRAS mutations in arteriovenous malformations of the brain[J]. N Engl J Med, 2018, 378(3):250-261. DOI: 10.1056/NEJMoa1709449.
[39]HongT, YanY, LiJ, et al. High prevalence of KRAS/BRAF somatic mutations in brain and spinal cord arteriovenous malformations[J]. Brain, 2019, 142(1):23-34. DOI: 10.1093/brain/awy307.
[40]ParkES, KimS, HuangS, et al. Selective endothelial hyperactivation of oncogenic KRAS induces brain arteriovenous malformations in mice[J]. Ann Neurol, 2021, 89(5):926-941. DOI: 10.1002/ana.26059.
[41]FishJE, Flores SuarezCP, BoudreauE, et al. Somatic gain of KRAS function in the endothelium is sufficient to cause vascular malformations that require MEK but not PI3K signaling[J]. Circ Res, 2020, 127(6):727-743. DOI: 10.1161/CIRCRESAHA.119.316500.
[42]PerataHJ, TomsickTA, TewJM. Feeding artery pedicle aneurysms: association with parenchymal hemorrhage and arteriovenous malformation in the brain[J]. J Neurosurg, 1994, 80(4):631-634. DOI: 10.3171/jns.1994.80.4.0631.
[43]ShankarJJ, MenezesRJ, Pohlmann-EdenB, et al. Angioarchitecture of brain AVM determines the presentation with seizures: proposed scoring system[J]. AJNR Am J Neuroradiol, 2013, 34(5):1028-1034. DOI: 10.3174/ajnr.A3361.
[44]GeibprasertS, PereiraV, KringsT, et al. Hydrocephalus in unruptured brain arteriovenous malformations: pathomechanical considerations, therapeutic implications, and clinical course[J]. J Neurosurg, 2009, 110(3):500-507. DOI: 10.3171/2008.7.JNS0815.
[45]FullertonHJ, AchrolAS, JohnstonSC, et al. Long-term hemorrhage risk in children versus adults with brain arteriovenous malformations[J]. Stroke, 2005, 36(10):2099-2104. DOI: 10.1161/01.STR.0000181746.77149.2b.
[46]MohrJP, Kejda-ScharlerJ, Pile-SpellmanJ. Diagnosis and treatment of arteriovenous malformations[J]. Curr Neurol Neurosci Rep, 2013, 13(2):324. DOI: 10.1007/s11910-012-0324-1.
[47]EvansRW. Diagnostic testing for the evaluation of headaches[J]. Neurol Clin, 1996, 14(1):1-26. DOI: 10.1016/s0733-8619(05)70240-1.
[48]FlemmingKD, LanzinoG. Management of unruptured intracranial aneurysms and cerebrovascular malformations[J]. Continuum (Minneap Minn), 2017, 23(1, Cerebrovascular Disease):181-210. DOI: 10.1212/CON.0000000000000418.
[49]GrossBA, DuR. Natural history of cerebral arteriovenous malformations: a meta-analysis[J]. J Neurosurg, 2013, 118(2):437-443. DOI: 10.3171/2012.10.JNS121280.
[50]KimH, Al-Shahi SalmanR, McCullochCE, et al. Untreated brain arteriovenous malformation: patient-level meta-analysis of hemorrhage predictors[J]. Neurology, 2014, 83(7):590-597. DOI: 10.1212/WNL.0000000000000688.
[51]HernesniemiJA, DashtiR, JuvelaS, et al. Natural history of brain arteriovenous malformations: a long-term follow-up study of risk of hemorrhage in 238 patients[J]. Neurosurgery, 2008, 63(5):823-829; discussion 829-831. DOI: 10.1227/01.NEU.0000330401.82582.5E.
[52]GuoY, SaundersT, SuH, et al. Silent intralesional microhemorrhage as a risk factor for brain arteriovenous malformation rupture[J]. Stroke, 2012, 43(5):1240-1246. DOI: 10.1161/STROKEAHA.111.647263.
[53]da CostaL, WallaceMC, Ter BruggeKG, et al. The natural history and predictive features of hemorrhage from brain arteriovenous malformations[J]. Stroke, 2009, 40(1):100-105. DOI: 10.1161/STROKEAHA.108.524678.
[54]MastH, YoungWL, KoenneckeHC, et al. Risk of spontaneous haemorrhage after diagnosis of cerebral arteriovenous malformation[J]. Lancet, 1997, 350(9084):1065-1068. DOI: 10.1016/s0140-6736(97)05390-7.
[55]StapfC, MastH, SciaccaRR, et al. Predictors of hemorrhage in patients with untreated brain arteriovenous malformation[J]. Neurology, 2006, 66(9):1350-1355. DOI: 10.1212/01.wnl.0000210524.68507.87.
[56]ChenY, HanH, MengX, et al. Development and validation of a scoring system for hemorrhage risk in brain arteriovenous malformations[J]. JAMA Netw Open, 2023, 6(3):e231070. DOI: 10.1001/jamanetworkopen.2023.1070.
[57]ChenY, ChenP, LiR, et al. Rupture-related quantitative hemodynamics of the supratentorial arteriovenous malformation nidus[J]. J Neurosurg, 2023, 138(3):740-749. DOI: 10.3171/2022.6.JNS212818.
[58]BurkhardtJK, ChenX, WinklerEA, et al. Delayed venous drainage in ruptured arteriovenous malformations based on quantitative color-coded digital subtraction angiography[J]. World Neurosurg, 2017, 104:619-627. DOI: 10.1016/j.wneu.2017.04.120.
[59]ChoiJH, MastH, SciaccaRR, et al. Clinical outcome after first and recurrent hemorrhage in patients with untreated brain arteriovenous malformation[J]. Stroke, 2006, 37(5):1243-1247. DOI: 10.1161/01.STR.0000217970.18319.7d.
[60]van BeijnumJ, LovelockCE, CordonnierC, et al. Outcome after spontaneous and arteriovenous malformation-related intracerebral haemorrhage: population-based studies[J]. Brain, 2009, 132(Pt 2):537-543. DOI: 10.1093/brain/awn318.
[61]RutledgeC, CookeDL, HettsSW, et al. Brain arteriovenous malformations[J]. Handb Clin Neurol, 2021, 176:171-178. DOI: 10.1016/B978-0-444-64034-5.00020-1.
[62]Al-Shahi SalmanR. The outlook for adults with epileptic seizure(s) associated with cerebral cavernous malformations or arteriovenous malformations[J]. Epilepsia, 2012, 53 Suppl 4∶34-42. DOI: 10.1111/j.1528-1167.2012.03611.x.
[63]HortonJC, ChambersWA, LyonsSL, et al. Pregnancy and the risk of hemorrhage from cerebral arteriovenous malformations[J]. Neurosurgery, 1990, 27(6):867-871; discussion 871-872. DOI: 10.1097/00006123-199012000-00002.
[64]LiuXJ, WangS, ZhaoYL, et al. Risk of cerebral arteriovenous malformation rupture during pregnancy and puerperium[J]. Neurology, 2014, 82(20):1798-1803. DOI: 10.1212/WNL.0000000000000436.
[65]GrossBA, DuR. Hemorrhage from arteriovenous malformations during pregnancy[J]. Neurosurgery, 2012, 71(2):349-355; discussion 355-356. DOI: 10.1227/NEU.0b013e318256c34b.
[66]PorrasJL, YangW, PhiladelphiaE, et al. Hemorrhage risk of brain arteriovenous malformations during pregnancy and puerperium in a North American cohort[J]. Stroke, 2017, 48(6):1507-1513. DOI: 10.1161/STROKEAHA.117.016828.
[67]SharsharT, LamyC, MasJL. Incidence and causes of strokes associated with pregnancy and puerperium. A study in public hospitals of Ile de France. Stroke in Pregnancy Study Group[J]. Stroke, 1995, 26(6):930-936. DOI: 10.1161/01.str.26.6.930.
[68]KittnerSJ, SternBJ, FeeserBR, et al. Pregnancy and the risk of stroke[J]. N Engl J Med, 1996, 335(11):768-774. DOI: 10.1056/NEJM199609123351102.
[69]ZhuD, ZhaoP, LvN, et al. Rupture risk of cerebral arteriovenous malformations during pregnancy and puerperium: a single-center experience and pooled data analysis[J]. World Neurosurg, 2018, 111:e308-e315. DOI: 10.1016/j.wneu.2017.12.056.
[70]AmiasAG. Cerebral vascular disease in pregnancy. I. Haemorrhage[J]. J Obstet Gynaecol Br Commonw, 1970, 77(2):100-120. DOI: 10.1111/j.1471-0528.1970.tb03487.x.
[71]RobinsonJL, HallCJ, SedzimirCB. Subarachnoid hemorrhage in pregnancy[J]. J Neurosurg, 1972, 36(1):27-33. DOI: 10.3171/jns.1972.36.1.0027.
[72]SadasivanB, MalikGM, LeeC, et al. Vascular malformations and pregnancy[J]. Surg Neurol, 1990, 33(5):305-313. DOI: 10.1016/0090-3019(90)90197-w.
[73]OgilvyCS, StiegPE, AwadI, et al. Recommendations for the management of intracranial arteriovenous malformations: a statement for healthcare professionals from a special writing group of the Stroke Council, American Stroke Association[J]. Circulation, 2001, 103(21):2644-2657. DOI: 10.1161/01.cir.103.21.2644.
[74]CanA, DuR. Neurosurgical Issues in Pregnancy[J]. Semin Neurol, 2017, 37(6):689-693. DOI: 10.1055/s-0037-1607430.
[75]LvX, LiW, HeH, et al. Known and unknown cerebral arteriovenous malformations in pregnancies: haemorrhage risk and influence on obstetric management[J]. Neuroradiol J,. DOI: 10.1177/1971400917712264.
[76]JosephNK, KumarS, BrownRD, et al. Influence of Pregnancy on Hemorrhage Risk in Women With Cerebral and Spinal Cavernous Malformations[J]. Stroke, 2021, 52(2):434-441. DOI: 10.1161/STROKEAHA.120.031761.
[77]DerdeynCP, ZipfelGJ, AlbuquerqueFC, et al. Management of brain arteriovenous malformations: a scientific statement for healthcare professionals from the American Heart Association/American Stroke Association[J]. Stroke, 2017, 48(8):e200-e224. DOI: 10.1161/STR.0000000000000134.
[78]BrazzelliM, SandercockPA, ChappellFM, et al. Magnetic resonance imaging versus computed tomography for detection of acute vascular lesions in patients presenting with stroke symptoms[J]. Cochrane Database Syst Rev, 2009, (4):CD007424. DOI: 10.1002/14651858.CD007424.pub2.
[79]Delgado AlmandozJE, SchaeferPW, ForeroNP, et al. Diagnostic accuracy and yield of multidetector CT angiography in the evaluation of spontaneous intraparenchymal cerebral hemorrhage[J]. AJNR Am J Neuroradiol, 2009, 30(6):1213-1221. DOI: 10.3174/ajnr.A1546.
[80]CordonnierC, Al-Shahi SalmanR, BhattacharyaJJ, et al. Differences between intracranial vascular malformation types in the characteristics of their presenting haemorrhages: prospective, population-based study[J]. J Neurol Neurosurg Psychiatry, 2008, 79(1):47-51. DOI: 10.1136/jnnp.2006.113753.
[81]CordonnierC, KlijnCJ, van BeijnumJ, et al. Radiological investigation of spontaneous intracerebral hemorrhage: systematic review and trinational survey[J]. Stroke, 2010, 41(4):685-690. DOI: 10.1161/STROKEAHA.109.572495.
[82]KimDJ, KringsT. Whole-brain perfusion CT patterns of brain arteriovenous malformations: a pilot study in 18 patients[J]. AJNR Am J Neuroradiol, 2011, 32(11):2061-2066. DOI: 10.3174/ajnr.A2659.
[83]SanelliPC, MifsudMJ, StiegPE. Role of CT angiography in guiding management decisions of newly diagnosed and residual arteriovenous malformations[J]. AJR Am J Roentgenol, 2004, 183(4):1123-1126. DOI: 10.2214/ajr.183.4.1831123.
[84]JosephsonCB, WhitePM, KrishanA, et al. Computed tomography angiography or magnetic resonance angiography for detection of intracranial vascular malformations in patients with intracerebral haemorrhage[J]. Cochrane Database Syst Rev, 2014, 2014(9):CD009372. DOI: 10.1002/14651858.CD009372.pub2.
[85]GoddardAJ, TanG, BeckerJ. Computed tomography angiography for the detection and characterization of intra-cranial aneurysms: current status[J]. Clin Radiol, 2005, 60(12):1221-1236. DOI: 10.1016/j.crad.2005.06.007.
[86]LinnJ, Ertl-WagnerB, SeelosKC, et al. Diagnostic value of multidetector-row CT angiography in the evaluation of thrombosis of the cerebral venous sinuses[J]. AJNR Am J Neuroradiol, 2007, 28(5):946-952.
[87]WillemsPW, TaeshineetanakulP, SchenkB, et al. The use of 4D-CTA in the diagnostic work-up of brain arteriovenous malformations[J]. Neuroradiology, 2012, 54(2):123-131. DOI: 10.1007/s00234-011-0864-0.
[88]IdeS, HiraiT, MoriokaM, et al. Usefulness of 3D DSA-MR fusion imaging in the pretreatment evaluation of brain arteriovenous malformations[J]. Acad Radiol, 2012, 19(11):1345-1352. DOI: 10.1016/j.acra.2012.07.001.
[89]HadizadehDR, KukukGM, SteckDT, et al. Noninvasive evaluation of cerebral arteriovenous malformations by 4D-MRA for preoperative planning and postoperative follow-up in 56 patients: comparison with DSA and intraoperative findings[J]. AJNR Am J Neuroradiol, 2012, 33(6):1095-1101. DOI: 10.3174/ajnr.A2921.
[90]MachetA, PortefaixC, KadziolkaK, et al. Brain arteriovenous malformation diagnosis: value of time-resolved contrast-enhanced MR angiography at 3.0T compared to DSA[J]. Neuroradiology, 2012, 54(10):1099-1108. DOI: 10.1007/s00234-012-1024-x.
[91]YuS, YanL, YaoY, et al. Noncontrast dynamic MRA in intracranial arteriovenous malformation (AVM), comparison with time of flight (TOF) and digital subtraction angiography (DSA)[J]. Magn Reson Imaging, 2012, 30(6):869-877. DOI: 10.1016/j.mri.2012.02.027.
[92]XuJ, ShiD, ChenC, et al. Noncontrast-enhanced four-dimensional MR angiography for the evaluation of cerebral arteriovenous malformation: a preliminary trial[J]. J Magn Reson Imaging, 2011, 34(5):1199-1205. DOI: 10.1002/jmri.22699.
[93]Pathological correlates of late-onset dementia in a multicentre, community-based population in England and Wales. Neuropathology Group of the Medical Research Council Cognitive Function and Ageing Study (MRC CFAS)[J]. Lancet, 2001, 357(9251):169-175. DOI: 10.1016/s0140-6736(00)03589-3.
[94]KakizawaY, NagashimaH, OyaF, et al. Compartments in arteriovenous malformation nidi demonstrated with rotational three-dimensional digital subtraction angiography by using selective microcatheterization. Report of three cases[J]. J Neurosurg, 2002, 96(4):770-774. DOI: 10.3171/jns.2002.96.4.0770.
[95]GailloudP, OishiS, CarpenterJ, et al. Three-dimensional digital angiography: new tool for simultaneous three-dimensional rendering of vascular and osseous information during rotational angiography[J]. AJNR Am J Neuroradiol, 2004, 25(4):571-573.
[96]CloftHJ, JosephGJ, DionJE. Risk of cerebral angiography in patients with subarachnoid hemorrhage, cerebral aneurysm, and arteriovenous malformation: a meta-analysis[J]. Stroke, 1999, 30(2):317-320. DOI: 10.1161/01.str.30.2.317.
[97]AlexanderMD, OliffMC, OlorunsolaOG, et al. Patient radiation exposure during diagnostic and therapeutic interventional neuroradiology procedures[J]. J Neurointerv Surg, 2010, 2(1):6-10. DOI: 10.1136/jnis.2009.000802.
[98]ChenX, CookeDL, SalonerD, et al. Higher flow is present in unruptured arteriovenous malformations with silent intralesional microhemorrhages[J]. Stroke, 2017, 48(10):2881-2884. DOI: 10.1161/STROKEAHA.117.017785.
[99]BhattacharyaJJ, LuoCB, SuhDC, et al. Wyburn-Mason or Bonnet-Dechaume-Blanc as cerebrofacial arteriovenous metameric syndromes (CAMS). A new concept and a new classification[J]. Interv Neuroradiol, 2001, 7(1):5-17. DOI: 10.1177/159101990100700101.
[100]MonizE.L′encéphalographie arterielle, son importance dans la localisation des tumeurs cérébrales[J]. Rev Neurol, 1927, 2: 72-89.
[101]KretzerRM, CoonAL, TamargoRJ. Walter E. Dandy′s contributions to vascular neurosurgery[J]. J Neurosurg, 2010, 112(6):1182-1191. DOI: 10.3171/2009.7.JNS09737.
[102]YaşargilMG. Intracranial microsurgery[J]. Clin Neurosurg, 1970, 17:250-256. DOI: 10.1093/neurosurgery/17.cn_suppl_1.250.
[103]SattariSA, ShahbandiA, YangW, et al. Microsurgery versus microsurgery with preoperative embolization for brain arteriovenous malformation treatment: a systematic review and meta-analysis[J]. Neurosurgery, 2023, 92(1):27-41. DOI: 10.1227/neu.0000000000002171.
[104]SpetzlerRF, MartinNA. A proposed grading system for arteriovenous malformations[J]. J Neurosurg, 1986, 65(4):476-483. DOI: 10.3171/jns.1986.65.4.0476.
[105]SpetzlerRF, PonceFA. A 3-tier classification of cerebral arteriovenous malformations. Clinical article[J]. J Neurosurg, 2011, 114(3):842-849. DOI: 10.3171/2010.8.JNS10663.
[106]KorjaM, BerviniD, AssaadN, et al. Role of surgery in the management of brain arteriovenous malformations: prospective cohort study[J]. Stroke, 2014, 45(12):3549-3555. DOI: 10.1161/STROKEAHA.114.007206.
[107]MorganMK, WiedmannM, AssaadNN, et al. Complication-effectiveness analysis for brain arteriovenous malformation surgery: a prospective cohort study[J]. Neurosurgery, 2016, 79(1):47-57. DOI: 10.1227/NEU.0000000000001144.
[108]LawtonMT. Spetzler-Martin Grade III arteriovenous malformations: surgical results and a modification of the grading scale[J]. Neurosurgery, 2003, 52(4):740-748; discussion 748-749. DOI: 10.1227/01.neu.0000053220.02268.9c.
