硬脑膜动静脉瘘介入诊断及治疗
硬脑膜动静脉瘘的介入诊断及治疗
NBCA
海绵窦DAVF
• 经静脉途径是首选的治愈性的方法
– 经岩下窦入路（闭塞时亦可通过） – 经眼上静脉入路 – 其它入路：岩上窦、对侧海绵窦、基底静脉丛
L-ECA
Spontaneous regression of a cavernous sinus DAVF
T2WI image shows multiple flow voids in the posterior cavernous sinus Left ECA angiogram shows a cavernous sinus dural AVF with posterior drainage into the inferior and superior petrosal sinuses Follow-up MR image shows resolution of the flow voids
L
TVE of DAVF via an occluded inferior petrosal sinus
Left ECA angiogram shows a cavernous sinus DAVF draining mainly into the inferior petrosal sinus and pterygopharyngeal plexus Follow-up angiogram obtained 3 months later shows that the inferior petrosal sinus is occluded, and the dural AVF now drains into the superior ophthalmic vein and the superficial middle cerebral vein .Although the patient’s symptoms were unchanged, occlusion of the DAVF was indicated
硬脑膜动静脉瘘介入诊治的新进展-最新年精选文档
硬脑膜动静脉瘘介入诊治的新进展1. 分型和临床表现鉴于DAVFs痿口位置和引流血管构筑的不同，其临床表现也有很大的差异[1] 。
这些临床表现主要包括突眼、颅内血管杂音、颅神经功能障碍、耳鸣、出血、颅内压升高、视神经乳头水肿，严重时甚至有发生充血性心衰的可能。
关于DAVFs的分型有几种，主要的两类分型分别以瘘口位置和引流静脉作为依据。
目前使用最多的分型是Cognard等人和Borden等人制定的分型。
这些分型的共同点是都以DAVFs的引流静脉作为区分的重点，单纯与静脉窦连接、血流为顺行的DAVFs其临床表现相对较轻微，而血流为逆流并有皮层静脉参与的DAVFs则表现出较严重的症状如颅内出血、颅神经功能障碍、颅内压升高等。
以1995 年Cognard等人制定的Cognard分型为例[2] : I型，DAVFs位于静脉窦内，血流为顺行，症状主要为搏动性耳鸣和颅内血管杂音；n 型，DAVFs位于静脉窦内，血流为逆流入静脉窦或皮层静脉，症状以颅内出血、颅神经功能障碍等为主；m型，皮层静脉直接引流，无静脉扩张，临床症状以颅内出血为主；W型，皮层静脉直接引流，有静脉扩张，具有占位效应，临床症状以中枢神经系统症状、颅高压为主，其发生颅内出血的可能性也最大；^型，血液引流入脊髓的髓周静脉，导致椎管内静脉压升高，脊髓缺血，临床表现为锥体束征阳性。
2.介入治疗的进展DAVFs的治疗应重视个体化治疗，充分考虑到疾病的病史、血管构筑情况和临床症状的严重程度。
其治疗原则为尽可能充分、彻底地闭塞瘘口，同时不影响正常的静脉回流[3]。
DAVFs 的治疗方法包括传统外科手术、放射外科、介入治疗以及综合治疗。
区别于前两种治疗方法，介入治疗可使栓塞材料直接到达病灶血管，闭塞瘘口，减少了一系列并发症。
随着技术和栓塞材料的不断进步，介入治疗逐渐成为治疗DAVFs的首选方法，尤其是在一些复杂的、高风险的DAVFs中，外科手术仅用于介入治疗无法实施的病患。
硬脑膜动静脉瘘及其治疗策略
主要辅助诊断
1．血管造影 2. TC D 由于动静脉间直接交通，缺乏血管阻力， 局部血流量增加，血液循环加快，使供血动脉 血流速度增高、搏动指数降低，这是TC D 识 别供血动脉的重要依据，脉动传递指数（PTI） 是确定硬脑膜动静脉瘘供血动脉的敏感指标； 3．CT 、CTA ; 4．M RI 、M RA ;
栓塞治疗的主要入路
1．动脉入路 ； 2．静脉入路； 3．局部钻孔穿刺硬脑膜窦 ； 4．联合入路 。①先行动脉入路栓塞，使D A VF 瘘口血流速度降低；②瘘口血流降 低后由静脉插管，将微导管逆行送至静 脉窦瘘口处填入可脱性球囊或微弹簧圈 闭塞瘘口。
静脉入路和直接穿刺静脉窦栓塞 两种方法的优点
①经动脉无法进入瘘口者可用此法栓塞； ②用此法栓塞剂通过瘘口的血管到正常毛 细血管床的可能性小； ③由于供血动脉未闭塞，必要时还可以经 动脉途径行二次栓塞。
DAVF的分型
（一） 瘘口部位 Herber 根据瘘口部位将D A V F 分为四类： ①后颅窝D A V F ， 供血动脉主要为枕动脉； ②中颅窝D A V F ，供血动脉主要为脑膜中动脉后支； ③前颅窝D A VF ，供血动脉主要为脑膜中动脉前支； ④海绵窦旁D A V F ，供血动脉主要为脑膜中动脉和颌 内动脉分支。
常见DAVF的部位分布及其治疗策略
（5） 早或双侧前颅窝、大脑镰区，占5.8%。 主要供血动脉来自单或双侧的颈内动脉眼动 脉的筛前动脉、筛后动脉的分支脑膜前动脉、 大脑镰硬脑膜的分支，颈外动脉的分支脑膜 中动脉的脑膜支。瘘回流入矢状窦、海绵窦、 蝶顶窦。宜选择血管内栓塞治疗和开颅手术。 结扎切除畸形血管。
常见DAVF的部位分布及其治疗策略
（2） 单或双侧海绵窦区， 占12 ％ 。 主要供血动脉来自单或双侧颈外动脉的分 支咽升动脉、颌内动脉的分支，颈内动 脉的脑膜支、脑膜垂体干、海绵窦下动 脉。瘘回流入单或双侧海绵窦。宜选择 血管内栓塞治疗，必要时配合经岩上 （下） 窦人路栓塞海绵窦，以阻断颈内 动脉海绵窦段的脑膜支。
硬脑膜动静脉瘘干预护理
疼痛程度：采用视觉模拟评分法评估患者疼痛程度 护理前后护理效果各指标对应的评价量表进行评价，分数越高，护理效果越好 患者对护理前后护理效果的满意度评价量表进行评价，分数越高，护理效果越好 患者生活质量评价量表进行评价，分数越高，护理效果越好
患者自我评估： 患者对护理效果 的主观感受和评 价
护理效果量表评 估：使用标准化 的量表对护理效 果进行客观评估
按病因分类：创伤性、自发性、医源性等 按瘘口大小分类：大瘘、小瘘 按病理特点分类：单纯性、复杂性 按病变部位分类：前部、后部、顶部、底部等
头痛：反复发作的头痛，通常在用力或咳嗽时加重
视力障碍：视野缺损、视物模糊等 颅内出血：硬脑膜动静脉瘘破裂导致颅内出血，出现意识障碍、偏瘫等症 状 癫痫：硬脑膜动静脉瘘刺激脑组织导致癫痫发作
创伤：颅脑外伤或手术损伤可能导致硬脑膜动静脉瘘的发生。 感染：颅内感染可能引起硬脑膜动静脉瘘。 肿瘤：部分肿瘤疾病可能导致硬脑膜动静脉瘘的发生。 先天性因素：部分患者可能由于先天性因素导致硬脑膜动静脉瘘。
关注患者情绪 变化，及时给 予心理支持和
疏导。
讲解疾病知识 和治疗过程， 增强患者信心
和配合度。
定期进行体检，及早发现硬脑膜 动静脉瘘。
避免过度劳累和精神压力，保持 心情愉悦。
保持健康的生活方式，如合理饮 食、适量运动等。
如有疑虑或出现相关症状，及时 就医检查。
定期进行脑部影像学检查，监测硬脑膜动静脉瘘的变化情况 密切关注患者症状和体征，如头痛、视力障碍等，及时发现异常情况 建立健康档案，记录患者病情和治疗情况，便于跟踪随访 加强患者教育，提高患者对硬脑膜动静脉瘘的认识和自我管理能力
汇报人：
目录
CONTENTS
硬脑膜动静脉瘘 是一种脑血管疾 病，发生在硬脑 膜上的动静脉之 间形成异常的交 通。
硬脑膜动静脉瘘的介入治疗
硬脑膜的解剖
DAVF形成的解剖学基础
• 双层结构 内骨膜层 与 脑膜层 • 在枕骨大孔区，外层形成环枕筋膜并延续成椎管的内骨膜
层，内层延续为硬脊膜 • 硬膜静脉和静脉窦位于两层之间，与椎管的硬膜外静脉丛
相对应 • 供应脑或脊髓的动脉在其穿过硬膜时，发出脑膜支硬膜动
脉，位于硬膜的外层，与硬膜静脉十分接近
• 禁忌证
–如超选择性插管不能避开危险吻合或正常脑组织的 供血动脉,则不能栓塞 。
–对前颅窝区DAVF ,其由眼动脉的筛前、后动脉供血, 虽然有经动脉栓塞的成功报道,但其往往会误栓眼 动脉而致失明,故大多数学者认为栓塞是禁忌的
介入治疗--动脉入路
• 仍是目前应用最多的入路。
• 导管尖端送到供血动脉远端的瘘口附近, 根据具体情况选用不同的栓塞材料来闭塞 瘘口, 栓塞材料越接近瘘口越好！
–胚胎发育过程中脑血管发育异常硬脑膜内的“生理性 动静脉交通”增加/静脉窦附近的血管异常增生硬脑 膜动静脉瘘
病因
• 获得性学说
– 与脑静脉窦血栓形成关系 – “恶性循环”学说 – 雌激素 – 新血管生成学说
脑静脉窦血栓形成DAVF
• 三种学说
“生理性动静脉交通”开放学说 肌源性自我调节障碍学说 血栓机化学说
–压力梯度再次发生逆转(如血栓发生部分再通或静 脉窦内血流发生大的变化等) 流入压再度
流入A - V 交通的血流 – ···A-V 交通血管阻力不可逆丧失通过AV 交通的
血流量 (∵Venturi 效应即 真空泵现象) 毛 细血管和微小动脉直径 生理性AV 交通形态 学改变病理性交通
其他
• 心功能不全：高流瘘，长期得不到有效的 治疗,可增加心脏负担
诊断
• 临床特征+辅助检查（ DSA/MRA/CTA /MRI/CT/TCD）
硬脑膜动静脉瘘的介入治疗- Neurology
Lin Bo Zhao,MDDae Chul Suh,MD,PhD Dong-Geun Lee,MD Sang Joon Kim,MD, PhDJae Kyun Kim,MD Seungbong Han,PhD Deok Hee Lee,MD,PhD Jong Sung Kim,MD, PhDCorrespondence toDr.Suh:dcsuh@amc.seoul.kr Association of pial venous reflux with hemorrhage or edema in dural arteriovenous fistulaABSTRACTObjective:We investigated whether pial venous reflux(PVR)is associated with hemorrhage or edema in dural arteriovenous fistula(DAVF).Methods:We evaluated the association of hemorrhage or edema with the occurrence of PVR or cortical venous reflux(CVR)in222patients with DAVF.We determined whether angiographic findings of PVR or CVR(more than Borden I or Cognard IIa)were associated with symptoms, lesion location,or brain lesion(hemorrhage or edema).We evaluated the lesion progression or the follow-up results after obliteration of the DAVF.Results:Hemorrhage or edema developed in18%(40/222)of the patients with DAVF and55% (40/72)of the patients with PVR.There were2patterns of PVR associated with hemorrhage or edema:(1)PVR in any particular CVR territory(75%),and(2)direct PVR not via CVR(25%).The presence of brain lesion increased the odds of presence of PVR by4.09times compared to