Abstract
目的
头颈部动脉夹层(cervicocerebral artery dissection，CAD)是导致中青年发生缺血性脑卒中的重要原因之一，病情凶险，不及时诊疗容易发生严重后果，早期确诊并及时干预可极大地改善预后。本研究的目的在于探讨CAD在高分辨率磁共振血管壁成像(high-resolution magnetic resonance vessel wall imaging，HRMR-VWI)中的影像学表现及CAD病变血管再通的影响因素。
方法
回顾性分析2017年4月至2019年12月间在中南大学湘雅医院放射科经HRMR-VWI确诊为CAD且有相关影像学复查资料的19例患者(共计26支病变血管)的临床及HRMR-VWI资料。将病变血管分为恢复组、未恢复组。经治疗后，无残留动脉夹层表现，管腔无残留狭窄的病变血管纳入恢复组；治疗后依然存在狭窄、闭塞或仍残留夹层改变的病变血管纳入未恢复组。根据病变血管供血区有无缺血性卒中，将病变血管分为缺血性卒中组和非缺血性卒中组。比较组间患者临床资料及影像学资料的差异。
结果
在26支受累血管中，颈内动脉颅外段夹层14支(53.8%)，椎动脉颅外段夹层8支(30.8%)，椎动脉颅内段夹层3支(11.5%)，基底动脉夹层1支(3.9%)；有16支病变血管供血区发生缺血性脑卒中。病变血管基线HRMR-VWI中均可观测到壁间血肿的影像学表现。恢复组共18支(69.2%)血管，未恢复组共8支(30.8%)血管，未恢复组血管较恢复组多见于颅内段(P<0.05)，但2组间性别、年龄、夹层影像学表现、病变血管长度、复查间隔时间、血管闭塞和抗血小板治疗情况差异均无统计学意义(均P>0.05)。缺血性卒中组与非缺血性卒中组间年龄，性别，合并高血压、高脂血症、糖尿病的情况，病变血管位置，血管闭塞情况，病变血管长度以及双腔征、内膜片及腔内血栓等影像学表现差异均统计学意义(均P>0.05)。
结论
壁间血肿为CAD常见的影像学表现，HRMR-VWI可清楚准确地显示壁间血肿。CAD病变血管的再通率高，发生于颅内段CAD较发生于颅外段CAD再通慢，可延长复查时间。
Keywords: 头颈部动脉夹层, 高分辨率磁共振血管壁成像, 缺血性脑卒中, 血管再通
Abstract
Objective
Cervicocerebral artery dissection (CAD) is one of the important causes for ischemic stroke in young and middle-aged people. CAD is dangerous and untimely diagnosis and treatment are likely to result in severe disability. Early diagnosis and timely intervention can greatly improve the prognosis of patients. This study was to investigate the imaging features of CAD on high-resolution magnetic resonance vessel wall imaging (HRMR-VWI) and to analyze the influential factors of vascular recanalization.
Methods
A total of 19 CAD patients with both baseline HRMR-VWI and follow-up data of vascular imaging in the period from April 2017 to December 2019 in Department of Radiology, Xiangya Hospital, Central South University were retrospectively analyzed. The diseased vessels were divided into a recovery group and a unrecovered group. After treatment, diseased vessels with no residual arterial dissection and no residual stenosis in the lumen were included in the recovery group. Diseased vessels with stenosis, occlusion or residual dissection were included in the unrecovered group. Diseased vessels were divided into a ischemic stroke group and a non-ischemic stroke group according to the presence or absence of ischemic stroke in the area supplied by the diseased vessels. Differences in clinical data and HRMR-VWI imaging findings were compared between the groups.
