椎动脉优势和基底动脉弯曲与后循环梗死部位的关系

目的 探讨椎动脉优势、基底动脉弯曲与后循环梗死的关系,分析后循环不同部位梗死患 者的椎动脉优势与基底动脉弯曲的关系。方法 选取临床表现为后循环梗死、头晕和眩晕、头痛等症状 患者156例,根据MRA检查结果分成椎动脉优势组（86例）及非优势组（70例）。比较两组间后循环各部位 的梗死发生率以及基底动脉弯曲的发生率,分析优势组各梗死部位后循环梗死侧与椎动脉优势侧的关 系,基底动脉弯曲方向与椎动脉优势侧相关性,基底动脉弯曲与后循环梗死的相关性。结果 85.1%（40/47） 基底动脉弯曲向椎动脉优势对侧,基底动脉弯曲方向与椎动脉优势方向呈负相关（r=-0.704,P ＜ 0.01）,优 势组后循环梗死的发生率明显高于对照组［51.2%（ 44/86） 比22.9%（ 16/70）,χ2=13.063,P＜0.01］。两组 间在小脑后下动脉（PICA）区和基底动脉（BA）区梗死发生率差异均有统计学意义,其余部位两组间的发 生率差异无统计学意义。基底动脉弯曲患者在PICA区和BA区梗死发生率与基底动脉呈直线患者差异 均有统计学意义,其余部位梗死的发生率差异无统计学意义。结论 椎动脉优势易于导致基底动脉弯曲 的发生,基底动脉易向优势对侧发生弯曲。椎动脉优势容易发生PICA供血区及BA脑桥支供血区的梗死, PICA供血区梗死部位多发生在椎动脉优势对侧,基底动脉弯曲侧;而BA脑桥支供血区的梗死多发生在 椎动脉优势侧,即基底动脉弯曲的对侧。     

椎动脉优势与后循环梗死的关系

目的 探讨椎动脉优势(vertebral artery dominance)与后循环梗死发生率及梗死侧的关系.同时了解椎动脉优势与基底动脉弯曲的相关性.方法 134例缺血性脑血管疾病、脑出血及突发性耳聋患者根据其是否存在椎动脉优势分为有椎动脉优势68例(优势组)和无椎动脉优势66例(对照组).比较两组间后循环梗死总发生率,后循环各部位的梗死发生率以及基底动脉弯曲的发生率.统计优势组各梗死部位后循环梗死侧与椎动脉优势侧的相关性,基底动脉弯曲方向与椎动脉优势侧的相关性,基底动脉弯曲与否与后循环梗死的相关性.结果 优势组后循环梗死发生率高于对照组[45.6％ (31/68)与21.2％(14/66),x2=8.922,P=0.003].优势组小脑后下动脉(PICA)供血区梗死及基底动脉供血区梗死发生率显著高于对照组[11.8％ (8/68)与0,x2=8.250,P=0.004;20.6％(14/68)与7.6％ (5/66),x2=4.660,P =0.031];两组的小脑上动脉供血区梗死率及大脑后动脉供血区梗死率差异无统计学意义.7例(7/8) PICA梗死患者梗死侧在椎动脉优势对侧.6例(6/14)基底动脉区梗死患者梗死侧与优势侧同侧.优势组基底动脉弯曲发生率显著高于对照组[50.0％(34/68)与9.1％ (6/66),x2=26.768,P=0.000].优势组基底动脉弯曲患者后循环梗死发生率与基底动脉呈直线的患者相仿,差异无统计学意义[ 52.9％ (18/34)与38.2％ (13/34),x2=1.482,P=0.223].优势组34例基底动脉弯曲的患者中,97.1％ (33/34)弯曲向椎动脉优势对侧.结论 椎动脉优势的患者较易发生后循环梗死,尤其是PICA和基底动脉供血区梗死,PICA供血区梗死部位一般在椎动脉优势对侧.椎动脉优势患者易致基底动脉弯曲,基底动脉一般弯向椎动脉优势对侧.     

基底动脉高密度征的研究进展

1 后循环脑梗死的临床 后循环系统主要的供血动脉是由双侧的椎动脉汇合组成的基底动脉及其分支供血.基底动脉及其分支缺血引起的梗死,其病变常局限于脑桥,也可同时引起脑干、小脑或枕叶的多处梗死.     

