《脑梗死的血管定位》课件.ppt

1、.脑梗死的血管定位.内容 脑供血动脉解剖 脑梗死的血管定位.人脑动脉解剖.脑动脉两大体系 颈内动脉系：大脑前部部分间脑 椎基底动脉系：大脑后部部分间脑脑干小脑小脑幕为界小脑幕为界顶枕沟为界（顶枕沟为界（3/2).脑动脉供血系统模式图.脑的主要供血动脉。(A)脑腹侧观。方块区域放大图 显示Willis动脉环。(B)脑外侧面观和(C)中间矢状面显示大脑中/前/后动脉。(D)冠状切面显示大脑中动脉行程。.颈内动脉系统MCAACA脉络丛前动脉.大脑中动脉（MCA）供血范围MCAACAPCAMCAMCA皮质支供应：皮质支供应：半球外侧面（额中回以下、中央前后回下半球外侧面（额中回以下、中央前后回下3/4

2、3/4、顶下小、顶下小叶、枕叶月状沟或枕外侧沟以前、颞下回上缘或上半以上的部分）；岛叶、枕叶月状沟或枕外侧沟以前、颞下回上缘或上半以上的部分）；岛叶；颞极内外侧；额叶眶面一部分。叶；颞极内外侧；额叶眶面一部分。.MCAMCA中央支供应：中央支供应：壳核、尾状核、内囊前肢、内囊膝的背外侧和内囊后肢的背壳核、尾状核、内囊前肢、内囊膝的背外侧和内囊后肢的背部区域。立体看，供应部区域。立体看，供应内囊上内囊上3/53/5.大脑中动脉（MCA）供血范围.大脑前动脉（ACA）血液供应ACAACA皮质支供应：皮质支供应：半球内侧面为顶枕裂以前皮质和胼胝体；在半球内侧面为顶枕裂以前皮质和胼胝体；在背外侧面达额

3、中回上缘或上半、额上回、中央前后回上背外侧面达额中回上缘或上半、额上回、中央前后回上1/41/4、顶上小叶及眶部内侧半等区域。顶上小叶及眶部内侧半等区域。ACAACA中央支供应：中央支供应：部分额叶眶面皮质、外囊、尾状核和豆状核前部分额叶眶面皮质、外囊、尾状核和豆状核前部、内囊前肢和内囊膝部和后肢前边部分。部、内囊前肢和内囊膝部和后肢前边部分。.脉络丛前动脉：脉络丛前动脉：侧脑室下角的脉络丛，并供应外侧膝侧脑室下角的脉络丛，并供应外侧膝状体、内囊后肢的后下部、大脑脚底的中状体、内囊后肢的后下部、大脑脚底的中1/31/3、苍白球、苍白球等，易形成血栓阻塞。等，易形成血栓阻塞。脉络膜前动脉的供血范

4、围左图详示：基底节区的血液供应。.脉络膜前动脉 脉络膜前动脉，14支，以3支最多，为一组较细小而恒定的血管，在后交通动脉起始远侧2 mm处由颈内动脉脉直接发出。该动脉在未穿入侧脑室下脚之前，除发13个皮质支外，还发出23个穿支，1支穿视神经内侧至大脑脚，另两支即为纹状体内囊动脉。此动脉主要营养尾状核尾，行程长，管径较小，易发生栓塞。.D.Axial T2-weighted image(2500/80)reveals the presence of an inhomogeneous mass in the right lateral ventricle.The low signal intens

5、ity suggets the presence of calcification and hemorrhage.E.Angiogram of the right internal carotid artery obtained on day 3 demonstrates a hypervascular mass fed from the right anterior choroidal artery(arrows).Which one is the Anterior Choroidal Artery?.脉络膜前动脉脉络膜前动脉闭塞常引起三偏症状闭塞常引起三偏症状群，特点为偏身感觉群，特点为偏