Results
A total of 26 vessels were involved, including 14 (53.8%) internal carotid artery extracranial segment, 8 (30.8%) vertebral artery extracranial segment, 3 (11.5%) vertebral artery intracranial segment, and 1 (3.9%) basilar artery. Ischemic stroke occurred in 16 diseased vascular supply areas. Intramural hematoma was all observed in the baseline HMR-VWI of the affected vessels. There were 18 vessels (69.2%) in the recovery group and 8 vessels (30.8%) in the unrecovered group. Compared with the vessels in the recovery group, the vessels in the unrecovered group were mostly found in the intracranial segment (P<0.05). However, there were no significant differences in gender, age, imaging findings of dissection, length of lesion involvement, time between reexamination, vascular occlusion, and antiplatelet therapy between the recovery group and the unrecovered group (all P>0.05).There were nosignificant differences in age, gender, complication of hypertension, hyperlipidemia, diabetes mellitus, lesion location, vascular occlusion, lesion involvement length, double lumen sign, internal membrane, and lumen thrombosis between the ischemic stroke group and the non-ischemic stroke group (all P>0.05).
Conclusion
Intramural hematoma is a common imaging manifestation of CAD and can be shown clearly and accurately on HRMR-VWI. Recanalization rate of CAD is high, and the recanalization of CAD in intracranial segment is slower than that of CAD in extracranial segment, which can prolong the review time.
Keywords: cervicocerebral artery dissection, high-resolution magnetic resonance vessel wall imaging, ischemic stroke, vascular recanalization
头颈部动脉夹层(cervicocerebral artery dissection，CAD)是指头颈部动脉血流通过破损的动脉内膜进入血管壁内或血管壁内滋养血管破裂形成壁间血肿的血管性疾病，可导致血管狭窄、闭塞或动脉瘤样扩张[1-2]。CAD是导致中青年发生缺血性脑卒中的重要原因之一[3-5]。本病病情凶险，诊疗不及时易导致严重残疾等后果[5]。高分辨率磁共振血管壁成像(high-resolution magnetic resonance vessel wall imaging，HRMR-VWI)技术既可清晰地显示壁间血肿、双腔征、内膜片等特征性影像学征象，还可很好地显示病变血管的管壁、管腔情况，近年来已被广泛应用于CAD的诊断及病情的评估[6-8]。本研究回顾性分析19例行HRMR-VWI的CAD患者的临床及影像学资料，以期提高医师对CAD患者HRMR-VWI影像学表现的认识水平，增加CAD的检出率；并试图发现与受累血管再通有关的影响因素，提供预后相关信息及指导治疗。
1. 对象与方法
1.1. 对象
回顾性分析2017年4月至2019年12月间在中南大学湘雅医院放射科经HRMR-VWI确诊为CAD且有相关影像学复查资料的19例患者(共计26支病变血管)。记录患者的性别，年龄，临床症状，治疗过程，复查时间间隔以及是否合并高血压、高脂血症、糖尿病等。
1.2. 扫描序列及参数
采用德国西门子Prisma 3.0T磁共振扫描仪与配备的64通道头颈联合线圈进行HRMR-VWI扫描，扫描期间嘱患者保持头颈部静止。首先获得常规三维时间飞跃法磁共振血管成像(three-dimensional time of flight magnetic resonance angiography，3D-TOF-MRA)的图像，再应用三维可变翻转角快速自旋回波加权成像技术(three-dimensional sampling perfection with application optimized contrasts using different flip angle evolutions，3D SPACE)获得3D SPACE T1WI、3D SPACE T2WI图像，最后用高压注射器经肘静脉注射钆喷酸葡胺(Gd-DTPA)0.2 mL/kg(1.5 mL/s)，在相同的参数下获得增强后的3D SPACE T1WI图像。