基底动脉闭塞的DSA分析

目的 探讨脑干梗死经DSA全脑血管造影证实基底动脉闭塞后的临床与预后,以期对临床治疗有一定的指导意义。方法 选取14例在临床中发现并经脑血管造影证实为基底动脉闭塞而临床症状轻微的患者。分析基底动脉闭塞后的临床表现与侧支代偿之间的关系。结果 （1）基底动脉近端闭塞,临床表现多以眩晕发作为主（占91％）;中段或远端闭塞,则多表现为间断性意识障碍（占66．7％）。（2）基底动脉近端闭塞,侧支血流多由颈外动脉和锁骨下动脉分支及椎动脉颅外段的肌支或脊髓前动脉代偿供血;基底动脉中、远段闭塞,侧支血流多由小脑后下动脉与小脑上动脉吻合（占100％）。结论 基底动脉闭塞若侧支代偿充分,可不表现明显的脑干缺血表现或表现轻微。内科治疗效果较好。     

症状性椎-基底动脉重度狭窄或闭塞致后循环缺血性卒中的血管重建治疗

目的探讨慢性椎-基底动脉重度狭窄或闭塞致后循环缺血性卒中血管重建治疗的有效性和安全性。方法纳入2018年1月至2021年1月天津市环湖医院诊断与治疗的11例慢性椎-基底动脉重度狭窄或闭塞致后循环缺血性卒中患者,采用MRI定位梗死部位,CTA确定血管狭窄或闭塞部位以及狭窄率,DSA明确侧支代偿情况,分别行枕动脉-椎动脉(OA-VA)搭桥术、颈外动脉-桡动脉-椎动脉(ECA-RA-VA)搭桥术、枕动脉-小脑后下动脉/小脑前下动脉(OA-PICA/AICA)搭桥术、颞浅动脉-大脑后动脉/小脑上动脉(STA-PCA/SCA)搭桥术等后循环血管重建治疗,采用改良Rankin量表(mRS)评价预后。结果 11例患者经CTA确定血管狭窄或闭塞部位,分别位于基底动脉占2/11,双侧椎动脉V4段-基底动脉串联病变占1/11,双侧椎动脉颅内段占2/11、颅外段占1/11,一侧椎动脉颅内段合并对侧颅外段占4/11,一侧椎动脉起始部闭塞合并另一侧椎动脉纤细占1/11。DSA明确侧支代偿情况,代偿血管分别为后交通动脉占7/11,小脑软膜吻合(包括小脑后下动脉、小脑前下动脉和小脑上动脉)占5/11,颈升动脉占4/11,大脑软膜吻合(大脑中动脉-大脑后动脉)占3/11,脊髓前动脉占1/11。11例患者顺利完成血管搭桥术,影像学检查(吲哚菁绿荧光血管造影术、DSA和CTA)均提示桥血管通畅。2例术后并发肺部感染,1例可疑颅内感染,均经抗生素治疗后好转。11例患者出院时mRS量表中位评分为1;术后平均随访8个月,9例预后良好(mRS评分为0～1)、2例预后中等(mRS评分为2～3)。结论血管重建治疗慢性椎-基底动脉重度狭窄或闭塞致后循环缺血性卒中有效性和安全性均较好,具备临床可行性。     

关于椎基底动脉走行变异或者发育异常的临床研究

<正>近些年关于椎基底动脉结构病变,如椎动脉发育不良或者一侧椎动脉优势以及关于基底动脉扩张迂曲的研究越来越多,本文将对于后循环主要动脉的变异及其意义进行阐述。1正常的椎基底动脉及其走形椎动脉起源于锁骨下动脉,左侧的锁骨下动脉直接起源于主动脉弓,右侧的锁骨下动脉起源于头臂干,左右两侧的椎动脉分别起源于左右两侧的锁骨下动脉,椎动脉在分支出下脑后下动脉后不久汇合成基底动脉,这些动脉供应着小脑     

