作者感谢所有的临床团队每天对 UCSD 的 AVM 患者的护理。

根据机构指南获得知情同意后, 以下所述的所有程序均作为脑车辆患者的护理标准执行. 
 1. 初始患者评估和成像 注意: 破裂车辆的患者通常在畸形被发现后出现在头痛或癫痫检查的影像上。车辆破裂的患者经常出现头痛、恶心、呕吐、虚弱、麻木和/或视力变化的急性发作. 
<ol> <li> 通过访问患者和/或家庭 (以确定以前的破裂状态、家族病史) 和执行详细的神经系统检查来获取完整的历史记录, 评估意识和方位、颅神经功能、下肢运动和感官功能, 和反射。这项检查可能会发现神经系统的缺陷, 由于隐性血管窃取, 局部质量效应, 和/或视觉变化 (与枕车辆)。在发生 AVM 破裂的情况下, 请将病人交给重症监护病房 (ICU), 并根据美国心脏协会 (阿哈)/美国中风协会 (ASA) 的指导方针与 neurocritical 护理小组一起。 9 </li> <li> 获得了平头计算机断层扫描 (CT) 每机构的协议, 以评估急性出血, 即, 一个地区的异常颅内 hyperdensity, 往往有质量效应。通过 CT 或磁共振 (MR)-血管造影, 以确定脑血管和任何潜在的血管异常的机构的协议。 10 对神经外科和放射科团队的所有图像进行解释. </li>
	<li> 如果患者神经稳定, 获得知情同意, 并通过六导管血管造影和 #177 对患者进行明确的血管成像; 栓塞 (见下文2和3节)。如果病人有渐进性的神经下降从出血, 放置颅内压监测和/或启动渗透疗法按照阿哈/ASA 准则 9 。进行血肿排空和 #177; AVM 切除术 (见下面4节) 在诊断六导管血管造影前或紧接后. </li>
</ol> 2。六血管造影 <ol> <li> 在麻醉组的帮助下, 如果稳定的话, 或全身麻醉下的病人仰卧在透视表上的位置 (典型的插管诱导与芬太尼 [5-10 心动/公斤], 咪达唑仑 [0.2-0.4 毫克/千克], 和0.5 毫克/千克罗库, 其次是麻醉维护与异丙酚在 50-150 心动/千克/分钟和瑞芬太尼在 0.1-0.5 心动/千克/分)。 11 </li> <li> 使用穿刺腹股沟访问套件和修改后的 Seldinger 技术来放置右股动脉鞘. 12 <ol> <li> 清洁 (含2% 氯己定的葡萄糖酸和70% 异丙醇) 和 sterilely 褶皱腹股沟. </li>
		<li> 触在腹股沟折痕处股动脉。注射1-2 毫升的1% 利多卡因 HCl 作为局部麻醉进入表面皮下组织。将微针插入股动脉腔内, 针在 45 #176; 角度对皮肤. </li>
		<li> 通过微针推进微丝, 取出微针保持微丝到位。做一个0.5cm 皮肤穿刺与11刀片在现场 microwire 退出皮肤. </li>
		<li> 插入容器扩张, 然后将该容器的微线和内部部分扩张, 使该容器的外部部分保持扩张. </li>
		<li> 在容器扩张的流明处插入一根 j 线, 并取出扩张, 保持 j 线到位. </li>
		<li> 在 J 线上插入一个5或 6-法国鞘到股动脉。取出 J 线, 保持鞘在动脉中的位置. </li>
	</ol> </li> <li> 将0.035 丝和 4-法国诊断导管头下单或双透视 (每秒3-5 帧) 提升主动脉, 并通过注射5-8 毫升不透明的造影剂来选择性 catheterize 和图像 (240毫克/毫升) 右侧颈内动脉、右椎动脉、左颈内动脉、左颈外动脉和左椎动脉. </li>
	<li> 复查记录的血管造影图象, 以确定该 AVM 的喂养血管和引流静脉. </li>
	<li> 如果不进行急性栓塞, 请卸下诊断导管和丝, 并按照制造商的说明, 用密封剂装置来固定股动脉, 13 或按住压力至少10分钟. </li>
</ol> 3。avm 栓塞 注意: 如果 avm 可以接受血管内和随后的外科治疗 (按照确定的评分标准, 1 , 8 以及外科医生和多学科会议评价), 最初的栓塞可能是在延迟的方式或与诊断血管造影的同一时段进行的。栓塞经常上演, 以减少破裂和中风的风险, 从迅速改变的流动动力学. 
<ol> <li> 获取知情同意。以协助从麻醉地方患者在一般麻醉之下和在 2.1, 并且安置患者仰卧在透视桌 (如果不同时作为最初的血管造影). </li>
	<li> 与神经监测组一起, 通过体感诱发电位 (SSEPs)、经颅运动诱发电位 (TcMEPs)、视觉诱发电位 (vep)、听觉脑干反应 (abr) 和/或脑电图 (eeg)。继续在整个案件的神经监测, 以跟踪 real-time 的功能, 关键的神经通路。SSEPs, TcMEPs 和脑电图作为标准的神经监测协议的一部分, 与 abr 椎/基底动脉病变, 和 vep 的视觉皮层病变。 14 </li> <li> 使用改进的 Seldinger 技术获取股动脉通路, 并在2.2 中插入 6-法国股骨鞘. </li>
	<li> 引入一个预轴系统, 由一个 6-法国导管 (一个更大的孔导管在系统的外面为稳定), 4 法国诊断导管 (一个更小的孔导管安置在6法国指南之内为选择性导管插管), 和一个0.035 丝 (定位在4法国诊断导管的腔内的系统指导) 作为一个单位进入股骨鞘. </li>
	<li> 如在2.3 前进, 轴系统头和有选择地 catheterize 大口径的颈血管 (即左或右内颈动脉或脊椎), 所期望的喂养 AVM 血管来源于诊断导管和将导导管推进至适当的宫颈段以支持。移除诊断导管, 通过小注射造影剂的快速分散来确保足够的血管径流, 并通过注射不透明造影 (5-8 毫升 240) 进行诊断血管造影 (在单声道或双透视下, 每秒3-5 帧)。毫克/毫升) 和 #160; 评估 AVM 的血液供应。叠加制导图像 (期望叠加船只运行与 real-time 透视) 或路线图图像 (船舶减法模板), 然后创建, 以协助微导管的目标 AVM 血管. </li>
	<li> 在腹股沟的导管中引入二甲基亚砜相容导管和 microwire, 并推进头选择性地 catheterize 所需的喂养动脉, 使用叠加或路标引导. </li>