[109]ViñuelaF, DionJE, DuckwilerG, et al. Combined endovascular embolization and surgery in the management of cerebral arteriovenous malformations: experience with 101 cases[J]. J Neurosurg, 1991, 75(6):856-864. DOI: 10.3171/jns.1991.75.6.0856.
[110]JafarJJ, DavisAJ, BerensteinA, et al. The effect of embolization with N-butyl cyanoacrylate prior to surgical resection of cerebral arteriovenous malformations[J]. J Neurosurg, 1993, 78(1):60-69. DOI: 10.3171/jns.1993.78.1.0060.
[111]DeMerittJS, Pile-SpellmanJ, MastH, et al. Outcome analysis of preoperative embolization with N-butyl cyanoacrylate in cerebral arteriovenous malformations[J]. AJNR Am J Neuroradiol, 1995, 16(9):1801-1807.
[112]Gutiérrez-GonzálezR, GilA, SernaC, et al. Normal perfusion pressure breakthrough phenomenon: what still remains unknown[J]. Br J Neurosurg, 2012, 26(3):403-405. DOI: 10.3109/02688697.2011.633637.
[113]SpetzlerRF, WilsonCB, WeinsteinP, et al. Normal perfusion pressure breakthrough theory[J]. Clin Neurosurg, 1978, 25:651-672. DOI: 10.1093/neurosurgery/25.cn_suppl_1.651.
[114]Liebman KmRR. The hemodynamic changes measured in cerebral arterio-venous malformations following endovascular treatment [J]. J Neurovasc Dis, 1997,
[115]LinF, WuJ, ZhaoB, et al. Preoperative functional findings and surgical outcomes in patients with motor cortical arteriovenous malformation[J]. World Neurosurg, 2016, 85:273-281. DOI: 10.1016/j.wneu.2015.10.002.
[116]EllisMJ, RutkaJT, KulkarniAV, et al. Corticospinal tract mapping in children with ruptured arteriovenous malformations using functionally guided diffusion-tensor imaging[J]. J Neurosurg Pediatr, 2012, 9(5):505-510. DOI: 10.3171/2012.1.PEDS11363.
[117]RussellSM, WooHH, JosefferSS, et al. Role of frameless stereotaxy in the surgical treatment of cerebral arteriovenous malformations: technique and outcomes in a controlled study of 44 consecutive patients[J]. Neurosurgery, 2002, 51(5):1108-1116; discussion 1116-1118. DOI: 10.1097/00006123-200211000-00002.
[118]PostN, RussellSM, HuangP, et al. Frame-based stereotactic resection of subcentimeter arteriovenous malformations in deep or eloquent regions of the brain: indications and technique with eight consecutive operations[J]. Minim Invasive Neurosurg, 2008, 51(2):114-118. DOI: 10.1055/s-2007-1022532.
[119]MunshiI, MacdonaldRL, WeirBK. Intraoperative angiography of brain arteriovenous malformations[J]. Neurosurgery, 1999, 45(3):491-497; discussion 497-499. DOI: 10.1097/00006123-199909000-00016.
[120]ZaidiHA, AblaAA, NakajiP, et al. Indocyanine green angiography in the surgical management of cerebral arteriovenous malformations: lessons learned in 130 consecutive cases[J]. Neurosurgery, 2014, 10 Suppl 2∶246-251; discussion 251. DOI: 10.1227/NEU.0000000000000318.
[121]BilbaoCJ, BhallaT, DalalS, et al. Comparison of indocyanine green fluorescent angiography to digital subtraction angiography in brain arteriovenous malformation surgery[J]. Acta Neurochir (Wien), 2015, 157(3):351-359. DOI: 10.1007/s00701-014-2287-2.
[122]林发, 王明泽, 仇汉诚, 等. 一站式复合手术对后循环参与供血的脑动静脉畸形手术风险和预后的影响[J]. 中华医学杂志, 2022, 102(21):1614-1620. DOI: 10.3760/cma.j.cn112137-20210910-02061.
[123]BarkerFG, ButlerWE, LyonsS, et al. Dose-volume prediction of radiation-related complications after proton beam radiosurgery for cerebral arteriovenous malformations[J]. J Neurosurg, 2003, 99(2):254-263. DOI: 10.3171/jns.2003.99.2.0254.
[124]SteinerL, LeksellL, GreitzT, et al. Stereotaxic radiosurgery for cerebral arteriovenous malformations. Report of a case [J]. Acta Chir Scand, 1972, 138(5): 459-464.
[125]AltschulerEM, LunsfordLD, CoffeyRJ, et al. Gamma knife radiosurgery for intracranial arteriovenous malformations in childhood and adolescence[J]. Pediatr Neurosci, 1989, 15(2):53-61. DOI: 10.1159/000120443.
[126]Skjøth-RasmussenJ, RoedH, OhlhuesL, et al. Complications following linear accelerator based stereotactic radiation for cerebral arteriovenous malformations[J]. Int J Radiat Oncol Biol Phys, 2010, 77(2):542-547. DOI: 10.1016/j.ijrobp.2009.05.048.
[127]FriedmanWA, BovaFJ, MendenhallWM. Linear accelerator radiosurgery for arteriovenous malformations: the relationship of size to outcome[J]. J Neurosurg, 1995, 82(2):180-189. DOI: 10.3171/jns.1995.82.2.0180.
[128]ColomboF, CavedonC, CasentiniL, et al. Early results of CyberKnife radiosurgery for arteriovenous malformations[J]. J Neurosurg, 2009, 111(4):807-819. DOI: 10.3171/2008.10.JNS08749.
[129]OermannEK, MurthyN, ChenV, et al. A multicenter retrospective study of frameless robotic radiosurgery for intracranial arteriovenous malformation[J]. Front Oncol, 2014, 4:298. DOI: 10.3389/fonc.2014.00298.
[130]NiwaR, IchiS, NomuraR, et al. Hypofractionated stereotactic radiotherapy with CyberKnife for large arteriovenous malformations and arteriovenous malformations located in eloquent areas[J]. Neurol Med Chir (Tokyo), 2022, 62(10):445-450. DOI: 10.2176/jns-nmc.2022-0033.
[131]PunyawaiP, RadomsutthikulN, DhanachaiM, et al. Long-term outcomes of 170 brain arteriovenous malformations treated by frameless image-guided robotic stereotactic radiosurgery: ramathibodi hospital experience[J]. Medicine (Baltimore), 2021, 100(19):e25752. DOI: 10.1097/MD.0000000000025752.
[132]BlamekS, TarnawskiR, MiszczykL. Linac-based stereotactic radiosurgery for brain arteriovenous malformations[J]. Clin Oncol (R Coll Radiol), 2011, 23(8):525-531. DOI: 10.1016/j.clon.2011.03.012.
[133]DingD, YenCP, StarkeRM, et al. Effect of prior hemorrhage on intracranial arteriovenous malformation radiosurgery outcomes[J]. Cerebrovasc Dis, 2015, 39(1):53-62. DOI: 10.1159/000369959.
[134]IlyasA, ChenCJ, DingD, et al. Radiation-induced changes after stereotactic radiosurgery for brain arteriovenous malformations: a systematic review and meta-analysis[J]. Neurosurgery, 2018, 83(3): 365-376.DOI: 10.1093/neuros/nyx502.
[135]DingD, StarkeRM, LiuKC, et al. Cortical plasticity in patients with cerebral arteriovenous malformations[J]. J Clin Neurosci, 2015, 22(12):1857-1861. DOI: 10.1016/j.jocn.2015.06.014.
[136]BörcekA, ÇeltikçiE, AksoğanY, et al. Clinical outcomes of stereotactic radiosurgery for cerebral arteriovenous malformations in pediatric patients: systematic review and meta-analysis [J]. Neurosurgery, 2019, 85(4): E629-E640.DOI: 10.1093/neuros/nyz146.
[137]StarkeRM, YenCP, DingD, et al. A practical grading scale for predicting outcome after radiosurgery for arteriovenous malformations: analysis of 1012 treated patients[J]. J Neurosurg, 2013, 119(4):981-987. DOI: 10.3171/2013.5.JNS1311.
[138]AoyamaH, ShiratoH, NishiokaT, et al. Treatment outcome of single or hypofractionated single-isocentric stereotactic irradiation (STI) using a linear accelerator for intracranial arteriovenous malformation[J]. Radiother Oncol, 2001, 59(3):323-328. DOI: 10.1016/s0167-8140(01)00303-6.
[139]YamamotoM, AkabaneA, MatsumaruY, et al. Long-term follow-up results of intentional 2-stage Gamma Knife surgery with an interval of at least 3 years for arteriovenous malformations larger than 10 cm³[J]. J Neurosurg, 2012, 117 Suppl:126-134. DOI: 10.3171/2012.6.GKS12757.
[140]DingD, StarkeRM, KanoH, et al. Stereotactic radiosurgery for Spetzler-Martin Grade III arteriovenous malformations: an international multicenter study[J]. J Neurosurg, 2017, 126(3):859-871. DOI: 10.3171/2016.1.JNS152564.
[141]FirlikAD, LevyEI, KondziolkaD, et al. Staged volume radiosurgery followed by microsurgical resection: a novel treatment for giant cerebral arteriovenous malformations: technical case report[J]. Neurosurgery, 1998, 43(5):1223-1228. DOI: 10.1097/00006123-199811000-00124.
[142]SirinS, KondziolkaD, NiranjanA, et al. Prospective staged volume radiosurgery for large arteriovenous malformations: indications and outcomes in otherwise untreatable patients[J]. Neurosurgery, 2006, 58(1):17-27; discussion 17-27. DOI: 10.1227/01.neu.0000190653.42970.6b.
[143]SeymourZA, ChanJW, SneedPK, et al. Dose response and architecture in volume staged radiosurgery for large arteriovenous malformations: A multi-institutional study[J]. Radiother Oncol, 2020, 144:180-188. DOI: 10.1016/j.radonc.2019.09.019.
[144]PollockBE, LinkMJ, StaffordSL, et al. Volume-staged stereotactic radiosurgery for intracranial arteriovenous malformations: outcomes based on an 18-year experience [J]. Neurosurgery, 2017, 80(4): 543-550.DOI: 10.1093/neuros/nyw107.
[145]FooteKD, FriedmanWA, EllisTL, et al. Salvage retreatment after failure of radiosurgery in patients with arteriovenous malformations[J]. J Neurosurg, 2003, 98(2):337-341. DOI: 10.3171/jns.2003.98.2.0337.
[146]ParkHR, LeeJM, KimJW, et al. Time-staged gamma knife stereotactic radiosurgery for large cerebral arteriovenous malformations: a preliminary report[J]. PLoS One, 2016, 11(11):e0165783. DOI: 10.1371/journal.pone.0165783.
[147]LunsfordLD, KondziolkaD, FlickingerJC, et al. Stereotactic radiosurgery for arteriovenous malformations of the brain[J]. J Neurosurg, 1991, 75(4):512-524. DOI: 10.3171/jns.1991.75.4.0512.
[148]SteinerL, LindquistC, AdlerJR, et al. Clinical outcome of radiosurgery for cerebral arteriovenous malformations[J]. J Neurosurg, 1992, 77(1):1-8. DOI: 10.3171/jns.1992.77.1.0001.
[149]ColomboF, PozzaF, ChieregoG, et al. Linear accelerator radiosurgery of cerebral arteriovenous malformations: an update[J]. Neurosurgery, 1994, 34(1):14-20; discussion 20-21.
[150]Cohen-InbarO, StarkeRM, KanoH, et al. Stereotactic radiosurgery for cerebellar arteriovenous malformations: an international multicenter study[J]. J Neurosurg, 2017, 127(3):512-521. DOI: 10.3171/2016.7.JNS161208.
[151]PatibandlaMR, DingD, KanoH, et al. Stereotactic radiosurgery for Spetzler-Martin Grade IV and V arteriovenous malformations: an international multicenter study[J]. J Neurosurg, 2018, 129(2):498-507. DOI: 10.3171/2017.3.JNS162635.
[152]HasegawaT, KatoT, NaitoT, et al. Long-term risks of hemorrhage and adverse radiation effects of stereotactic radiosurgery for brain arteriovenous malformations[J]. Neurosurgery, 2022, 90(6):784-792. DOI: 10.1227/neu.0000000000001913.
[153]ChenCJ, DingD, LeeCC, et al. Stereotactic radiosurgery with versus without embolization for brain arteriovenous malformations[J]. Neurosurgery, 2021, 88(2): 313-321.DOI: 10.1093/neuros/nyaa418
[154]HasegawaT, KatoT, NaitoT, et al. Effect of embolization before stereotactic radiosurgery for brain arteriovenous malformations: a case-control study with propensity score matching[J]. J Neurosurg, 2023, 138(4):955-961. DOI: 10.3171/2022.7.JNS221343.
[155]de OliveiraE, TedeschiH, RasoJ. Comprehensive management of arteriovenous malformations[J]. Neurol Res, 1998, 20(8):673-683. DOI: 10.1080/01616412.1998.11740583.
[156]KarlssonB, LindquistC, SteinerL. Prediction of obliteration after gamma knife surgery for cerebral arteriovenous malformations[J]. Neurosurgery, 1997, 40(3):425-430; discussion 430-431. DOI: 10.1097/00006123-199703000-00001.
[157]SchwartzM, SixelK, YoungC, et al. Prediction of obliteration of arteriovenous malformations after radiosurgery: the obliteration prediction index[J]. Can J Neurol Sci, 1997, 24(2):106-109. DOI: 10.1017/s0317167100021417.
[158]PollockBE, FlickingerJC. A proposed radiosurgery-based grading system for arteriovenous malformations[J]. J Neurosurg, 2002, 96(1):79-85. DOI: 10.3171/jns.2002.96.1.0079.
[159]PollockBE, FlickingerJC. Modification of the radiosurgery-based arteriovenous malformation grading system[J]. Neurosurgery, 2008, 63(2):239-243; discussion 243. DOI: 10.1227/01.NEU.0000315861.24920.92.
[160]SeifertV, StolkeD, MehdornHM, et al. Clinical and radiological evaluation of long-term results of stereotactic proton beam radiosurgery in patients with cerebral arteriovenous malformations[J]. J Neurosurg, 1994, 81(5):683-689. DOI: 10.3171/jns.1994.81.5.0683.
[161]SunDQ, CarsonKA, RazaSM, et al. The radiosurgical treatment of arteriovenous malformations: obliteration, morbidities, and performance status[J]. Int J Radiat Oncol Biol Phys, 2011, 80(2):354-361. DOI: 10.1016/j.ijrobp.2010.01.049.
[162]FlickingerJC, KondziolkaD, MaitzAH, et al. An analysis of the dose-response for arteriovenous malformation radiosurgery and other factors affecting obliteration[J]. Radiother Oncol, 2002, 63(3):347-354. DOI: 10.1016/s0167-8140(02)00103-2.
[163]BowdenG, CavaleriJ, KanoH, et al. Radiosurgery for arteriovenous malformations and the impact on headaches[J]. Headache, 2017, 57(5):737-745. DOI: 10.1111/head.13055.
[164]PrzybylowskiCJ, DingD, StarkeRM, et al. Seizure and anticonvulsant outcomes following stereotactic radiosurgery for intracranial arteriovenous malformations[J]. J Neurosurg, 2015, 122(6):1299-1305. DOI: 10.3171/2014.11.JNS141388.
[165]PollockBE, KondziolkaD, FlickingerJC, et al. Magnetic resonance imaging: an accurate method to evaluate arteriovenous malformations after stereotactic radiosurgery[J]. J Neurosurg, 1996, 85(6):1044-1049. DOI: 10.3171/jns.1996.85.6.1044.
[166]FlickingerJC, KondziolkaD, LunsfordLD, et al. Development of a model to predict permanent symptomatic postradiosurgery injury for arteriovenous malformation patients. Arteriovenous Malformation Radiosurgery Study Group[J]. Int J Radiat Oncol Biol Phys, 2000, 46(5):1143-1148. DOI: 10.1016/s0360-3016(99)00513-1.
[167]CetinIA, AtesR, DhaensJ, et al. Retrospective analysis of linac-based radiosurgery for arteriovenous malformations and testing of the Flickinger formula in predicting radiation injury[J]. Strahlenther Onkol, 2012, 188(12):1133-1138. DOI: 10.1007/s00066-012-0180-6.
[168]FlickingerJC, KondziolkaD, LunsfordLD, et al. A multi-institutional analysis of complication outcomes after arteriovenous malformation radiosurgery[J]. Int J Radiat Oncol Biol Phys, 1999, 44(1):67-74. DOI: 10.1016/s0360-3016(98)00518-5.
[169]HaraM, NakamuraM, ShiokawaY, et al. Delayed cyst formation after radiosurgery for cerebral arteriovenous malformation: two case reports[J]. Minim Invasive Neurosurg, 1998, 41(1):40-45. DOI: 10.1055/s-2008-1052014.
[170]KanoH, FlickingerJC, TonettiD, et al. Estimating the risks of adverse radiation effects after gamma knife radiosurgery for arteriovenous malformations[J]. Stroke, 2017, 48(1):84-90. DOI: 10.1161/STROKEAHA.116.014825.
[171]IzawaM, HayashiM, ChernovM, et al. Long-term complications after gamma knife surgery for arteriovenous malformations[J]. J Neurosurg, 2005, 102 Suppl:34-37. DOI: 10.3171/jns.2005.102.s_supplement.0034.
[172]LUESSENHOPAJ, SPENCEWT. Artificial embolization of cerebral arteries. Report of use in a case of arteriovenous malformation[J]. J Am Med Assoc, 1960, 172:1153-1155. DOI: 10.1001/jama.1960.63020110001009.
[173]DoppmanJL, ZapolW, PierceJ. Transcatheter embolization with a silicone rubber preparation. Experimental observations[J]. Invest Radiol, 1971, 6(5):304-309. DOI: 10.1097/00004424-197109000-00002.
[174]KerberC. Balloon catheter with a calibrated leak. A new system for superselective angiography and occlusive catheter therapy[J]. Radiology, 1976, 120(3):547-550. DOI: 10.1148/120.3.547.
[175]Fernández-AlvarezV, SuárezC, de BreeR, et al. Management of extracranial arteriovenous malformations of the head and neck[J]. Auris Nasus Larynx, 2020, 47(2):181-190. DOI: 10.1016/j.anl.2019.11.008.
[176]YuSC, ChanMS, LamJM, et al. Complete obliteration of intracranial arteriovenous malformation with endovascular cyanoacrylate embolization: initial success and rate of permanent cure[J]. AJNR Am J Neuroradiol, 2004, 25(7):1139-1143.