选择脑微出血与椎-基底动脉形态在脑干梗死中的相关性研究

目的选择脑微出血与椎-基底动脉形态在脑干梗死中的相关性研究。方法从本院选择92例脑干梗死患者采用MRI与SWI进行检查,并根据检查结果分为阴性组与阳性组,对比两组患者的椎-基底动脉形态特点,并就脑微出血与椎-基底动脉形态的相关性进行分析。结果阴性组与阳性组在基底动脉迂曲、椎动脉狭窄、基底动脉狭窄以及椎动脉发育不良方面差异明显(P0.05);阳性组椎-基底动脉异常发生率比阴性组高,P0.05。结论脑干梗死患者大多伴有椎-基底动脉形态异常,从而提高了脑微出血的发生率。此外,基底脑微出血与基底动脉延长、椎动脉发育不良具有极为密切的联系。     

脑微出血与椎-基底动脉形态在脑干梗死中的相关性研究

目的研究脑干梗死患者脑微出血(CMBs)与椎-基底动脉形态的关系。方法对204例脑干梗死患者行头颅MRI+磁敏感加权成像(SWI)及头颈MRA检查,根据CMBs情况将患者分为脑干CMBs阳性组与阴性组。比较两组椎-基底动脉形态特点,分析脑干梗死患者CMBs与椎-基底动脉形态独立相关因素。结果头颅SWI检查结果显示,112例患者有脑干CMBs(阳性组),92例脑干无CMBs(阴性组)。阳性组椎-基底动脉异常发生率(78.6%)显著高于阴性组(58.7%)(χ~2=9.432,P=0.002)。与阴性组比较,阳性组椎动脉狭窄、椎动脉发育不良及基底动脉迂曲、延长的比率显著增高(均P0.05)。Logistic回归分析显示,椎动脉发育不良、基底动脉迂曲延长是脑干脑CMBs的独立危险因素(OR=1.859,95CI%:1.056~3.270,P=0.032;OR=1.745,95CI%:1.010~3.018,P=0.046)。结论伴有椎-基底动脉形态异常脑干梗死患者脑干CMBs发生率高。脑干CMBs与椎动脉发育不良、基底动脉迂曲延长独立相关。     

椎动脉优势与脑血管疾病、面肌痉挛、三叉神经痛相关性的临床分析

目的探讨椎动脉优势(VAD)与面肌痉挛、三叉神经痛及脑血管疾病的相关性。方法收集在辽宁省人民医院神经科就诊并同时行头部MRI和MRA检查的后循环梗死、单纯头晕、突发性眩晕伴平衡障碍、偏头痛、面肌痉挛、三叉神经痛患者。根据有无VAD分为椎动脉优势组和非椎动脉优势组。收集患者的一般资料,记录疾病的发生率;记录后循环梗死的发生率、发生位置;分析VAD与基底动脉弯曲发生率及弯曲方向的关系;Pearson检验分析椎动脉直径差异与三叉神经痛患者的症状评分、基底动脉弯曲长度(BL)的相关性。结果本研究共纳入413例患者,VAD的发生率为52.3%;优势组中后循环梗死患者105例(105/413,25.42%),突发性眩晕伴平衡障碍患者39例(39/413,9.44%)、面肌痉挛患者12例(12/413,2.91%)、三叉神经痛患者11例(11/413,2.66%),与非优势组相比具有统计学差异(P<0.05);在199例后循环梗死患者中,优势组梗死主要发生在小脑后下动脉供血区(PICA)(27/199,13.57%)和基底动脉供血区(BA)(45/199,22.61%)。PICA区梗死发生在VAD对侧的比例(20/105,19.05%)高于同侧(7/105,6.67%),BA区梗死主要发生在椎动脉优势同侧,其差异均具有统计学意义(P<0.05);优势组中有117例存在基底动脉弯曲,明显高于非优势组(P<0.05),143例左侧VAD患者中,有92例患者椎动脉向右侧弯曲;73例右侧优势患者中有20例患者基底动脉向左侧弯曲。椎动脉直径差异与三叉神经痛患者的症状评分呈正相关(r=0.336,P=0.001),与基底动脉弯曲长度呈正相关(r=0.432,P=0.004)。结论椎动脉优势人群后循环梗死、三叉神经痛、面肌痉挛的发生率较非优势人群高;椎动脉优势合并后循环梗死中以PICA和BA支配区多见;椎动脉优势患者基底动脉弯曲发生概率高,其弯曲方向与椎动脉优势方向相反;椎动脉直径差异越大,基底动脉弯曲长度越长,三叉神经痛患者的症状评分越高。     