the group without brain lesion(95%confidence interval51.570–11.394,p50.004).Brain edema caused by PVR was reversible after obliteration of the fistula and may have progressed to hem-orrhage without proper patient management performed within several weeks after the initial presentation.Conclusions:Our results show that PVR is more closely associated with the hemorrhage or edema than CVR in patients with DAVF.PVR can occur not only as a part of CVR but also directly in cer-tain types of DAVF.Neurology®2014;82:1897–1904GLOSSARYCVR5cortical venous reflux;DAVF5dural arteriovenous fistula;GK5gamma knife;mRS5modified Rankin Scale;PVR5 pial venous reflux;SAH5subarachnoid hemorrhage.Current classifications of dural arteriovenous fistula(DAVF)are focused primarily on the pres-ence of cortical venous reflux(CVR)related to cerebral venous hypertension leading to cerebral infarction or hemorrhage.1–3CVR is known to be related to the so-called aggressive type of DAVF because29%to46%of patients with CVR may develop cerebral hemorrhage.4–6How-ever,it has not been precisely determined why hemorrhage or edema in certain brain areas is related to CVR.Pial venous reflux(PVR),a part of CVR,has not been clearly identified or differentiated from CVR.7However,there have been only a few descriptions of the relationship of PVR to CVR and the location of their anatomical junction.The aim of this study was to investigate the relationship of PVR vs CVR to hemorrhage or edema.To achieve this,we assessed serial angiographic and cross-sectional imaging findings of CVR and PVR associated with hemorrhage or edema.We then present a concept regarding how PVR occurring in patients with CVR is related to hemorrhage or edema.METHODS We reviewed prospectively collected records of222consecutive patients diagnosed with DAVF at a single medical insti-tution(Asan Medical Center,Seoul,Korea)between July1998and October2012.We analyzed the patients’angiographic findings andFrom the Department of Radiology and Research Institute of Radiology(L.B.Z.,D.C.S.,D.-G.L.,S.J.K.,D.H.L.)and Department of Neurology (J.S.K.),University of Ulsan,College of Medicine,and Department of Epidemiology and Biostatistics(S.H.),Asan Medical Center,Seoul,Korea; Department of Radiology(L.B.Z.),First Affiliated Hospital of Nanjing Medical University,Nanjing,China;and Department of Radiology(J.K.K.), Chung-Ang University,College of Medicine,Seoul,Korea.Go to for full disclosures.Funding information and disclosures deemed relevant by the authors,if any,are provided at the end of the article.©2014American Academy of Neurology1897medical records to assess the patient demographics,the presence of brain lesions(hemorrhage or edema),shunt localization,and the presence of CVR or PVR.We excluded pial-type brain arteriovenous malformations with a dural supply.Selective angiography of the internal carotid artery,external carotid artery,and vertebral arteries was obtained using high-resolution, biplane,digital subtraction angiography(AXIOM Artis zee biplane angiography system;Siemens AG Medical Solutions, Erlangen,Germany).The clinical symptoms were separated into2groups,i.e., benign and aggressive.8The benign group consisted of an inci-dental diagnosis,nonspecific headaches,cranial nerve deficits, chemosis/proptosis,bruit or pulsatile tinnitus,mass lesions,and cardiac insufficiency.The aggressive group included seizures, intracranial hemorrhage,motor or sensory deficits,visual field defects,aphasia,global neurologic deficits(dementia,delayed psychomotor development,macrocrania),and other nonhemor-rhagic neurologic deficits such as incontinence.We did not mea-sure the venous pressure either directly or indirectly.Standard protocol approvals,registrations,and patient consents.The institutional review board approved the study, and written informed consent was obtained from each patient.MRI/CT findings.Patients who presented with hemorrhage or edema seen on MRI/CT obtained before treatment were analyzed and classified into3subgroups:(1)hemorrhage,defined as paren-chymal or subarachnoid hemorrhage(SAH)with little or no edema;(2)edema,defined as parenchymal edema with no evi-dence of hemorrhage;or(3)edema combined with hemorrhage, defined as both edema and hemorrhage,with the edema being disproportionate to the amount that would be expected surround-ing a parenchymal hemorrhage.We correlated symptoms,lesion locations,and angiographic types.The patients who presented with acute neurologic deficits underwent an imaging study accord-ing to our acute stroke protocol,and which therefore included fluid-attenuated inversion recovery imaging(n528),diffusion-weighted imaging(n524),apparent diffusion coefficient imaging (n520),and perfusion imaging(n55).One patient who presented with a brainstem sign showed MRI findings mimicking brainstem tumor and thus underwent magnetic resonance spectroscopy.Because the application of MRI/CT studies varied according to the attending physician or patient’s presenting symptom,analysis of imaging studies was based on the neuroradiologist’s report and was additionally reviewed by consensus of2experienced neuroradiologists(S.J.K.and D.C.S.). Angiographic typing.Angiographically,benign and aggressive lesions were defined according to the absence or presence of CVR9and were also grouped using the