[177]PierotL, CognardC, HerbreteauD, et al. Endovascular treatment of brain arteriovenous malformations using a liquid embolic agent: results of a prospective, multicentre study (BRAVO)[J]. Eur Radiol, 2013, 23(10):2838-2845. DOI: 10.1007/s00330-013-2870-6.
[178]DurstCR, StarkeRM, GaughenJ, et al. A method for complete angiographic obliteration of a brain arteriovenous malformation in a single session through a single pedicle[J]. J Clin Neurosci, 2015, 22(2):391-395. DOI: 10.1016/j.jocn.2014.07.030.
[179]WillinskyR, GoyalM, TerbruggeK, et al. Embolisation of small (<3 cm) brain arteriovenous malformations. correlation of angiographic results to a proposed angioarchitecture grading system[J]. Interv Neuroradiol, 2001, 7(1):19-27. DOI: 10.1177/159101990100700102.
[180]DmytriwAA, Ter BruggeKG, KringsT, et al. Endovascular treatment of head and neck arteriovenous malformations[J]. Neuroradiology, 2014, 56(3):227-236. DOI: 10.1007/s00234-014-1328-0.
[181]HakJF, BoulouisG, KerlerouxB, et al. Pediatric brain arteriovenous malformation recurrence: a cohort study, systematic review and meta-analysis[J]. J Neurointerv Surg, 2022, 14(6):611-617. DOI: 10.1136/neurintsurg-2021-017777.
[182]HeY, BaiW, LiT, et al. Curative transvenous embolization for ruptured brain arteriovenous malformations: a single-center experience from China[J]. World Neurosurg, 2018, 116:e421-e428. DOI: 10.1016/j.wneu.2018.04.223.
[183]FangYB, ByunJS, LiuJM, et al. Transvenous embolization of brain arteriovenous malformations: a systematic review and meta-analysis[J]. J Neurosurg Sci, 2019, 63(4):468-472. DOI: 10.23736/S0390-5616.18.04342-4.
[184]KoyanagiM, MosimannPJ, NordmeyerH, et al. The transvenous retrograde pressure cooker technique for the curative embolization of high-grade brain arteriovenous malformations[J]. J Neurointerv Surg, 2021, 13(7):637-641. DOI: 10.1136/neurintsurg-2020-016566.
[185]BatistaS, Almeida FilhoJA, OliveiraLB, et al. Evaluating the safety and efficacy of transvenous embolization for brain arteriovenous malformation: a systematic review and meta-analysis[J]. Interv Neuroradiol, 2023:15910199231204922. DOI: 10.1177/15910199231204922.
[186]ChenCJ, NoratP, DingD, et al. Transvenous embolization of brain arteriovenous malformations: a review of techniques, indications, and outcomes[J]. Neurosurg Focus, 2018, 45(1):E13. DOI: 10.3171/2018.3.FOCUS18113.
[187]HeY, DingY, BaiW, et al. Safety and efficacy of transvenous embolization of ruptured brain arteriovenous malformations as a last resort: a prospective single-arm study[J]. AJNR Am J Neuroradiol, 2019, 40(10):1744-1751. DOI: 10.3174/ajnr.A6197.
[188]VianaDC, de Castro-AfonsoLH, NakiriGS, et al. Extending the indications for transvenous approach embolization for superficial brain arteriovenous malformations[J]. J Neurointerv Surg, 2017, 9(11):1053-1059. DOI: 10.1136/neurintsurg-2017-013113.
[189]ChapotR, StrackeP, VelascoA, et al. The pressure cooker technique for the treatment of brain AVMs[J]. J Neuroradiol, 2014, 41(1):87-91. DOI: 10.1016/j.neurad.2013.10.001.
[190]AbudDG, de Castro-AfonsoLH, NakiriGS, et al. Modified pressure cooker technique: an easier way to control onyx reflux[J]. J Neuroradiol, 2016, 43(3):218-222. DOI: 10.1016/j.neurad.2016.01.146.
[191]PereiraVM, Marcos-GonzalezA, RadovanovicI, et al. Transvenous embolization of a ruptured deep cerebral arteriovenous malformation. A technical note[J]. Interv Neuroradiol, 2013, 19(1):27-34. DOI: 10.1177/159101991301900104.
[192]MaimonS, StraussI, FrolovV, et al. Brain arteriovenous malformation treatment using a combination of Onyx and a new detachable tip microcatheter, SONIC: short-term results[J]. AJNR Am J Neuroradiol, 2010, 31(5):947-954. DOI: 10.3174/ajnr.A1959.
[193]KringsT, HansFJ, GeibprasertS, et al. Partial "targeted" embolisation of brain arteriovenous malformations[J]. Eur Radiol, 2010, 20(11):2723-2731. DOI: 10.1007/s00330-010-1834-3.
[194]BrownRD, WiebersDO, ForbesGS. Unruptured intracranial aneurysms and arteriovenous malformations: frequency of intracranial hemorrhage and relationship of lesions[J]. J Neurosurg, 1990, 73(6):859-863. DOI: 10.3171/jns.1990.73.6.0859.
[195]AlexanderMD, HippeDS, CookeDL, et al. targeted embolization of aneurysms associated with brain arteriovenous malformations at high risk for surgical resection: a case-control study [J]. Neurosurgery, 2018, 82(3): 343-349.DOI: 10.1093/neuros/nyx167
[196]XiaochuanH, YuhuaJ, XianliL, et al. Targeted embolization reduces hemorrhage complications in partially embolized cerebral AVM combined with gamma knife surgery[J]. Interv Neuroradiol, 2015, 21(1):80-87. DOI: 10.15274/inr-2014-10090.
[197]PierotL, KadziolkaK, LitréF, et al. Combined treatment of brain AVMs with use of Onyx embolization followed by radiosurgery[J]. AJNR Am J Neuroradiol, 2013, 34(7):1395-1400. DOI: 10.3174/ajnr.A3409.
[198]LvX, WuZ, LiY, et al. Hemorrhage risk after partial endovascular NBCA and ONYX embolization for brain arteriovenous malformation[J]. Neurol Res, 2012, 34(6):552-556. DOI: 10.1179/1743132812Y.0000000044.
[199]HanPP, PonceFA, SpetzlerRF. Intention-to-treat analysis of Spetzler-Martin grades IV and V arteriovenous malformations: natural history and treatment paradigm[J]. J Neurosurg, 2003, 98(1):3-7. DOI: 10.3171/jns.2003.98.1.0003.
[200]BatjerHH, SrDMD, SeibertGB, et al. Intracranial arteriovenous malformation: relationships between clinical and radiographic factors and ipsilateral steal severity[J]. Neurosurgery, 1988, 23(3):322-328. DOI: 10.1227/00006123-198809000-00006.
[201]KusskeJA, KellyWA. Embolization and reduction of the "steal" syndrome in cerebral arteriovenous malformations[J]. J Neurosurg, 1974, 40(3):313-321. DOI: 10.3171/jns.1974.40.3.0313.
[202]FelicianoCE, de León-BerraR, Hernández-GaitánMS, et al. A proposal for a new arteriovenous malformation grading scale for neuroendovascular procedures and literature review[J]. P R Health Sci J, 2010, 29(2):117-120.
[203]DumontTM, KanP, SnyderKV, et al. A proposed grading system for endovascular treatment of cerebral arteriovenous malformations: Buffalo score[J]. Surg Neurol Int, 2015, 6:3. DOI: 10.4103/2152-7806.148847.
[204]LopesDK, MoftakharR, StrausD, et al. Arteriovenous malformation embocure score: AVMES[J]. J Neurointerv Surg, 2016, 8(7):685-691. DOI: 10.1136/neurintsurg-2015-011779.
[205]BellDL, Leslie-MazwiTM, YooAJ, et al. Application of a novel brain arteriovenous malformation endovascular grading scale for transarterial embolization[J]. AJNR Am J Neuroradiol, 2015, 36(7):1303-1309. DOI: 10.3174/ajnr.A4286.
[206]JinH, JiangY, GeH, et al. Comparison of grading scales regarding perioperative complications and clinical outcomes of brain arteriovenous malformations after endovascular therapy-multicenter study[J]. World Neurosurg, 2017, 106:394-401. DOI: 10.1016/j.wneu.2017.07.020.
[207]PulliB, StapletonCJ, WalcottBP, et al. Comparison of predictive grading systems for procedural risk in endovascular treatment of brain arteriovenous malformations: analysis of 104 consecutive patients[J]. J Neurosurg, 2019:1-9. DOI: 10.3171/2019.4.JNS19266.
[208]LeonardiM, BarbaraC, SimonettiL, et al. Glubran 2: a new acrylic glue for neuroradiological endovascular use. Experimental study on animals[J]. Interv Neuroradiol, 2002, 8(3):245-250. DOI: 10.1177/159101990200800304.
[209]中华医学会神经外科学分会介入学组, 《脑动静脉畸形介入治疗中国专家共识》编写委员会. 脑动静脉畸形介入治疗中国专家共识[J]. 中华神经外科杂志, 2017, 33(12):1195-1203. DOI: 10.3760/cma.j.issn.1001-2346.2017.12.003.
[210]GailloudP. Endovascular treatment of cerebral arteriovenous malformations[J]. Tech Vasc Interv Radiol, 2005, 8(3):118-128. DOI: 10.1053/j.tvir.2005.10.003.
[211]高旭, 于春泳, 李志清, 等. 弹簧圈近端辅助Onyx胶栓塞技术治疗脑动静脉畸形(附22例报告)[J]. 中华神经外科杂志, 2014, 30(3):221-224. DOI: 10.3760/cma.j.issn.1001-2346.2014.03.002.
[212]AsadiH, KokHK, LoobyS, et al. Outcomes and complications after endovascular treatment of brain arteriovenous malformations: a prognostication attempt using artificial intelligence[J]. World Neurosurg, 2016, 96:562-569.e1. DOI: 10.1016/j.wneu.2016.09.086.
[213]BaharvahdatH, BlancR, TermechiR, et al. Hemorrhagic complications after endovascular treatment of cerebral arteriovenous malformations[J]. AJNR Am J Neuroradiol, 2014, 35(5):978-983. DOI: 10.3174/ajnr.A3906.
[214]JordanJA, LlibreJC, VázquezF, et al. Predictors of hemorrhagic complications from endovascular treatment of cerebral arteriovenous malformations[J]. Interv Neuroradiol, 2014, 20(1):74-82. DOI: 10.15274/INR-2014-10011.
[215]PottsMB, LauD, AblaAA, et al. Current surgical results with low-grade brain arteriovenous malformations[J]. J Neurosurg, 2015, 122(4):912-920. DOI: 10.3171/2014.12.JNS14938.
[216]GraffeoCS, SahgalA, De SallesA, et al. Stereotactic radiosurgery for Spetzler-Martin Grade I and II arteriovenous malformations: international society of stereotactic radiosurgery (ISRS) practice guideline[J]. Neurosurgery, 2020, 87(3):442-452. DOI: 10.1093/neuros/nyaa004.
[217]KanoH, LunsfordLD, FlickingerJC, et al. Stereotactic radiosurgery for arteriovenous malformations, Part 1: management of Spetzler-Martin Grade I and II arteriovenous malformations[J]. J Neurosurg, 2012, 116(1):11-20. DOI: 10.3171/2011.9.JNS101740.
[218]GamiA, FeghaliJ, RapaportS, et al. Microsurgical resection versus stereotactic radiosurgery for low-grade intracranial arteriovenous malformations: a 27-year institutional experience[J]. J Clin Neurosci, 2021, 94:209-215. DOI: 10.1016/j.jocn.2021.10.036.
[219]SattariSA, ShahbandiA, KimJE, et al. Microsurgery versus stereotactic radiosurgery for treatment of patients with brain arteriovenous malformation: a systematic review and meta-analysis[J]. Neurosurgery, 2023, 93(3):510-523. DOI: 10.1227/neu.0000000000002460.
[220]TalaatM, ShotarE, PrematK, et al. Safety and effectiveness of first-line endovascular management of low-grade brain arteriovenous malformations: single center experience in 145 patients[J]. Clin Neuroradiol, 2022, 32(4):1019-1029. DOI: 10.1007/s00062-022-01176-9.
[221]BaharvahdatH, BlancR, FahedR, et al. Endovascular treatment for low-grade (Spetzler-Martin I-II) brain arteriovenous malformations[J]. AJNR Am J Neuroradiol, 2019, 40(4):668-672. DOI: 10.3174/ajnr.A5988.
[222]IosifC, de LucenaAF, Abreu-MattosLG, et al. Curative endovascular treatment for low-grade Spetzler-Martin brain arteriovenous malformations: a single-center prospective study[J]. J Neurointerv Surg, 2019, 11(7):699-705. DOI: 10.1136/neurintsurg-2018-014390.
[223]CatapanoJS, SrinivasanVM, RumallaK, et al. Effects of preoperative embolization on Spetzler-Martin grade I and II arteriovenous malformations: a propensity-adjusted analysis[J]. Neurosurgery, 2022, 90(1):92-98. DOI: 10.1227/NEU.0000000000001741.
[224]MorganMK, AssaadN, KorjaM. Surgery for unruptured Spetzler-Martin grade 3 brain arteriovenous malformations: a prospective surgical cohort[J]. Neurosurgery, 2015, 77(3):362-369; discussion 369-370. DOI: 10.1227/NEU.0000000000000774.
[225]DingD. Microsurgery versus radiosurgery as the definitive intervention for Spetzler-Martin grade III arteriovenous malformations[J]. Clin Neurol Neurosurg, 2015, 133:103-104. DOI: 10.1016/j.clineuro.2015.03.021.
[226]BurelJ, PapagiannakiC, SourourN, et al. Endovascular treatment as first-line therapy in Spetzler-Martin grade III brain arteriovenous malformations: a multicenter retrospective study[J]. J Neurosurg, 2023, 139(4):1070-1077. DOI: 10.3171/2023.1.JNS222745.
[227]HassanT, RefaatM, IssaAM, et al. Geometrical characteristics of grade III arteriovenous malformations that contribute to better outcomes in endovascular treatment[J]. World Neurosurg, 2023, 180:e749-e755. DOI: 10.1016/j.wneu.2023.10.019.
[228]NguyenBT, TranHM, HuynhCT, et al. Gamma knife radiosurgery for Spetzler-Martin grade iii brain arteriovenous malformations[J]. World Neurosurg, 2023, 175:e796-e803. DOI: 10.1016/j.wneu.2023.04.022.
[229]JiaoY, WuJ, ChenX, et al. Spetzler-Martin grade IV and V arteriovenous malformations: treatment outcomes and risk factors for negative outcomes after surgical resection[J]. J Clin Neurosci, 2019, 61:166-173. DOI: 10.1016/j.jocn.2018.10.101.
[230]JiangH, TangX, WengR, et al. Long-term outcome of a tailored embolization strategy with Gamma Knife radiosurgery for high-grade brain arteriovenous malformations: a single-center experience[J]. J Neurosurg, 2023, 139(1):176-183. DOI: 10.3171/2022.11.JNS221363.
[231]ChangH, SilvaMA, WengJ, et al. The impact of embolization on radiosurgery obliteration rates for brain arteriovenous malformations: a systematic review and meta-analysis[J]. Neurosurg Rev, 2022, 46(1):28. DOI: 10.1007/s10143-022-01935-9.
[232]RussellD, PeckT, DingD, et al. Stereotactic radiosurgery alone or combined with embolization for brain arteriovenous malformations: a systematic review and meta-analysis[J]. J Neurosurg, 2018, 128(5):1338-1348. DOI: 10.3171/2016.11.JNS162382.
[233]DingD, YenCP, StarkeRM, et al. Outcomes following single-session radiosurgery for high-grade intracranial arteriovenous malformations[J]. Br J Neurosurg, 2014, 28(5):666-674. DOI: 10.3109/02688697.2013.872227.
[234]TongX, WuJ, PanJ, et al. Microsurgical resection for persistent arteriovenous malformations following Gamma Knife radiosurgery: a case-control study[J]. World Neurosurg, 2016, 88:277-288. DOI: 10.1016/j.wneu.2016.01.027.
[235]FleetwoodIG, MarcellusML, LevyRP, et al. Deep arteriovenous malformations of the basal ganglia and thalamus: natural history[J]. J Neurosurg, 2003, 98(4):747-750. DOI: 10.3171/jns.2003.98.4.0747.
[236]PottsMB, JahangiriA, JenM, et al. Deep arteriovenous malformations in the basal ganglia, thalamus, and insula: multimodality management, patient selection, and results[J]. World Neurosurg, 2014, 82(3-4):386-394. DOI: 10.1016/j.wneu.2014.03.033.
[237]JiZ, XiangS, LiJ, et al. Multimodality treatment of deep-seated cerebral arteriovenous malformations: the experiences of one center[J]. Curr Neurovasc Res, 2022, 19(5):476-486. DOI: 10.2174/1567202620666221114111512.
[238]SasakiT, KuritaH, SaitoI, et al. Arteriovenous malformations in the basal ganglia and thalamus: management and results in 101 cases[J]. J Neurosurg, 1998, 88(2):285-292. DOI: 10.3171/jns.1998.88.2.0285.
[239]OhadiM, IranmehrA, ChavoshiM, et al. Stereotactic radiosurgery outcome for deep-seated cerebral arteriovenous malformations in the brainstem and thalamus/basal ganglia: systematic review and meta-analysis[J]. Neurosurg Rev, 2023, 46(1):148. DOI: 10.1007/s10143-023-02059-4.
[240]BroderickJ, ConnollyS, FeldmannE, et al. Guidelines for the management of spontaneous intracerebral hemorrhage in adults: 2007 update: a guideline from the American Heart Association/American Stroke Association Stroke Council, High Blood Pressure Research Council, and the Quality of Care and Outcomes in Research Interdisciplinary Working Group[J]. Circulation, 2007, 116(16):e391-413. DOI: 10.1161/CIRCULATIONAHA.107.183689.
[241]MorgensternLB, HemphillJC, AndersonC, et al. Guidelines for the management of spontaneous intracerebral hemorrhage: a guideline for healthcare professionals from the American Heart Association/American Stroke Association[J]. Stroke, 2010, 41(9):2108-2129. DOI: 10.1161/STR.0b013e3181ec611b.
[242]AounSG, BendokBR, BatjerHH. Acute management of ruptured arteriovenous malformations and dural arteriovenous fistulas[J]. Neurosurg Clin N Am, 2012, 23(1):87-103. DOI: 10.1016/j.nec.2011.09.013.
[243]HartmannA, MohrJP. Acute management of brain arteriovenous malformations[J]. Curr Treat Options Neurol, 2015, 17(5):346. DOI: 10.1007/s11940-015-0346-5.
[244]JafarJJ, RezaiAR. Acute surgical management of intracranial arteriovenous malformations[J]. Neurosurgery, 1994, 34(1):8-12; discussion 12-13.
