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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,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,MCA,ACA,PCA,MCA皮质支供应:半球外侧面(额中回以下、中央前后回下3/4、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;颞极内外侧;额叶眶面一部分。,MCA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部区域。立体看,供应内囊上3/5,大脑中动脉(MCA)供血范围,大脑前动脉(ACA)血液供应,ACA皮质支供应:半球内侧面为顶枕裂以前皮质和胼胝体;在背外侧面达额中回上缘或上半、额上回、中央前后回上1/4、顶上小叶及眶部内侧半等区域。,ACA中央支供应: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。,脉络丛前动脉: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1/3、苍白球等,易形成血栓阻塞。,脉络膜前动脉的供血范围,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2mm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.AxialT2-weightedimage(2500/80)revealsthepresenceofaninhomogeneousmassintherightlateralventricle.Thelowsignalintensitysuggetsthepresenceofcalcificationandhemorrhage.E.Angiogramoftherightinternalcarotidarteryobtainedonday3demonstratesahypervascularmassfedfromtherightanteriorchoroidalartery(arrows).,WhichoneistheAnteriorChoroidalArtery?,脉络膜前动脉闭塞常引起三偏症状群,特点为偏身感觉障碍重于偏瘫,而对侧同向偏盲又重于偏身感觉障碍,有的尚有感觉过度、丘脑手、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。,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,椎动脉行程,图A:斜侧位观;图B:前后位观;图C:俯观。,1.左椎动脉2.脑膜后动脉3.小脑后下动脉(PICA)4.基底动脉5.小脑前下动脉(AICA)6.脑桥外侧支7.小脑上动脉(SCA)8.大脑后动脉9.小脑半球支大水平裂10.SCA的小脑半球分支11.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):,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:丘脑、下丘脑、底丘脑、膝状体以及大部分中脑。此外,分支到侧脑室及第三脑室脉络丛。,变异大。主要来自PCA(72.5-88.3%);来自ICA(6.8-20.2%);两部分平均参加(4.3-11%)。,PCA供血区模式图,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、舌回、窟窿回峡、楔叶、楔前叶后1/3及顶上小叶后部),Bloodsupplyofthethreesubdivisionsofthebrainstem.Diagramofmajorsupply.Sectionsthroughdifferentlevelsofthebrainstemindicatingtheterritorysuppliedbyeachofthemajorbrainstemarteries.,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,Patientswithunilateralparamedianinfarctionstypicallypresentedapuremotorhemiparesisthatprogressedoverthefirst3daysandwasaccompaniedbydysarthriaandhomolateralataxia.,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(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-GublerSyndrome),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(FovilleSyndrome),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(Wallenbergsyndrome),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。,Magneticresonanceimageofthefluidattenuatedinversionrecoverysequencefortheaxial(left)andT2weightedcoronal(right)sections.Thereisawelldemarcatedunilateralmedialmedullaryinfarctjustbelowthepontomedullaryjunction.Therightsideofeachimagecorrespondstotheleftsideofthebrain.,大脑动脉血管供血分区CT解剖(图文),脑的供血模式图,左枕叶梗死。(PCA终末支),Figure1:(a)NormalinitialCTofthepatient;(b)ThecranialCTtwodaysaftertheincidentshowssignalchangesconsistentwithsimultaneousinfarctsintherightMCAandPCAareas;(c)InthedigitalsubtractionangiographyoftherightICA,PCAisseentooriginatefromtherightICAthroughPCoAi.e.fetaltypePCA,PICAOntheleftCT-imagesofaleft-sidedPICA-infarction.Noticetheposteriorextention.Theinfarctionwastheresultofadissection(bluearrow).,OntheleftCT-imagesofaleft-sidedPICA-infarction.Inunilateralinfarctsthereisalwaysasharpdelineationinthemidlinebecausethesuperiorvermianbranchesdonotcrossthemidline,buthaveasagittalcourse.Thissharpdelineationmaynotbeevidentuntilthelatephaseofinfarction.Intheearlyphase,edemamaycrossthemidlineandcreatediagnosticdifficulties.Infarctionsatpontinelevelareusuallyparamedianandsharplydefinedbecausethebranchesofthebasilarareryhaveasagittalcourseanddonotcrossthemidline.Bilateralinfarctsarerarelyobservedbecausethesepatientsdonotsurvivelongenoughtobestudied,butsometimessmallbilateralinfarctscanbeseen.,SCAOntheleftCT-imagesofacerebellarinfarctionintheregionofthesuperiorcerebellararteryandalsointhebrainstemintheterritoryofthePCA.Noticethelimitationtothemidline.,ACA:A1segment:fromorigintoanteriorcommunicatingarteryandgivesrisetomediallenticulostriatearteries(inferiorpartsoftheheadofthecaudateandtheanteriorlimboftheinternalcapsule).A2segment:fromanteriorcommunicatingarterytobifurcationofpericallosalandcallosomarginalarteries.A3segment:majorbranches(medialportionsoffrontallobes,superiormedialpartofparietallobes,anteriorpartofthecorpuscallosum).,AnteriorchoroidalarteryTheterritoryoftheanteriorchoroidalarteryencompassespartofthehippocampus,theposteriorlimboftheinternalcapsuleandextendsupwardstoanarealateraltotheposteriorpartofthecellamedia.ThewholeareaisrarelyinvolvedinAChAinfarcts.Ontheleftanuncommoninfarctioninthehippocampalregion.PartoftheterritoryoftheanteriorchoroidalarteryandthePCAareinvolved.,MiddlecerebralarteryTheMCAhascorticalbranchesanddeeppenetratingbranches,whicharecalledthelaterallenticulo-striatearteries.Theterritoryofthelaterallenticulo-striateperforatingarteriesoftheMCAisindicatedwithadifferentcolorfromtherestoftheterritoryoftheMCAbecauseitisawell-definedareasuppliedbypenetratingbranches,whichmaybeinvolvedorsparedininfarctsseparatelyfromthemaincorticalterritoryoftheMCA.OntheleftaT2W-imageofapatientwithaninfarctionintheterritoryofthemiddlecerebralartery(MCA).Noticethatthelaterallenticulo-striateperforatingarteriesoftheMCAarealsoinvolved(orangearrow).,OntheleftimagesofahemorrhagicinfarctionintheareaofthedeepperforatinglenticulostriatebranchesoftheMCA.,OntheleftenhancedCT-imagesofapatientwithaninfarctionintheterritoryofthemiddlecerebralartery(MCA).Thereisextensivegyralenhancement(luxuryperfusion).Sometimesthisluxuryperfusionmayleadtoconfusionwithtumoralenhancement.,Posteriorcerebralartery(PCA)DeeporproximalPCAstrokescauseischemiainthethalamusand/ormidbrain,aswellasinthecortex.SuperficialordistalPCAinfarctionsinvolveonlycorticalstructures(4).Ontheleftapatientwithacutevisionlossintherighthalfofthevisualfield.TheCTdemonstratesaninfarctioninthecontralateralvisualcortex,i.eleftoccipitallobe.,Therearetwopatternsofborderzoneinfarcts:1.CorticalborderzoneinfarctionsInfarctionsofthecortexandadjacentsubcorticalwhitematterlocatedattheborderzoneofACA/MCAandMCA/PCA2.InternalborderzoneinfarctionsInfarctionsofthedeepwhitematterofthecentrumsemiovaleandcoronaradiataattheborderzonebetweenlenticulostriateperforatorsandthedeeppenetratingcorticalbranchesoftheMCAorattheborderzoneofdeepwhitematterbranchesoftheMCAandtheACA.,OntheleftthreeconsecutiveCT-imagesofapatientwithanocclusionoftherightinternalcarotidartery.Thehypoperfusionintherighthemisphereresultedinmultipleinternalborderzoneinfarctions.Thispatternofdeepwatershedinfarctionisquitecommonandshouldurgeyoutoexaminethecarotids.,Ontheleftimagesofapatientwhohassmallinfarctionsintherighthemisphereinthedeepborderzone(bluearrowheads)andalsointhecorticalborderzonebetweentheMCA-andPCA-territory(yellowarrows).Thereisabnormalsignalintherightcarotid(redarrow)asaresultofocclusion.Inpatientswithabnormalitiesthatmayindicateborderzoneinfarcts,alwaysstudytheimagesofthecarotidarterytolookforabnormalsignal.,OntheleftanotherexampleofsmallinfarctionsinthedeepborderzoneandinthecorticalborderzonebetweentheMCA-andPCA-territoryinthelefthemisphere.,OntheleftanexampleofinfarctionsinthedeepborderzoneandinthecorticalborderzonebetweentheACA-andMCA-territory.Theabnormalsignalintensityintherightcarotidistheresultofanocclusion.Thiscombinationoffindingsissocommon,thatonceyouknowthepattern,youwillseeitmanytimes.,脉络膜前动脉供血区梗死,A9-year-oldpreviouslyhealthygirlwasadmittedtotheEmergencyRoomwithaneight-hourhistoryofsuddenonsetofsevereheadache.Thepainwaspulsatileandbilateralandnotaccompaniedbyothersymptoms.Thereisnohistoryofmigraine,epilepsyorstroke.Parentsreportedthatsoonaftertheonsetoftheheadachethepatientbecamedrowsyforaboutonehour.Notriggerfactorwasidentified.Ontheneurologicalexamination,thepatientwasalertandwellorientedwithnootherabnormalitiesbutmildnuchalrigidity.Computedtomographyofthebrainrevealedhemorrhageintherightlateralventricle(Fig1)andgadolinium-enhancedmagneticresonanceimagingstudyofthebraindisclosedaheterogeneouslesioninthemesialportionoftherighttemporallobe,aboveandinsidethetemporalhornofthelateralventricle.Thelesionextendeduntilthesubependimaryareaofthetrigonooftherightventricle.ThelesionwashypointenseonT1andT2-weightedimagesandenhancedwiththecontrast.OtherhyperintenseT1andT2-weightedimageslesionswereseenintherightlateralventriclesuggestingbleeding.Magneticresonanceangiographyandcerebralangiographydisclosedanarteriovenousmalformationinpartofthechoroidplexus,suppliedbytheanteriorchoroidalartery(Figs2and3).TheAVMwasclassifiedaccordingtoSpetzlergradingsystemasgrade3(deepvenousdrainage:1;eloquencearea:0andsize:2).,Lacunesmaybeconfusedwithotheremptyspaces,suchasenlargedperivascularVirchow-Robinspaces(VRS).TheVRSareextensionsofthesubarachnoidspacethataccompanyvesselsenteringthebrainparenchyma.WideningofVRSoftenfirstoccursaroundpenetratingarteriesinthesubstantiaperforataandcanbeseenontransverseMRIslicesaroundtheanteriorcommisure,eveninyoungsubjects(5).OntheleftCT-andMR-imagesattheleveloftheanteriorcommisure(bluearrows).OntheCTthereisahypodenseareaintherighthemisphere,whi

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