6、身感觉障碍重于偏瘫，而对障碍重于偏瘫，而对侧同向偏盲又重于偏侧同向偏盲又重于偏身感觉障碍，有的尚身感觉障碍，有的尚有感觉过度、丘脑手、有感觉过度、丘脑手、患肢水肿等。患肢水肿等。.内囊额状断面脑后片图显示各部位血液供应来源。内囊额状断面脑后片图显示各部位血液供应来源。.中央前回及中央后回的血液供应图.椎基底动脉系统VABA.椎动脉（VA）V1（骨外）段：向上进C6横突孔。V2（椎间孔段V3（脊椎外）段：V4（硬膜内段）：过枕骨大孔，在脑桥及延髓交界处合成基底动脉。近侧椎动脉段解剖（A侧位；B前后位；C颏顶位）：骨外段（V1）横突孔段（V2）椎外段（V3）4.硬膜内段（V4）5.枕骨髁的大概位置

7、 椎动脉行程图图A A：斜侧位观；图：斜侧位观；图B B：前：前后位观；图后位观；图C C：俯观。：俯观。.1.1.左椎动脉左椎动脉2.2.脑膜后动脉脑膜后动脉3.3.小脑后下动脉（小脑后下动脉（PICAPICA）4.4.基底动脉基底动脉5.5.小脑前下动脉小脑前下动脉(AICA)(AICA)6.6.脑桥外侧支脑桥外侧支7.7.小脑上动脉（小脑上动脉（SCASCA）8.8.大脑后动脉大脑后动脉9.9.小脑半球支大水平裂小脑半球支大水平裂10.SCA10.SCA的小脑半球分支的小脑半球分支11.11.小脑蚓上动脉小脑蚓上动脉椎基底动脉系统及其分支解剖（侧位）：.椎基底动脉系统及其分支解剖（正位）

8、：1.右椎动脉2.左椎动脉3.脊髓前动脉4.小脑后下动脉（PICA）5.基底动脉6.小脑前下动脉（AICA）7.脑桥外侧支8.小脑上动脉（SCA）9.大脑后动脉10.后交通动脉11.颈内动脉.大脑后动脉（PCA）血液供应中央支：中央支：丘脑、下丘脑、底丘脑、膝状体丘脑、下丘脑、底丘脑、膝状体以及大部分中脑。此外，分支到侧脑室及以及大部分中脑。此外，分支到侧脑室及第三脑室脉络丛。第三脑室脉络丛。变异大。变异大。主要来自主要来自PCAPCA（72.5-88.3%72.5-88.3%）；来自）；来自ICAICA（6.8-20.2%6.8-20.2%）；两部分平均参加（）；两部分平均参加（4.3-4.

9、3-11%11%）。）。.PCAPCA供血区模式图供血区模式图皮质支：皮质支：半球底面和内侧面一部分（包括：海马回、梭状回、颞下回、半球底面和内侧面一部分（包括：海马回、梭状回、颞下回、舌回、窟窿回峡、楔叶、楔前叶后舌回、窟窿回峡、楔叶、楔前叶后1/31/3及顶上小叶后部）及顶上小叶后部）.Blood supply of the three subdivisions of the brainstem.Diagram of major supply.Sections through different levels of the brainstem indicating the territor

10、y supplied by each of the major brainstem arteries.脑桥的血液供应特点 桥脑的血供源自椎基底动脉，桥脑基底外侧和被盖部由短旋动脉供应；桥脑基底部内侧由基底动脉中央支供应，旁正中支供应桥脑被盖部正中部分脑室底部、外展神经核、内侧纵束和网状结构；桥脑基底部和被盖部最外侧为长旋动脉供应。由于外侧区侧支循环丰富，发生梗塞概率较低。而桥脑旁正中动脉、短旋动脉呈直角起自基底动脉，易受高血压的影响而出现动脉粥样硬化，易出现梗塞。.脑桥梗死的临床特点 貌似大脑半球病变的纯运动性偏瘫占桥脑梗塞的60.9%。这是因为锥体束位于桥脑基底部，基底部由基底动脉的旁正中深