[245]JinH, LenckS, KringsT, et al. Interval angioarchitectural evolution of brain arteriovenous malformations following rupture[J]. J Neurosurg, 2018, 131(1):96-103. DOI: 10.3171/2018.2.JNS18128.
[246]ZhangY, ChenY, HanH, et al. Timing of microsurgical resection for ruptured brain arteriovenous malformations: a propensity score-matched analysis using prospective single-center registry data[J]. J Neurosurg, 2024, 140(1):164-171. DOI: 10.3171/2023.5.JNS222666.
[247]XuF, ZhongJ, RayA, et al. Stereotactic radiosurgery with and without embolization for intracranial arteriovenous malformations: a systematic review and meta-analysis[J]. Neurosurg Focus, 2014, 37(3):E16. DOI: 10.3171/2014.6.FOCUS14178.
[248]EnglotDJ, YoungWL, HanSJ, et al. Seizure predictors and control after microsurgical resection of supratentorial arteriovenous malformations in 440 patients[J]. Neurosurgery, 2012, 71(3):572-580; discussion 580. DOI: 10.1227/NEU.0b013e31825ea3ba.
[249]HeikkinenER, KonnovB, MelnikovL, et al. Relief of epilepsy by radiosurgery of cerebral arteriovenous malformations[J]. Stereotact Funct Neurosurg, 1989, 53(3):157-166. DOI: 10.1159/000099532.
[250]ChenCJ, ChivukulaS, DingD, et al. Seizure outcomes following radiosurgery for cerebral arteriovenous malformations[J]. Neurosurg Focus, 2014, 37(3):E17. DOI: 10.3171/2014.6.FOCUS1454.
[251]BaranoskiJF, GrantRA, HirschLJ, et al. Seizure control for intracranial arteriovenous malformations is directly related to treatment modality: a meta-analysis[J]. J Neurointerv Surg, 2014, 6(9):684-690. DOI: 10.1136/neurintsurg-2013-010945.
[252]HyunSJ, KongDS, LeeJI, et al. Cerebral arteriovenous malformations and seizures: differential impact on the time to seizure-free state according to the treatment modalities[J]. Acta Neurochir (Wien), 2012, 154(6):1003-1010. DOI: 10.1007/s00701-012-1339-8.
[253]FennellVS, MartirosyanNL, AtwalGS, et al. Hemodynamics associated with intracerebral arteriovenous malformations: the effects of treatment modalities [J]. Neurosurgery, 2018, 83(4): 611-621.DOI: 10.1093/neuros/nyx560.
[254]CaoY, WangR, YangL, et al. Bipolar electrocoagulation on cortex after AVMs lesionectomy for seizure control[J]. Can J Neurol Sci, 2011, 38(1):48-53.
[255]Bustuchina VlaicuM. New approaches for brain arteriovenous malformations-related epilepsy[J]. Rev Neurol (Paris), 2023, 179(3):188-200. DOI: 10.1016/j.neurol.2022.05.011.
[256]JosephsonCB, LeachJP, DuncanR, et al. Seizure risk from cavernous or arteriovenous malformations: prospective population-based study[J]. Neurology, 2011, 76(18):1548-1554. DOI: 10.1212/WNL.0b013e3182190f37.
[257]StephenLJ, KwanP, BrodieMJ. Does the cause of localisation-related epilepsy influence the response to antiepileptic drug treatment?[J]. Epilepsia, 2001, 42(3):357-362. DOI: 10.1046/j.1528-1157.2001.29000.x.
[258]SturialeCL, PucaA, SebastianiP, et al. Single nucleotide polymorphisms associated with sporadic brain arteriovenous malformations: where do we stand?[J]. Brain, 2013, 136(Pt 2):665-681. DOI: 10.1093/brain/aws180.
[259]HolashJ, MaisonpierrePC, ComptonD, et al. Vessel cooption, regression, and growth in tumors mediated by angiopoietins and VEGF[J]. Science, 1999, 284(5422):1994-1998. DOI: 10.1126/science.284.5422.1994.
[260]JaysonGC, KerbelR, EllisLM, et al. Antiangiogenic therapy in oncology: current status and future directions[J]. Lancet, 2016, 388(10043):518-529. DOI: 10.1016/S0140-6736(15)01088-0.
[261]SandalciogluIE, WendeD, EggertA, et al. Vascular endothelial growth factor plasma levels are significantly elevated in patients with cerebral arteriovenous malformations[J]. Cerebrovasc Dis, 2006, 21(3):154-158. DOI: 10.1159/000090526.
[262]LarrivéeB, PrahstC, GordonE, et al. ALK1 signaling inhibits angiogenesis by cooperating with the Notch pathway[J]. Dev Cell, 2012, 22(3):489-500. DOI: 10.1016/j.devcel.2012.02.005.
[263]del ToroR, PrahstC, MathivetT, et al. Identification and functional analysis of endothelial tip cell-enriched genes[J]. Blood, 2010, 116(19):4025-4033. DOI: 10.1182/blood-2010-02-270819.
[264]WangY, FeiD, VanderlaanM, et al. Biological activity of bevacizumab, a humanized anti-VEGF antibody in vitro[J]. Angiogenesis, 2004, 7(4):335-345. DOI: 10.1007/s10456-004-8272-2.
[265]JubbAM, HarrisAL. Biomarkers to predict the clinical efficacy of bevacizumab in cancer[J]. Lancet Oncol, 2010, 11(12):1172-1183. DOI: 10.1016/S1470-2045(10)70232-1.
[266]KarnezisTT, DavidsonTM. Treatment of hereditary hemorrhagic telangiectasia with submucosal and topical bevacizumab therapy[J]. Laryngoscope, 2012, 122(3):495-497. DOI: 10.1002/lary.22501.
[267]SimondsJ, MillerF, MandelJ, et al. The effect of bevacizumab (Avastin) treatment on epistaxis in hereditary hemorrhagic telangiectasia[J]. Laryngoscope, 2009, 119(5):988-992. DOI: 10.1002/lary.20159.
[268]Dupuis-GirodS, AmbrunA, DecullierE, et al. ELLIPSE Study: a Phase 1 study evaluating the tolerance of bevacizumab nasal spray in the treatment of epistaxis in hereditary hemorrhagic telangiectasia[J]. MAbs, 2014, 6(3):794-799. DOI: 10.4161/mabs.28025.
[269]Dupuis-GirodS, AmbrunA, DecullierE, et al. Effect of bevacizumab nasal spray on epistaxis duration in hereditary hemorrhagic telangectasia: a randomized clinical trial[J]. JAMA, 2016, 316(9):934-942. DOI: 10.1001/jama.2016.11387.
[270]MusterR, KoN, SmithW, et al. Proof-of-concept single-arm trial of bevacizumab therapy for brain arteriovenous malformation[J]. BMJ Neurol Open, 2021, 3(1):e000114. DOI: 10.1136/bmjno-2020-000114.
[271]TanvetyanonT, MurtaghR, BeplerG. Rupture of a cerebral arteriovenous malformation in a patient treated with bevacizumab[J]. J Thorac Oncol, 2009, 4(2):268-269. DOI: 10.1097/JTO.0b013e318195a642.
[272]WinklerEA, KimCN, RossJM, et al. A single-cell atlas of the normal and malformed human brain vasculature[J]. Science, 2022, 375(6584):eabi7377. DOI: 10.1126/science.abi7377.
[273]HashimotoT, MatsumotoMM, LiJF, et al. Suppression of MMP-9 by doxycycline in brain arteriovenous malformations[J]. BMC Neurol, 2005, 5(1):1. DOI: 10.1186/1471-2377-5-1.
[274]FrenzelT, LeeCZ, KimH, et al. Feasibility of minocycline and doxycycline use as potential vasculostatic therapy for brain vascular malformations: pilot study of adverse events and tolerance[J]. Cerebrovasc Dis, 2008, 25(1-2):157-163. DOI: 10.1159/000113733.
[275]BurrowsPE, MullikenJB, FishmanSJ, et al. Pharmacological treatment of a diffuse arteriovenous malformation of the upper extremity in a child[J]. J Craniofac Surg, 2009, 20 Suppl 1∶597-602. DOI: 10.1097/SCS.0b013e3181927f1e.
[276]MengJS, OkedaR. Histopathological structure of the pial arteriovenous malformation in adults: observation by reconstruction of serial sections of four surgical specimens[J]. Acta Neuropathol, 2001, 102(1):63-68. DOI: 10.1007/s004010000351.
[277]ChenW, GuoY, WalkerEJ, et al. Reduced mural cell coverage and impaired vessel integrity after angiogenic stimulation in the Alk1-deficient brain[J]. Arterioscler Thromb Vasc Biol, 2013, 33(2):305-310. DOI: 10.1161/ATVBAHA.112.300485.
[278]BaeyensN, LarrivéeB, OlaR, et al. Defective fluid shear stress mechanotransduction mediates hereditary hemorrhagic telangiectasia[J]. J Cell Biol, 2016, 214(7):807-816. DOI: 10.1083/jcb.201603106.
[279]LebrinF, SrunS, RaymondK, et al. Thalidomide stimulates vessel maturation and reduces epistaxis in individuals with hereditary hemorrhagic telangiectasia[J]. Nat Med, 2010, 16(4):420-428. DOI: 10.1038/nm.2131.
[280]InvernizziR, QuagliaF, KlersyC, et al. Efficacy and safety of thalidomide for the treatment of severe recurrent epistaxis in hereditary haemorrhagic telangiectasia: results of a non-randomised, single-centre, phase 2 study[J]. Lancet Haematol, 2015, 2(11):e465-473. DOI: 10.1016/S2352-3026(15)00195-7.
[281]GeZZ, ChenHM, GaoYJ, et al. Efficacy of thalidomide for refractory gastrointestinal bleeding from vascular malformation[J]. Gastroenterology, 2011, 141(5):1629-1637.e1-4. DOI: 10.1053/j.gastro.2011.07.018.
[282]TsengS, PakG, WashenikK, et al. Rediscovering thalidomide: a review of its mechanism of action, side effects, and potential uses[J]. J Am Acad Dermatol, 1996, 35(6):969-979. DOI: 10.1016/s0190-9622(96)90122-x.
[283]CoutoJA, HuangAY, KonczykDJ, et al. Somatic MAP2K1 mutations are associated with extracranial arteriovenous malformation[J]. Am J Hum Genet, 2017, 100(3):546-554. DOI: 10.1016/j.ajhg.2017.01.018.
[284]EdwardsEA, PhelpsAS, CookeD, et al. Monitoring arteriovenous malformation response to genotype-targeted therapy[J]. Pediatrics, 2020, 146(3):e20193206 [pii]. DOI: 10.1542/peds.2019-3206.
[285]NicholsonCL, FlanaganS, MuratiM, et al. Successful management of an arteriovenous malformation with trametinib in a patient with capillary-malformation arteriovenous malformation syndrome and cardiac compromise[J]. Pediatr Dermatol, 2022, 39(2):316-319. DOI: 10.1111/pde.14912.
[286]LekwuttikarnR, LimYH, AdmaniS, et al. Genotype-guided medical treatment of an arteriovenous malformation in a child[J]. JAMA Dermatol, 2019, 155(2):256-257. DOI: 10.1001/jamadermatol.2018.4653.
[287]Al-SamkariH, EngW. A precision medicine approach to hereditary hemorrhagic telangiectasia and complex vascular anomalies[J]. J Thromb Haemost, 2022, 20(5):1077-1088. DOI: 10.1111/jth.15715.
[288]ScherschinskiL, RahmaniR, SrinivasanVM, et al. Genetics and emerging therapies for brain arteriovenous malformations[J]. World Neurosurg, 2022, 159:327-337. DOI: 10.1016/j.wneu.2021.10.127.
[289]LiH, JingC, WuJ, et al. Circulating tumor DNA detection: a potential tool for colorectal cancer management[J]. Oncol Lett, 2019, 17(2):1409-1416. DOI: 10.3892/ol.2018.9794.
[290]Pérez-AlfayateR, GrassoG. State of the art and future direction in diagnosis, molecular biology, genetics, and treatment of brain arteriovenous malformations[J]. World Neurosurg, 2022, 159:362-372. DOI: 10.1016/j.wneu.2021.08.111.
[291]PriemerDS, VortmeyerAO, ZhangS, et al. Activating KRAS mutations in arteriovenous malformations of the brain: frequency and clinicopathologic correlation[J]. Hum Pathol, 2019, 89:33-39. DOI: 10.1016/j.humpath.2019.04.004.
[292]PalmieriM, CurròA, TommasiA, et al. Cell-free DNA next-generation sequencing liquid biopsy as a new revolutionary approach for arteriovenous malformation[J]. JVS Vasc Sci, 2020, 1:176-180. DOI: 10.1016/j.jvssci.2020.08.002.
[293]FengL, SternDM, Pile-SpellmanJ. Human endothelium: endovascular biopsy and molecular analysis[J]. Radiology, 1999, 212(3):655-664. DOI: 10.1148/radiology.212.3.r99au28655.
[294]AlexanderMD, SunZ, ConradMB, et al. Assessment of cell yield among different devices for endovascular biopsy to harvest vascular endothelial cells[J]. Biotechniques, 2019, 66(1):34-36. DOI: 10.2144/btn-2018-0099.
[295]WinklerE, WuD, GilE, et al. Endoluminal biopsy for molecular profiling of human brain vascular malformations[J]. Neurology, 2022, 98(16):e1637-e1647. DOI: 10.1212/WNL.0000000000200109.
[1]LawtonMT, RutledgeWC, KimH, et al. Brain arteriovenous malformations[J]. Nat Rev Dis Primers, 2015, 1:15008. DOI: 10.1038/nrdp.2015.8.
[2]Al-ShahiR, WarlowC. A systematic review of the frequency and prognosis of arteriovenous malformations of the brain in adults[J]. Brain, 2001, 124(Pt 10):1900-1926. DOI: 10.1093/brain/124.10.1900.
[3]Arteriovenous Malformation Study Group.Arteriovenous malformations of the brain in adults[J]. N Engl J Med, 1999, 340(23):1812-1818. DOI: 10.1056/NEJM199906103402307.
[4]van BeijnumJ, van der WorpHB, BuisDR, et al. Treatment of brain arteriovenous malformations: a systematic review and meta-analysis[J]. JAMA, 2011, 306(18):2011-2019. DOI: 10.1001/jama.2011.1632.
[5]MohrJP, ParidesMK, StapfC, et al. Medical management with or without interventional therapy for unruptured brain arteriovenous malformations (ARUBA): a multicentre, non-blinded, randomised trial[J]. Lancet, 2014, 383(9917):614-621. DOI: 10.1016/S0140-6736(13)62302-8.
[6]Al-Shahi SalmanR, WhitePM, CounsellCE, et al. Outcome after conservative management or intervention for unruptured brain arteriovenous malformations[J]. JAMA, 2014, 311(16):1661-1669. DOI: 10.1001/jama.2014.3200.
[7]MohrJP, OverbeyJR, HartmannA, et al. Medical management with interventional therapy versus medical management alone for unruptured brain arteriovenous malformations (ARUBA): final follow-up of a multicentre, non-blinded, randomised controlled trial[J]. Lancet Neurol, 2020, 19(7):573-581. DOI: 10.1016/S1474-4422(20)30181-2.
[8]HemphillJC, GreenbergSM, AndersonCS, et al. Guidelines for the management of spontaneous intracerebral hemorrhage: a guideline for healthcare professionals from the American Heart Association/American Stroke Association[J]. Stroke, 2015, 46(7):2032-2060. DOI: 10.1161/STR.0000000000000069.
[9]HofmeisterC, StapfC, HartmannA, et al. Demographic, morphological, and clinical characteristics of 1289 patients with brain arteriovenous malformation[J]. Stroke, 2000, 31(6):1307-1310. DOI: 10.1161/01.str.31.6.1307.
[10]Al-ShahiR, FangJS, LewisSC, et al. Prevalence of adults with brain arteriovenous malformations: a community based study in Scotland using capture-recapture analysis[J]. J Neurol Neurosurg Psychiatry, 2002, 73(5):547-551. DOI: 10.1136/jnnp.73.5.547.
[11]BrownRD, WiebersDO, TornerJC, et al. Incidence and prevalence of intracranial vascular malformations in Olmsted County, Minnesota, 1965 to 1992[J]. Neurology, 1996, 46(4):949-952. DOI: 10.1212/wnl.46.4.949.
[12]StapfC, MastH, SciaccaRR, et al. The New York Islands AVM Study: design, study progress, and initial results[J]. Stroke, 2003, 34(5):e29-33. DOI: 10.1161/01.STR.0000068784.36838.19.
[13]HillmanJ. Population-based analysis of arteriovenous malformation treatment[J]. J Neurosurg, 2001, 95(4):633-637. DOI: 10.3171/jns.2001.95.4.0633.
[14]Al-ShahiR, BhattacharyaJJ, CurrieDG, et al. Prospective, population-based detection of intracranial vascular malformations in adults: the Scottish Intracranial Vascular Malformation Study (SIVMS)[J]. Stroke, 2003, 34(5):1163-1169. DOI: 10.1161/01.STR.0000069018.90456.C9.
[15]JessurunGA, KamphuisDJ, van der ZandeFH, et al. Cerebral arteriovenous malformations in The Netherlands Antilles. High prevalence of hereditary hemorrhagic telangiectasia-related single and multiple cerebral arteriovenous malformations[J]. Clin Neurol Neurosurg, 1993, 95(3):193-198. DOI: 10.1016/0303-8467(93)90123-x.
[16]GabrielRA, KimH, SidneyS, et al. Ten-year detection rate of brain arteriovenous malformations in a large, multiethnic, defined population[J]. Stroke, 2010, 41(1):21-26. DOI: 10.1161/STROKEAHA.109.566018.
[17]StapfC, LabovitzDL, SciaccaRR, et al. Incidence of adult brain arteriovenous malformation hemorrhage in a prospective population-based stroke survey[J]. Cerebrovasc Dis, 2002, 13(1):43-46. DOI: 10.1159/000047745.
[18]MorrisZ, WhiteleyWN, LongstrethWT, et al. Incidental findings on brain magnetic resonance imaging: systematic review and meta-analysis[J]. BMJ, 2009, 339:b3016. DOI: 10.1136/bmj.b3016.
[19]WillinskyRA, LasjauniasP, TerbruggeK, et al. Multiple cerebral arteriovenous malformations (AVMs). review of our experience from 203 patients with cerebral vascular lesions[J]. Neuroradiology, 1990, 32(3):207-210. DOI: 10.1007/BF00589113.