3D SPACE T1WI扫描参数：重复时间(time of repetition，TR)/回波时间(time of echo，TE)=700 ms/20 ms，带宽(band width，BW)=488 kHz，视野(field of view，FOV)=170.00 mm×170.00 mm×135.68 mm，矩阵=320×320×320(12.5%区域过采样)，空间分辨率0.53 mm×0.53 mm×0.53 mm(不采用零点填充技术)，回波链(echo train length，ETL)=52，ETL持续时间=283 ms，部分傅里叶采集=6/8，全局自动校准部分并行采集(generalized auto-calibrating partially parallel acquisition，GRAPPA)加速比=2。3DSPACE T2WI扫描参数：TR/TE=1 300 ms/84 ms，BW=539 kHz，FOV=170.00 mm×170.00 mm×135.68 mm，矩阵=320×320×320(12.5%区域过采样)，空间分辨率 0.53 mm×0.53 mm×0.53 mm(不采用零点填充技术)，ETL=73，ETL持续时间=267 ms，部分傅里叶采集=6/8，GRAPPA加速比=3。通过西门子后处理软件，对原始图像进行多平面重建(multiple planar reconstruction，MPR)及曲面重建(curve planar reconstruction，CPR)。
1.3. 图像分析
由2名高年资放射科医师采用双盲法分别对HRMR-VWI图像进行阅片，阅片时主要观察病变血管位置、累及范围、狭窄程度、夹层特征性影像学特征(壁间血肿、双腔征、内膜片)，瘤样扩张、腔内血栓等其他影像学特征，意见不一致时经讨论得到一致结论。
将CAD病变血管分为颈内动脉颅内段及颅外段、椎动脉颅内段及颅外段、基底动脉共5个血管节段进行观察和分析。在CPR图像上测量病变血管累及范围，以cm为单位。
按照北美症状性颈动脉内膜剥离术临床试验(North American Symptomatic Carotid Endarterectomy，NASCET)方法测量颅外段血管狭窄率，狭窄率=1-(狭窄处管腔直径/狭窄远端正常管腔直径×100%)；按照华法林-阿司匹林治疗症状性颅内动脉狭窄(Warfarin-Aspirin Symptomatic Intracranial Disease，WASID)试验测量颅内段血管狭窄率，狭窄率=1-(狭窄处管腔直径/狭窄近端正常管腔直径×100%)[9-10]。在本研究中，血管狭窄程度仅分为有无闭塞。
内膜片定义为在任何序列图像上穿过血管腔延伸至血管侧壁的等信号线影；双腔征定义为血流分别进入真腔和假腔；壁间血肿定义为新月形动脉壁增厚，且无血液流动，信号随血肿时期不同可呈高-等信号；瘤样扩张定义为管腔较正常动脉扩张约1.5倍；腔内血栓定义为在增强前序列上管腔内填充的高信号灶，增强后可见强化[11-13]。
对比复查的影像学资料，将病变血管分为恢复组、未恢复组。经治疗后，将无残留动脉夹层表现，管腔无残留狭窄的病变血管纳入恢复组；依然存在狭窄、闭塞或仍残留夹层改变的病变血管纳入未恢复组。根据病变血管供血区有无缺血性卒中，将病变血管分为缺血性卒中组和非缺血性卒中组。由2位放射科医师独立评估，当意见不一致时经讨论得到一致结论。比较2组患者临床资料及影像学资料的差异。
1.4. 统计学处理
采用SPSS 22.0统计软件行数据处理，计量资料以均数±标准差( ±s)表示，计数资料以例或支(%)表示。符合正态分布的计量资料比较使用独立样本t检验，不符合正态分布的计量资料使用Wilcoxon秩和检验，各组间的计数资料比较使用Fisher确切概率检验，均以P<0.05为差异有统计学意义。
2. 结 果
2.1. 临床特征及夹层病变位置
19例CAD患者年龄22~55(40.2±7.6)岁，其中男性16例(84.2%)，女性3例(15.8%)。5例(26.3%)患者合并高血压，1例(5.2%)合并高脂血症，1例(5.2%)合并糖尿病，1例(5.2%)患者合并高血压和高脂血症。共26支血管受累，其中颈内动脉颅外段夹层14支(53.8%)，椎动脉颅外段夹层8支(30.8%)，椎动脉颅内段夹层3支(11.5%)，基底动脉夹层1支(3.9%)；16支病变血管供血区发生缺血性脑卒中，主要表现为一侧肢体无力伴言语不清，余病变血管供血区未发生缺血性脑卒中。4例患者同时有2支血管受累，1例患者同时有4支血管受累。
2.2. 基线HRMR-VWI表现及复查血管改变
基线HRMR-VWI示：26支病变血管均有壁间血肿，9支(34.6%)有双腔征及内膜片影像学特征，7支(26.9%)有腔内血栓。在19例CAD患者中，4例患者使用抗凝药物治疗，14例患者使用抗血小板治疗，1例患者行保守治疗。
恢复组(图1)纳入18支(69.2%)血管(属于15例患者)，未恢复组(图2~3)纳入8支(30.8%)血管(属于6例患者)，有3例患者同时属于恢复组和未恢复组。与恢复组相比，未恢复组血管多见于颅内段(P<0.05)；但2组间性别、年龄、夹层影像学表现、病变血管长度、复查间隔时间、血管闭塞和抗血小板治疗情况差异均无统计学意义(均P>0.05，表1)。
图1.