后循环梗死与椎基底动脉狭窄的相关性分析

目的 探讨MRI所示的后循环梗死灶与DSA发现的椎基底动脉狭窄的相关性.方法 回顾分析30例后循环梗死患者的临床资料,将每例后循环梗死患者头部MRI发现的梗死灶与DSA所见的椎基底动脉狭窄血管进行对照.结果 MRI示单发性梗死22例(其中脑干梗死10例,小脑梗死8例,丘脑梗死2例,枕叶梗死2例),多发性梗死8例.DSA...     

Embolism from vertebral artery origin occlusive disease.

We report 10 patients with severe occlusive disease of the vertebral artery (VA) origin in the neck with intra-arterial embolism to the posterior circulation. The VA lesions in seven patients were complete occlusions, and three patients had severe atherostenosis. All patients had strokes in the vertebrobasilar territory. The most frequent recipient sites of intra-arterial embolism were the intracranial VA-posterior inferior cerebellar artery region (8), and the distal basilar artery (BA) and its superior cerebellar and posterior cerebral artery branches (7). Two patients had pontine infarction due to BA embolism. The most common clinical signs were due to cerebellar infarction. Atherosclerotic disease of the VA origin has features in common with disease of the internal carotid artery origin. Both have similar risk factors and demography, and each can cause strokes by intracranial intra-arterial embolism.     

The clinical and topographic spectrum of cerebellar infarcts: A clinical—magnetic resonance imaging correlation study

We studied 34 consecutive patients with non–mass-producing cerebellar infarcts using a standard protocol of investigations including magnetic resonance imaging (MRI). We analyzed the topography of infarcts to determine the involved arterial territories and we correlated the findings with neurological dysfunction and potential causes of stroke. Sixteen patients had an infarct in the territory of the posterior inferior cerebellar artery (PICA); 2, in the territory of the anterior inferior cerebellar artery (AICA); 13, in the territory of the superior cerebellar artery (SCA); and 8 had junctional infarcts between the territories of the medial and lateral branches of the PICA or PICA/SCA territories. PICA or medial PICA territory infarcts were manifested by acute vertigo and truncal ataxia, while the patients with lateral PICA territory infarcts presented with unsteadiness, limb ataxia and dysmetria without dysarthria. Patients with infarcts in the AICA territory were characterized by limb and trunk ataxia associated with signs of lateropontine involvement. Patients with SCA territory infarcts presented with dysarthria, unsteadiness and/or vertigo, limb ataxia, and dysmetria. Cardiac embolism was the main cause of large infarcts in the territories of the PICA (8/16) or SCA (4/7). Multiple small infarcts were associated with vertebrobasilar atherosclerosis (8/12). These clinical–MRI correlations allow better definition of the topographic and etiological spectrum of cerebellar infarction, which was previously based on pathological studies in subjects with severe infarction.     

Infarcts in the territory of the lateral branch of the posterior inferior cerebellar artery.

The territory of the lateral branch of the posterior inferior cerebellar artery (1PICA) supplies the anterolateral region of the caudal part of the cerebellar hemisphere. Because infarcts in the territory of the 1PICA have rarely been studied specifically, 10 patients with this type of infarct are reported. An 1PICA infarct was isolated in only three patients, whereas it was associated with brainstem infarct in four, with occipital infarct in one, and with multiple infarcts in two patients. The most common symptom at onset was acute unsteadiness and gait ataxia without rotatory vertigo (six patients). Unilateral cerebellar dysfunction was found in all patients, with limb ataxia (nine patients), dysdiadochokinesia (five patients), and ipsilateral body sway (four patients), but dysarthria and primary position nystagmus were notably absent. In the patients with a coexisting infarct in the brainstem, cranial nerve and sensorimotor dysfunction was prominent and often masked the signs of cerebellar dysfunction. Unlike other infarcts in the PICA territory, 1PICA territory infarcts were mainly associated with vertebral artery atherosclerosis (six patients), whereas cardiac embolism was less common (three patients). Unilateral limb ataxia without dysarthria or vestibular signs suggests isolated 1PICA territory infarction and should allow its differentiation from other cerebellar infarcts.     