	<li> 一旦栓塞的位置达到与导管它是冲洗与 (亚甲基亚砜)。一旦冲洗, 栓塞的 AVM 病灶和理想的喂养动脉通过控制注射的无线电不透明液体栓塞剂下的负面路线图图像, 直到达到回流耐受。总体积的 embolisate 使用的是由大小的病变, 渗透的病灶, 并允许回流。注意避免 embolisate 回流到非 AVM 动脉, 或远端栓塞到引流静脉。一旦栓塞完成, 背部吸入的栓塞注射器举行和导管被删除下透视可视化. </li>
	<li> 根据需要重复栓塞其他喂养血管, 目标至少50% 术前尼达尔栓塞。 15 一般情况下, 只有一个或两个喂食容器和和 #60; 40% 的病灶是栓塞在一个单一的程序, 使分期栓塞常见. </li>
	<li> 在步骤3.5 中通过引导导管通过造影剂注入最终血管造影, 以评估 AVM 栓塞并确保母血管通畅. </li>
	<li> 在步骤2.5 中取出导导管并闭合股动脉。如果病人被直接送往或切除, 股骨鞘可以留在术血管造影 (在步骤4.8 中描述). </li>
</ol> 4。avm 切除术 <ol> <li> 获得知情同意, 在麻醉的协助下, 将患者置于全身麻醉下, 如步骤2.1 所示, 并根据 avm 的位置和所需的开颅手术定位病人。获得血液同意和产品. </li>
	<li> 与 neuromonitoring 团队一起, 按照3.2 中的说明建立基线 neuromonitoring, 并在整个案例中继续进行监视. </li>
	<li> 同步术前成像与术神经导航系统使用表面匹配, 标记, 或指针注册, 根据导航系统的规范. </li>
	<li> 如果鞘尚未到位, 则在步骤2.2 中获得腹股沟通道. </li>
	<li> 使用高功率钻孔系统对颅骨内特定的 AVM 位置进行开颅手术, 确保大骨外露。
	<ol> <li> 使用 #15 刀片切割皮肤和盔瓣。通过在皮肤边缘上放置骨架夹和/或使用凝固设置 (烧灼医疗产品, 清水, FL), 获得止血烧灼电。如果计划的切口涉及部下的肌肉, 用电切割筋膜/肌肉。用骨膜升降梯从骨上切开软组织瓣, 使颅骨显露。另外, 周嫁接可以在这个时候单独收获, 以帮助以后关闭。钩子用于软组织缩回. #160; 冲洗并获得止血. </li>
		<li> 在所需开颅的外围创建一个或多个毛刺孔, 并使用高功率钻孔系统在 3 mm 直径的火柴钻头上进行。额外的毛刺孔将允许更短的骨切割和硬脑膜被剥离 multifocally 之前执行开颅手术. </li>
		<li> 将硬脑膜从颅骨内侧剥离, 用骨升降机或踏板附着在骨内表面, 完成开颅手术, 用锥形钻头与踏板附着的硬脑膜连接毛刺孔。保护.如果可能的话, 计划开颅手术, 以确保早期进入脑脊液 (CSF) 蓄水池排水. </li>
		<li> 另一种方法是, 在弗雷泽和 #39 或科克和 #39 点 (在创建一个小的毛刺孔, 如在 4.5.1, 用 #11 刀片切开硬脑膜) 进行脑脊液引流时, 将外部心室引流置于侧脑室。腰椎引流放置在腰椎膜囊穿刺后与大口径陶西针在大约 L3-L4 或 L4-L5 间隙也可用于脑脊液排水. </li>
	</ol> </li> <li> 取出骨瓣并通过双极电进行止血后, 将硬脑膜 tack-up 缝合以关闭硬膜外间隙, 用 C1 钻头在骨开颅周围的小孔中钻孔, 并确保硬脑膜这些部位的骨骼使用4-0 缝合线。然后, 使用 #11 或 #15 刀片打开硬脑膜。注意不要伤害皮层或皮质血管。一旦一个小 durotomy 已经创建, 打开其余裸露的硬脑膜, 无论是十字交叉或 c 形的时尚使用 Metzenbaum 剪刀, 用杰拉尔德钳, 以提高硬脑膜边缘和可视化剪刀的秘诀, 而切割保存下属皮质结构. </li>
	<li> 使用具有1.5X 至17.0X 的可变放大容量的操作显微镜和10X 目镜, 对 AVM 进行切除。 5 其他形式的手术放大倍数, 如 exoscope, 也可以使用。
	<ol> <li> 开始显微外科切除术首先解剖在蛛网膜下腔 (使用钝和尖锐技术与双极钳, 弯曲解剖, 和 microscissors) 定义 AVM 解剖和揭露它的边缘, 自由引流静脉, 并获得近端控制通过识别和解剖免费的所有喂养动脉. </li>
		<li> 非常小心地识别和保存在 avm 早期的引流静脉, 因为阻断静脉引流前的动脉馈线导致充血的 avm 和增加的破裂风险. </li>
		<li> 在定义这一解剖后, 通过在双极性钳的尖端和使用高达30瓦特的功率, 或通过在双极电之间轻轻地夹住血管, 将动脉供血动脉凝结成近远端的 AVM。放置小动脉瘤夹. </li>
		<li> 使用双极性钳 (用于解剖和电) 和可变动作吸入尖端, 在病灶周围的脑实质内立即解剖圆周。脑牵引器可用于促进深部解剖的可视化. </li>
		<li> 在完成 AVM 解剖后, 使用双极性电作为步骤4.7.3 和/或修剪任何引流静脉。从切除腔中取出 AVM。清除整个病灶以消除未来出血风险是至关重要的. </li>
		<li> 如果正在尝试 post-hemorrhage 手术切除, 则从 AVM 病灶中取出远端的血肿, 直到脑部减压, 并确定喂养血管和引流静脉。这些地标之后被识别, 继续 AVM 尼达尔切除术4.7 步. </li>
	</ol> </li> <li> 在 AVM 移除后, 执行术血管造影, 如步骤 2.1-2.4 所示, 使用在步骤4.4 中放置的动脉鞘。使用术中或双平面血管造影或 C 臂透视, 确保完全尼达尔切除. </li>
	<li> 采用双极性电作为阶梯 4.7.4, 用可吸收止血剂轻轻排入切除腔, 获得细致止血。用4-0 缝合线关闭或 re-approximate 硬脑膜, 如果需要的话, 用围颅或人工硬脑膜移植。用电镀系统代替和固定骨瓣, 并用间断的可吸收缝合线关闭盔瓣和皮肤, 用于深层, 或者是主食或为皮肤缝合。取出腹股沟鞘, 并在2.5 步中固定腹股沟. </li>
	<li> Extubate 如果能够, 并将病人转移到 ICU 进行严密的神经监测和恢复. </li>
</ol> 5。长期随访 <ol> <li> 在学确认完整的 AVM 切除 (通过术或术后导管造影) 后, 通过导管血管造影在1和5年后的后处理中获得远程成像. </li> </ol>