classification systems of Borden2and Cognard.1Borden I(sinus drainage only),Cognard I (antegrade sinus drainage without CVR),and Cognard IIa(retro-grade sinus drainage without CVR)were considered as“benign”DAVFs,whereas all of the higher grades that have cortical and spinal drainage with or without sinus drainage were grouped as“aggressive”DAVFs.10,11The main locations of DAVFs were categorized as the cavernous sinus,the transverse-sigmoid sinus,the superior sagittal sinus,the ethmoidal roof,and the petrous area.We also identified a new type of DAVF lesion in the parietotemporal convexity and defined it as parietotemporal convexity DAVF.CVR vs PVR.The presence of cortical and pial venous drainage was determined.Veins were defined as“cortical”when they coursed along the cortical surface draining into the venous sinus and as“pial”when the fine and tortuous veins were within the brain or on the brain surface,as seen on cerebral angiography (figure1E)and/or MRI.Presence of PVR was also decided by comparison with cortical veins in the venous phase of the ipsilat-eral internal carotid arteriogram(figure2,G and J).Compared with cortical veins,which are regarded as the main leptomeningeal veins draining into sinus,the fine pial veins or the intracortical veins beneath the pial membrane were regarded as having a corkscrew-like appearance or intraparenchymal course,12which cannot be seen on a routine normal angiogram(figures1E,2I,and3J).We did not apply any size criteria for the differentiation because the pial vein is much smaller and more peripherally located than the cortical vein. In patients who underwent serial imaging studies,their presenting symptom pattern was compared with the development of a brain lesion according to the time interval.Follow-up.Follow-up data for the222study patients were col-lected from the time of their admission until the end of2012.A complete history was obtained from each patient,and a neurologic examination was performed by independent neurologists who were not involved in the interventional procedure.If a patient was not followed up or the patient’s status was not exactly mentioned in an outpatient clinic,an experienced nurse telephoned the patients to evaluate the possibility of any clinically relevant event.Functional outcome was assessed with the modified Rankin Scale(mRS).13 Median clinical follow-up of all patients was15months (range1–178months),and final outcome was evaluated using the mRS,as shown in the table.The40patients with hemorrhage or edema were followed for a median of12months(range1–155 months).Treatment included embolization in23,gamma knife (GK)irradiation in6,surgical resection in5,and no treatment in 6patients.14Good(mRS score#2)vs poor(mRS score.2) outcome was compared for each treatment modality. Statistical methods.Cross-tabulations using patient sex,age, angio-type(benign vs aggressive),clinical symptoms group (benign vs aggressive),lesion location,brain lesion(hemorrhage or edema),and the presence of CVR or PVR were performed. Statistical significance was calculated for each group using the Fisher exact test and t test for categorical variables and continuous variables,respectively.We conducted univariate and multivariable analyses using variables that were significant in frequency or mean comparison between the presence and absence of PVR compared with the presence of CVR without PVR.Because lesion location was the cavernous sinus in62%of patients and the frequency of some category levels for the other lesion locations was small,we regrouped lesion location into a smaller number of categories(the cavernous sinus vs others).15Similarly,we regrouped135patients with the presence of CVR into presence or absence groups of the brain lesion.The univariate and multivariable logistic regression model proposed by Firth was fitted for the binary outcome variable.This method can handle the separation problem occurring when some categorical levels have zero counts of brain lesion as in the patients with CVR but without PVR.16All statistical analyses were performed using SPSS18software(SPSS Inc., Chicago,IL)and R software(R Foundation for Statistical Computing,Vienna,Austria;).The R package “logistf”was used to fit the bias-reduced logistic regression model.17 Significance was determined at p,0.05.We retrospectively computed the statistical power under some assumptions.Group sample sizes of42in group1with brain lesion and84in group2without brain lesion achieve90%power to detect a difference between the group proportions of0.3.The pro-portion in group1is assumed to be0.3under the null hypothesis and0.6under the alternative hypothesis.The proportion in group 2is0.3.The test statistic used was the2-sided z test with pooled variance.The significance level of the test was targeted at0.05.1898Neurology82May27,2014RESULTS Baseline characteristics.The baseline clini-cal and angiographic features of the 222patients with intracranial DAVF are summarized in the table.There were 134women (60%)and 88men (40%)with a mean age at admission of 57years (range 14–85years).The most common DAVF location was the cavernous sinus region (137patients [62%])followed by the transverse and sigmoid sinus regions (38pa-tients [17%]).Major presenting symptoms or signs in patients who presented with hemorrhage or edema were altered