恢复组病例HRMR-VWI
Figure 1 HRMR-VWI of case in the recovery group
A: Baseline axial HRMR-VWI results. Extracranial segment of the right internal carotid artery intramural hematoma (white arrow); B: Baseline curve planar reconstruction image; C: Results of axial HRMR-VWI reexamination in 84 days. The intermural hematoma is completely absorbed.
图2.
未恢复组病例1的HRMR-VWI
Figure 2 HRMR-VWI of case 1 in the unrecovered group
A: Baseline axial HRMR-VWI. Intracranial segment of bilateral vertebral artery intramural hematoma (white arrow); B: Baseline curve planar reconstruction image showing right vertebral artery extracranial segment and basilar artery intramural hematoma(asterisk); C: Axial HRMR-VWI reexamination in 135 days. The intermural hematoma of bilateral vertebral artery is partially absorbed.
图3.
未恢复组病例2的HRMR-VWI
Figure 3 HRMR-VWI of case 2 in the unrecovered group
A: Baseline axial HRMR-VWI. Intracranial thrombosis in the extracranial segment of the left internal carotid artery (white arrow); B: Baseline axial HRMR-VWI showing extracranial segment of the left internal carotid artery intramural hematoma (red arrow); C: Coronal HRMR-VWI reexamination in 118 days. The intermural hematoma is same with the former; D: Axial HRMR-VWI reexamination in 118 days.
表1.
CAD病变血管再通影响因素
Table 1 Analysis of influential factors of vascular recanalization in CAD patients
| 组别 | n | 年龄/岁 | 性别/[例(%)] |
高血压/ [例(%)] |
高脂血症/ [例(%)] |
糖尿病/ [例(%)] |
复查间隔 时间/d |
血管闭塞/ [支(%)] |
|---|---|---|---|---|---|---|---|---|
| P | 0.226 | 0.529 | 1.000 | 1.000 | 0.529 | 0.468 | 0.072 | |
| 恢复组 | 18 | 42.8±7.3 | 15(83.3) | 4(22.2) | 2(11.1) | 1(5.6) | 95.4±40.3 | 1(5.6) |
| 未恢复组 | 8 | 39.1±5.8 | 8(100.0) | 2(25.0) | 0(0) | 1(12.5) | 108.6±46.1 | 3(37.5) |
| 组别 | 颅内段/[支(%)] | 病变血管/cm |
壁间血肿/ [支(%)] |
腔内血栓/ [支(%)] |
内膜片/[支(%)] |
双腔征/ [支(%)] |
抗血小板药物/[例(%)]) |
|---|---|---|---|---|---|---|---|
| 恢复组 | 0(0) | 3.4±2.0 | 18(100) | 3(16.7) | 15(83.3) | 6(33.3) | 12(66.7) |
| 未恢复组 | 4(50) | 3.8±3.3 | 8(100) | 4(50.0) | 8(100.0) | 3(37.5) | 7(87.5) |
| P | 0.005 | 0.696 | NA | 0.149 | 1.000 | 1.000 | 0.739 |
NA: Not applicable.