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M., et al. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Multimodality+intraoperative+neurophysiological+monitoring+during+Onyx+embolization+of+cerebrovascular+malformations.">Multimodality intraoperative neurophysiological monitoring during Onyx embolization of cerebrovascular malformations.</a> Neurodiagn J. 55 (1), 12-24 (2015).</li><li>Vi&#241;uela, F., et al. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Combined+endovascular+embolization+and+surgery+in+the+management+of+cerebral+arteriovenous+malformations:+experience+with+101+cases.">Combined endovascular embolization and surgery in the management of cerebral arteriovenous malformations: experience with 101 cases.</a> J Neurosurg. 75 (6), 856-864 (1991).</li></ol>

科持有 Covidien 医师培训的咨询安排。科没有与这项工作有关的直接财务利益。其余的作者对本研究中使用的材料或方法或本文所述的结果没有披露。

在这里, 我们展示了一个综合的方法, 脑车辆通过联合血管内和开放式手术管理。导管血管造影是成像车辆的金标准, 对手术评估和规划具有重要的价值。手术前栓塞可以简化手术切除, 但需要与外科和介入治疗组之间的沟通, 以制定一个最佳的战略方法。例如, AVM 动脉馈线最容易栓塞也可能是最外科手术。然而, 如果他们是栓塞之前制定一个全面的治疗计划, 只留下更深更难获得动脉馈线, 手术变得...

脑动静脉畸形 (车辆), 动脉和静脉之间的异常连接不干预正常毛细血管床, 目前独特的神经外科的挑战。根据大小, 存在深引流静脉, 并参与雄辩皮质,1出血的风险以前破裂车辆范围从0.9 到8% 每年,2 , 每年平均破裂风险为3%。3车辆的出血与近10% 的死亡率和显著的发病率有关, 其中多达34% 的患者有中度至严重残疾。4先前破裂的车辆增加了年出血率,2 , 但复的即时风险相对较低。除非血肿的质量影响需要急性干预, 否则治疗通常是在权衡了预期的自然病史与治疗相关的风险之后进行的。5,6
外科手术切除是治疗选择的小车辆, 因为它立即和明确地消除未来出血的风险。然而, 高流速的车辆, 以及增加风险的 AVM 相关动脉瘤,4,7 , 使外科手术切除最具挑战性的所有神经外科病例。术前栓塞车辆, 以减少血流量和消除高危 AVM 的特点, 可以大大减少技术挑战的切除。
综合训练的血管外科是唯一的定位, 以明确治疗车辆通过进行术前血管造影和血管内栓塞, 以及开放手术切除。在这里, 我们描述的管理协议的外科手术可及性脑车辆 (根据确定的评分等级1,8以及外科医生和多学科会议评价) 在我们的机构。