consciousness (n 511),orbital/ocular symptoms related to the brain/brainstem (n 55),neurologic deficit (n 511),seizure (n 56),severe headache (n 56),and dizziness (n 51).Seizure developed in patients with edema in the parietal lobe due to the DAVF of the parietotemporal convexity (n 55)or superior sagittal sinus (n 51)(figure 2).MRI/CT findings.Forty patients presented with hem-orrhage or edema,as seen on MRI/CT.Twenty-nine patients revealed hemorrhage associated with (n 523)or without (n 56)surrounding edema (figure 1).Eleven patients only had edema without evidence of hemorrhage (figure 2).Among the 29patients with hemorrhage,27presented with parenchymal hemorrhage,one presented with intracerebral hemorrhage followed by massive SAH,and one presented with massive SAH with acute hydrocephalus.The location of the hemorrhage was lobar (n 518),the cerebellar hemisphere (n 56),and the brainstem (n 54).One patient who presented with a brainstem sign showed MRI findings mimicking brainstem tumor,but magnetic resonance spectroscopy did not reveal any evidence of tumor or ischemia (figure 3).CVR vs PVR.The distribution of CVR and PVR in222patients is presented in the table.There was no CVR in 39%,CVR only in 28%,CVR and PVR in 28%,and PVR only in 5%.Presence of PVR in 72patients (32%)was associated with hemorrhage or edema (p ,0.001).Among 40patients (18%)who developed hemorrhage or edema,30patients (75%)revealed the presence of CVR and PVR (figure 1).Ten patients (25%)revealed direct filling of PVR not via CVR (figure 2).Univariate analysis revealed that the presence of brain lesion (hemorrhage or edema)increased the odds of the presence of PVR by 5.68times compared with the group without brain lesion (95%confidence interval 52.571–13.369,p ,0.001).Compared with the cavernous sinus location,other locations increased the odds of presence of PVR by 2.80times.Focal cerebral edema with development of subsequent hemorrhage in a 66-year-old woman who presented with neurologic deficit.A magnetic resonance fluid-attenuated inversion recovery image (A)shows localized high signal intensity in the right parietal subcortical area.(B)CT imaging obtained 10days later showed focal hemorrhage surrounded by edema in the same area of the right parietal lobe.Anteroposterior (C)and lateral (D)views of the right external carotid arteriogram show a dural arteriovenous fistula in the superior sagittal sinus (SSS)supplied by the middle meningeal and superficial temporal arteries.There is occlusion of the SSS (white arrows in D and E).Note the diffuse corkscrew-like tortuous,fine pial venous engorge-ment (black arrows)in the late venous phase (E).Her neurologic deficit remained after obliteration of the fistula by intrao-perative coil embolization.Neurology 82May 27,20141899Moreover,aggressive symptoms increased the odds of presence of PVR by 3.23times compared with the benign symptom group.In the multivariable analysis,after adjusting for location and aggressive symptoms,presence of brain lesion was still significant and increased the odds of presence of PVR by 4.09times compared with the group without brain lesion (95%confidence interval 51.570–11.394,p 50.004).Follow-up results.During median 15months offollow-up,there was no difference in good vs poor outcome,likely because the patients with aggressive angio-type underwent active treatment while the others did not (table).During the follow-up period,there were 3patients who developed hemorrhage (n 52)in patients with PVR and hydrocephalus (n 51)in a patient with CVR.A successful treatment outcome (mRS score #2)was obtained in 33of the 40patients:20by emboli-zation,5by GK irradiation,4after surgery,and 4who received no treatment.18There was a poor treatment outcome (mRS score .2,n 57)in 3patients who underwent embolization,one who had surgery,one after GK irradiation,and in 2patients with no treat-ment.Of 29patients who presented with hemorrhage,26were treated using endovascular techniques (n 521,transarterial or transvenous or both),DAVF-resection surgery (n 53),or by GK irradiation (n 52)as the first treatment option.Five patients under-went combined therapy because of incomplete removal of the fistula using GK treatment (n 51)or surgery (n 51)followed by embolization or embolization fol-lowed by surgery (n 52)or GK treatment (n 51).The patients who had presented with hemorrhage showed complete resolution of the hemorrhage on follow-up imaging,and no patient revealed recurrent hemorrhage during the follow-up period.Of the 11patients who presented with brain edema only,8underwent endovascular treatment and 3were lost to follow-up after either GK treatment (n 52)or no treatment (n 51).The edema resolved completely in 7of these patients,as seen on MRIs obtained 2months after treatment (figures 2and 3);edema decreased in one patient after a follow-up period of 1month.Progression of brain lesions.Eight patients developedbrain lesions during the follow-up period.Brain edema (n 52,both 3months after their initial diagnosis)or hemorrhage (n 52,1and 8months after the initial diagnosis)appeared after initial MRI studies were normal.In the patients whopresentedLocalized cerebral edema in a 62-year-old man who presented with right-side myoclonus and tonic seizure.A gradient echo image obtained at the time of the seizure (A)shows a