2.3. CAD所致缺血性卒中发生的影响因素
缺血性卒中组纳入16支(61.5%)血管(属于13例患者)，非缺血性卒中组纳入10支(38.5%)血管(属于6例患者)。2组间年龄，性别，合并高血压、高脂血症、糖尿病的情况，病变血管位置，血管闭塞情况，病变血管长度以及双腔征、内膜片及腔内血栓等影像学表现差异均无统计学意义(均P>0.05，表2)。
表2.
CAD所致缺血性脑卒中影响因素的分析
Table 2 Analysis of influential factors of ischemic stroke due to CAD
| 组别 | n | 年龄/岁 | 性别/[例(%)] | 高血压[例(%)] | 高脂血症[例(%)] | 糖尿病/[例(%)] | 血管闭塞/[支(%)] |
|---|---|---|---|---|---|---|---|
| P | 0.296 | 1.000 | 0.053 | 0.508 | 0.508 | 1.000 | |
| 缺血性卒中组 | 16 | 40.5±8.1 | 14(87.5) | 6(37.5) | 2(12.5) | 2(12.5) | 3(18.8) |
| 非缺血性卒中组 | 10 | 43.5±4.5 | 9(90.0) | 0(0) | 0(0) | 0(0) | 1(10.0) |
| 组别 | 颅内段/[支(%)] | 累及长度/cm | 壁间血肿/[支(%)] | 腔内血栓/[支(%)] | 内膜片/[支(%)] | 双腔征/[支(%)] |
|---|---|---|---|---|---|---|
| 缺血性卒中组 | 1(6.3) | 3.7±2.5 | 16(100) | 6(37.5) | 5(31.2) | 5(31.2) |
| 非缺血性卒中组 | 3(30.0) | 3.2±2.2 | 10(100) | 1(10.0) | 4(40.0) | 4(40.0) |
| P | 0.264 | 0.642 | NA | 0.149 | 0.692 | 0.692 |
NA: Not applicable.
3. 讨 论
本研究发现：CAD以颅外段血管病变较为常见，占84.6%；病变的颅内段血管(椎动脉颅内段夹层3支，基底动脉夹层1支)均为后循环血管，与既往研究[1-2, 14-15]相符。本研究中的患者年龄22~55岁，26.3%的患者合并高血压，5.2%的合并高脂血症，5.2%的合并糖尿病，5.2%的同时合并高血压和高脂血症，合并脑血管病危险因素的比例并不高，但缺血性卒中的发生率为68.4%，与其他研究[3-5]结果类似。
本研究中CAD病变血管的再通率达69.2%，仅8支病变血管管腔仍见狭窄、闭塞；且与恢复组相比，未恢复组血管多见于颅内段，这可能是由于颅内段夹层较颅外段夹层需要更长的时间来恢复。本研究中所有再通病变血管发生在(95.4±40.3) d内。既往研究[16-17]报道CAD病变血管再通率可达37%~75%，通常发生在3~6个月内。这提示临床上治疗CAD时，对颅外段夹层患者建议3个月后复查，颅内段夹层患者应延长复查时间至4~6个月，以避免低估CAD再通率和更好地指导个体化治疗。
本研究发现：未恢复组与恢复组之间性别、年龄、夹层影像学表现、病变血管长度、复查间隔时间、血管闭塞和抗血小板治疗情况差异均无统计学意义。而既往对CAD的超声研究[18-19]发现年龄、高血压病史、动脉管腔的狭窄程度等因素可能影响CAD病变血管的再通。造成此差异的原因可能为在应用超声对CAD进行诊断、评估时，可能会遗漏某些病变及影像学特征；且本研究的样本量较小，无法排除相关混杂因素的影响。但是，本研究中所有病变血管在基线HRMR-VWI上均可见到壁间血肿，这有助于CAD的诊断，也再一次验证了HRMR-VWI对CAD的诊断作用。
本研究发现多根血管受累、颅外段夹层向颅内段夹层延伸的现象。大多数的研究[20-21]将CAD病例分为颅内段、颅外段进行描述，忽略了CAD常累及多个动脉节段，由颅外段向颅内段延伸、发展，并且向颅内段延伸的CAD往往有着更高的卒中风险的特点。因此，笔者建议对CAD患者采用头颈一体化线圈的三维HR-MRI，以覆盖更大范围的血管，更全面地评价颅内、颅外血管。
CAD是青年缺血性脑卒中常见的病因，本研究对CAD所致缺血性卒中的影响因素进行了分析，结果发现：缺血性卒中组和非缺血性卒中组之间年龄，性别，合并高血压、高脂血症、糖尿病的情况，病变血管位置，血管闭塞情况，病变血管长度以及双腔征、内膜片及腔内血栓等影像学表现差异均未见统计学意义。既往一多中心颈动脉夹层合并缺血性卒中的研究[22]认为高血压是CAD患者发生缺血性脑卒中的危险因素。造成这种结果差异的原因可能与混杂因素干扰有关，需要更大样本的多中心研究。
本研究未发现CAD治疗方式对病变血管再通的影响。由于目前对于CAD的最佳治疗方法还未达成一致。对CAD合并脑梗死的患者，治疗的主要目的是降低脑卒中的发生及再发风险，可采用抗血小板治疗、抗凝治疗、血管内治疗等方式。既往的多中心临床随机试验[23-24]表明：抗血小板治疗和抗凝治疗两者均可有效地减少缺血性卒中的再发，且在病变血管再通、预防缺血性卒中再发、降低死亡风险方面差异无统计学意义。
本研究中的大多数CAD病例由于合并短暂性脑缺血发作或急性缺血性脑卒中选择药物治疗，且以抗血小板药物为主，在复查期间均未发生急性缺血性脑卒中。对于CAD患者的治疗，需要根据患者的首发症状及临床特征来选择治疗方式，各治疗方式的优缺点需要大样本的前瞻性研究来确定。