<table border="1" fo:keep-together.within-page="1" fo:keep-with-next.within-page="always">
	<tbody>
		<tr>
			<td>ChloraPrep Sterilization Solution</td>
			<td>BD, Franklin Lakes, NJ</td>
			<td>260815</td>
			<td>For skin sterilization</td>
		</tr>
		<tr>
			<td>Lidocaine Hcl 1%&#160;</td>
			<td>ACE Surgical Supply, Inc, Brockton, MA</td>
			<td>001-1421</td>
			<td>For local anesthetic</td>
		</tr>
		<tr>
			<td>Micropuncture Groin Access Kit</td>
			<td>Cook Medical, Bloomington, IN</td>
			<td>G56202</td>
			<td>Used for femoral artery access</td>
		</tr>
		<tr>
			<td>0.035 Guidewire&#160;</td>
			<td>Terumo Medical, Somerset, NJ</td>
			<td>GR3506</td>
			<td>Used in conjunction with diagnostic catheters for cerebral angiography</td>
		</tr>
		<tr>
			<td>Cerebral Angiography Diagnostic Catheters&#160;</td>
			<td>Terumo Medical, Somerset, NJ</td>
			<td>CG416</td>
			<td>Used in conjunction with guidewire for cerebral angiography</td>
		</tr>
		<tr>
			<td>Omnipaque Contrast Agent</td>
			<td>GE Healthcare, Chicago, IL&#160;</td>
			<td>Q9965</td>
			<td>Contrast agent for cerebral vessel imaging</td>
		</tr>
		<tr>
			<td>Microcatheter and Microwire</td>
			<td>Covidian, Plymouth, MN</td>
			<td>105-5091-150, 103-0608</td>
			<td>Used for distal arterial catheterization</td>
		</tr>
		<tr>
			<td>Onyx Liquid Embolic</td>
			<td>Covidian, Plymouth, MN</td>
			<td>105-7100-060</td>
			<td>Used for AVM embolization</td>
		</tr>
		<tr>
			<td>Angio-Seal Vascular Closure Device</td>
			<td>St. Jude Medical, St Paul, MN</td>
			<td>610130</td>
			<td>Used for femoral artery closure following angiography/intra-arterial embolization</td>
		</tr>
		<tr>
			<td>Midas Rex High Power Drill System</td>
			<td>Medtronic, Minneapolis, MN</td>
			<td>PM700</td>
			<td>Used for craniotomy&#160;</td>
		</tr>
		<tr>
			<td>Matchstick Drill Bit</td>
			<td>Medtronic, Minneapolis, MN</td>
			<td>10MH30-MN</td>
			<td>Used to create burr hole for craniotomy&#160;</td>
		</tr>
		<tr>
			<td>Tapered Drill Bit</td>
			<td>Medtronic, Minneapolis, MN</td>
			<td>F1/8TA15</td>
			<td>Used to complete craniotomy&#160;</td>
		</tr>
		<tr>
			<td>#11 and 15 Blade Surgical Scalpels</td>
			<td>BD Bard-Parker, Franklin Lakes, NJ</td>
			<td>372615&#160;</td>
			<td>Used for groin incision for angiography and dural opening for external ventricular drain placement or AVM resection</td>
		</tr>
		<tr>
			<td>Metzenbaum Dissecting Scissors</td>
			<td>Stoelting Co, Wood Dale, IL</td>
			<td>52134-01P</td>
			<td>Used for dural opening</td>
		</tr>
		<tr>
			<td>Bone Elevator</td>
			<td>Stoelting Co, Wood Dale, IL</td>
			<td>52169</td>
			<td>Used for separating dura from the inner skull</td>
		</tr>
		<tr>
			<td>Gerald Forceps</td>
			<td>Stoelting Co, Wood Dale, IL</td>
			<td>52106-52</td>
			<td>Used for dural opening and manipulation</td>
		</tr>
		<tr>
			<td>Microsurgical Instruments&#160;</td>
			<td>Accurate Surgical &#38; Scientific Instruments Corporation, Westbury, NY</td>
			<td>ASSI.BML1</td>
			<td>Used for AVM microsurgical resection</td>
		</tr>
		<tr>
			<td>Bipolar Forceps&#160;</td>
			<td>Accurate Surgical &#38; Scientific Instruments Corporation, Westbury, NY</td>
			<td>ASSI.BPNS20423FP</td>
			<td>Used for AVM microsurgical resection</td>
		</tr>
		<tr>
			<td>Electrosurgery Generator</td>
			<td>Bovie Medical Products, Clearwater, FL&#160;</td>
			<td>IDS-200&#160;</td>
			<td>Used for electrosurgical cutting/coagulation</td>
		</tr>
		<tr>
			<td>Small Aneurysm Clips</td>
			<td>Codman Neuro, Raynham, MA</td>
			<td>20-1801</td>
			<td>Used for occlusion of arterial AVM feeders not amenable to coagulation</td>
		</tr>
		<tr>
			<td>Brain Retractors</td>
			<td>Medicon, Tuttlingen, Germany</td>
			<td>22.00.06</td>
			<td>For brain retraction for deep AVM dissection/resection</td>
		</tr>
		<tr>
			<td>Variable Action Suction tip</td>
			<td>Millennium Surgical, Narberth, PA</td>
			<td>6-8607</td>
			<td>For suction with AVM dissection/resection</td>
		</tr>
		<tr>
			<td>Fibrillar Absorbable Hemostatic Agent</td>
			<td>Ethicon, Somerville, NJ</td>
			<td>63713-0019-61</td>
			<td>For hemostatis within surgical cavity</td>
		</tr>
		<tr>
			<td>4-0 Suture</td>
			<td>Ethicon, Somerville, NJ</td>
			<td>C554D</td>
			<td>For dural closure</td>
		</tr>
		<tr>
			<td>2-0 Absorbable Suture</td>
			<td>Ethicon, Somerville, NJ</td>
			<td>J286G</td>
			<td>For deep tissue closure</td>
		</tr>
		<tr>
			<td>3-0 Nylon Suture</td>
			<td>Ethicon, Somerville, NJ</td>
			<td>ET-663G</td>
			<td>For skin closure</td>
		</tr>
		<tr>
			<td>Surgical Staples&#160;</td>
			<td>Medline, Mundelein, IL</td>
			<td>STAPLER35RB</td>
			<td>For skin closure</td>
		</tr>
		<tr>
			<td>Bone Plating System</td>
			<td>Biomet, Warsaw, IN</td>
			<td>15-7378-12</td>
			<td>For bone flap securement</td>
		</tr>
		<tr>
			<td>Operating Microscope</td>
			<td>Leica Microsystems, Buffalo Grove, IL</td>
			<td>M720 OH5</td>
			<td>Used for AVM microsurgical resection</td>
		</tr>
		<tr>
			<td>BrainLab Neuronavigation Imaging System</td>
			<td>Brainlab, Inc, Chicago, IL</td>
			<td>Brainlab Curve&#160;</td>
			<td>Used for AVM microsurgical resection</td>
		</tr>
		<tr>
			<td>Lumbar External Drainage System</td>
			<td>Codman Neuro, Raynham, MA</td>
			<td>K964923</td>
			<td>Used for placement of lumbar drain for CSF drainage</td>
		</tr>
		<tr>
			<td>External Ventricular Drainage Catheter</td>
			<td>Medtronic, Minneapolis, MN</td>
			<td></td>
			<td>Used for placement of ventricular catheter for CSF drainage</td>
		</tr>
		<tr>
			<td>Disposable Raney Scalp Clips</td>
			<td>A&#38;E Medical Corporation, Farmingdale, NJ</td>
			<td>070-001</td>
			<td>Used for scalp hemostasis</td>
		</tr>
	</tbody>
</table>