[20]PanP, WeinsheimerS, CookeD, et al. Review of treatment and therapeutic targets in brain arteriovenous malformation[J]. J Cereb Blood Flow Metab, 2021, 41(12):3141-3156. DOI: 10.1177/0271678X211026771.
[21]Barbosa Do PradoL, HanC, OhSP, et al. Recent advances in basic research for brain arteriovenous malformation[J]. Int J Mol Sci, 2019, 20(21):5324. DOI: 10.3390/ijms20215324.
[22]ChenW, ChoiEJ, McDougallCM, et al. Brain arteriovenous malformation modeling, pathogenesis, and novel therapeutic targets[J]. Transl Stroke Res, 2014, 5(3):316-329. DOI: 10.1007/s12975-014-0343-0.
[23]KühnelT, WirschingK, WohlgemuthW, et al. Hereditary hemorrhagic telangiectasia[J]. Otolaryngol Clin North Am, 2018, 51(1):237-254. DOI: 10.1016/j.otc.2017.09.017.
[24]FaughnanME, PaldaVA, Garcia-TsaoG, et al. International guidelines for the diagnosis and management of hereditary haemorrhagic telangiectasia[J]. J Med Genet, 2011, 48(2):73-87. DOI: 10.1136/jmg.2009.069013.
[25]GuttmacherAE, MarchukDA, WhiteRI. Hereditary hemorrhagic telangiectasia[J]. N Engl J Med, 1995, 333(14):918-924. DOI: 10.1056/NEJM199510053331407.
[26]KringsT, KimH, PowerS, et al. Neurovascular manifestations in hereditary hemorrhagic telangiectasia: imaging features and genotype-phenotype correlations[J]. AJNR Am J Neuroradiol, 2015, 36(5):863-870. DOI: 10.3174/ajnr.A4210.
[27]SabbàC, PasculliG, LenatoGM, et al. Hereditary hemorrhagic telangiectasia: clinical features in ENG and ALK1 mutation carriers[J]. J Thromb Haemost, 2007, 5(6):1149-1157. DOI: 10.1111/j.1538-7836.2007.02531.x.
[28]GallioneC, AylsworthAS, BeisJ, et al. Overlapping spectra of SMAD4 mutations in juvenile polyposis (JP) and JP-HHT syndrome[J]. Am J Med Genet A, 2010, 152A(2):333-339. DOI: 10.1002/ajmg.a.33206.
[29]SorensenLK, BrookeBS, LiDY, et al. Loss of distinct arterial and venous boundaries in mice lacking endoglin, a vascular-specific TGFbeta coreceptor[J]. Dev Biol, 2003, 261(1):235-250. DOI: 10.1016/s0012-1606(03)00158-1.
[30]UrnessLD, SorensenLK, LiDY. Arteriovenous malformations in mice lacking activin receptor-like kinase-1[J]. Nat Genet, 2000, 26(3):328-331. DOI: 10.1038/81634.
[31]ParkSO, WankhedeM, LeeYJ, et al. Real-time imaging of de novo arteriovenous malformation in a mouse model of hereditary hemorrhagic telangiectasia[J]. J Clin Invest, 2009, 119(11):3487-3496. DOI: 10.1172/JCI39482.
[32]Bayrak-ToydemirP, StevensonDA. Capillary Malformation-Arteriovenous Malformation Syndrome [M]//ADAM MP, FELDMAN J, MIRZAA GM, et al. GeneReviews(®). Seattle (WA); University of Washington, Seattle Copyright © 1993-2023, University of Washington, Seattle. GeneReviews is a registered trademark of the University of Washington, Seattle. All rights reserved. 1993.
[33]LapinskiPE, LubeckBA, ChenD, et al. RASA1 regulates the function of lymphatic vessel valves in mice[J]. J Clin Invest, 2017, 127(7):2569-2585. DOI: 10.1172/JCI89607.
[34]BurrowsPE, Gonzalez-GarayML, RasmussenJC, et al. Lymphatic abnormalities are associated with RASA1 gene mutations in mouse and man[J]. Proc Natl Acad Sci U S A, 2013, 110(21):8621-8626. DOI: 10.1073/pnas.1222722110.
[35]AmyereM, RevencuN, HelaersR, et al. Germline loss-of-function mutations in EPHB4 cause a second form of capillary malformation-arteriovenous malformation (CM-AVM2) deregulating RAS-MAPK signaling[J]. Circulation, 2017, 136(11):1037-1048. DOI: 10.1161/CIRCULATIONAHA.116.026886.
[36]HigaG, PacanowskiJP, JeckDT, et al. Vertebral artery aneurysms and cervical arteriovenous fistulae in patients with neurofibromatosis 1[J]. Vascular, 2010, 18(3):166-177. DOI: 10.2310/6670.2010.00032.
[37]TurnbullMM, HumeniukV, SteinB, et al. Arteriovenous malformations in Cowden syndrome[J]. J Med Genet, 2005, 42(8):e50. DOI: 10.1136/jmg.2004.030569.
[38]NikolaevSI, VetiskaS, BonillaX, et al. Somatic activating KRAS mutations in arteriovenous malformations of the brain[J]. N Engl J Med, 2018, 378(3):250-261. DOI: 10.1056/NEJMoa1709449.
[39]HongT, YanY, LiJ, et al. High prevalence of KRAS/BRAF somatic mutations in brain and spinal cord arteriovenous malformations[J]. Brain, 2019, 142(1):23-34. DOI: 10.1093/brain/awy307.
[40]ParkES, KimS, HuangS, et al. Selective endothelial hyperactivation of oncogenic KRAS induces brain arteriovenous malformations in mice[J]. Ann Neurol, 2021, 89(5):926-941. DOI: 10.1002/ana.26059.
[41]FishJE, Flores SuarezCP, BoudreauE, et al. Somatic gain of KRAS function in the endothelium is sufficient to cause vascular malformations that require MEK but not PI3K signaling[J]. Circ Res, 2020, 127(6):727-743. DOI: 10.1161/CIRCRESAHA.119.316500.
[42]PerataHJ, TomsickTA, TewJM. Feeding artery pedicle aneurysms: association with parenchymal hemorrhage and arteriovenous malformation in the brain[J]. J Neurosurg, 1994, 80(4):631-634. DOI: 10.3171/jns.1994.80.4.0631.
[43]ShankarJJ, MenezesRJ, Pohlmann-EdenB, et al. Angioarchitecture of brain AVM determines the presentation with seizures: proposed scoring system[J]. AJNR Am J Neuroradiol, 2013, 34(5):1028-1034. DOI: 10.3174/ajnr.A3361.
[44]GeibprasertS, PereiraV, KringsT, et al. Hydrocephalus in unruptured brain arteriovenous malformations: pathomechanical considerations, therapeutic implications, and clinical course[J]. J Neurosurg, 2009, 110(3):500-507. DOI: 10.3171/2008.7.JNS0815.
[45]FullertonHJ, AchrolAS, JohnstonSC, et al. Long-term hemorrhage risk in children versus adults with brain arteriovenous malformations[J]. Stroke, 2005, 36(10):2099-2104. DOI: 10.1161/01.STR.0000181746.77149.2b.
[46]MohrJP, Kejda-ScharlerJ, Pile-SpellmanJ. Diagnosis and treatment of arteriovenous malformations[J]. Curr Neurol Neurosci Rep, 2013, 13(2):324. DOI: 10.1007/s11910-012-0324-1.
[47]EvansRW. Diagnostic testing for the evaluation of headaches[J]. Neurol Clin, 1996, 14(1):1-26. DOI: 10.1016/s0733-8619(05)70240-1.
[48]FlemmingKD, LanzinoG. Management of unruptured intracranial aneurysms and cerebrovascular malformations[J]. Continuum (Minneap Minn), 2017, 23(1, Cerebrovascular Disease):181-210. DOI: 10.1212/CON.0000000000000418.
[49]GrossBA, DuR. Natural history of cerebral arteriovenous malformations: a meta-analysis[J]. J Neurosurg, 2013, 118(2):437-443. DOI: 10.3171/2012.10.JNS121280.
[50]KimH, Al-Shahi SalmanR, McCullochCE, et al. Untreated brain arteriovenous malformation: patient-level meta-analysis of hemorrhage predictors[J]. Neurology, 2014, 83(7):590-597. DOI: 10.1212/WNL.0000000000000688.
[51]HernesniemiJA, DashtiR, JuvelaS, et al. Natural history of brain arteriovenous malformations: a long-term follow-up study of risk of hemorrhage in 238 patients[J]. Neurosurgery, 2008, 63(5):823-829; discussion 829-831. DOI: 10.1227/01.NEU.0000330401.82582.5E.
[52]GuoY, SaundersT, SuH, et al. Silent intralesional microhemorrhage as a risk factor for brain arteriovenous malformation rupture[J]. Stroke, 2012, 43(5):1240-1246. DOI: 10.1161/STROKEAHA.111.647263.
[53]da CostaL, WallaceMC, Ter BruggeKG, et al. The natural history and predictive features of hemorrhage from brain arteriovenous malformations[J]. Stroke, 2009, 40(1):100-105. DOI: 10.1161/STROKEAHA.108.524678.
[54]MastH, YoungWL, KoenneckeHC, et al. Risk of spontaneous haemorrhage after diagnosis of cerebral arteriovenous malformation[J]. Lancet, 1997, 350(9084):1065-1068. DOI: 10.1016/s0140-6736(97)05390-7.
[55]StapfC, MastH, SciaccaRR, et al. Predictors of hemorrhage in patients with untreated brain arteriovenous malformation[J]. Neurology, 2006, 66(9):1350-1355. DOI: 10.1212/01.wnl.0000210524.68507.87.
[56]ChenY, HanH, MengX, et al. Development and validation of a scoring system for hemorrhage risk in brain arteriovenous malformations[J]. JAMA Netw Open, 2023, 6(3):e231070. DOI: 10.1001/jamanetworkopen.2023.1070.
[57]ChenY, ChenP, LiR, et al. Rupture-related quantitative hemodynamics of the supratentorial arteriovenous malformation nidus[J]. J Neurosurg, 2023, 138(3):740-749. DOI: 10.3171/2022.6.JNS212818.
[58]BurkhardtJK, ChenX, WinklerEA, et al. Delayed venous drainage in ruptured arteriovenous malformations based on quantitative color-coded digital subtraction angiography[J]. World Neurosurg, 2017, 104:619-627. DOI: 10.1016/j.wneu.2017.04.120.
[59]ChoiJH, MastH, SciaccaRR, et al. Clinical outcome after first and recurrent hemorrhage in patients with untreated brain arteriovenous malformation[J]. Stroke, 2006, 37(5):1243-1247. DOI: 10.1161/01.STR.0000217970.18319.7d.
[60]van BeijnumJ, LovelockCE, CordonnierC, et al. Outcome after spontaneous and arteriovenous malformation-related intracerebral haemorrhage: population-based studies[J]. Brain, 2009, 132(Pt 2):537-543. DOI: 10.1093/brain/awn318.
[61]RutledgeC, CookeDL, HettsSW, et al. Brain arteriovenous malformations[J]. Handb Clin Neurol, 2021, 176:171-178. DOI: 10.1016/B978-0-444-64034-5.00020-1.
[62]Al-Shahi SalmanR. The outlook for adults with epileptic seizure(s) associated with cerebral cavernous malformations or arteriovenous malformations[J]. Epilepsia, 2012, 53 Suppl 4∶34-42. DOI: 10.1111/j.1528-1167.2012.03611.x.
[63]HortonJC, ChambersWA, LyonsSL, et al. Pregnancy and the risk of hemorrhage from cerebral arteriovenous malformations[J]. Neurosurgery, 1990, 27(6):867-871; discussion 871-872. DOI: 10.1097/00006123-199012000-00002.
[64]LiuXJ, WangS, ZhaoYL, et al. Risk of cerebral arteriovenous malformation rupture during pregnancy and puerperium[J]. Neurology, 2014, 82(20):1798-1803. DOI: 10.1212/WNL.0000000000000436.
[65]GrossBA, DuR. Hemorrhage from arteriovenous malformations during pregnancy[J]. Neurosurgery, 2012, 71(2):349-355; discussion 355-356. DOI: 10.1227/NEU.0b013e318256c34b.
[66]PorrasJL, YangW, PhiladelphiaE, et al. Hemorrhage risk of brain arteriovenous malformations during pregnancy and puerperium in a North American cohort[J]. Stroke, 2017, 48(6):1507-1513. DOI: 10.1161/STROKEAHA.117.016828.
[67]SharsharT, LamyC, MasJL. Incidence and causes of strokes associated with pregnancy and puerperium. A study in public hospitals of Ile de France. Stroke in Pregnancy Study Group[J]. Stroke, 1995, 26(6):930-936. DOI: 10.1161/01.str.26.6.930.
[68]KittnerSJ, SternBJ, FeeserBR, et al. Pregnancy and the risk of stroke[J]. N Engl J Med, 1996, 335(11):768-774. DOI: 10.1056/NEJM199609123351102.
[69]ZhuD, ZhaoP, LvN, et al. Rupture risk of cerebral arteriovenous malformations during pregnancy and puerperium: a single-center experience and pooled data analysis[J]. World Neurosurg, 2018, 111:e308-e315. DOI: 10.1016/j.wneu.2017.12.056.
[70]AmiasAG. Cerebral vascular disease in pregnancy. I. Haemorrhage[J]. J Obstet Gynaecol Br Commonw, 1970, 77(2):100-120. DOI: 10.1111/j.1471-0528.1970.tb03487.x.
[71]RobinsonJL, HallCJ, SedzimirCB. Subarachnoid hemorrhage in pregnancy[J]. J Neurosurg, 1972, 36(1):27-33. DOI: 10.3171/jns.1972.36.1.0027.
[72]SadasivanB, MalikGM, LeeC, et al. Vascular malformations and pregnancy[J]. Surg Neurol, 1990, 33(5):305-313. DOI: 10.1016/0090-3019(90)90197-w.
[73]OgilvyCS, StiegPE, AwadI, et al. Recommendations for the management of intracranial arteriovenous malformations: a statement for healthcare professionals from a special writing group of the Stroke Council, American Stroke Association[J]. Circulation, 2001, 103(21):2644-2657. DOI: 10.1161/01.cir.103.21.2644.
[74]CanA, DuR. Neurosurgical Issues in Pregnancy[J]. Semin Neurol, 2017, 37(6):689-693. DOI: 10.1055/s-0037-1607430.
[75]LvX, LiW, HeH, et al. Known and unknown cerebral arteriovenous malformations in pregnancies: haemorrhage risk and influence on obstetric management[J]. Neuroradiol J,. DOI: 10.1177/1971400917712264.
[76]JosephNK, KumarS, BrownRD, et al. Influence of Pregnancy on Hemorrhage Risk in Women With Cerebral and Spinal Cavernous Malformations[J]. Stroke, 2021, 52(2):434-441. DOI: 10.1161/STROKEAHA.120.031761.
[77]DerdeynCP, ZipfelGJ, AlbuquerqueFC, et al. Management of brain arteriovenous malformations: a scientific statement for healthcare professionals from the American Heart Association/American Stroke Association[J]. Stroke, 2017, 48(8):e200-e224. DOI: 10.1161/STR.0000000000000134.
[78]BrazzelliM, SandercockPA, ChappellFM, et al. Magnetic resonance imaging versus computed tomography for detection of acute vascular lesions in patients presenting with stroke symptoms[J]. Cochrane Database Syst Rev, 2009, (4):CD007424. DOI: 10.1002/14651858.CD007424.pub2.
[79]Delgado AlmandozJE, SchaeferPW, ForeroNP, et al. Diagnostic accuracy and yield of multidetector CT angiography in the evaluation of spontaneous intraparenchymal cerebral hemorrhage[J]. AJNR Am J Neuroradiol, 2009, 30(6):1213-1221. DOI: 10.3174/ajnr.A1546.
[80]CordonnierC, Al-Shahi SalmanR, BhattacharyaJJ, et al. Differences between intracranial vascular malformation types in the characteristics of their presenting haemorrhages: prospective, population-based study[J]. J Neurol Neurosurg Psychiatry, 2008, 79(1):47-51. DOI: 10.1136/jnnp.2006.113753.
[81]CordonnierC, KlijnCJ, van BeijnumJ, et al. Radiological investigation of spontaneous intracerebral hemorrhage: systematic review and trinational survey[J]. Stroke, 2010, 41(4):685-690. DOI: 10.1161/STROKEAHA.109.572495.
[82]KimDJ, KringsT. Whole-brain perfusion CT patterns of brain arteriovenous malformations: a pilot study in 18 patients[J]. AJNR Am J Neuroradiol, 2011, 32(11):2061-2066. DOI: 10.3174/ajnr.A2659.
[83]SanelliPC, MifsudMJ, StiegPE. Role of CT angiography in guiding management decisions of newly diagnosed and residual arteriovenous malformations[J]. AJR Am J Roentgenol, 2004, 183(4):1123-1126. DOI: 10.2214/ajr.183.4.1831123.
[84]JosephsonCB, WhitePM, KrishanA, et al. Computed tomography angiography or magnetic resonance angiography for detection of intracranial vascular malformations in patients with intracerebral haemorrhage[J]. Cochrane Database Syst Rev, 2014, 2014(9):CD009372. DOI: 10.1002/14651858.CD009372.pub2.
[85]GoddardAJ, TanG, BeckerJ. Computed tomography angiography for the detection and characterization of intra-cranial aneurysms: current status[J]. Clin Radiol, 2005, 60(12):1221-1236. DOI: 10.1016/j.crad.2005.06.007.
[86]LinnJ, Ertl-WagnerB, SeelosKC, et al. Diagnostic value of multidetector-row CT angiography in the evaluation of thrombosis of the cerebral venous sinuses[J]. AJNR Am J Neuroradiol, 2007, 28(5):946-952.
[87]WillemsPW, TaeshineetanakulP, SchenkB, et al. The use of 4D-CTA in the diagnostic work-up of brain arteriovenous malformations[J]. Neuroradiology, 2012, 54(2):123-131. DOI: 10.1007/s00234-011-0864-0.
[88]IdeS, HiraiT, MoriokaM, et al. Usefulness of 3D DSA-MR fusion imaging in the pretreatment evaluation of brain arteriovenous malformations[J]. Acad Radiol, 2012, 19(11):1345-1352. DOI: 10.1016/j.acra.2012.07.001.
[89]HadizadehDR, KukukGM, SteckDT, et al. Noninvasive evaluation of cerebral arteriovenous malformations by 4D-MRA for preoperative planning and postoperative follow-up in 56 patients: comparison with DSA and intraoperative findings[J]. AJNR Am J Neuroradiol, 2012, 33(6):1095-1101. DOI: 10.3174/ajnr.A2921.