11、穿支供应血流，该部位动脉易有动脉硬化性改变和透明变性，其近端闭塞时导致基底部正中梗塞，使未交叉的锥体束受损。PICA和SCA引起的梗塞通常仅累及小脑；而AICA（供应脑桥外侧被盖部和小脑中脚）不同，它引起的梗塞灶多累及脑干和小脑中脚。.桥脑梗塞时交叉性瘫及颅神经麻痹并不常见，因桥脑的颅神经核多分部于被盖部，由较丰富的长旋动脉及小脑上动脉供应血流，后交通动脉、大脑后动脉和小脑上动脉有侧枝循环，所以颅神经可不受影响。脑桥梗死的临床特点.脑桥上/中部旁中线综合征 由基底动脉旁中央支血供障碍引起；病变对侧中枢性舌瘫对侧中枢性上下肢瘫痪同侧小脑性共济失调Patients with unilateral

12、paramedian infarctions typically presented a pure motor hemiparesis that progressed over the first 3 days and was accompanied by dysarthriaand homolateral ataxia.桥脑上外侧综合征 小脑上动脉闭塞引起；眩晕、恶心、呕吐、眼球震颤（前庭核损害）两眼向病灶侧水平凝视不能（脑桥侧视中枢损害）同侧肢体共济失调（脑桥臂、结合臂、小脑齿状核损害）；同侧Horner综合征（下行交感神经损害）同侧面部感觉障碍（三叉神经感觉束损害）和对侧痛觉、温度觉障碍

13、（脊髓丘脑束损害）；对侧下肢深感觉障碍（内侧丘系外侧部分损害）双侧听力障碍，对侧较重。.少见SCA综合征出现病变对侧感音性耳聋.脑桥腹下部综合征（Millard-Gubler Syndrome)同侧外展N麻痹同侧周围性面瘫 对侧中枢性舌瘫一；对侧肢体瘫。也其它位置不同的突出症状可能出现 小脑前下动脉阻塞引起。.脑桥基底内侧综合征（Foville Syndrome)病灶侧周围性面瘫；两眼向病灶侧同向注视麻痹；病灶对侧偏瘫；基底动脉旁正中支闭塞引起。.小脑后下动脉综合征（Wallenberg syndrome)现证实10由PICA引起，75由一侧椎动脉闭塞引起。余下由基底动脉闭塞引起。.延髓内侧综

14、合征（Dejerine综合征）椎动脉及其分支或基底动脉后部血管阻塞，引起延髓锥体发生梗死时产生同侧舌肌麻痹（XII脑神经损害）和萎缩，对侧上下肢中枢性瘫痪以及触觉、位置觉、振动觉减退或丧失。.Magneticresonance image of the fluid attenuated inversion recovery sequence for the axial(left)and T2 weighted coronal(right)sections.There is a well demarcated unilateral medial medullary infarct just be

15、low the pontomedullary junction.The right side of each image corresponds to the left side of the brain.大脑动脉血管供血分区大脑动脉血管供血分区CT解剖解剖(图文图文).MCA 终末支ACA终末支PCA终末支.MCA 终末支ACA终末支PCA终末支脉胳膜前动脉.MCA 终末支ACA终末支PCA终末支脉胳膜前动脉ACA穿支PCA穿支及PCoA.MCA 终末支ACA终末支PCA终末支脉胳膜前动脉ACA穿支PCA穿支及PCoAMCA穿支.MCA 终末支ACA终末支PCA终末支脉胳膜前动脉ACA穿支P

16、CA穿支及PCoAMCA穿支.MCA 终末支ACA终末支PCA终末支脉胳膜前动脉ACA穿支PCA穿支及PCoAMCA穿支.MCA 终末支ACA终末支PCA终末支.MCA 终末支ACA终末支PCA终末支.MCA 终末支ACA终末支PCA终末支.MCA 终末支ACA终末支.ACA终末支.脑的供血模式图脑的供血模式图.左枕叶梗死。（PCA终末支）.Figure 1:(a)Normal initial CT of the patient;(b)The cranial CT two days after the incident shows signal changes consistent with