目前，考虑到壁间血肿是CAD特征性影像学表现，而大部分CAD的壁间血肿是可以自发吸收、好转的，在CAD合并脑梗死的临床治疗中，初始治疗侧重于使用抗血小板或抗凝药物。当药物治疗失败后，如在临床随访期间持续发生缺血性或血栓栓塞事件时应考虑进行血管内治疗，以获得短期和/或长期的临床和影像学改善[25-26]。
本研究存在以下局限性。首先，因为这是一项回顾性分析，样本量少，复查间隔时间不同，并且无法根据血管狭窄程度分层分析，所以还需要更多的、更大样本量的前瞻性研究来确定CAD再通的影响因素。其次，各患者基线扫描时期各不相同，由于夹层可在短期内变化，从而导致某些影像学特征改变，由此可产生误差。
综上，本研究评估了19例26支CAD血管的基线HRMR-VWI影像学特征和复查时病变血管的改善情况，国内的研究较少有此类报道。本研究结果发现壁间血肿为CAD的常见影像学表现，HRMR-VWI可清楚准确地显示壁间血肿，CAD病变血管的再通率高，颅内段夹层较颅外段夹层再通慢，可延长复查时间。
利益冲突声明
作者声称无任何利益冲突。
原文网址
http://xbyxb.csu.edu.cn/xbwk/fileup/PDF/202105467.pdf
参考文献
- 1. Debette S, Compter A, Labeyrie MA, et al. Epidemiology, pathophysiology, diagnosis, and management of intracranial artery dissection[J]. Lancet Neurol, 2015, 14(6): 640-654. [DOI] [PubMed] [Google Scholar]
- 2. Debette S, Leys D. Cervical-artery dissections: predisposing factors, diagnosis, and outcome[J]. Lancet Neurol, 2009, 8(7): 668-678. [DOI] [PubMed] [Google Scholar]
- 3. Ekker MS, Boot EM, Singhal AB, et al. Epidemiology, aetiology, and management of ischaemic stroke in young adults[J]. Lancet Neurol, 2018, 17(9): 790-801. [DOI] [PubMed] [Google Scholar]
- 4. Debette S. Pathophysiology and risk factors of cervical artery dissection: what have we learnt from large hospital-based cohorts?[J]. Curr Opin Neurol, 2014, 27(1): 20-28. [DOI] [PubMed] [Google Scholar]
- 5. Putaala J, Metso AJ, Metso TM, et al. Analysis of 1008 consecutive patients aged 15 to 49 with first-ever ischemic stroke: the Helsinki young stroke registry[J]. Stroke, 2009, 40(4): 1195-1203. [DOI] [PubMed] [Google Scholar]
- 6. Edjlali M, Roca P, Rabrait C, et al. 3D fast spin-echo T1 black-blood imaging for the diagnosis of cervical artery dissection[J]. AJNR Am J Neuroradiol, 2013, 34(9): E103-106. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 7. Han M, Rim NJ, Lee JS, et al. Feasibility of high-resolution MR imaging for the diagnosis of intracranial vertebrobasilar artery dissection[J]. Eur Radiol, 2014, 24(12): 3017-3024. [DOI] [PubMed] [Google Scholar]
- 8. Jung SC, Kim HS, Choi CG, et al. Quantitative analysis using high-resolution 3T MRI in acute intracranial artery dissection[J]. J Neuroimaging, 2016, 26(6): 612-617. [DOI] [PubMed] [Google Scholar]
