1、MRA正常表现MRA正常表现MRV正常表现DSA正常表现DSA正常表现动脉分叉部、分支处、动脉转弯处等，对颈内动脉瘤，尤其是海绵窦段，难以排除骨性解剖结构的干扰，往往导致颈内动脉海绵窦段的前、后、内侧壁均无法显示，同时，动脉瘤周围分支动脉n及瘤腔穿动脉具有较低的敏感度。n为无创性检查，具有安全、快速的特点。患者容易接受。且无X线辐射，所用对比剂安全性高，用量较少。nMRA图像与DSA有良好的相关性能任意方向显示动脉瘤与瘤颈关系，并能较准确测量动脉瘤大小、瘤颈及载瘤动脉直径，对血管内栓塞治疗或手术方案的选择具有极大帮助，因而易于被临床医师接受MRA的局限性n不能显示动脉瘤的钙化及动脉瘤与鞍区颅骨
2、的解剖关系，n对直径3 mm的动脉瘤常难以显示；n走行于扫描层面而非垂直的血管、扭曲的血管及分叉的血管因饱和作用造成信号丢失；n局部狭窄或扩张的血管及大的动脉瘤，由于血流的不均匀性，因湍流或涡流造成血液中质子群失散，导致信号丧失，致使上述性质的血管显示差，导致信号丧失或出现夸大效应。1、可明确动脉瘤的部位、是单发还是多发，对瘤体、瘤颈及其与载瘤动脉之间解剖关系的显示最为准确，对微小动脉瘤的发现和对巨大动脉瘤腔内有无“危险”动脉分支的辨别等，均有明显优势。n2、还可以模拟内镜功能观察血管腔内的情况。显示动脉瘤瘤颈开口、瘤内血栓、有无动脉分支从瘤体发出等信息。n3、了解脑底动脉环的侧支循环情况。n
3、但是，DSA也存在假阴性，原因与动脉瘤内血栓形成、载瘤动脉痉挛、动脉瘤与其他血管重叠以及操作者的技术因素和影像结果的判读等有关。前交通动脉瘤左侧M1末端动脉瘤右侧大脑前动脉A1段动脉瘤Thrombosis of Cerebral Venous Sinuses)n脑静脉窦血栓形成是一种特殊类型的急性脑血管病，发病急，病情重，诊断和治疗不及时死亡率高。其临床表现无特异性，单凭临床症状难以做出明确诊断，诊断有赖于影像学检查。n以往文献认为CT平扫检查阳性率低，明确诊断多需要进一步行CTV、MRV或DSA检查。但CT平扫也可见特异性的直接征象和较为特征的间接征象，结合间接征象对大部分病例可以做出较明确
4、的诊断。n直接征象：静脉窦密度增高，CT值一般超过60Hu，局部密度可均匀或不均匀。n间接征象：静脉性脑梗死、脑出血、脑肿胀、脑水肿。n直接征象：受累静脉窦流空影消失，T1WI呈高信号或中等信号，T2WI呈高信号或等低信号。n间接征象：静脉性脑梗死、脑出血、脑肿胀、脑水肿，出现相应的MR表现。表现为受累的脑静脉窦内完全或不完全充盈缺损，其边缘部分可见强化，部分相应区域脑表面浅静脉扩张。n受累静脉窦完全不显影或部分显示，脑静脉期循环时间延长，局部或广泛侧支静脉代偿性开放n 烟雾病(Moyamoya disease，MMD)又称脑底异常血管网症，是一组颈内动脉末端、大脑前动脉和(或)大脑中动脉近端
5、狭窄或闭塞，导致脑底或基底节区出现异常血管网的慢性进行性血管性疾病。脑血管造影呈现“烟雾”状，1967年由日本学者Suzuki发现并命名为“烟雾病”。目前病因不明。n流行病学：好发于东亚、东南亚，尤其是日本，女性多于男性，好发年龄为0一10岁以及3040岁。有文献报道10属于家族性发病。n临床表现:可分为短暂性脑缺血发作、梗死、出血、癫痫等四型。儿童以脑缺血症状为主，成人以脑出血症状为主。n对于烟雾病的诊断，国内外学者多认为血管闭塞或狭窄必须是两侧同时受累，而且无明显病因。n对于单侧血管受累或者有明显病因的(如动脉炎、动脉硬化等)称为烟雾综合征。n不用对比剂即可显示烟雾病的血管，且无副作用，故
6、MRI结合MRA逐渐取代传统的DSA，成为烟雾病诊断的主要诊断方法。n但是，MRA常高估血管狭窄程度，对早期或较轻的不典型的异常血管网的显示有一定困难，在显示颅内、外侧支循环及继发的微小动脉瘤方面敏感性较低。不但可以清晰显示病变脑血管狭窄或闭塞的部位和程度、颅底异常新生血管，而且对于颅内外血管代偿、脑循环时间长短等情况均可准确判断。n临床无明显症状患者，年龄普遍偏高，多介于3040岁之间或左右，颅底新生血管茂盛，颅内、外吻合支建立丰富而杂乱，部分代偿血管迂曲、扩张。n临床症状明显患者则相反，颅底新生血管相对稀疏，吻合支建立情况相对较差，甚至无吻合支建立，且年龄相对偏小，脑循环时间明显延长。可伴
7、发脑梗死或脑出血。Figure1.Typical appearance of capillary telangiectasia in the pons.(a)Axial T1WI(500/22)shows subtle T1 prolongation in the ventral middle part of the pons(arrow).(b)Axial T2WI(2,500/80)correspondingly shows a subtle hyperintense lesion.No hypointense signal is present.(c)Coronal gadolinium
8、-enhanced T1WI(500/22)shows a well-circumscribed,enhancing,round lesion in the ventral middle part of the pons(arrow).(d)Coronal GRE image(800/35,20 flip angle)shows corresponding,marked,susceptibility-related signal intensity loss,presumably from a blood oxygen-level-dependent(BOLD)effect due to de
9、oxyhemoglobin.Figure 2.Capillary telangiectasiain the might temporal tip.(a)Axial T1WI(600/15)is unremarkable,although in retrospect the right temporal tip lesion may be subtly detected.(b)Axial gadolinium-enhanced T1WI(600/15)clearly demonstrates the enhancing,round,7-mm lesion(arrow).Note the brus