17、simultaneous infarcts in the right MCA and PCA areas;(c)In the digital subtraction angiography of the right ICA,PCA is seen to originate from the right ICA through PCoA i.e.fetal type PCA.PICAOn the left CT-images of a left-sided PICA-infarction.Notice the posterior extention.The infarction was the

18、result of a dissection(blue arrow).On the left CT-images of a left-sided PICA-infarction.In unilateral infarcts there is always a sharp delineation in the midline because the superior vermian branches do not cross the midline,but have a sagittal course.This sharp delineation may not be evident until

19、 the late phase of infarction.In the early phase,edema may cross the midline and create diagnostic difficulties.Infarctions at pontine level are usually paramedian and sharply defined because the branches of the basilar arery have a sagittal course and do not cross the midline.Bilateral infarcts are

20、 rarely observed because these patients do not survive long enough to be studied,but sometimes small bilateral infarcts can be seen.SCAOn the left CT-images of a cerebellar infarction in the region of the superior cerebellar artery and also in the brainstem in the territory of the PCA.Notice the lim

21、itation to the midline.ACA：A1 segment:from origin to anterior communicating artery and gives rise to medial lenticulostriate arteries(inferior parts of the head of the caudate and the anterior limb of the internal capsule).A2 segment:from anterior communicating artery to bifurcation of pericallosal

22、and callosomarginal arteries.A3 segment:major branches(medial portions of frontal lobes,superior medial part of parietal lobes,anterior part of the corpus callosum).Anterior choroidal arteryThe territory of the anterior choroidal artery encompasses part of the hippocampus,the posterior limb of the i

23、nternal capsule and extends upwards to an area lateral to the posterior part of the cella media.The whole area is rarely involved in AChA infarcts.On the left an uncommon infarction in the hippocampal region.Part of the territory of the anterior choroidal artery and the PCA are involved.Middle cereb

24、ral arteryThe MCA has cortical branches and deep penetrating branches,which are called the lateral lenticulo-striate arteries.The territory of the lateral lenticulo-striate perforating arteries of the MCA is indicated with a different color from the rest of the territory of the MCA because it is a w

25、ell-defined area supplied by penetrating branches,which may be involved or spared in infarcts separately from the main cortical territory of the MCA.On the left a T2W-image of a patient with an infarction in the territory of the middle cerebral artery(MCA).Notice that the lateral lenticulo-striate p

26、erforating arteries of the MCA are also involved(orange arrow).On the left images of a hemorrhagic infarction in the area of the deep perforating lenticulostriate branches of the MCA.On the left enhanced CT-images of a patient with an infarction in the territory of the middle cerebral artery(MCA).Th

27、ere is extensive gyral enhancement(luxury perfusion).Sometimes this luxury perfusion may lead to confusion with tumoral enhancement.Posterior cerebral artery(PCA)Deep or proximal PCA strokes cause ischemia in the thalamus and/or midbrain,as well as in the cortex.Superficial or distal PCA infarctions

28、 involve only cortical structures(4).On the left a patient with acute vision loss in the right half of the visual field.The CT demonstrates an infarction in the contralateral visual cortex,i.e left occipital lobe.There are two patterns of border zone infarcts:1.Cortical border zone infarctionsInfarc

29、tions of the cortex and adjacent subcortical white matter located at the border zone of ACA/MCA and MCA/PCA 2.Internal border zone infarctions Infarctions of the deep white matter of the centrum semiovale and corona radiata at the border zone between lenticulostriate perforators and the deep penetra

30、ting cortical branches of the MCA or at the border zone of deep white matter branches of the MCA and the ACA.On the left three consecutive CT-images of a patient with an occlusion of the right internal carotid artery.The hypoperfusion in the right hemisphere resulted in multiple internal border zone