- 9. Chen L, Zhan Q, Ma C, et al. Reproducibility of middle cerebral artery stenosis measurements by DSA: Comparison of the NASCET and WASID methods[J]. PLoS One, 2015, 10(6): e0130991. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 10. Huang J, Degnan AJ, Liu Q, et al. Comparison of NASCET and WASID criteria for the measurement of intracranial stenosis using digital subtraction and computed tomography angiography of the middle cerebral artery[J]. J Neuroradiol, 2012, 39(5): 342-345. [DOI] [PubMed] [Google Scholar]
- 11. Hunter MA, Santosh C, Teasdale E, et al. High-resolution double inversion recovery black-blood imaging of cervical artery dissection using 3T MR imaging[J]. AJNR Am J Neuroradiol, 2012, 33(11): E133-E137. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 12. Park KJ, Jung SC, Kim HS, et al. Multi-contrast high-resolution magnetic resonance findings of spontaneous and unruptured intracranial vertebral artery dissection: qualitative and quantitative analysis according to stages[J]. Cerebrovasc Dis, 2016, 42(1/2): 23-31. [DOI] [PubMed] [Google Scholar]
- 13. Wu Y, Wu F, Liu Y, et al. High-resolution magnetic resonance imaging of cervicocranial artery dissection: imaging features associated with stroke[J]. Stroke, 2019, 50(11): 3101-3107. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 14. 中华医学会神经病学分会, 中华医学会神经病学分会脑血管病学组 . 中国颈部动脉夹层诊治指南2015[J]. 中华神经科杂志, 2015, 48(8): 644-651. [Google Scholar]; Chinese Academy of Neurology, Chinese Academy of Neurology, Chinese academy of cerebrovascular diseases . Chinese guidelines for the diagnosis and treatment of cervical artery dissection 2015[J]. Chinese journal of neurology, 2015, 48(8): 644-651. [Google Scholar]
- 15. 中国医师协会神经外科医师分会神经介入专家委员会, 中国卒中学会神经介入分会, 中国医师协会神经外科医师分会青年医师委员会 . 颅内动脉夹层的影像学诊断中国专家共识[J]. 中华神经外科杂志, 2016, 32(11): 1085-1094. [Google Scholar]; Committee of Neurointerventional Specialists of Neurosurgeon Branch of Chinese Physicians Association, Chinese Stroke Society Neurointerventional Branch, Committee of Young Physicians of Neurosurgeon Branch of Chinese Physicians Association . Chinese expert consensus on imaging diagnosis of intracranial arterial dissection [J]. Chinese Journal of Neurosurgery, 2016, 32(11): 1085-1094. [Google Scholar]
- 16. Nedeltchev K, Bickel S, Arnold M, et al. R2-recanalization of spontaneous carotid artery dissection[J]. Stroke, 2009, 40(2): 499-504. [DOI] [PubMed] [Google Scholar]
- 17. Vicenzini E, Toscano M, Maestrini I, et al. Predictors and timing of recanalization in intracranial carotid artery and siphon dissection: an ultrasound follow-up study[J]. Cerebrovasc Dis, 2013, 35(5): 476-482. [DOI] [PubMed] [Google Scholar]