focal edema and dark signal along the left frontoparietal cortex.MRI obtained 3months later shows aggravated edema on T2-weighted image (B)and on T1-weighted image (C).Gadolinium-enhanced image shows slight enhancement along the cortical margin (D).T2-weighted image obtained 4years after embolization (E)shows normalized brain parenchyma without any other neurologic deficit.Note only a faint iron deposition along the cortical margin.Anteroposterior (F)and lateral (G)views of the external carotid angiogram show the superficial temporal artery supplying a dural arteriovenous fis-tula over the left parietal convexity via the emissary artery (thick,short arrows)into the pial veins (thick,long arrows).Note collateral filling of a remote pial vein (thin,long arrow in G –K)via the intracortical veins (thin,short arrows in G –K).Selective anteroposterior (H)and lateral (I)angiograms obtained at the emissary artery show pial venous reflux filling to the intracortical veins (thin,short arrows in G –K)as well as intraparenchymal collateral to the other pial vein (thin,long arrows in G –K).The venous phase of the internal carotid arteriogram (J),in contrast to pial venous reflux,shows no visible abnormality in the cortical venous drainage.Schematic drawing (K)shows a shunt filling the pial vein (thick,long arrow)and the other pial vein filling (thin,long arrow)via the intraparenchymal veins (thin,short arrows).Note cortical veins in the subarachnoid space (pink-colored space).The reason the fistular shunt flow remains in the pial venous system is suggested by thrombosed disconnection (asterisk)of pial-cortical venous drainage.1900Neurology 82May 27,2014with brain edema,there was aggravation of the edema (n 52,1and 3months after initial MRI)(figure 2),development of hemorrhage (n 51,10days after initial MRI)(figure 1),or even improvement with some residual encephalomalacia (n 51,1.5years after initial MRI).The locations of these lesions were the parietotemporal convexity (n 54),cavernous sinus (n 52),superior sagittal sinus (n 51),and transverse-sigmoid sinus (n 51).DISCUSSION Our study suggests that PVR is moreclosely related to hemorrhage or edema.PVR was associated with hemorrhage or edema in 75%of pa-tients and was related to a certain brain area,whereas CVR occurred in a wide vascular territory.Our study also revealed that PVR was found without filling of the cortical vein in a certain type of DAVF in 25%of patients with hemorrhage or edema.Therefore,presence of PVR should be identified in addition to the CVR,which is currently known as a risk factor for hemorrhage in DAVF.19–21In addition,DAVF diagnosis needs to be considered when there is corkscrew-like pial venous engorgement in patients who reveal brain lesion associated with seizure or neurologic deficit.In contrast to arterial ischemic infarction,many parenchymal abnormalities secondary to venous con-gestion are reversible.22If venous hypertension can be relieved before cell death or intracranial hemor-rhage,the parenchymal changes may partially or com-pletely resolve.However,if venous pressure continues to increase,with a consequent reduction in arterial perfusion pressure,cell death may ensue.Our study revealed that edema after embolization was progres-sively completely resolved,although the edema re-mained during the initial short-term follow-up period.Three levels of cortical veins have been described,i.e.,the main leptomeningeal veins,the fine pial net-work,and the intracortical veins.12The main lepto-meningeal veins are located in the pia matter on the surface of the cortex.Pial veins form a dense superfi-cial network 23and they have been found to pass over sulci without entering them.24If the DAVF hemor-rhage is caused by rupture of the main leptomenin-geal veins,it should present more frequently with SAH than with hemorrhage.25This anatomical aspect also demonstrates that it is the intracortical veins or pial veins rather than the main leptomeningeal veins that rupture secondary to venous hypertension in pa-tients with cerebral DAVF.20The diameters oftheA 49-year-old man presented with diplopia,dizziness,and mild dysarthria.A T2-weighted image (A)shows high signal intensities in the left cerebellar pedun-cle and pons.There are no definite signal changes on diffusion-weighted imaging (B)and slightly increased signal intensity on apparent diffusion coefficient image (C).Susceptibility-weighted imaging (D)shows the dilated petrosal vein in the left cerebellopontine angle (long,white arrow)and intracortical venous engorgement (short,white arrow).A perfusion imaging study shows increased mean transit time (E),decreased cerebral blood flow (F),and decreased cere-bral blood volume (G)at the areas of round cursors on the high signal intensities on panel A.Perfusion curve (H)shows decreased perfusion status in the brain edema area (red line)compared with the contralateral normal side (blue line).Single-voxel spectroscopy (I)obtained at the left middle cerebellar peduncle with marked gadolinium enhancement shows decreased choline (Cho)and creatine peak and relatively preserved N -acetyl aspartate (NAA)peak with decreased Cho/NAA ratio suggesting a nontumorous condition.Preembolization (J)and postembolization (K)external carotid angiograms show disappear-ance of a fistular shunt and the engorged