双侧小脑梗死模式的探讨

目的探寻双侧小脑梗死的模式和机制。方法经MRI弥散成像(DWI)证实急性期小脑梗死的患者,根据梗死灶的分布将患者分为单侧小脑梗死组(UCI)和双侧小脑梗死组(BCI),并对两组的人口学特征、血管分布、小脑以外梗死灶以及病因进行了比较。结果因急性卒中入院的115例后循环脑梗死患者中,56例为小脑梗死或小脑合并其它部位梗死,其中单侧小脑梗死36例(64.3%),双侧小脑梗死20例(35.7%)。基线资料比较显示,脑卒中史(P=0.002)、纤维蛋白元水平(P=0.036)和入院时NIHSS评分(P=0.001)在双侧小脑梗死组明显高于单侧小脑梗死组。按血管分布区划分,小脑后下动脉(PICA)供血区小脑梗死发生率最高,且更多发生单侧小脑梗死(P=0.006);而双侧小脑梗死更常见于PICA+小脑上动脉(SCA)供血区(P=0.004)。双侧小脑梗死组合并小脑以外梗死灶的发生率明显高于单侧小脑梗死组(P=0.002),特别是合并幕下梗死灶常见(P=0.022)。在卒中机制上,双侧小脑梗死以大动脉粥样硬化性病变更多见(P=0.041),责任动脉病变主要是在椎动脉V4段、V4段与BA接合处的重度狭窄或闭塞。结论双侧小脑梗死并不少见,常见于PICA+SCA供血区;大动脉粥样硬化所致动脉源性栓塞是其卒中重要机制之一。     

Spectrum of the posterior inferior cerebellar artery territory infarcts. Clinical-diffusion-weighted imaging correlates

BACKGROUND AND PURPOSE: The clinical, etiological and stroke mechanisms are defined well before but the detailed clinical and etiologic mechanisms regarding to all clinical spectrum of posterior inferior cerebellar artery (PICA) infarcts were not systematically studied by diffusion-weighted imaging (DWI). METHODS: Seventy-four patients with PICA territory ischemic lesion proved by DWI with decreased apparent diffusion coefficient and FLAIR (fluid attenuation inversion recovery) included in our Registry, corresponding to 2% of 3,650 patients with ischemic stroke, were studied. The presence of steno-occlusive lesions in the posterior circulation were sought by magnetic resonance angiography, and reviewed with a three-dimensional rotating cineangiographic method. RESULTS: We found six subgroups of PICA territory infarcts according clinico-topographical relationship: (1) 9 patients with lesion in the territory lateral branch of PICA; (2) 23 patients with an infarct in the territory of medial branch of PICA; (3) 9 patients with a lesion involving both medial and lateral branches of the PICA; (4) 9 patients with cortical infarcts at the boundary zones either between medial and lateral branches of the PICA or between PICA and m/l superior cerebellar artery (SCA); (5) 10 patients with a lesion at the deep boundary zones either between medial and lateral PICA, or between PICA and medial/lateral SCA; (6)14 patients with concomitant multiple lesions in the PICA and in other vertebrobasilar artery territories. The main cause of PICA infarcts was extracranial large-artery disease in 30 patients (41%) patients, cardioembolism and in situ branch disease in 15 patients (20%) each. CONCLUSIONS: Multiple PICA territory lesions on DWI were not uncommon and could be caused by multiple emboli originating from break-up of atherosclerotic plaque in the subclavian/innominate-vertebral arterial system. DWI findings of single or multiple small lesions could account for some cases with transient and subtle cerebellar symptoms which have been considered before as 'vertebrobasilar insufficiency' without morphologic lesion. Different clinical-DWI correlations allow us to determine better definition of the topographical and etiological spectrum of acute PICA territory lesions, which was previously defined by pathological and conventional MRI studies.     