comprehensive endovascular and open surgical management of cerebral arteriovenous malformations

Arteriovenious 畸形 (车辆) 与显著的发病率和死亡率相关, 并有每年3% 的破裂风险。治疗车辆必须专门针对病变, 手术切除是金标准的小, 容易接近的病变。预手术栓塞车辆可以减少尼达尔血流量, 消除高危的 AVM 功能, 如 intranidal 或静脉动脉瘤, 从而简化了一个具有挑战性的神经外科手术。在此, 我们描述了我们的方法进行分期血管内栓塞和开放切除车辆, 并强调了优势, 有全面训练的神经血管外科医生领导一个多学科的临床团队。这包括计划开颅手术和切除术, 立即跟随最后的栓塞阶段, 从而使用一个单一的麻醉期, 积极栓塞, 并迅速切除。最后, 我们提供了一个有代表性的情况下, 22-year-old 女性与破裂右额动静脉畸形诊断在癫痫发作检查, 谁成功治疗通过分期栓塞后, 开放手术切除。

一个 22-year-old 前健康女性提出新的发作发作。非对比头颅 CT 对急性出血呈阴性, 但表现为右额病变不完全特征。MRI 显示在右上额脑回 (图 1) 内有大约 2.9 x 2.4 cm Spetzler-马丁级 3 AVM, 有大量引流皮质静脉到上矢状窦, 通过右大分支的动脉供血大脑中动脉病人进行了多次分期血管内栓塞, 最终在栓塞的右脑前动脉蒂 (图 2)。在完成这些分期栓塞有剩余供...

Watch this Scientific Journal Video about Comprehensive Endovascular and Open Surgical Management of Cerebral Arteriovenous Malformations at JoVE.com

Comprehensive Endovascular and Open Surgical Management of Cerebral Arteriovenous Malformations

手术是 arteriovenious 畸形 (车辆) 的金标准, 术前栓塞可以简化这一过程。我们描述我们的方法进行分期血管内栓塞和开放切除车辆, 并提供一个有代表性的临床例子突出的优势, 全面训练的神经血管外科医生领导的多学科临床团队.

脑动静脉畸形的综合血管内和开放性手术治疗

Arteriovenious malformations (AVMs) are associated with significant morbidity and mortality, and have a rupture risk of ~3% per year. Treatment of AVMs ...

comprehensive-endovascular-open-surgical-management-cerebral

Research

JoVE Journal

Neuroscience

9.5K 次观看.  University of California, San Diego. 手术是 arteriovenious 畸形 (车辆) 的金标准, 术前栓塞可以简化这一过程。我们描述我们的方法进行分期血管内栓塞和开放切除车辆, 并提供一个有代表性的临床例子突出的优势, 全面训练的神经血管外科医生领导的多学科临床团队.

视频: Comprehensive Endovascular and Open Surgical Management of Cerebral Arteriovenous Malformations

Focal Cerebral Ischemia Model by Endovascular Suture Occlusion of the Middle Cerebral Artery in the Rat

Stroke is the leading cause of disability and the third leading cause of death in adults worldwide1. In human stroke, there exists a highly variable clinical state; in the development of animal models of focal ischemia, however, achieving reproducibility of experimentally induced infarct volume is essential. The rat is a widely used animal model for stroke due to its relatively low animal husbandry costs and to the similarity of its cranial circulation to that of humans2,3. In humans, the middle cerebral artery (MCA) is most commonly affected in stroke syndromes and multiple methods of MCA occlusion (MCAO) have been described to mimic this clinical syndrome in animal models. Because recanalization commonly occurs following an acute stroke in the human, reperfusion after a period of occlusion has been included in many of these models. In this video, we demonstrate the transient endovascular suture MCAO model in the spontaneously hypertensive rat (SHR). A filament with a silicon tip coating is placed intraluminally at the MCA origin for 60 minutes, followed by reperfusion. Note that the optimal occlusion period may vary in other rat strains, such as Wistar or Sprague-Dawley. Several behavioral indicators of stroke in the rat are shown. Focal ischemia is confirmed using T2-weighted magnetic resonance images and by staining brain sections with 2,3,5-triphenyltetrazolium chloride (TTC) 24 hours after MCAO.

Surgical induction of ischemic brain damage in the rat is a widely used model for stroke research. Here we demonstrate the induction of focal cerebral ischemia by occlusion of the middle cerebral artery. Visualization of the resulting infarct by histological staining and magnetic resonance imaging is also shown.

焦距脑缺血模型大鼠大脑中动脉的血管内缝合闭塞

Stroke is the leading cause of disability and the third leading cause of death in adults worldwide1. In human stroke, there exists a highly variable ...