petrosal vein (long arrow in J).Note fine corkscrew-like pial veins (short arrows).Fluid-attenuated inversion recovery image obtained 8months after embolization (L)shows normalized brain parenchyma without any other neurologic deficit.Neurology 82May 27,20141901intracortical veins measured by photon microscopy studies were ,80m m,26which could not be detected on 3-tesla MRI or on cerebral digital subtraction angi-ography.Until now,there have been no literature reports describing the diameters of intracranial veins in patients with DAVF.The presence of susceptibility-weighted imaging hyperintensity within the venous structure could be a useful indicator of retrograde leptomeningeal venous drainage in patients with DAVF,although it did not distinguish the 3levels of the cortical vein.27There must be a subarachnoid-pial junction as seen in the cortical veno-dural junction that has a particular role in the cor-tical venous drainage of the brain.This subarachnoid-pial junction was also well demonstrated in a recent embryo-logic study in which it was seen that vessels penetrated the glial membrane into the brain substance.28Because our study is limited by its retrospective design even though we prospectively collected the data at the time of enrollment,we could not provide pro-spective sample size calculation.In addition,we did not obtain the imaging follow-up results especially for the benign symptom group or CVR without brain lesion.Although we described the association of PVR with cerebral hemorrhage or edema,we could not provide a distinctive anatomical demarcation of the cortico-pial venous junction because there was a smooth continuation of the venous drainage at the junctional zone at the pial membrane to the cortical vein,which is located in the subarachnoid space.High-resolution MRI obtained at more than 7tesla may demonstrate the anatomical relationship in the future study.We assumed that there must bearachnoid-duro-pialAbbreviations:CVR 5cortical venous reflux;FU 5follow-up;mRS 5modified Rankin Scale;P-T 5parietotemporal;PVR 5pial venous reflux;SSS 5superior sagittal sinus;Sx 5symptom;T-S 5transverse sigmoid.Data are n (%)unless otherwise indicated.15presence;25absence.aBorden type I or Cognard I 1IIa.bBorden type II and III or Cognard type more than IIb.cThree patients with osseous dural arteriovenous fistula,one patient with multiple dural arteriovenous fistulae.dMultivariable analysis,after adjusting for location and aggressive symptom group,revealed that the presence of brain lesion is still significant and increases the odds of presence of PVR by 4.09times compared with the group without brain lesion (95%confidence interval 51.570–11.394,p 50.004).1902Neurology 82May 27,2014adhesion or occlusion of the cortico-pial junction pre-cluding cortical venous drainage and diverting angioge-netic shunt flow into the pial veins.29However,further anatomical or pathologic studies will be required to support this hypothesis.Our study suggests that PVR is more closely related to brain lesions,such as hemorrhage or edema,than CVR in patients with DAVF.PVR can occur not only as a part of CVR but also directly in certain types of DAVF.Hemorrhage may be secondary to venous edema or the rupture of small cortical veins,especially intracortical veins,because PVR,as a newly proposed concept,may be more closely correlated with venous edema and hemorrhage.Further studies will be required to support the concept and to demonstrate the close relationship between PVR and the aggressive clinical behavior seen in patients with cerebral DAVF. AUTHOR CONTRIBUTIONSDr.Lin Bo Zhao:acquisition and analysis of data,literature review. Dr.Dae Chul Suh:study concept and design,study supervision,final revision.Dr.Dong-Geun Lee:analysis and interpretation of data. Dr.Sang Joon Kim:critical revision of the manuscript for important intellectual content.Dr.Jae Kyun Kim and Mr.Seungbong Han:statis-tical analysis.Dr.Deok Hee Lee:interpretation of data.Dr.Jong Sung Kim:critical revision of the manuscript.ACKNOWLEDGMENTThe authors acknowledge the assistance of Min-ju Kim,Department of Clinical Epidemiology and Biostatistics,Asan Medical Center,with statis-tical analysis.STUDY FUNDINGNo targeted funding reported.DISCLOSUREL.Zhao reports no disclosures relevant to the manuscript.D.Suh serves as an executive committee member of World Federation of Interventional and Therapeutic Neuroradiology and holds patents on an intravascular occlusion device.D.Lee,S.Kim,J.K.Kim,and S.Han report no disclo-sures relevant to the manuscript.D.Lee holds patents on a stroke treat-ment device and guidewire.J.S.Kim serves as an associate editor of the International Journal of Stroke,an editorial board member of Stroke,asso-ciate editor of Cerebrovascular Diseases,and an editorial board member of Neurocritical Care.Go to for full disclosures.Received August29,2013.Accepted in final form February24,2014.REFERENCES1.Cognard C,Gobin YP,Pierot L,et al.Cerebral duralarteriovenous fistulas:clinical and angiographic correlation with a revised classification of venous drainage.Radiology 1995;194:671–680.2.Borden JA,Wu JK,Shucart WA.A proposed classificationfor spinal and cranial dural arteriovenous fistulous malfor-mations and implications for treatment.J Neurosurg 1995;82:166–179.3.Houdart E,Gobin