[90]MachetA, PortefaixC, KadziolkaK, et al. Brain arteriovenous malformation diagnosis: value of time-resolved contrast-enhanced MR angiography at 3.0T compared to DSA[J]. Neuroradiology, 2012, 54(10):1099-1108. DOI: 10.1007/s00234-012-1024-x.
[91]YuS, YanL, YaoY, et al. Noncontrast dynamic MRA in intracranial arteriovenous malformation (AVM), comparison with time of flight (TOF) and digital subtraction angiography (DSA)[J]. Magn Reson Imaging, 2012, 30(6):869-877. DOI: 10.1016/j.mri.2012.02.027.
[92]XuJ, ShiD, ChenC, et al. Noncontrast-enhanced four-dimensional MR angiography for the evaluation of cerebral arteriovenous malformation: a preliminary trial[J]. J Magn Reson Imaging, 2011, 34(5):1199-1205. DOI: 10.1002/jmri.22699.
[93]Pathological correlates of late-onset dementia in a multicentre, community-based population in England and Wales. Neuropathology Group of the Medical Research Council Cognitive Function and Ageing Study (MRC CFAS)[J]. Lancet, 2001, 357(9251):169-175. DOI: 10.1016/s0140-6736(00)03589-3.
[94]KakizawaY, NagashimaH, OyaF, et al. Compartments in arteriovenous malformation nidi demonstrated with rotational three-dimensional digital subtraction angiography by using selective microcatheterization. Report of three cases[J]. J Neurosurg, 2002, 96(4):770-774. DOI: 10.3171/jns.2002.96.4.0770.
[95]GailloudP, OishiS, CarpenterJ, et al. Three-dimensional digital angiography: new tool for simultaneous three-dimensional rendering of vascular and osseous information during rotational angiography[J]. AJNR Am J Neuroradiol, 2004, 25(4):571-573.
[96]CloftHJ, JosephGJ, DionJE. Risk of cerebral angiography in patients with subarachnoid hemorrhage, cerebral aneurysm, and arteriovenous malformation: a meta-analysis[J]. Stroke, 1999, 30(2):317-320. DOI: 10.1161/01.str.30.2.317.
[97]AlexanderMD, OliffMC, OlorunsolaOG, et al. Patient radiation exposure during diagnostic and therapeutic interventional neuroradiology procedures[J]. J Neurointerv Surg, 2010, 2(1):6-10. DOI: 10.1136/jnis.2009.000802.
[98]ChenX, CookeDL, SalonerD, et al. Higher flow is present in unruptured arteriovenous malformations with silent intralesional microhemorrhages[J]. Stroke, 2017, 48(10):2881-2884. DOI: 10.1161/STROKEAHA.117.017785.
[99]BhattacharyaJJ, LuoCB, SuhDC, et al. Wyburn-Mason or Bonnet-Dechaume-Blanc as cerebrofacial arteriovenous metameric syndromes (CAMS). A new concept and a new classification[J]. Interv Neuroradiol, 2001, 7(1):5-17. DOI: 10.1177/159101990100700101.
[100]MonizE.L′encéphalographie arterielle, son importance dans la localisation des tumeurs cérébrales[J]. Rev Neurol, 1927, 2: 72-89.
[101]KretzerRM, CoonAL, TamargoRJ. Walter E. Dandy′s contributions to vascular neurosurgery[J]. J Neurosurg, 2010, 112(6):1182-1191. DOI: 10.3171/2009.7.JNS09737.
[102]YaşargilMG. Intracranial microsurgery[J]. Clin Neurosurg, 1970, 17:250-256. DOI: 10.1093/neurosurgery/17.cn_suppl_1.250.
[103]SattariSA, ShahbandiA, YangW, et al. Microsurgery versus microsurgery with preoperative embolization for brain arteriovenous malformation treatment: a systematic review and meta-analysis[J]. Neurosurgery, 2023, 92(1):27-41. DOI: 10.1227/neu.0000000000002171.
[104]SpetzlerRF, MartinNA. A proposed grading system for arteriovenous malformations[J]. J Neurosurg, 1986, 65(4):476-483. DOI: 10.3171/jns.1986.65.4.0476.
[105]SpetzlerRF, PonceFA. A 3-tier classification of cerebral arteriovenous malformations. Clinical article[J]. J Neurosurg, 2011, 114(3):842-849. DOI: 10.3171/2010.8.JNS10663.
[106]KorjaM, BerviniD, AssaadN, et al. Role of surgery in the management of brain arteriovenous malformations: prospective cohort study[J]. Stroke, 2014, 45(12):3549-3555. DOI: 10.1161/STROKEAHA.114.007206.
[107]MorganMK, WiedmannM, AssaadNN, et al. Complication-effectiveness analysis for brain arteriovenous malformation surgery: a prospective cohort study[J]. Neurosurgery, 2016, 79(1):47-57. DOI: 10.1227/NEU.0000000000001144.
[108]LawtonMT. Spetzler-Martin Grade III arteriovenous malformations: surgical results and a modification of the grading scale[J]. Neurosurgery, 2003, 52(4):740-748; discussion 748-749. DOI: 10.1227/01.neu.0000053220.02268.9c.
[109]ViñuelaF, DionJE, DuckwilerG, et al. Combined endovascular embolization and surgery in the management of cerebral arteriovenous malformations: experience with 101 cases[J]. J Neurosurg, 1991, 75(6):856-864. DOI: 10.3171/jns.1991.75.6.0856.
[110]JafarJJ, DavisAJ, BerensteinA, et al. The effect of embolization with N-butyl cyanoacrylate prior to surgical resection of cerebral arteriovenous malformations[J]. J Neurosurg, 1993, 78(1):60-69. DOI: 10.3171/jns.1993.78.1.0060.
[111]DeMerittJS, Pile-SpellmanJ, MastH, et al. Outcome analysis of preoperative embolization with N-butyl cyanoacrylate in cerebral arteriovenous malformations[J]. AJNR Am J Neuroradiol, 1995, 16(9):1801-1807.
[112]Gutiérrez-GonzálezR, GilA, SernaC, et al. Normal perfusion pressure breakthrough phenomenon: what still remains unknown[J]. Br J Neurosurg, 2012, 26(3):403-405. DOI: 10.3109/02688697.2011.633637.
[113]SpetzlerRF, WilsonCB, WeinsteinP, et al. Normal perfusion pressure breakthrough theory[J]. Clin Neurosurg, 1978, 25:651-672. DOI: 10.1093/neurosurgery/25.cn_suppl_1.651.
[114]Liebman KmRR. The hemodynamic changes measured in cerebral arterio-venous malformations following endovascular treatment [J]. J Neurovasc Dis, 1997,
[115]LinF, WuJ, ZhaoB, et al. Preoperative functional findings and surgical outcomes in patients with motor cortical arteriovenous malformation[J]. World Neurosurg, 2016, 85:273-281. DOI: 10.1016/j.wneu.2015.10.002.
[116]EllisMJ, RutkaJT, KulkarniAV, et al. Corticospinal tract mapping in children with ruptured arteriovenous malformations using functionally guided diffusion-tensor imaging[J]. J Neurosurg Pediatr, 2012, 9(5):505-510. DOI: 10.3171/2012.1.PEDS11363.
[117]RussellSM, WooHH, JosefferSS, et al. Role of frameless stereotaxy in the surgical treatment of cerebral arteriovenous malformations: technique and outcomes in a controlled study of 44 consecutive patients[J]. Neurosurgery, 2002, 51(5):1108-1116; discussion 1116-1118. DOI: 10.1097/00006123-200211000-00002.
[118]PostN, RussellSM, HuangP, et al. Frame-based stereotactic resection of subcentimeter arteriovenous malformations in deep or eloquent regions of the brain: indications and technique with eight consecutive operations[J]. Minim Invasive Neurosurg, 2008, 51(2):114-118. DOI: 10.1055/s-2007-1022532.
[119]MunshiI, MacdonaldRL, WeirBK. Intraoperative angiography of brain arteriovenous malformations[J]. Neurosurgery, 1999, 45(3):491-497; discussion 497-499. DOI: 10.1097/00006123-199909000-00016.
[120]ZaidiHA, AblaAA, NakajiP, et al. Indocyanine green angiography in the surgical management of cerebral arteriovenous malformations: lessons learned in 130 consecutive cases[J]. Neurosurgery, 2014, 10 Suppl 2∶246-251; discussion 251. DOI: 10.1227/NEU.0000000000000318.
[121]BilbaoCJ, BhallaT, DalalS, et al. Comparison of indocyanine green fluorescent angiography to digital subtraction angiography in brain arteriovenous malformation surgery[J]. Acta Neurochir (Wien), 2015, 157(3):351-359. DOI: 10.1007/s00701-014-2287-2.
[122]林发, 王明泽, 仇汉诚, 等. 一站式复合手术对后循环参与供血的脑动静脉畸形手术风险和预后的影响[J]. 中华医学杂志, 2022, 102(21):1614-1620. DOI: 10.3760/cma.j.cn112137-20210910-02061.
[123]BarkerFG, ButlerWE, LyonsS, et al. Dose-volume prediction of radiation-related complications after proton beam radiosurgery for cerebral arteriovenous malformations[J]. J Neurosurg, 2003, 99(2):254-263. DOI: 10.3171/jns.2003.99.2.0254.
[124]SteinerL, LeksellL, GreitzT, et al. Stereotaxic radiosurgery for cerebral arteriovenous malformations. Report of a case [J]. Acta Chir Scand, 1972, 138(5): 459-464.
[125]AltschulerEM, LunsfordLD, CoffeyRJ, et al. Gamma knife radiosurgery for intracranial arteriovenous malformations in childhood and adolescence[J]. Pediatr Neurosci, 1989, 15(2):53-61. DOI: 10.1159/000120443.
[126]Skjøth-RasmussenJ, RoedH, OhlhuesL, et al. Complications following linear accelerator based stereotactic radiation for cerebral arteriovenous malformations[J]. Int J Radiat Oncol Biol Phys, 2010, 77(2):542-547. DOI: 10.1016/j.ijrobp.2009.05.048.
[127]FriedmanWA, BovaFJ, MendenhallWM. Linear accelerator radiosurgery for arteriovenous malformations: the relationship of size to outcome[J]. J Neurosurg, 1995, 82(2):180-189. DOI: 10.3171/jns.1995.82.2.0180.
[128]ColomboF, CavedonC, CasentiniL, et al. Early results of CyberKnife radiosurgery for arteriovenous malformations[J]. J Neurosurg, 2009, 111(4):807-819. DOI: 10.3171/2008.10.JNS08749.
[129]OermannEK, MurthyN, ChenV, et al. A multicenter retrospective study of frameless robotic radiosurgery for intracranial arteriovenous malformation[J]. Front Oncol, 2014, 4:298. DOI: 10.3389/fonc.2014.00298.
[130]NiwaR, IchiS, NomuraR, et al. Hypofractionated stereotactic radiotherapy with CyberKnife for large arteriovenous malformations and arteriovenous malformations located in eloquent areas[J]. Neurol Med Chir (Tokyo), 2022, 62(10):445-450. DOI: 10.2176/jns-nmc.2022-0033.
[131]PunyawaiP, RadomsutthikulN, DhanachaiM, et al. Long-term outcomes of 170 brain arteriovenous malformations treated by frameless image-guided robotic stereotactic radiosurgery: ramathibodi hospital experience[J]. Medicine (Baltimore), 2021, 100(19):e25752. DOI: 10.1097/MD.0000000000025752.
[132]BlamekS, TarnawskiR, MiszczykL. Linac-based stereotactic radiosurgery for brain arteriovenous malformations[J]. Clin Oncol (R Coll Radiol), 2011, 23(8):525-531. DOI: 10.1016/j.clon.2011.03.012.
[133]DingD, YenCP, StarkeRM, et al. Effect of prior hemorrhage on intracranial arteriovenous malformation radiosurgery outcomes[J]. Cerebrovasc Dis, 2015, 39(1):53-62. DOI: 10.1159/000369959.
[134]IlyasA, ChenCJ, DingD, et al. Radiation-induced changes after stereotactic radiosurgery for brain arteriovenous malformations: a systematic review and meta-analysis[J]. Neurosurgery, 2018, 83(3): 365-376.DOI: 10.1093/neuros/nyx502.
[135]DingD, StarkeRM, LiuKC, et al. Cortical plasticity in patients with cerebral arteriovenous malformations[J]. J Clin Neurosci, 2015, 22(12):1857-1861. DOI: 10.1016/j.jocn.2015.06.014.
[136]BörcekA, ÇeltikçiE, AksoğanY, et al. Clinical outcomes of stereotactic radiosurgery for cerebral arteriovenous malformations in pediatric patients: systematic review and meta-analysis [J]. Neurosurgery, 2019, 85(4): E629-E640.DOI: 10.1093/neuros/nyz146.
[137]StarkeRM, YenCP, DingD, et al. A practical grading scale for predicting outcome after radiosurgery for arteriovenous malformations: analysis of 1012 treated patients[J]. J Neurosurg, 2013, 119(4):981-987. DOI: 10.3171/2013.5.JNS1311.
[138]AoyamaH, ShiratoH, NishiokaT, et al. Treatment outcome of single or hypofractionated single-isocentric stereotactic irradiation (STI) using a linear accelerator for intracranial arteriovenous malformation[J]. Radiother Oncol, 2001, 59(3):323-328. DOI: 10.1016/s0167-8140(01)00303-6.
[139]YamamotoM, AkabaneA, MatsumaruY, et al. Long-term follow-up results of intentional 2-stage Gamma Knife surgery with an interval of at least 3 years for arteriovenous malformations larger than 10 cm³[J]. J Neurosurg, 2012, 117 Suppl:126-134. DOI: 10.3171/2012.6.GKS12757.
[140]DingD, StarkeRM, KanoH, et al. Stereotactic radiosurgery for Spetzler-Martin Grade III arteriovenous malformations: an international multicenter study[J]. J Neurosurg, 2017, 126(3):859-871. DOI: 10.3171/2016.1.JNS152564.
[141]FirlikAD, LevyEI, KondziolkaD, et al. Staged volume radiosurgery followed by microsurgical resection: a novel treatment for giant cerebral arteriovenous malformations: technical case report[J]. Neurosurgery, 1998, 43(5):1223-1228. DOI: 10.1097/00006123-199811000-00124.
[142]SirinS, KondziolkaD, NiranjanA, et al. Prospective staged volume radiosurgery for large arteriovenous malformations: indications and outcomes in otherwise untreatable patients[J]. Neurosurgery, 2006, 58(1):17-27; discussion 17-27. DOI: 10.1227/01.neu.0000190653.42970.6b.
[143]SeymourZA, ChanJW, SneedPK, et al. Dose response and architecture in volume staged radiosurgery for large arteriovenous malformations: A multi-institutional study[J]. Radiother Oncol, 2020, 144:180-188. DOI: 10.1016/j.radonc.2019.09.019.
[144]PollockBE, LinkMJ, StaffordSL, et al. Volume-staged stereotactic radiosurgery for intracranial arteriovenous malformations: outcomes based on an 18-year experience [J]. Neurosurgery, 2017, 80(4): 543-550.DOI: 10.1093/neuros/nyw107.
[145]FooteKD, FriedmanWA, EllisTL, et al. Salvage retreatment after failure of radiosurgery in patients with arteriovenous malformations[J]. J Neurosurg, 2003, 98(2):337-341. DOI: 10.3171/jns.2003.98.2.0337.
[146]ParkHR, LeeJM, KimJW, et al. Time-staged gamma knife stereotactic radiosurgery for large cerebral arteriovenous malformations: a preliminary report[J]. PLoS One, 2016, 11(11):e0165783. DOI: 10.1371/journal.pone.0165783.
[147]LunsfordLD, KondziolkaD, FlickingerJC, et al. Stereotactic radiosurgery for arteriovenous malformations of the brain[J]. J Neurosurg, 1991, 75(4):512-524. DOI: 10.3171/jns.1991.75.4.0512.
[148]SteinerL, LindquistC, AdlerJR, et al. Clinical outcome of radiosurgery for cerebral arteriovenous malformations[J]. J Neurosurg, 1992, 77(1):1-8. DOI: 10.3171/jns.1992.77.1.0001.
[149]ColomboF, PozzaF, ChieregoG, et al. Linear accelerator radiosurgery of cerebral arteriovenous malformations: an update[J]. Neurosurgery, 1994, 34(1):14-20; discussion 20-21.
[150]Cohen-InbarO, StarkeRM, KanoH, et al. Stereotactic radiosurgery for cerebellar arteriovenous malformations: an international multicenter study[J]. J Neurosurg, 2017, 127(3):512-521. DOI: 10.3171/2016.7.JNS161208.
[151]PatibandlaMR, DingD, KanoH, et al. Stereotactic radiosurgery for Spetzler-Martin Grade IV and V arteriovenous malformations: an international multicenter study[J]. J Neurosurg, 2018, 129(2):498-507. DOI: 10.3171/2017.3.JNS162635.
[152]HasegawaT, KatoT, NaitoT, et al. Long-term risks of hemorrhage and adverse radiation effects of stereotactic radiosurgery for brain arteriovenous malformations[J]. Neurosurgery, 2022, 90(6):784-792. DOI: 10.1227/neu.0000000000001913.
[153]ChenCJ, DingD, LeeCC, et al. Stereotactic radiosurgery with versus without embolization for brain arteriovenous malformations[J]. Neurosurgery, 2021, 88(2): 313-321.DOI: 10.1093/neuros/nyaa418
[154]HasegawaT, KatoT, NaitoT, et al. Effect of embolization before stereotactic radiosurgery for brain arteriovenous malformations: a case-control study with propensity score matching[J]. J Neurosurg, 2023, 138(4):955-961. DOI: 10.3171/2022.7.JNS221343.
[155]de OliveiraE, TedeschiH, RasoJ. Comprehensive management of arteriovenous malformations[J]. Neurol Res, 1998, 20(8):673-683. DOI: 10.1080/01616412.1998.11740583.
[156]KarlssonB, LindquistC, SteinerL. Prediction of obliteration after gamma knife surgery for cerebral arteriovenous malformations[J]. Neurosurgery, 1997, 40(3):425-430; discussion 430-431. DOI: 10.1097/00006123-199703000-00001.
[157]SchwartzM, SixelK, YoungC, et al. Prediction of obliteration of arteriovenous malformations after radiosurgery: the obliteration prediction index[J]. Can J Neurol Sci, 1997, 24(2):106-109. DOI: 10.1017/s0317167100021417.
[158]PollockBE, FlickingerJC. A proposed radiosurgery-based grading system for arteriovenous malformations[J]. J Neurosurg, 2002, 96(1):79-85. DOI: 10.3171/jns.2002.96.1.0079.
[159]PollockBE, FlickingerJC. Modification of the radiosurgery-based arteriovenous malformation grading system[J]. Neurosurgery, 2008, 63(2):239-243; discussion 243. DOI: 10.1227/01.NEU.0000315861.24920.92.