Rotational vertebral artery syndrome

Whether the rotational vertebral artery syndrome (RVAS), consisting of attacks of vertigo, nystagmus and tinnitus elicited by head-rotation induced compression of the dominant vertebral artery (VA), reflects ischemic dysfunction of uni- or bilateral peripheral or central vestibular structures, is still debated. We report on a patient with bilateral high-grade carotid stenoses, in whom rightward headrotation led to RVAS symptoms including a prominent nystagmus. Three-dimensional kinematic analysis of the nystagmus pattern, recorded with search coils, revealed major downbeat nystagmus with minor horizontal and torsional components. Magnetic resonance angiography demonstrated a hypoplastic right VA terminating in the posterior inferior cerebellar artery, a dominant left VA, and a hypoplastic P1-segment of the left posterior cerebral artery (PCA) that was supplied by the left posterior communicating artery (PCoA). The right PCA and both anterior inferior cerebellar arteries were supplied by the basilar artery. The right PCoA originated from the right internal carotid artery. Color duplex sonography showed severe reduction of diastolic blood flow velocities in the left VA during RVAS attacks. The nystagmus pattern can be best explained by vectorial addition of 3D sensitivity vectors of stimulated right and left anterior and horizontal semicircular canals with slightly stronger stimulation on the left side. We hypothesize that in RVAS, compression of dominant VA leads to acute vertebrobasilar insufficiency with bilateral, but asymmetric ischemia of the superior labyrinth. With regard to RVAS etiology, our case illustrates a type of pure vascular RVAS. Severity of attacks markedly decreased after successful bilateral carotid endarterectomy.     

Bilateral Cerebellar Infarctions Caused by a Stenosis of a Congenitally Unpaired Posterior Inferior Cerebellar Artery

Bilateral symmetrical cerebellar infarcts in the territory supplied by the medial posterior inferior cerebellar artery (PICA) branches are extremely rare. In the few cases published, it has not been possible to clearly pinpoint the cause of this infarct pattern. The authors present the case history of a 58-year-old man who had acute headaches accompanied by pronounced rotatory vertigo with nausea and vomiting. The neurological examination revealed bilateral cerebellar signs. Cranial magnetic resonance imaging showed bilateral, nearly symmetrical infarcts in the territory of the medial branches of both PICAs. These bilateral PICA infarctions were caused by a stenosis of an unpaired PICA originating from the left vertebral artery supplying both cerebellar hemispheres.     

Stroke in patients with fusiform vertebrobasilar aneurysms

We studied seven patients with brainstem infarction and large fusiform vertebrobasilar (VB) aneurysms to clarify the clinical, radiologic, and pathologic features. All presented with pontine infarcts; one also had a cerebellar infarct. VB TIAs preceded brainstem infarction in four patients. Angiography and CT documented VB fusiform aneurysmal dilatation. Four had intraluminal thrombi and one had severe basilar artery stenosis. Two distinct clinical pictures emerged: unilateral pontine infarcts with favorable outcome, presumably related to obstruction of a pontine penetrating artery at its origin from the posterior wall of the aneurysmal basilar artery, and major fatal bilateral pontine infarcts from basilar artery occlusion. Two patients came to autopsy. One had thrombus in the dilated basilar artery and a posterior cerebral artery branch embolus with hemorrhagic occipital infarction; the other had basilar artery thrombus with aneurysmal rupture and subarachnoid hemorrhage. Fusiform VB aneurysms caused brainstem stroke by intraluminal thrombus, local embolism, atherostenosis, and obstruction of paramedian penetrating arteries. Subarachnoid hemorrhage is an uncommon complication.     

A case of bow hunter's stroke caused by non-dominant vertebral artery

Rotational movements in the territory of vertebrobasilar artery of the head and neck can induce vertebrobasilar insufficiency (VBI) or infarction. The term "bow hunter's stroke" or "rotational VBI" has been used to describe this clinical syndrome. In most cases, symptoms were provoked because of involvement of a dominant vertebral artery (VA) with hypoplasia or occlusion of the contralateral VA. The author presented a case in which bow hunter's stroke was caused by occlusion of a non-dominant VA ending in the posterior inferior cerebellar artery (PICA). Diagnosis of rotational VBI was based on stereotypical clinical symptoms related to head rotation and hemodynamic study of the effects of head rotation. VA compression was documented in dynamic ultrasonography including the disappearance of end-diastolic flow in extracranial portion of VA and marked reduction in blood flow velocity (more than 50%) in the intracranial portion of VA upon head rotation. We emphasize that rotational occlusion of this anatomical variation is an important cause of VBI. This may cause permanent neurological deficits if left undiagnosed.