科研

神经科学

Comprehensive Profiling of Dopamine Regulation in Substantia Nigra and Ventral Tegmental Area

Dopamine is a vigorously studied neurotransmitter in the CNS. Indeed, its involvement in locomotor activity and reward-related behaviour has fostered five decades of inquiry into the molecular deficiencies associated with dopamine regulation. The majority of these inquiries of dopamine regulation in the brain focus upon the molecular basis for its regulation in the terminal field regions of the nigrostriatal and mesoaccumbens pathways; striatum and nucleus accumbens. Furthermore, such studies have concentrated on analysis of dopamine tissue content with normalization to only wet tissue weight. Investigation of the proteins that regulate dopamine, such as tyrosine hydroxylase (TH) protein, TH phosphorylation, dopamine transporter (DAT), and vesicular monoamine transporter 2 (VMAT2) protein often do not include analysis of dopamine tissue content in the same sample. The ability to analyze both dopamine tissue content and its regulating proteins (including post-translational modifications) not only gives inherent power to interpreting the relationship of dopamine with the protein level and function of TH, DAT, or VMAT2, but also extends sample economy. This translates into less cost, and yet produces insights into the molecular regulation of dopamine in virtually any paradigm of the investigators' choice.
We focus the analyses in the midbrain. Although the SN and VTA are typically neglected in most studies of dopamine regulation, these nuclei are easily dissected with practice. A comprehensive readout of dopamine tissue content and TH, DAT, or VMAT2 can be conducted. There is burgeoning literature on the impact of dopamine function in the SN and VTA on behavior, and the impingements of exogenous substances or disease processes therein 1-5. Furthermore, compounds such as growth factors have a profound effect on dopamine and dopamine-regulating proteins, to a comparatively greater extent in the SN or VTA 6-8. Therefore, this methodology is presented for reference to laboratories that want to extend their inquiries on how specific treatments modulate behaviour and dopamine regulation. Here, a multi-step method is presented for the analyses of dopamine tissue content, the protein levels of TH, DAT, or VMAT2, and TH phosphorylation from the substantia nigra and VTA from rodent midbrain. The analysis of TH phosphorylation can yield significant insights into not only how TH activity is regulated, but also the signaling cascades affected in the somatodendritic nuclei in a given paradigm.
We will illustrate the dissection technique to segregate these two nuclei and the sample processing of dissected tissue that produces a profile revealing molecular mechanisms of dopamine regulation in vivo, specific for each nuclei (Figure 1).

Dopamine is distinctly regulated in the midbrain nuclei, which contain the cell bodies and dendrites of the dopamine neurons. Here we describe a dissection and sample-handling approach to maximize results, and thus conclusions and insights, on dopamine regulation in the midbrain nuclei of the substantia nigra (SN) and ventral tegmental area (VTA) in rodents.

在黑质和腹侧被盖区多巴胺调控的综合性能分析

Dopamine is a vigorously studied neurotransmitter in the CNS. Indeed, its involvement in locomotor activity and reward-related behaviour has fostered five ...

Dual Electrophysiological Recordings of Synaptically-evoked Astroglial and Neuronal Responses in Acute Hippocampal Slices

Astrocytes form together with neurons tripartite synapses, where they integrate and modulate neuronal activity. Indeed, astrocytes sense neuronal inputs through activation of their ion channels and neurotransmitter receptors, and process information in part through activity-dependent release of gliotransmitters. Furthermore, astrocytes constitute the main uptake system for glutamate, contribute to potassium spatial buffering, as well as to GABA clearance. These cells therefore constantly monitor synaptic activity, and are thereby sensitive indicators for alterations in synaptically-released glutamate, GABA and extracellular potassium levels. Additionally, alterations in astroglial uptake activity or buffering capacity can have severe effects on neuronal functions, and might be overlooked when characterizing physiopathological situations or knockout mice. Dual recording of neuronal and astroglial activities is therefore an important method to study alterations in synaptic strength associated to concomitant changes in astroglial uptake and buffering capacities. Here we describe how to prepare hippocampal slices, how to identify stratum radiatum astrocytes, and how to record simultaneously neuronal and astroglial electrophysiological responses. Furthermore, we describe how to isolate pharmacologically the synaptically-evoked astroglial currents.

The preparation of acute brain slices from isolated hippocampi, as well as the simultaneous electrophysiological recordings of astrocytes and neurons in stratum radiatum during stimulation of schaffer collaterals is described. The pharmacological isolation of astroglial potassium and glutamate transporter currents is demonstrated.

双突触诱发的星形胶质细胞和神经元的反应，在急性海马脑片电生理记录

Astrocytes form together with neurons tripartite synapses, where they integrate and modulate neuronal activity. Indeed, astrocytes sense neuronal inputs ...

Isolation and Cannulation of Cerebral Parenchymal Arterioles

Intracerebral parenchymal arterioles (PAs), which include parenchymal arterioles, penetrating arterioles and pre-capillary arterioles, are high resistance blood vessels branching out from pial arteries and arterioles and diving into the brain parenchyma. Individual PA perfuse a discrete cylindrical territory of the parenchyma and the neurons contained within. These arterioles are a central player in the regulation of cerebral blood flow both globally (cerebrovascular autoregulation) and locally (functional hyperemia). PAs are part of the neurovascular unit, a structure that matches regional blood flow to metabolic activity within the brain and also includes neurons, interneurons, and astrocytes. Perfusion through PAs is directly linked to the activity of neurons in that particular territory and increases in neuronal metabolism lead to an augmentation in local perfusion caused by dilation of the feed PA. Regulation of PAs differs from that of better-characterized pial arteries. Pressure-induced vasoconstriction is greater in PAs and vasodilatory mechanisms vary. In addition, PAs do not receive extrinsic innervation from perivascular nerves &#8212; innervation is intrinsic and indirect in nature through contact with astrocytic endfeet. Thus, data regarding contractile regulation accumulated by studies using pial arteries does not directly translate to understanding PA function. Further, it remains undetermined how pathological states, such as hypertension and diabetes, affect PA structure and reactivity. This knowledge gap is in part a consequence of the technical difficulties pertaining to PA isolation and cannulation. In this manuscript we present a protocol for isolation and cannulation of rodent PAs. Further, we show examples of experiments that can be performed with these arterioles, including agonist-induced constriction and myogenic reactivity. Although the focus of this manuscript is on PA cannulation and pressure myography, isolated PAs can also be used for biochemical, biophysical, molecular, and imaging studies.