[160]SeifertV, StolkeD, MehdornHM, et al. Clinical and radiological evaluation of long-term results of stereotactic proton beam radiosurgery in patients with cerebral arteriovenous malformations[J]. J Neurosurg, 1994, 81(5):683-689. DOI: 10.3171/jns.1994.81.5.0683.
[161]SunDQ, CarsonKA, RazaSM, et al. The radiosurgical treatment of arteriovenous malformations: obliteration, morbidities, and performance status[J]. Int J Radiat Oncol Biol Phys, 2011, 80(2):354-361. DOI: 10.1016/j.ijrobp.2010.01.049.
[162]FlickingerJC, KondziolkaD, MaitzAH, et al. An analysis of the dose-response for arteriovenous malformation radiosurgery and other factors affecting obliteration[J]. Radiother Oncol, 2002, 63(3):347-354. DOI: 10.1016/s0167-8140(02)00103-2.
[163]BowdenG, CavaleriJ, KanoH, et al. Radiosurgery for arteriovenous malformations and the impact on headaches[J]. Headache, 2017, 57(5):737-745. DOI: 10.1111/head.13055.
[164]PrzybylowskiCJ, DingD, StarkeRM, et al. Seizure and anticonvulsant outcomes following stereotactic radiosurgery for intracranial arteriovenous malformations[J]. J Neurosurg, 2015, 122(6):1299-1305. DOI: 10.3171/2014.11.JNS141388.
[165]PollockBE, KondziolkaD, FlickingerJC, et al. Magnetic resonance imaging: an accurate method to evaluate arteriovenous malformations after stereotactic radiosurgery[J]. J Neurosurg, 1996, 85(6):1044-1049. DOI: 10.3171/jns.1996.85.6.1044.
[166]FlickingerJC, KondziolkaD, LunsfordLD, et al. Development of a model to predict permanent symptomatic postradiosurgery injury for arteriovenous malformation patients. Arteriovenous Malformation Radiosurgery Study Group[J]. Int J Radiat Oncol Biol Phys, 2000, 46(5):1143-1148. DOI: 10.1016/s0360-3016(99)00513-1.
[167]CetinIA, AtesR, DhaensJ, et al. Retrospective analysis of linac-based radiosurgery for arteriovenous malformations and testing of the Flickinger formula in predicting radiation injury[J]. Strahlenther Onkol, 2012, 188(12):1133-1138. DOI: 10.1007/s00066-012-0180-6.
[168]FlickingerJC, KondziolkaD, LunsfordLD, et al. A multi-institutional analysis of complication outcomes after arteriovenous malformation radiosurgery[J]. Int J Radiat Oncol Biol Phys, 1999, 44(1):67-74. DOI: 10.1016/s0360-3016(98)00518-5.
[169]HaraM, NakamuraM, ShiokawaY, et al. Delayed cyst formation after radiosurgery for cerebral arteriovenous malformation: two case reports[J]. Minim Invasive Neurosurg, 1998, 41(1):40-45. DOI: 10.1055/s-2008-1052014.
[170]KanoH, FlickingerJC, TonettiD, et al. Estimating the risks of adverse radiation effects after gamma knife radiosurgery for arteriovenous malformations[J]. Stroke, 2017, 48(1):84-90. DOI: 10.1161/STROKEAHA.116.014825.
[171]IzawaM, HayashiM, ChernovM, et al. Long-term complications after gamma knife surgery for arteriovenous malformations[J]. J Neurosurg, 2005, 102 Suppl:34-37. DOI: 10.3171/jns.2005.102.s_supplement.0034.
[172]LUESSENHOPAJ, SPENCEWT. Artificial embolization of cerebral arteries. Report of use in a case of arteriovenous malformation[J]. J Am Med Assoc, 1960, 172:1153-1155. DOI: 10.1001/jama.1960.63020110001009.
[173]DoppmanJL, ZapolW, PierceJ. Transcatheter embolization with a silicone rubber preparation. Experimental observations[J]. Invest Radiol, 1971, 6(5):304-309. DOI: 10.1097/00004424-197109000-00002.
[174]KerberC. Balloon catheter with a calibrated leak. A new system for superselective angiography and occlusive catheter therapy[J]. Radiology, 1976, 120(3):547-550. DOI: 10.1148/120.3.547.
[175]Fernández-AlvarezV, SuárezC, de BreeR, et al. Management of extracranial arteriovenous malformations of the head and neck[J]. Auris Nasus Larynx, 2020, 47(2):181-190. DOI: 10.1016/j.anl.2019.11.008.
[176]YuSC, ChanMS, LamJM, et al. Complete obliteration of intracranial arteriovenous malformation with endovascular cyanoacrylate embolization: initial success and rate of permanent cure[J]. AJNR Am J Neuroradiol, 2004, 25(7):1139-1143.
[177]PierotL, CognardC, HerbreteauD, et al. Endovascular treatment of brain arteriovenous malformations using a liquid embolic agent: results of a prospective, multicentre study (BRAVO)[J]. Eur Radiol, 2013, 23(10):2838-2845. DOI: 10.1007/s00330-013-2870-6.
[178]DurstCR, StarkeRM, GaughenJ, et al. A method for complete angiographic obliteration of a brain arteriovenous malformation in a single session through a single pedicle[J]. J Clin Neurosci, 2015, 22(2):391-395. DOI: 10.1016/j.jocn.2014.07.030.
[179]WillinskyR, GoyalM, TerbruggeK, et al. Embolisation of small (<3 cm) brain arteriovenous malformations. correlation of angiographic results to a proposed angioarchitecture grading system[J]. Interv Neuroradiol, 2001, 7(1):19-27. DOI: 10.1177/159101990100700102.
[180]DmytriwAA, Ter BruggeKG, KringsT, et al. Endovascular treatment of head and neck arteriovenous malformations[J]. Neuroradiology, 2014, 56(3):227-236. DOI: 10.1007/s00234-014-1328-0.
[181]HakJF, BoulouisG, KerlerouxB, et al. Pediatric brain arteriovenous malformation recurrence: a cohort study, systematic review and meta-analysis[J]. J Neurointerv Surg, 2022, 14(6):611-617. DOI: 10.1136/neurintsurg-2021-017777.
[182]HeY, BaiW, LiT, et al. Curative transvenous embolization for ruptured brain arteriovenous malformations: a single-center experience from China[J]. World Neurosurg, 2018, 116:e421-e428. DOI: 10.1016/j.wneu.2018.04.223.
[183]FangYB, ByunJS, LiuJM, et al. Transvenous embolization of brain arteriovenous malformations: a systematic review and meta-analysis[J]. J Neurosurg Sci, 2019, 63(4):468-472. DOI: 10.23736/S0390-5616.18.04342-4.
[184]KoyanagiM, MosimannPJ, NordmeyerH, et al. The transvenous retrograde pressure cooker technique for the curative embolization of high-grade brain arteriovenous malformations[J]. J Neurointerv Surg, 2021, 13(7):637-641. DOI: 10.1136/neurintsurg-2020-016566.
[185]BatistaS, Almeida FilhoJA, OliveiraLB, et al. Evaluating the safety and efficacy of transvenous embolization for brain arteriovenous malformation: a systematic review and meta-analysis[J]. Interv Neuroradiol, 2023:15910199231204922. DOI: 10.1177/15910199231204922.
[186]ChenCJ, NoratP, DingD, et al. Transvenous embolization of brain arteriovenous malformations: a review of techniques, indications, and outcomes[J]. Neurosurg Focus, 2018, 45(1):E13. DOI: 10.3171/2018.3.FOCUS18113.
[187]HeY, DingY, BaiW, et al. Safety and efficacy of transvenous embolization of ruptured brain arteriovenous malformations as a last resort: a prospective single-arm study[J]. AJNR Am J Neuroradiol, 2019, 40(10):1744-1751. DOI: 10.3174/ajnr.A6197.
[188]VianaDC, de Castro-AfonsoLH, NakiriGS, et al. Extending the indications for transvenous approach embolization for superficial brain arteriovenous malformations[J]. J Neurointerv Surg, 2017, 9(11):1053-1059. DOI: 10.1136/neurintsurg-2017-013113.
[189]ChapotR, StrackeP, VelascoA, et al. The pressure cooker technique for the treatment of brain AVMs[J]. J Neuroradiol, 2014, 41(1):87-91. DOI: 10.1016/j.neurad.2013.10.001.
[190]AbudDG, de Castro-AfonsoLH, NakiriGS, et al. Modified pressure cooker technique: an easier way to control onyx reflux[J]. J Neuroradiol, 2016, 43(3):218-222. DOI: 10.1016/j.neurad.2016.01.146.
[191]PereiraVM, Marcos-GonzalezA, RadovanovicI, et al. Transvenous embolization of a ruptured deep cerebral arteriovenous malformation. A technical note[J]. Interv Neuroradiol, 2013, 19(1):27-34. DOI: 10.1177/159101991301900104.
[192]MaimonS, StraussI, FrolovV, et al. Brain arteriovenous malformation treatment using a combination of Onyx and a new detachable tip microcatheter, SONIC: short-term results[J]. AJNR Am J Neuroradiol, 2010, 31(5):947-954. DOI: 10.3174/ajnr.A1959.
[193]KringsT, HansFJ, GeibprasertS, et al. Partial "targeted" embolisation of brain arteriovenous malformations[J]. Eur Radiol, 2010, 20(11):2723-2731. DOI: 10.1007/s00330-010-1834-3.
[194]BrownRD, WiebersDO, ForbesGS. Unruptured intracranial aneurysms and arteriovenous malformations: frequency of intracranial hemorrhage and relationship of lesions[J]. J Neurosurg, 1990, 73(6):859-863. DOI: 10.3171/jns.1990.73.6.0859.
[195]AlexanderMD, HippeDS, CookeDL, et al. targeted embolization of aneurysms associated with brain arteriovenous malformations at high risk for surgical resection: a case-control study [J]. Neurosurgery, 2018, 82(3): 343-349.DOI: 10.1093/neuros/nyx167
[196]XiaochuanH, YuhuaJ, XianliL, et al. Targeted embolization reduces hemorrhage complications in partially embolized cerebral AVM combined with gamma knife surgery[J]. Interv Neuroradiol, 2015, 21(1):80-87. DOI: 10.15274/inr-2014-10090.
[197]PierotL, KadziolkaK, LitréF, et al. Combined treatment of brain AVMs with use of Onyx embolization followed by radiosurgery[J]. AJNR Am J Neuroradiol, 2013, 34(7):1395-1400. DOI: 10.3174/ajnr.A3409.
[198]LvX, WuZ, LiY, et al. Hemorrhage risk after partial endovascular NBCA and ONYX embolization for brain arteriovenous malformation[J]. Neurol Res, 2012, 34(6):552-556. DOI: 10.1179/1743132812Y.0000000044.
[199]HanPP, PonceFA, SpetzlerRF. Intention-to-treat analysis of Spetzler-Martin grades IV and V arteriovenous malformations: natural history and treatment paradigm[J]. J Neurosurg, 2003, 98(1):3-7. DOI: 10.3171/jns.2003.98.1.0003.
[200]BatjerHH, SrDMD, SeibertGB, et al. Intracranial arteriovenous malformation: relationships between clinical and radiographic factors and ipsilateral steal severity[J]. Neurosurgery, 1988, 23(3):322-328. DOI: 10.1227/00006123-198809000-00006.
[201]KusskeJA, KellyWA. Embolization and reduction of the "steal" syndrome in cerebral arteriovenous malformations[J]. J Neurosurg, 1974, 40(3):313-321. DOI: 10.3171/jns.1974.40.3.0313.
[202]FelicianoCE, de León-BerraR, Hernández-GaitánMS, et al. A proposal for a new arteriovenous malformation grading scale for neuroendovascular procedures and literature review[J]. P R Health Sci J, 2010, 29(2):117-120.
[203]DumontTM, KanP, SnyderKV, et al. A proposed grading system for endovascular treatment of cerebral arteriovenous malformations: Buffalo score[J]. Surg Neurol Int, 2015, 6:3. DOI: 10.4103/2152-7806.148847.
[204]LopesDK, MoftakharR, StrausD, et al. Arteriovenous malformation embocure score: AVMES[J]. J Neurointerv Surg, 2016, 8(7):685-691. DOI: 10.1136/neurintsurg-2015-011779.
[205]BellDL, Leslie-MazwiTM, YooAJ, et al. Application of a novel brain arteriovenous malformation endovascular grading scale for transarterial embolization[J]. AJNR Am J Neuroradiol, 2015, 36(7):1303-1309. DOI: 10.3174/ajnr.A4286.
[206]JinH, JiangY, GeH, et al. Comparison of grading scales regarding perioperative complications and clinical outcomes of brain arteriovenous malformations after endovascular therapy-multicenter study[J]. World Neurosurg, 2017, 106:394-401. DOI: 10.1016/j.wneu.2017.07.020.
[207]PulliB, StapletonCJ, WalcottBP, et al. Comparison of predictive grading systems for procedural risk in endovascular treatment of brain arteriovenous malformations: analysis of 104 consecutive patients[J]. J Neurosurg, 2019:1-9. DOI: 10.3171/2019.4.JNS19266.
[208]LeonardiM, BarbaraC, SimonettiL, et al. Glubran 2: a new acrylic glue for neuroradiological endovascular use. Experimental study on animals[J]. Interv Neuroradiol, 2002, 8(3):245-250. DOI: 10.1177/159101990200800304.
[209]中华医学会神经外科学分会介入学组, 《脑动静脉畸形介入治疗中国专家共识》编写委员会. 脑动静脉畸形介入治疗中国专家共识[J]. 中华神经外科杂志, 2017, 33(12):1195-1203. DOI: 10.3760/cma.j.issn.1001-2346.2017.12.003.
[210]GailloudP. Endovascular treatment of cerebral arteriovenous malformations[J]. Tech Vasc Interv Radiol, 2005, 8(3):118-128. DOI: 10.1053/j.tvir.2005.10.003.
[211]高旭, 于春泳, 李志清, 等. 弹簧圈近端辅助Onyx胶栓塞技术治疗脑动静脉畸形(附22例报告)[J]. 中华神经外科杂志, 2014, 30(3):221-224. DOI: 10.3760/cma.j.issn.1001-2346.2014.03.002.
[212]AsadiH, KokHK, LoobyS, et al. Outcomes and complications after endovascular treatment of brain arteriovenous malformations: a prognostication attempt using artificial intelligence[J]. World Neurosurg, 2016, 96:562-569.e1. DOI: 10.1016/j.wneu.2016.09.086.
[213]BaharvahdatH, BlancR, TermechiR, et al. Hemorrhagic complications after endovascular treatment of cerebral arteriovenous malformations[J]. AJNR Am J Neuroradiol, 2014, 35(5):978-983. DOI: 10.3174/ajnr.A3906.
[214]JordanJA, LlibreJC, VázquezF, et al. Predictors of hemorrhagic complications from endovascular treatment of cerebral arteriovenous malformations[J]. Interv Neuroradiol, 2014, 20(1):74-82. DOI: 10.15274/INR-2014-10011.
[215]PottsMB, LauD, AblaAA, et al. Current surgical results with low-grade brain arteriovenous malformations[J]. J Neurosurg, 2015, 122(4):912-920. DOI: 10.3171/2014.12.JNS14938.
[216]GraffeoCS, SahgalA, De SallesA, et al. Stereotactic radiosurgery for Spetzler-Martin Grade I and II arteriovenous malformations: international society of stereotactic radiosurgery (ISRS) practice guideline[J]. Neurosurgery, 2020, 87(3):442-452. DOI: 10.1093/neuros/nyaa004.
[217]KanoH, LunsfordLD, FlickingerJC, et al. Stereotactic radiosurgery for arteriovenous malformations, Part 1: management of Spetzler-Martin Grade I and II arteriovenous malformations[J]. J Neurosurg, 2012, 116(1):11-20. DOI: 10.3171/2011.9.JNS101740.
[218]GamiA, FeghaliJ, RapaportS, et al. Microsurgical resection versus stereotactic radiosurgery for low-grade intracranial arteriovenous malformations: a 27-year institutional experience[J]. J Clin Neurosci, 2021, 94:209-215. DOI: 10.1016/j.jocn.2021.10.036.
[219]SattariSA, ShahbandiA, KimJE, et al. Microsurgery versus stereotactic radiosurgery for treatment of patients with brain arteriovenous malformation: a systematic review and meta-analysis[J]. Neurosurgery, 2023, 93(3):510-523. DOI: 10.1227/neu.0000000000002460.
[220]TalaatM, ShotarE, PrematK, et al. Safety and effectiveness of first-line endovascular management of low-grade brain arteriovenous malformations: single center experience in 145 patients[J]. Clin Neuroradiol, 2022, 32(4):1019-1029. DOI: 10.1007/s00062-022-01176-9.
[221]BaharvahdatH, BlancR, FahedR, et al. Endovascular treatment for low-grade (Spetzler-Martin I-II) brain arteriovenous malformations[J]. AJNR Am J Neuroradiol, 2019, 40(4):668-672. DOI: 10.3174/ajnr.A5988.
[222]IosifC, de LucenaAF, Abreu-MattosLG, et al. Curative endovascular treatment for low-grade Spetzler-Martin brain arteriovenous malformations: a single-center prospective study[J]. J Neurointerv Surg, 2019, 11(7):699-705. DOI: 10.1136/neurintsurg-2018-014390.
[223]CatapanoJS, SrinivasanVM, RumallaK, et al. Effects of preoperative embolization on Spetzler-Martin grade I and II arteriovenous malformations: a propensity-adjusted analysis[J]. Neurosurgery, 2022, 90(1):92-98. DOI: 10.1227/NEU.0000000000001741.
[224]MorganMK, AssaadN, KorjaM. Surgery for unruptured Spetzler-Martin grade 3 brain arteriovenous malformations: a prospective surgical cohort[J]. Neurosurgery, 2015, 77(3):362-369; discussion 369-370. DOI: 10.1227/NEU.0000000000000774.
[225]DingD. Microsurgery versus radiosurgery as the definitive intervention for Spetzler-Martin grade III arteriovenous malformations[J]. Clin Neurol Neurosurg, 2015, 133:103-104. DOI: 10.1016/j.clineuro.2015.03.021.
[226]BurelJ, PapagiannakiC, SourourN, et al. Endovascular treatment as first-line therapy in Spetzler-Martin grade III brain arteriovenous malformations: a multicenter retrospective study[J]. J Neurosurg, 2023, 139(4):1070-1077. DOI: 10.3171/2023.1.JNS222745.