YP,Casasco A,Aymard A,Herbreteau D,Merland JJ.A proposed angiographic clas-sification of intracranial arteriovenous fistulae and malfor-mations.Neuroradiology1993;35:381–385.4.Lucas CdP,Caldas JG,Prandini MN.Do leptomeningealvenous drainage and dysplastic venous dilation predicthemorrhage in dural arteriovenous fistula?Surg Neurol 2006;66(suppl3):S2–S5.5.Singh V,Smith WS,Lawton MT,Halbach VV,Young WL.Risk factors for hemorrhagic presentation in patients with dural arteriovenous fistulae.Neurosurgery2008;62:628–635.6.Piippo A,Laakso A,Seppa K,et al.Early and long-termexcess mortality in227patients with intracranial dural arteriovenous fistulas.J Neurosurg2013;119:164–171.7.Willinsky R,Terbrugge K,Montanera W,Mikulis D,Wallace MC.Venous congestion:an MR finding in dural arteriovenous malformations with cortical venous drain-age.Am J Neuroradiol1994;15:1501–1507.sjaunias P,Chiu M,ter Brugge K,Tolia A,Hurth M,Bernstein M.Neurological manifestations of intracranial dural arteriovenous malformations.J Neurosurg1986;64: 724–730.sjaunias P,TerBrugge K,Chiu M.Dural AVM.Neurosurgery1985;16:435–436.10.Davies MA,Saleh J,Ter Brugge K,Willinsky R,Wallace MC.The natural history and management of intracranial dural arteriovenous fistulae:part1:benign lesions.Interv Neuroradiol1997;3:295–302.11.Davies MA,Ter Brugge K,Willinsky R,Wallace MC.Thenatural history and management of intracranial dural arte-riovenous fistulae:part2:aggressive lesions.Interv Neuro-radiol1997;3:303–311.12.Duvernoy HM.Vascularization of the cerebral cortex[inFrench].Rev Neurol1999;155:684–687.13.Sulter G,Steen C,De Keyser e of the Barthel Indexand modified Rankin Scale in acute stroke trials.Stroke 1999;30:1538–1541.14.Chung SJ,Kim JS,Kim JC,et al.Intracranial dural arte-riovenous fistulas:analysis of60patients.Cerebrovasc Dis 2002;13:79–88.15.Suh DC,Lee JH,Kim SJ,et al.New concept in cavernoussinus dural arteriovenous fistula:correlation with present-ing symptom and venous drainage patterns.Stroke2005;36:1134–1139.16.Heinze G,Schemper M.A solution to the problem ofseparation in logistic regression.Stat Med2002;21: 2409–2419.17.Heinze G,Ploner M,Dunkler D,Southworth H.Logistf:Firth’s bias reduced logistic regression.R package version1.21[online].Available at:/package5logistf.Accessed December5,2013.18.Choi BS,Park JW,Kim JL,et al.Treatment strategy basedon multimodal management outcome of cavernous sinus dural arteriovenous fistula(CSDAVF).Neurointervention 2011;6:6–12.19.van Dijk JMC,terBrugge KG,Willinsky RA,Wallace MC.Clinical course of cranial dural arteriovenous fistulas with long-term persistent cortical venous reflux.Stroke2002;33:1233–1236.20.Daniels DJ,Vellimana AK,Zipfel GJ,Lanzino G.Intra-cranial hemorrhage from dural arteriovenous fistulas:clin-ical features and outcome.Neurosurg Focus2013;34:E15.21.Davies MA,TerBrugge K,Willinsky R,Coyne T,Saleh J,Wallace MC.The validity of classification for the clinical presentation of intracranial dural arteriovenous fistulas.J Neurosurg1996;85:830–837.22.Leach JL,Fortuna RB,Jones BV,Gaskill-Shipley MF.Imaging of cerebral venous thrombosis:current techni-ques,spectrum of findings,and diagnostic pitfalls.Radio-graphics2006;26(suppl1):S19–S41.Neurology82May27,20141903。
硬脑膜动静脉瘘诊断与治疗PPT
保持良好的生活习惯，避免过度劳累和熬夜 保持良好的饮食习惯，避免高脂肪、高糖、高盐的食物 保持良好的心理状态，避免过度紧张和焦虑 定期进行体检，及时发现并治疗相关疾病
保持良好的生活习惯，避免过度劳 累和熬夜
保持良好的心理状态，避免过度紧 张和焦虑
保持良好的饮食习惯，避免辛辣刺 激性食物
生活方式调整：保 持良好的生活习惯， 避免过度劳累
手术治疗：对于复 发性硬脑膜动静脉 瘘，可以考虑再次 手术治疗
症状：头痛、 恶心、呕吐、
意识障碍等
原因：动静脉 瘘破裂，血液
流入脑组织
处理：立即进 行手术治疗， 清除血肿，修
复瘘口
预防：定期复 查，及时发现 和处理并发症
症状：头痛、发热、恶心、呕吐等 原因：细菌、病毒、真菌等感染 治疗：抗生素、抗病毒药物、抗真菌药物等 预防：保持良好的卫生习惯，避免感染源
症状改善：头痛、 头晕、耳鸣等症状 是否减轻或消失
影像学检查：CT、 MRI等检查结果， 观察瘘口大小、血 流速度等变化
血流动力学监测： 监测脑血流量、血 压等指标，评估治 疗效果
药物治疗效果：观 察药物治疗后症状 改善情况，评估药 物疗效
治疗后症状改善情况 影像学检查结果 复发率 并发症发生率 患者生活质量改善情况
症状：头痛、恶心、呕吐、视力下降等 原因：硬脑膜动静脉瘘导致脑脊液循环障碍 治疗：手术治疗，如分流术、栓塞术等 预防：定期体检，及时发现并治疗硬脑膜动静脉瘘
颅内出血：需要立即进行手术 治疗，防止病情恶化
脑积水：可以通过引流或分流 手术进行治疗
癫痫发作：可以使用抗癫痫药 物进行治疗
认知功能障碍：可以通过康复 训练和药物治疗进行改善
治疗效果：手术成功率、并发症发生率、复发率等 功能恢复：语言、运动、认知等功能恢复情况 生活质量：日常生活能力、社会适应能力等 心理状态：焦虑、抑郁等情绪变化及应对策略 长期随访：定期复查、监测病情变化及治疗效果
经眼上静脉介入治疗海绵窦区硬脑膜动静脉瘘
眶 上 内侧 缘 切 开 穿 刺 眼 上静 脉 使 用 微 弹簧 圈 介 入 栓 塞海 绵 窦 区 硬 脑 膜 Ａ Ｖ Ｆ １ ６例 。 结 果
所 有 患 者 均 临床 治 愈 ， １ 例虽 将 海 绵 窦致 密填 塞 ， 但 仍 有 少 量翼 丛 引流 ， 压颈 １ 个 月后 消失 。 栓塞 术 后 并 发
Ｗａ ｓ ｄ ｏ ｃ ｕ ｍｅ ｎ ｔ ｅ ｄ ｉ ｎ １ ５ ｐ ａ ｔ ｉ ｅ ｎ ｔ ｓ（ ９ ４ ％） ． Ｒ ｅ ｓ ｉ ｄ ｕ ｌ ａ ｉ ｆ ｓ ｔ ｕ ｌ ａ ｗ ａ ｓ ｌ ｅ ｆ ｔ ｉ ｎ １ ｐ ａ ｔ ｉ ｅ ｎ ｔ ｓ ｗ ｉ ｔ ｈ ｃ ｏ ｍｐ ａ ｃ ｔ ｏ ｃ ｃ ｌ ｕ ｓ ｉ ｏ ｎ ｖ ｉ ａ
经 眼上静脉介入治疗海绵 窦 区硬脑膜 动静脉瘘
陈怀 瑞 ， 白如 林 ， 黄承 光 ， 李 宾 ， 张光 霁
【 摘要 】 目的
和疗 效 。 方法
探 讨 眶 上 内侧缘 切 开 穿 刺 眼 上 静脉 介 入 栓 塞海 绵 窦 区硬 脑 膜 动 静 脉 瘘 （ Ａ Ｖ Ｆ ） 的方 法
．
Ｍｅ ｈｏ ｔ ｄ ｓ Ｓ ｕ 哂ｃ ｌ ａ ｅ ｘ ｐ ｏ ｓ ｕ ｒ ｅ ｏ ｆ ｔ ｈ ｅ ｓ ｕ ｐ ｅ ｉ ｒ ｏ ｒ ｏ ｐ ｈ ｔ ｈ ａ ｌ ｍｉ ｃ ｖ ｅ ｉ ｎ ｗ ａ ｓ ｐ ｅ ｒ ｆ ｏ ｒ ｍｅ ｄ ｂ ｙ ｅ ｙ ｅ ｌ ｉ ｄ ｉ ｎ ｃ ｉ ｓ ｉ ｏ ｎ ａ ｎ ｄ ｆ ｏ ｌ ｌ ｏ ｗｅ ｄ ｂ ｙ
岩上窦区硬脑膜动静脉瘘诊治一例
岩上窦区硬脑膜动静脉瘘诊治一例王全;李静伟;孙力泳;陈圣攀;李桂林;张鸿祺【期刊名称】《中国脑血管病杂志》【年(卷),期】2015(000)010【总页数】3页(P534-536)【关键词】硬脑膜动静脉瘘;脑膜垂体干;岩静脉【作者】王全;李静伟;孙力泳;陈圣攀;李桂林;张鸿祺【作者单位】内蒙古自治区赤峰市宝山医院神经外科024076;100053北京，首都医科大学宣武医院神经外科;100053北京，首都医科大学宣武医院神经外科;100053北京，首都医科大学宣武医院神经外科;100053北京，首都医科大学宣武医院神经外科;100053北京，首都医科大学宣武医院神经外科【正文语种】中文患者女，54岁，主因“颈部疼痛1个月余，四肢无力伴二便障碍20 d，加重1周”于2015年5月18日入住首都医科大学宣武医院。
患者1个月前无明显诱因出现颈枕部持续性胀痛，未予以诊治，20 d前出现四肢无力伴二便困难，就诊于当地医院，诊断为“颈椎病”，接受药物保守治疗后症状无缓解。
1周前就诊于外院神经内科，考虑为“急性脊髓炎”而接受大剂量激素[注射用甲泼尼龙琥珀酸钠(商品名：甲强龙)1 g/d]冲击治疗2 d后，四肢肌力明显下降，并伴二便无法自行排出，为进一步诊治入住本院。
入院体格检查示：颈后部压痛，胸7以下浅深感觉减退，腹壁反射减退，双上肢肌力Ⅲ级，左下肢肌力Ⅱ- 级，右下肢肌力Ⅱ级。
双侧霍夫曼征阳性，双侧巴宾斯基征阳性。