- 18. 李兆强, 华扬, 贾凌云, 等. 颈部动脉夹层管腔不全再通的影响因素分析[J]. 中华医学超声杂志(电子版), 2019, 16(6): 401-406. [Google Scholar]; LI Zhaoqiang, HUA Yang, JIA Lingyun, et al. Analysis of influencing factors of incomplete recanalization of cervical artery dissection[J]. Chinese Journal of Medical Ultrasound. Electronic Version, 2019, 16(6): 401-406. [Google Scholar]
- 19. Lee WJ, Jung KH, Moon J, et al. Prognosis of spontaneous cervical artery dissection and transcranial doppler findings associated with clinical outcomes[J]. Eur Radiol, 2016, 26(5): 1284-1291. [DOI] [PubMed] [Google Scholar]
- 20. Béjot Y, Aboa-Eboulé C, Debette S, et al. Characteristics and outcomes of patients with multiple cervical artery dissection[J]. Stroke, 2014, 45(1): 37-41. [DOI] [PubMed] [Google Scholar]
- 21. Di Meglio L, Mazighi M, Reiner P, et al. Intracranial extension of extracranial vertebral dissection is associated with an increased risk of ischemic events[J]. Stroke, 2019, 50(8): 2231-2233. [DOI] [PubMed] [Google Scholar]
- 22. Debette S, Metso T, Pezzini A, et al. Association of vascular risk factors with cervical artery dissection and ischemic stroke in young adults[J]. Circulation, 2011, 123(14): 1537-1544. [DOI] [PubMed] [Google Scholar]
- 23. CADISS trial investigators, Markus HS, Hayter E, et al. Antiplatelet treatment compared with anticoagulation treatment for cervical artery dissection (CADISS): A randomised trial[J]. Lancet Neurol, 2015, 14(4): 361-367. [DOI] [PubMed] [Google Scholar]
- 24. Markus HS, Levi C, King A, et al. Antiplatelet therapy vs anticoagulation therapy in cervical artery dissection: the cervical artery dissection in stroke study (CADISS) randomized clinical trial final results[J]. JAMA Neurol, 2019, 76(6): 657-664. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 25. Kernan WN, Ovbiagele B, Black HR, et al. Guidelines for the prevention of stroke in patients with stroke and transient ischemic attack: a guideline for healthcare professionals from the American Heart Association/American Stroke Association[J]. Stroke, 2014, 45(7): 2160-2236. [DOI] [PubMed] [Google Scholar]
- 26. Asif KS, Lazzaro MA, Teleb MS, et al. Endovascular reconstruction for progressively worsening carotid artery dissection[J]. J Neurointerv Surg, 2015, 7(1): 32-39. [DOI] [PubMed] [Google Scholar]