31、 infarctions.This pattern of deep watershed infarction is quite common and should urge you to examine the carotids.On the left images of a patient who has small infarctions in the right hemisphere in the deep borderzone(blue arrowheads)and also in the cortical borderzone between the MCA-and PCA-terr

32、itory(yellow arrows).There is abnormal signal in the right carotid(red arrow)as a result of occlusion.In patients with abnormalities that may indicate borderzone infarcts,always study the images of the carotid artery to look for abnormal signal.On the left another example of small infarctions in the

33、 deep borderzone and in the cortical borderzone between the MCA-and PCA-territory in the left hemisphere.On the left an example of infarctions in the deep borderzone and in the cortical borderzone between the ACA-and MCA-territory.The abnormal signal intensity in the right carotid is the result of a

34、n occlusion.This combination of findings is so common,that once you know the pattern,you will see it many times.脉络膜前动脉供血区梗死脉络膜前动脉供血区梗死.A 9-year-old previously healthy girl was admitted to the Emergency Room with an eight-hour history of sudden onset of severe headache.The pain was pulsatile and bila

35、teral and not accompanied by other symptoms.There is no history of migraine,epilepsy or stroke.Parents reported that soon after the onset of the headache the patient became drowsy for about one hour.No trigger factor was identified.On the neurological examination,the patient was alert and well orien

36、ted with no other abnormalities but mild nuchal rigidity.Computed tomography of the brain revealed hemorrhage in the right lateral ventricle(Fig 1)and gadolinium-enhanced magnetic resonance imaging study of the brain disclosed a heterogeneous lesion in the mesial portion of the right temporal lobe,a

37、bove and inside the temporal horn of the lateral ventricle.The lesion extended until the subependimary area of the trigono of the right ventricle.The lesion was hypointense on T1 and T2-weighted images and enhanced with the contrast.Other hyperintense T1 and T2-weighted images lesions were seen in t

38、he right lateral ventricle suggesting bleeding.Magnetic resonance angiography and cerebral angiography disclosed an arteriovenous malformation in part of the choroid plexus,supplied by the anterior choroidal artery(Figs 2 and 3).The AVM was classified according to Spetzler grading system as grade 3(

39、deep venous drainage:1;eloquence area:0 and size:2).Lacunes may be confused with other empty spaces,such as enlarged perivascular Virchow-Robin spaces(VRS).The VRS are extensions of the subarachnoid space that accompany vessels entering the brain parenchyma.Widening of VRS often first occurs around

40、penetrating arteries in the substantia perforata and can be seen on transverse MRI slices around the anterior commisure,even in young subjects(5).On the left CT-and MR-images at the level of the anterior commisure(blue arrows).On the CT there is a hypodense area in the right hemisphere,which follows

41、 the signal intensity of CSF on T2W-and FLAIR-images,which is typical for widened VRS.PRES PRES is short for Posterior Reversible Encephalopathy Syndrome.It is also known as reversible posterior Leukoencephalopathy syndrome RPLS.It classically consists of potentially reversible vasogenic edema in th

42、e posterior circulation territories,but anterior circulation structures can also be involved(6).Many causes have been described including hypertension,eclampsia and preeclampsia,immunosuppressive medications such as cyclosporine.The mechanism is not entirely understood but is thought to be related t

43、o a hyperperfusion state,with blood-brain-barrier breakthrough,extravasation of fluid potentially containing blood or macromolecules,and resulting cortical or subcortical edema.The typical imaging findings of PRES are most apparent as hyperintensity on FLAIR images in the parietooccipital and poster

44、ior frontal cortical and subcortical white matter;less commonly,the brainstem,basal ganglia,and cerebellum are involved.On the left images of a patient with reversible neurological symptoms.The abnormalities are seen both in the posterior circulation as well as in the basal ganglia.Continue.Diagnosis:MELAS.