This manuscript describes a simple and reproducible protocol for isolation of intracerebral arterioles (a group of blood vessels encompassing parenchymal arterioles, penetrating arterioles and pre-capillary arterioles) from mice, to be used in pressure myography, immunofluorescence, biochemistry, and molecular studies.

分离及脑实质小动脉插管

Intracerebral parenchymal arterioles (PAs), which include parenchymal arterioles, penetrating arterioles and pre-capillary arterioles, are high resistance ...

Optimized Management of Endovascular Treatment for Acute Ischemic Stroke

This manuscript describes a streamlined protocol for the management of patients with acute ischemic stroke, which aims at the minimization of time from hospital admission to reperfusion. Rapid restoration of cerebral blood flow is essential for the outcomes of patients with acute ischemic stroke. Endovascular treatment (EVT) has become the standard of care to accomplish this in patients with acute stroke due to large vessel occlusion (LVO). To achieve reperfusion of ischemic brain regions as fast as possible, all in-hospital time delays have to be carefully avoided. Therefore, management of patients with acute ischemic stroke was optimized with an interdisciplinary standard operating procedure (SOP). Stroke neurologists, diagnostic as well as interventional neuroradiologists, and anesthesiologists streamlined all necessary processes from patient admission and diagnosis to EVT of eligible patients. Target times for every step were established. Actually achieved times were prospectively recorded along with clinical data and imaging scores for all endovascularly treated stroke patients. These data were regularly analyzed and discussed in interdisciplinary team meetings. Potential issues were evaluated and all staff involved was trained to adhere to the SOP. This streamlined patient management approach and enhanced interdisciplinary collaboration reduced time from patient admission to reperfusion significantly and was accompanied by a beneficial effect on clinical outcomes.

The outcome of patients with acute ischemic stroke depends on swift restoration of cerebral blood flow. This protocol aims at optimizing the management of such patients by minimizing peri-procedural timings and rendering the time from hospital admission to reperfusion as short as possible.

急性缺血性中风血管内治疗的优化管理

This manuscript describes a streamlined protocol for the management of patients with acute ischemic stroke, which aims at the minimization of time from ...

A Rat Model of Mild Intrauterine Hypoperfusion with Microcoil Stenosis

Intrauterine hypoperfusion/ischemia is one of the major causes of intrauterine/fetal growth restriction, preterm birth, and low birth weight. Most studies of this phenomenon have been performed in either models with severe intrauterine ischemia or models with gradient degree of intrauterine hypoperfusion. No study has been performed in a model on uniform mild intrauterine hypoperfusion (MIUH). Two models have been used for studies of MIUH: a model based on suture ligation of either side of the arterial arcade formed with the uterine and ovarian arteries, and a transient model based on clipping the bilateral ovarian arteries and aorta having patency. Those two rodent models of MIUH have some limitations, e.g., not all fetuses are subjected to MIUH, depending on their position in the uterine horn. In our MIUH model, all fetuses are subjected to a comparable level of intrauterine hypoperfusion. MIUH was achieved by mild stenosis of all four arteries feeding the uterus, i.e., the bilateral uterine and ovarian arteries.
Arterial stenosis was induced by metal microcoils wrapped around the feeding arteries. Producing arterial stenosis with microcoils allowed us to control, optimize, and reproduce decreased blood flow with very little inter-animal variability and a low mortality rate, thus enabling accurate evaluation. When microcoils with an inner diameter of 0.24 mm were used, the blood flow in both the placenta and fetus was mildly decreased (approximately 30% from the pre-stenosis level in the placenta). The offspring of our MIUH model clearly demonstrates long-lasting alterations in neurological, neuroanatomical and behavioral test results.

Mild intrauterine hypoperfusion was produced by artery stenosis with metal microcoils wrapped around the uterine and ovarian arteries in rats at embryonic day 17. This procedure produced prenatal hypoperfusion and intrauterine growth restriction.

轻度宫内灌注圈狭窄的大鼠模型

Intrauterine hypoperfusion/ischemia is one of the major causes of intrauterine/fetal growth restriction, preterm birth, and low birth weight. Most studies ...