10、hlike appearance of the anterior border of the lesion.A tiny left vemmian venous angioma is incidentally noted(arrowhead).(c)Axial T2WI(2,500/80)shows no definite abnormality.In particular,no hypointense signal is seen.(d)Axial GRE image(850/35,10 flip angle)shows markedly increased susceptibilitybl
11、ooming(arrow)of the capillary telangiectasia lesion that corresponds to the region of enhancement.Figure 5.Large capillary telangiectasia lesion.(a)Axial T1WI(700/15)and(b,c)consecutive axial 5-mm T2WI(2,500/80)demonstrate no abnormality,except for a possible small draining vein in the ventral left
12、part of the pons(arrow in a).In particular,no hypointense or hyperintense signal is seen on the T2WI.(d)Gadolinium-enhanced T1Wi(600/15)shows a large region of enhancement(arrows)that involves the entire right side of the pons and extends into the posterior left side of the pons.(e)Susceptibility-se
13、nsitive GRE image(500/20,20flip angle)shows markedly increased susceptibility dephasing that corresponds to the region of enhancement in d.(f)Proton-density-weighted image(2,500/20)shows subtle T2 prolongation that corresponds to this same distribution.The reason that the lesion is invisible in b an
14、d c is that the mild T2 prolongation evidenced here is counteracted by the T2 shortening(presumably owing to the BOLD effect of deoxyhemoglobin in capillary telangiectasia)in e.FIG 1.Left vertebral angiography(arterial phase,lateral view)showing VGAM supplied from medial posterior choroidal artery a
15、nd drained to an old embryonic falcine sinus(A).Panel B(internal carotid angiogramvenous phase,lateral view)shows the venous drainage pattern of the patient after endovascular aneurysm embolization.Normal drainage of the internal cerebral vein(black arrow)to the median prosencephalic vein and then i
16、nto the accessory embryonic falcine sinus(white arrow)is evident.Rotational 3D digital subtraction angiography with volume rendering,anteroposterior(C)and lateral(D)views,show the feeding artery from MPChA,MPChAaneurysm,and preaneurysmal stenosis.Greatly dilated old embryonic median prosencephalic v
17、ein and an associated hypoplastic left posterior cerebral artery are also clearly seen.FIG 1.Images from the case of a 19-month-old patient with mild hydrocephalusand engorged scalp veins.A,Sagittal view T1WI shows the markedly enlarged median prosencephalic vein of Markowski,charac-teristic of VGAM(arrow).Arterial feeders can be seen along the anterior wall of the vein.B,The complex arterial maze(arrows)is well seen on this conventional angiogramobtained with injection of the left vertebral artery.Coils can be seen along the right side of the varix,occluding several arterial feeders.谢谢！