[227]HassanT, RefaatM, IssaAM, et al. Geometrical characteristics of grade III arteriovenous malformations that contribute to better outcomes in endovascular treatment[J]. World Neurosurg, 2023, 180:e749-e755. DOI: 10.1016/j.wneu.2023.10.019.
[228]NguyenBT, TranHM, HuynhCT, et al. Gamma knife radiosurgery for Spetzler-Martin grade iii brain arteriovenous malformations[J]. World Neurosurg, 2023, 175:e796-e803. DOI: 10.1016/j.wneu.2023.04.022.
[229]JiaoY, WuJ, ChenX, et al. Spetzler-Martin grade IV and V arteriovenous malformations: treatment outcomes and risk factors for negative outcomes after surgical resection[J]. J Clin Neurosci, 2019, 61:166-173. DOI: 10.1016/j.jocn.2018.10.101.
[230]JiangH, TangX, WengR, et al. Long-term outcome of a tailored embolization strategy with Gamma Knife radiosurgery for high-grade brain arteriovenous malformations: a single-center experience[J]. J Neurosurg, 2023, 139(1):176-183. DOI: 10.3171/2022.11.JNS221363.
[231]ChangH, SilvaMA, WengJ, et al. The impact of embolization on radiosurgery obliteration rates for brain arteriovenous malformations: a systematic review and meta-analysis[J]. Neurosurg Rev, 2022, 46(1):28. DOI: 10.1007/s10143-022-01935-9.
[232]RussellD, PeckT, DingD, et al. Stereotactic radiosurgery alone or combined with embolization for brain arteriovenous malformations: a systematic review and meta-analysis[J]. J Neurosurg, 2018, 128(5):1338-1348. DOI: 10.3171/2016.11.JNS162382.
[233]DingD, YenCP, StarkeRM, et al. Outcomes following single-session radiosurgery for high-grade intracranial arteriovenous malformations[J]. Br J Neurosurg, 2014, 28(5):666-674. DOI: 10.3109/02688697.2013.872227.
[234]TongX, WuJ, PanJ, et al. Microsurgical resection for persistent arteriovenous malformations following Gamma Knife radiosurgery: a case-control study[J]. World Neurosurg, 2016, 88:277-288. DOI: 10.1016/j.wneu.2016.01.027.
[235]FleetwoodIG, MarcellusML, LevyRP, et al. Deep arteriovenous malformations of the basal ganglia and thalamus: natural history[J]. J Neurosurg, 2003, 98(4):747-750. DOI: 10.3171/jns.2003.98.4.0747.
[236]PottsMB, JahangiriA, JenM, et al. Deep arteriovenous malformations in the basal ganglia, thalamus, and insula: multimodality management, patient selection, and results[J]. World Neurosurg, 2014, 82(3-4):386-394. DOI: 10.1016/j.wneu.2014.03.033.
[237]JiZ, XiangS, LiJ, et al. Multimodality treatment of deep-seated cerebral arteriovenous malformations: the experiences of one center[J]. Curr Neurovasc Res, 2022, 19(5):476-486. DOI: 10.2174/1567202620666221114111512.
[238]SasakiT, KuritaH, SaitoI, et al. Arteriovenous malformations in the basal ganglia and thalamus: management and results in 101 cases[J]. J Neurosurg, 1998, 88(2):285-292. DOI: 10.3171/jns.1998.88.2.0285.
[239]OhadiM, IranmehrA, ChavoshiM, et al. Stereotactic radiosurgery outcome for deep-seated cerebral arteriovenous malformations in the brainstem and thalamus/basal ganglia: systematic review and meta-analysis[J]. Neurosurg Rev, 2023, 46(1):148. DOI: 10.1007/s10143-023-02059-4.
[240]BroderickJ, ConnollyS, FeldmannE, et al. Guidelines for the management of spontaneous intracerebral hemorrhage in adults: 2007 update: a guideline from the American Heart Association/American Stroke Association Stroke Council, High Blood Pressure Research Council, and the Quality of Care and Outcomes in Research Interdisciplinary Working Group[J]. Circulation, 2007, 116(16):e391-413. DOI: 10.1161/CIRCULATIONAHA.107.183689.
[241]MorgensternLB, HemphillJC, AndersonC, et al. Guidelines for the management of spontaneous intracerebral hemorrhage: a guideline for healthcare professionals from the American Heart Association/American Stroke Association[J]. Stroke, 2010, 41(9):2108-2129. DOI: 10.1161/STR.0b013e3181ec611b.
[242]AounSG, BendokBR, BatjerHH. Acute management of ruptured arteriovenous malformations and dural arteriovenous fistulas[J]. Neurosurg Clin N Am, 2012, 23(1):87-103. DOI: 10.1016/j.nec.2011.09.013.
[243]HartmannA, MohrJP. Acute management of brain arteriovenous malformations[J]. Curr Treat Options Neurol, 2015, 17(5):346. DOI: 10.1007/s11940-015-0346-5.
[244]JafarJJ, RezaiAR. Acute surgical management of intracranial arteriovenous malformations[J]. Neurosurgery, 1994, 34(1):8-12; discussion 12-13.
[245]JinH, LenckS, KringsT, et al. Interval angioarchitectural evolution of brain arteriovenous malformations following rupture[J]. J Neurosurg, 2018, 131(1):96-103. DOI: 10.3171/2018.2.JNS18128.
[246]ZhangY, ChenY, HanH, et al. Timing of microsurgical resection for ruptured brain arteriovenous malformations: a propensity score-matched analysis using prospective single-center registry data[J]. J Neurosurg, 2024, 140(1):164-171. DOI: 10.3171/2023.5.JNS222666.
[247]XuF, ZhongJ, RayA, et al. Stereotactic radiosurgery with and without embolization for intracranial arteriovenous malformations: a systematic review and meta-analysis[J]. Neurosurg Focus, 2014, 37(3):E16. DOI: 10.3171/2014.6.FOCUS14178.
[248]EnglotDJ, YoungWL, HanSJ, et al. Seizure predictors and control after microsurgical resection of supratentorial arteriovenous malformations in 440 patients[J]. Neurosurgery, 2012, 71(3):572-580; discussion 580. DOI: 10.1227/NEU.0b013e31825ea3ba.
[249]HeikkinenER, KonnovB, MelnikovL, et al. Relief of epilepsy by radiosurgery of cerebral arteriovenous malformations[J]. Stereotact Funct Neurosurg, 1989, 53(3):157-166. DOI: 10.1159/000099532.
[250]ChenCJ, ChivukulaS, DingD, et al. Seizure outcomes following radiosurgery for cerebral arteriovenous malformations[J]. Neurosurg Focus, 2014, 37(3):E17. DOI: 10.3171/2014.6.FOCUS1454.
[251]BaranoskiJF, GrantRA, HirschLJ, et al. Seizure control for intracranial arteriovenous malformations is directly related to treatment modality: a meta-analysis[J]. J Neurointerv Surg, 2014, 6(9):684-690. DOI: 10.1136/neurintsurg-2013-010945.
[252]HyunSJ, KongDS, LeeJI, et al. Cerebral arteriovenous malformations and seizures: differential impact on the time to seizure-free state according to the treatment modalities[J]. Acta Neurochir (Wien), 2012, 154(6):1003-1010. DOI: 10.1007/s00701-012-1339-8.
[253]FennellVS, MartirosyanNL, AtwalGS, et al. Hemodynamics associated with intracerebral arteriovenous malformations: the effects of treatment modalities [J]. Neurosurgery, 2018, 83(4): 611-621.DOI: 10.1093/neuros/nyx560.
[254]CaoY, WangR, YangL, et al. Bipolar electrocoagulation on cortex after AVMs lesionectomy for seizure control[J]. Can J Neurol Sci, 2011, 38(1):48-53.
[255]Bustuchina VlaicuM. New approaches for brain arteriovenous malformations-related epilepsy[J]. Rev Neurol (Paris), 2023, 179(3):188-200. DOI: 10.1016/j.neurol.2022.05.011.
[256]JosephsonCB, LeachJP, DuncanR, et al. Seizure risk from cavernous or arteriovenous malformations: prospective population-based study[J]. Neurology, 2011, 76(18):1548-1554. DOI: 10.1212/WNL.0b013e3182190f37.
[257]StephenLJ, KwanP, BrodieMJ. Does the cause of localisation-related epilepsy influence the response to antiepileptic drug treatment?[J]. Epilepsia, 2001, 42(3):357-362. DOI: 10.1046/j.1528-1157.2001.29000.x.
[258]SturialeCL, PucaA, SebastianiP, et al. Single nucleotide polymorphisms associated with sporadic brain arteriovenous malformations: where do we stand?[J]. Brain, 2013, 136(Pt 2):665-681. DOI: 10.1093/brain/aws180.
[259]HolashJ, MaisonpierrePC, ComptonD, et al. Vessel cooption, regression, and growth in tumors mediated by angiopoietins and VEGF[J]. Science, 1999, 284(5422):1994-1998. DOI: 10.1126/science.284.5422.1994.
[260]JaysonGC, KerbelR, EllisLM, et al. Antiangiogenic therapy in oncology: current status and future directions[J]. Lancet, 2016, 388(10043):518-529. DOI: 10.1016/S0140-6736(15)01088-0.
[261]SandalciogluIE, WendeD, EggertA, et al. Vascular endothelial growth factor plasma levels are significantly elevated in patients with cerebral arteriovenous malformations[J]. Cerebrovasc Dis, 2006, 21(3):154-158. DOI: 10.1159/000090526.
[262]LarrivéeB, PrahstC, GordonE, et al. ALK1 signaling inhibits angiogenesis by cooperating with the Notch pathway[J]. Dev Cell, 2012, 22(3):489-500. DOI: 10.1016/j.devcel.2012.02.005.
[263]del ToroR, PrahstC, MathivetT, et al. Identification and functional analysis of endothelial tip cell-enriched genes[J]. Blood, 2010, 116(19):4025-4033. DOI: 10.1182/blood-2010-02-270819.
[264]WangY, FeiD, VanderlaanM, et al. Biological activity of bevacizumab, a humanized anti-VEGF antibody in vitro[J]. Angiogenesis, 2004, 7(4):335-345. DOI: 10.1007/s10456-004-8272-2.
[265]JubbAM, HarrisAL. Biomarkers to predict the clinical efficacy of bevacizumab in cancer[J]. Lancet Oncol, 2010, 11(12):1172-1183. DOI: 10.1016/S1470-2045(10)70232-1.
[266]KarnezisTT, DavidsonTM. Treatment of hereditary hemorrhagic telangiectasia with submucosal and topical bevacizumab therapy[J]. Laryngoscope, 2012, 122(3):495-497. DOI: 10.1002/lary.22501.
[267]SimondsJ, MillerF, MandelJ, et al. The effect of bevacizumab (Avastin) treatment on epistaxis in hereditary hemorrhagic telangiectasia[J]. Laryngoscope, 2009, 119(5):988-992. DOI: 10.1002/lary.20159.
[268]Dupuis-GirodS, AmbrunA, DecullierE, et al. ELLIPSE Study: a Phase 1 study evaluating the tolerance of bevacizumab nasal spray in the treatment of epistaxis in hereditary hemorrhagic telangiectasia[J]. MAbs, 2014, 6(3):794-799. DOI: 10.4161/mabs.28025.
[269]Dupuis-GirodS, AmbrunA, DecullierE, et al. Effect of bevacizumab nasal spray on epistaxis duration in hereditary hemorrhagic telangectasia: a randomized clinical trial[J]. JAMA, 2016, 316(9):934-942. DOI: 10.1001/jama.2016.11387.
[270]MusterR, KoN, SmithW, et al. Proof-of-concept single-arm trial of bevacizumab therapy for brain arteriovenous malformation[J]. BMJ Neurol Open, 2021, 3(1):e000114. DOI: 10.1136/bmjno-2020-000114.
[271]TanvetyanonT, MurtaghR, BeplerG. Rupture of a cerebral arteriovenous malformation in a patient treated with bevacizumab[J]. J Thorac Oncol, 2009, 4(2):268-269. DOI: 10.1097/JTO.0b013e318195a642.
[272]WinklerEA, KimCN, RossJM, et al. A single-cell atlas of the normal and malformed human brain vasculature[J]. Science, 2022, 375(6584):eabi7377. DOI: 10.1126/science.abi7377.
[273]HashimotoT, MatsumotoMM, LiJF, et al. Suppression of MMP-9 by doxycycline in brain arteriovenous malformations[J]. BMC Neurol, 2005, 5(1):1. DOI: 10.1186/1471-2377-5-1.
[274]FrenzelT, LeeCZ, KimH, et al. Feasibility of minocycline and doxycycline use as potential vasculostatic therapy for brain vascular malformations: pilot study of adverse events and tolerance[J]. Cerebrovasc Dis, 2008, 25(1-2):157-163. DOI: 10.1159/000113733.
[275]BurrowsPE, MullikenJB, FishmanSJ, et al. Pharmacological treatment of a diffuse arteriovenous malformation of the upper extremity in a child[J]. J Craniofac Surg, 2009, 20 Suppl 1∶597-602. DOI: 10.1097/SCS.0b013e3181927f1e.
[276]MengJS, OkedaR. Histopathological structure of the pial arteriovenous malformation in adults: observation by reconstruction of serial sections of four surgical specimens[J]. Acta Neuropathol, 2001, 102(1):63-68. DOI: 10.1007/s004010000351.
[277]ChenW, GuoY, WalkerEJ, et al. Reduced mural cell coverage and impaired vessel integrity after angiogenic stimulation in the Alk1-deficient brain[J]. Arterioscler Thromb Vasc Biol, 2013, 33(2):305-310. DOI: 10.1161/ATVBAHA.112.300485.
[278]BaeyensN, LarrivéeB, OlaR, et al. Defective fluid shear stress mechanotransduction mediates hereditary hemorrhagic telangiectasia[J]. J Cell Biol, 2016, 214(7):807-816. DOI: 10.1083/jcb.201603106.
[279]LebrinF, SrunS, RaymondK, et al. Thalidomide stimulates vessel maturation and reduces epistaxis in individuals with hereditary hemorrhagic telangiectasia[J]. Nat Med, 2010, 16(4):420-428. DOI: 10.1038/nm.2131.
[280]InvernizziR, QuagliaF, KlersyC, et al. Efficacy and safety of thalidomide for the treatment of severe recurrent epistaxis in hereditary haemorrhagic telangiectasia: results of a non-randomised, single-centre, phase 2 study[J]. Lancet Haematol, 2015, 2(11):e465-473. DOI: 10.1016/S2352-3026(15)00195-7.
[281]GeZZ, ChenHM, GaoYJ, et al. Efficacy of thalidomide for refractory gastrointestinal bleeding from vascular malformation[J]. Gastroenterology, 2011, 141(5):1629-1637.e1-4. DOI: 10.1053/j.gastro.2011.07.018.
[282]TsengS, PakG, WashenikK, et al. Rediscovering thalidomide: a review of its mechanism of action, side effects, and potential uses[J]. J Am Acad Dermatol, 1996, 35(6):969-979. DOI: 10.1016/s0190-9622(96)90122-x.
[283]CoutoJA, HuangAY, KonczykDJ, et al. Somatic MAP2K1 mutations are associated with extracranial arteriovenous malformation[J]. Am J Hum Genet, 2017, 100(3):546-554. DOI: 10.1016/j.ajhg.2017.01.018.
[284]EdwardsEA, PhelpsAS, CookeD, et al. Monitoring arteriovenous malformation response to genotype-targeted therapy[J]. Pediatrics, 2020, 146(3):e20193206 [pii]. DOI: 10.1542/peds.2019-3206.
[285]NicholsonCL, FlanaganS, MuratiM, et al. Successful management of an arteriovenous malformation with trametinib in a patient with capillary-malformation arteriovenous malformation syndrome and cardiac compromise[J]. Pediatr Dermatol, 2022, 39(2):316-319. DOI: 10.1111/pde.14912.
[286]LekwuttikarnR, LimYH, AdmaniS, et al. Genotype-guided medical treatment of an arteriovenous malformation in a child[J]. JAMA Dermatol, 2019, 155(2):256-257. DOI: 10.1001/jamadermatol.2018.4653.
[287]Al-SamkariH, EngW. A precision medicine approach to hereditary hemorrhagic telangiectasia and complex vascular anomalies[J]. J Thromb Haemost, 2022, 20(5):1077-1088. DOI: 10.1111/jth.15715.
[288]ScherschinskiL, RahmaniR, SrinivasanVM, et al. Genetics and emerging therapies for brain arteriovenous malformations[J]. World Neurosurg, 2022, 159:327-337. DOI: 10.1016/j.wneu.2021.10.127.
[289]LiH, JingC, WuJ, et al. Circulating tumor DNA detection: a potential tool for colorectal cancer management[J]. Oncol Lett, 2019, 17(2):1409-1416. DOI: 10.3892/ol.2018.9794.
[290]Pérez-AlfayateR, GrassoG. State of the art and future direction in diagnosis, molecular biology, genetics, and treatment of brain arteriovenous malformations[J]. World Neurosurg, 2022, 159:362-372. DOI: 10.1016/j.wneu.2021.08.111.
[291]PriemerDS, VortmeyerAO, ZhangS, et al. Activating KRAS mutations in arteriovenous malformations of the brain: frequency and clinicopathologic correlation[J]. Hum Pathol, 2019, 89:33-39. DOI: 10.1016/j.humpath.2019.04.004.
[292]PalmieriM, CurròA, TommasiA, et al. Cell-free DNA next-generation sequencing liquid biopsy as a new revolutionary approach for arteriovenous malformation[J]. JVS Vasc Sci, 2020, 1:176-180. DOI: 10.1016/j.jvssci.2020.08.002.
[293]FengL, SternDM, Pile-SpellmanJ. Human endothelium: endovascular biopsy and molecular analysis[J]. Radiology, 1999, 212(3):655-664. DOI: 10.1148/radiology.212.3.r99au28655.
[294]AlexanderMD, SunZ, ConradMB, et al. Assessment of cell yield among different devices for endovascular biopsy to harvest vascular endothelial cells[J]. Biotechniques, 2019, 66(1):34-36. DOI: 10.2144/btn-2018-0099.
[295]WinklerE, WuD, GilE, et al. Endoluminal biopsy for molecular profiling of human brain vascular malformations[J]. Neurology, 2022, 98(16):e1637-e1647. DOI: 10.1212/WNL.0000000000200109.
声明：脑医汇旗下神外资讯、神介资讯、脑医咨询、Ai Brain 所发表内容之知识产权为脑医汇及主办方、原作者等相关权利人所有。
投稿邮箱：NAOYIHUI@163.com
未经许可，禁止进行转载、摘编、复制、裁切、录制等。经许可授权使用，亦须注明来源。欢迎转发、分享。
投稿/会议发布，请联系400-888-2526转3。