Comprehensive Autopsy Program for Individuals with Multiple Sclerosis

We describe a rapid tissue donation program for individuals with multiple sclerosis (MS) that requires scientists and technicians to be on-call 24/7, 365 days a year. Participants consent to donate their brain and spinal cord. Most patients were followed by neurologists at the Cleveland Clinic Mellen Center for MS Treatment and Research. Their clinical courses and neurological disabilities are well-characterized. Soon after death, the body is transported to the MS Imaging Center, where the brain is scanned in situ by 3 T magnetic resonance imaging (MRI). The body is then transferred to the autopsy room, where the brain and spinal cord are removed. The brain is divided into two hemispheres. One hemisphere is immediately placed in a slicing box and alternate 1 cm-thick slices are either fixed in 4% paraformaldehyde for two days or rapidly frozen in dry ice and 2-methylbutane. The short-fixed brain slices are stored in a cryopreservation solution and used for histological analyses and immunocytochemical detection of sensitive antigens. Frozen slices are stored at -80 &#176;C and used for molecular, immunocytochemical, and in situ hybridization/RNA scope studies. The other hemisphere is placed in 4% paraformaldehyde for several months, placed in the slicing box, re-scanned in the 3 T magnetic resonance (MR) scanner and sliced into centimeter-thick slices. Postmortem in situ MR images (MRIs) are co-registered with 1 cm-thick brain slices to facilitate MRI-pathology correlations. All brain slices are photographed and brain white-matter lesions are identified. The spinal cord is cut into 2 cm segments. Alternate segments are fixed in 4% paraformaldehyde or rapidly frozen. The rapid procurement of postmortem MS tissues allows pathological and molecular analyses of MS brains and spinal cords and pathological correlations of brain MRI abnormalities. The quality of these rapidly-processed postmortem tissues (usually within 6 h of death) is of great value to MS research and has resulted in many high-impact discoveries.

Multiple sclerosis is an inflammatory demyelinating disease with no cure. Analysis of brain tissue provides important clues to understanding the pathogenesis of the disease. Here we discuss the methodology and downstream analysis of MS brain tissue collected through a unique rapid autopsy program in operation at the Cleveland Clinic.

多发性硬化患者综合解剖计划

We describe a rapid tissue donation program for individuals with multiple sclerosis (MS) that requires scientists and technicians to be on-call 24/7, 365 ...

Simulator Training for Endovascular Neurosurgery

Simulation-based training has become common practice across medical specialties, especially for learning complex skills performed in high-risk environments. In the field of endovascular neurosurgery, the demand for consequence- and risk-free learning environments led to the development of simulation devices valuable for medical trainees. The goal of this protocol is to provide instructive guidelines for the use of an endovascular neurosurgery simulator in an academic setting. The simulator provides trainees with the opportunity to receive realistic feedback on their knowledge of anatomy, as well as haptic feedback indicative of their success in handling the catheter-based systems without negative consequences. The utility of this specific protocol in relation to other neuroendovascular training modalities is also discussed.

Simulation of complex, high-risk procedures is critical to the education of medical trainees. A protocol for simulator-based endovascular neurosurgery training in a controlled academic environment is described. The protocol includes stepwise guidelines for trainees of varying levels, with a discussion of the advantages and limitations of this model.

血管内神经外科模拟器培训

Simulation-based training has become common practice across medical specialties, especially for learning complex skills performed in high-risk ...

Endovascular Perforation Model for Subarachnoid Hemorrhage Combined with Magnetic Resonance Imaging (MRI)

The endovascular filament perforation model to mimic subarachnoid hemorrhage (SAH) is a commonly used model - however, the technique can cause a high mortality rate as well as an uncontrollable volume of SAH and other intracranial complications such as stroke or intracranial hemorrhage. In this protocol, a standardized SAH mouse model is presented, induced by endovascular filament perforation, combined with magnetic resonance imaging (MRI) 24 h after operation to ensure the correct bleeding site and exclude other relevant intracranial pathologies. Briefly, C57BL/6J mice are anesthetized with an intraperitoneal ketamine/xylazine (70 mg/16 mg/kg body weight) injection and placed in a supine position. After midline neck incision, the common carotid artery (CCA) and carotid bifurcation are exposed, and a 5-0 non-absorbable monofilament polypropylene suture is inserted in a retrograde fashion into the external carotid artery (ECA) and advanced into the common carotid artery. Then, the filament is invaginated into the internal carotid artery (ICA) and pushed forward to perforate the anterior cerebral artery (ACA). After recovery from surgery, mice undergo a 7.0 T MRI 24 h later. The volume of bleeding can be quantified and graded via postoperative MRI, enabling a robust experimental SAH group with the option to perform further subgroup analyses based on blood quantity.

Endovascular Perforation Model for Subarachnoid Hemorrhage Combined with Magnetic Resonance Imaging MRI

Here we present a standardized SAH mouse model, induced by endovascular filament perforation, combined with magnetic resonance imaging (MRI) 24 h after operation to ensure the correct bleeding site and exclude other relevant intracranial pathologies.

蛛网膜下腔出血结合磁共振成像（MRI）的血管内穿孔模型

The endovascular filament perforation model to mimic subarachnoid hemorrhage (SAH) is a commonly used model - however, the technique can cause a high ...

Comprehensive Understanding of Inactivity-Induced Gait Alteration in Rodents

It is well known that disuse affects neural systems and that joint motions become altered; however, which outcomes properly exhibit these characteristics is still unclear. The present study describes a motion analysis approach that utilizes three-dimensional (3D) reconstruction from video captures. Using this technology, disuse-evoked alterations of walking performances were observed in rodents exposed to a simulated microgravity environment by unloading their hindlimb by their tail. After 2 weeks of unloading, the rats walked on a treadmill, and their gait motions were captured with four charge-coupled device (CCD) cameras. 3D motion profiles were reconstructed and compared to those of control subjects using the image processing software. The reconstructed outcome measures successfully portrayed distinct aspects of distorted gait motion: hyperextension of the knee and ankle joints and higher position of the hip joints during the stance phase. Motion analysis is useful for several reasons. First, it enables quantitative behavioral evaluations instead of subjective observations (e.g., pass/fail in certain tasks). Second, multiple parameters can be extracted to fit specific needs once the fundamental datasets are obtained. Despite hurdles for broader application, the disadvantages of this method, including labor intensity and cost, may be alleviated by determining comprehensive measurements and experimental procedures.

The present protocol describes three-dimensional motion tracking/evaluation to depict gait motion alteration of rats after exposure to a simulated disuse environment.

全面了解啮齿动物不活动引起的步态改变

It is well known that disuse affects neural systems and that joint motions become altered; however, which outcomes properly exhibit these characteristics ...