术前头颈部MRI示延髓至胸3椎体水平脊髓明显增粗水肿，伴延颈髓腹侧髓周流空影(图1a)。
三维时间飞跃法(time of flight, TOF)MR血管成像(MRA)示迂曲扩张的脑膜垂体干小脑幕缘支起自右侧颈内动脉海绵窦段并沿小脑幕缘行至岩尖部(图1b)。
入院后于局部麻醉下行全脑DSA，右侧颈内动脉造影示瘘口位于岩尖部，由脑膜垂体干小脑幕缘支供血并向岩上静脉引流，引流静脉沿脑干小脑侧方向下走行，经寰枕交界区后汇入脊髓前、后静脉并向下引流(图2)。
硬脑膜动静脉瘘介入诊断治疗PPT
分型
• 按静脉引流方向分型：与临床表现及预后密切 相关
• 按DAVF部位分型：与血供来源及治疗途径密切 相关
• 静脉引流方向与病变部位相结合分型
按静脉引流方向分型
Borden classification
1 Venous drainage directly into dural venous sinus or meningeal vein 2 Venous drainage into dural venous sinus with CVR 3 Venous drainage directly into subarachnoid veins(CVR only)
L-ICA
Male,49 DAVF of anterior cranial fossa （Cognard Ⅳ）
The left lateral internal carotid arteriogram demonstrates a DAVF supplied by the anterior ethmoidal branches of the ophthalmic artery and the draining intracranial vein with a focal aneurysmal dilatation at the site of parenchymal hemorrhage
CVR=cortical venous reflux（可能与静脉窦闭塞有关）
按DAVF部位分型
• 海绵窦DAVF • 横窦－乙状窦DAVF • 小脑幕DAVF • 上矢状窦DAVF • 前颅窝DAVF • 边缘窦DAVF • 岩上/下窦DAVF • 舌下神经管DAVF
经动脉入路栓塞硬脑膜动静脉瘘中的辅助超选技术
—
—
９ ８－ ２ ・— —
介入放射学杂志 ２１ ０ ０年 １ ２月第 １ 第 １ ９卷 ２期
ＪＩｔ ｖｎ ａｉｌ ０ ０ Ｖｏ． Ｎ ．２ ｎｅ ｅｔ ｄｏ ２ １ ， １ ９， ｏ１ ｒ Ｒ １
・
神经介人
Ｎ ｕｏ ｔ ｖｎｉ ・ ｅｒｉ ｅ ｅｔ ｎ ｎｒ ｏ
经动脉入路栓塞硬脑膜动静脉瘘 中的 辅助超选技术
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【 ｂ ｔａｔ Ｏｂｅｔ ｅ Ｔ ｖ ｕ ｔ ｔｅａｓ ｔ ｔｅｈ ｉｕｓｉ ｐｒ ｒ ｎ ａｓｒ ｒ ｌ ｍｂｌ ａｏ ｆ Ａ ｓ ｃ】 ｒ ｊｃｉ ｏｅａ ａ ｓｉａ ｃ ｎ ｅ ｅ ｏｍｉｇｔ ｎａｔ ｉ ｏｉ ｔｎｏ ｖ ｌ ｅｈ ｓｎｔ ｑ ｎ ｆ ｒ ｅａ ｅ ｚｉ
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经岩下窦介入栓塞海绵窦区硬脑膜动静脉瘘三例临床体会
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而改变 剧 烈活动后增强 ， 压迫患侧颈 总动脉减轻或消失 。本
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时， 可停止静脉栓塞 ， 残余 的少许供血用正 丁基氰基丙烯 酸异
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床症状和判断预后 。Ｃ Ａ Ｆ 多涉及双侧的动脉 系统分支供 Ｄ Ｖｓ
血 。本组 ３ 例患 者中有 ２ 例双侧颈 内动脉 和颈外动脉 的分支 供血 ， 而单纯单侧动脉系统供血者仅 １ 向岩下窦或岩上窦 例。
管弹性较差 ， 易破裂形成瘘 。④ 医源性海绵窦 内血栓形成 ， 也
可能是形成瘘的原因。
１１ 临床资料 ： ． 本组患者男性 １ ，女性 ２例 ，年龄 ４ ～ ４ 例 ２７
岁， 平均 ５ ３岁。临床表现 ： 例有球结膜充血水肿 、 ２ １ 头痛 、 眼 球突 出； 例结膜充血水肿 、 １ 视力下降伴眼球运动障碍 ； １例右
的 ［ 近 年来 随 着介 入 技术 的 发展 ， 脉 入 路 血 管 内栓 塞 已 成 ２ １ 。 静
硬脑膜动静脉瘘
正常颈内动脉DSA
Internal Carotid Artery
DSA动脉期
DSA动脉期
DSA动脉期
DSA窦期
DSA动态
DSA动态
治疗经过
❖ 入院后给予脱水降颅压、神经营养、抗血小板、中药活 血、抗感染、保肝及对症治疗，病情好转。
❖ 住院期间，患者曾出现头痛、恶心、呕吐症状，左侧肢 体无力，肌力3级，考虑高颅压，静脉性脑梗死不除外， 加强脱水、抗血小板治疗后，症状明显缓解，肌力恢复 至5级减。
长T1长T2信号，以白质受累为主，轻度不规则强化；DWI显示大脑小脑 半球表面广泛点状低信号；MRA显示血管走行基本正常。 ➢ 2006年1月25日：胸片提示上腔静脉略增宽，其余(-)
辅助检查
❖ 2006年1月26日：肝功：ALT 184 IU/L，AST 96 IU/L，ALP 205 IU/L，TP 55.8g/L，GLB 19.4g/L。乙肝六项：HBsAb（＋）， HBcAb（＋）；复查肝功：ALT 65 IU/L，AST 39 IU/L；D-Dimer： 0.8mg/L（正常<0.3mg/L）
➢ 2006年2月7日：头MRI平扫＋增强＋MRA＋MRV：双侧大脑、 小脑半球表面异常信号：浅静脉扩张可能性大，双侧额顶枕脑白 质水肿，增强扫描脑内未见明显强化影；MRV提示右侧乙状窦 狭窄，左侧乙状窦闭塞，左侧外囊软化灶，双侧筛窦蝶窦炎。 MRA动脉走行未见异常。
➢ 2006年2月8日：胸部CT提示左下肺感染，双侧胸膜增厚，伴右 侧少量胸腔积液。
DAVF典型临床表现
• DAVF 的临床表现复杂多样，主要与静脉引流 的方向、流速、流量和瘘口部位有关。
1 、颅内杂音
DAVF分类－2
根据病变范围：
经股静脉栓塞海绵窦—硬脑膜动静脉瘘一例报告
－ 一量≯ ～ 毒囊 ｛ ＼ 参 霉．
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2020/7/16
硬脑膜动静脉瘘（DAVF)
• 发生于硬脑膜及其附属结构如静脉窦、大脑镰、 小%-15% • 可见于任何年龄，成人多见
2020/7/16
硬脑膜动静脉瘘（DAVF)
• 硬脑膜窦畸形伴动静脉瘘
– 新生儿或婴儿，常为巨大囊袋或硬膜湖，与其它窦或大脑 静脉以缓流交通，多累及上矢状窦，常伴栓塞、闭锁或一 侧颈内静脉球发育低下
• CT与MRI:对良性DAVF敏感性较低；对侵袭性 DAVF，可显示异常血管，颅内出血，局部占位 效应，脑水肿，脑积水，静脉窦血栓形成及颅骨 骨质异常等征象
• CTA与MRA：可清楚显示异常增粗的供血动脉和 扩张的引流静脉及静脉窦，对瘘口位置及“危险 吻合”显示欠佳
2020/7/16
诊断
• DSA
• 支架植入：其支撑力可恢复静脉窦正常引流并可封 闭位于静脉窦壁上的瘘口；远期效果待进一步观察
2020/7/16
海绵窦DAVF
• 保守 • 放疗 • TAE－微粒
• TVE • TAE－
女，10岁 进行性脑神经缺失（婴儿型DAVF） CT强化： 上矢状窦扩张，脑皮质钙化，白质变薄 MR T1WI：上矢状窦及窦汇巨大流空影，小脑扁桃体下移
2020/7/16
成人型DAVF
2020/7/16
硬脑膜动脉
• 前颅窝
– 脑膜中动脉前支 – 筛前、后动脉 – 脑膜返动脉 – 蝶腭动脉
• 中颅窝
2020/7/16
2020/7/16
❖颅内出血 ❖头痛
❖搏动性突眼 ❖球结膜水肿 和充血 ❖眶周杂音 ❖进行性视力 下降 ❖颅神经麻痹
2020/7/16
❖头痛 ❖颅内出血 ❖中枢神经缺失，痴呆
❖杂音，耳鸣 ❖颅内出血 ❖中枢神经缺失
❖杂音，耳鸣，头痛 ❖眼部症状 ❖颅内出血（少见）
诊断
• 经颅多普勒：可探测血流动力学改变，特异性较 低
2020/7/16
2020/7/16
R-ICA
tentorial DAVF（Cognard Ⅲ）
女，37 肾移植术后，左横窦DAVF（Cognard Ⅱa+b）
术后1年MR示上矢状窦血栓形成，3年后自感颅内杂音， MR示脑表多发迂曲血管流空影；左侧颈外动脉造影侧位， 左侧横窦DAVF伴CVR，同侧乙状窦闭塞
• 两种假说
– “生理性动静脉交通”开放：硬脑膜动静脉之间存“生理性 动静脉交通”（dormant channels)或“裂隙样血管”（ crack-like vessels），某些病理状态使其开放，形成DAVF
– 新生血管：某些血管生长因子异常释放促使硬脑膜新生血管 形成，致使DAVF形成
2020/7/16
2020/7/16
介入治疗策略
• 经动脉微粒栓塞（TAE-微粒）：难以达到完全栓塞 ，通常用于缓解症状或辅助治疗
• 经静脉弹簧圈栓塞(TVE)：治愈性手段，必须致密 栓塞，否则可使症状恶化；可并发静脉壁损伤，颅 内出血
• 经动脉NBCA/Onyx栓塞(TAE)：用于复杂DAVF不 能通过静脉途径栓塞时，完全栓塞率较高；可造成 异位栓塞，对操作技术要求高
2020/7/16
岩上窦DAVF（Cognard Ⅴ)向脊髓静脉引流 右脑膜中动脉后支，右枕动脉脑膜支及右侧脑膜垂体干供血
2020/7/16
男，58 右眼球结膜充血水 R－ECA造影：肿右侧海绵窦DAVF，引流至眼上静脉及皮层静脉
2020/7/16
治疗
• 保守治疗 • 立体定向放射治疗 • 血管内介入治疗 • 外科手术
分型
• 按静脉引流方向分型：与临床表现及预后密切 相关
• 按DAVF部位分型：与血供来源及治疗途径密切 相关
• 静脉引流方向与病变部位相结合分型
2020/7/16
2020/7/16
2020/7/16
2020/7/16
按DAVF部位分型
• 海绵窦DAVF • 横窦－乙状窦DAVF • 小脑幕DAVF • 上矢状窦DAVF • 前颅窝DAVF • 边缘窦DAVF • 岩上/下窦DAVF • 舌下神经管DAVF
2020/7/16
L-ICA
Male,49 DAVF of anterior cranial fossa （Cognard Ⅳ）
The left lateral internal carotid arteriogram demonstrates a DAVF supplied by the anterior ethmoidal branches of the ophthalmic artery and the draining intracranial vein with a focal aneurysmal dilatation at the site of parenchymal hemorrhage
– 供血动脉 – 瘘口位置 – 引流静脉 – 静脉窦扩张与闭塞 – 脑循环异常
2020/7/16
L-ICA
Male,62 tentorial DAVF（Cognard Ⅳ）
The left lateral ICA angiogram shows a tentorial DAVF fed by an inferior marginal tentorial artery draining into a cortical vein
– 脑膜中/副动脉 – 颈内动脉下外侧干 – 咽升动脉脑膜支
• 后颅窝
– 椎动脉脑膜支 – 脑膜垂体干 – 枕动脉脑膜支 – 脑膜中动脉后支 – 咽升动脉脑膜支 – 大脑后动脉分支 – 小脑上动脉分支 – 小脑下后动脉分支
2020/7/16
2020/7/16
发病机制
• DAVF与手术、头外伤、感染、硬脑膜窦血栓形成、 雌激素等因素有关，但确切发病机制不明
• 婴儿型DAVF
– 高流速，高流量，多灶性，表现为大的窦及多发的局部动 静脉瘘和大的供血血管，常继发引起皮层－软膜分流，直 窦常缺如；静脉出口闭塞可引起颅压增高，脑室积水
• 成人型DAVF
2020/7/16
2020/7/16
婴儿型DAVF
• 多支供血动脉 • 静脉窦瘤样扩张 • 梗塞性脑积水 • 直窦缺如 • 骨皮质改变