分水嶺區(qū)梗死及影像學(xué)表現(xiàn)

分水嶺區(qū)梗死及影像學(xué)表現(xiàn)演示文稿本文檔共34頁；當(dāng)前第1頁；編輯于星期五\23點49分優(yōu)選分水嶺區(qū)梗死及影像學(xué)表現(xiàn)本文檔共34頁；當(dāng)前第2頁；編輯于星期五\23點49分本文檔共34頁；當(dāng)前第3頁；編輯于星期五\23點49分本文檔共34頁；當(dāng)前第4頁；編輯于星期五\23點49分本文檔共34頁；當(dāng)前第5頁；編輯于星期五\23點49分WatershedInfarcts

www.radiologyassistant.nl/images/48e9bb7f02d66Basis-waterscheiding2.pngasaresultofhypoperfusion.

Therearetwopatternsofborderzoneinfarcts:

Corticalborderzoneinfarctions

InfarctionsofthecortexandadjacentsubcorticalwhitematterlocatedattheborderzoneofACA/MCAandMCA/PCA

Internalborderzoneinfarctions

InfarctionsofthedeepwhitematterofthecentrumsemiovaleandcoronaradiataattheborderzonebetweenlenticulostriateperforatorsandthedeeppenetratingcorticalbranchesoftheMCAorattheborderzoneofdeepwhitematterbranchesoftheMCAandtheACA.本文檔共34頁；當(dāng)前第6頁；編輯于星期五\23點49分Corticawatershedstrokes(CWS),orouterbraininfarcts,arelocatedbetweenthecorticalterritoriesoftheanteriorcerebralartery(ACA),middlecerebralartery(MCA),andposteriorcerebralartery(PCA).Internalwatershedstrokes(IWS),orsubcorticalbraininfarcts,arelocatedinthewhitematter,alongandslightlyabovethelateralventricle,betweenthedeepandthesuperficialarterialsystemsoftheMCA,orbetweenthesuperficialsystemsoftheMCAandACA.本文檔共34頁；當(dāng)前第7頁；編輯于星期五\23點49分本文檔共34頁；當(dāng)前第8頁；編輯于星期五\23點49分本文檔共34頁；當(dāng)前第9頁；編輯于星期五\23點49分

Watershedsorborderzonesareareasthatlieatthejunctionoftwodifferentdrainage

areas.Thevascularsupplyofthecerebralparenchymacanbeenvisionedinasimilarmanner,withdefinedboundariesbetweendifferentarterialsystems.Cerebralinfarctsinborderzoneswerefirstdiscussedin1883andweredefinedasischemiclesionsinanareabetweentwo

neighboringvascularterritories.Theseterritoriescanbefurtherclassifiedintwobroadcategoriesas(a)external(cortical)or(b)internal(subcortical)borderzones.Borderzoneinfarctsconstituteapproximately10%ofallcerebralinfarcts.Varioustheorieshavebeenproposedtoexplaintheirpathogenesis.Itisbelievedthatrepeatedepisodesofseveresystemichypotensionarethemostfrequentcause.Susceptibilityofborderzonestoischemiawasprovedinanautopsystudyofpatientswithborderzoneinfarcts.Variousneuropathologicstudieshaveshownneuronalnecrosisfromhypotensionintheseregionsandhaveadvancedourunderstandingofthepreferentialdistributionofborderzoneinfarcts.本文檔共34頁；當(dāng)前第10頁；編輯于星期五\23點49分

Theappearancesofborderzoneinfarctsdepictedbystandardimagingmodalitiesarewelldescribed.Advancedimagingtechniquescanhelpidentifyareasofmiseryperfusionassociatedwiththeseinfarcts.Miseryperfusion(低灌注)representsachronicfailureofcerebralautoregulationassociatedwithdecreased

cerebralperfusionpressuresinthepresenceofextracranialandintracranialatheromatousdisease.Theimportantinformationderivedfromimagingcanbeusefulforpatientmanagementanddiseaseprognosis本文檔共34頁；當(dāng)前第11頁；編輯于星期五\23點49分

Theexternalorcorticalborderzonesarelocatedatthejunctionsoftheanterior,middle,andposteriorcerebralarteryterritories.Infarctsintheanteriorexternalborderzonesandparamedianwhitematterarefoundatthejunctionoftheterritoriessuppliedbytheanteriorandmiddlecerebralarteries,andthoseintheparieto-occipitalareas(posteriorexternalborderzones)arefoundatthejunctionoftheterritoriessuppliedbythemiddleandposteriorcerebralarteries.本文檔共34頁；當(dāng)前第12頁；編輯于星期五\23點49分Theinternalorsubcorticalborderzonesarelocatedatthejunctionsoftheanterior,middle,andposteriorcerebralarteryterritorieswiththeHeubner,lenticulostriate,andanteriorchoroidalarteryterritories.Internalborderzoneinfarctsthusmaybedesignatedasinfarctsofthelenticulostriate–middlecerebralartery,lenticulostriate–anterior

cerebralartery,Heubner–anteriorcerebralartery,anteriorchoroidal–middlecerebralartery,andanteriorchoroidal–posteriorcerebralarteryterritories.Infarctsofthelenticulostriate–middlecerebralarteryborderzone,whichissuppliedbytheendbranchesofdeepperforatinglenticulostriatearteriesandmedullarypenetratorsfromthepial–middlecerebralartery,arethemostcommonlyseenatimagingandaredescribedindetailinthisarticle.本文檔共34頁；當(dāng)前第13頁；編輯于星期五\23點49分

ColoroverlaysonaxialT2-weightedmagneticresonance(MR)imagesofnormalcerebrumshowprobablelocationsofexternal(blue)andinternal(red)borderzoneinfarcts.本文檔共34頁；當(dāng)前第14頁；編輯于星期五\23點49分

Borderzoneinfarctsinvolvethejunctionofthedistalfieldsoftwononanastomosingarterialsystems.Theconventionaltheoryimplicateshemodynamiccompromiseproducedbyrepeatedepisodesofhypotensioninthepresenceofaseverearterialstenosisorocclusion.Thelowerperfusionpressurefoundwithintheborderzoneareasinthissettingconfersanincreasedsusceptibilitytoischemia,whichcanleadtoinfarction.Thiscausalroleofseverearterialhypotensionhasbeenwelldescribedandconfirmedbytheresultsofexperimentalstudiesinanimals.Thetypicalclinicalmanifestationsofsyncope（暈厥）,hypotension,andepisodicfluctuating（情感波動）orprogressiveweaknessofthehandsarealsosupportiveofthistheoryofhemodynamicfailure.RadiologicstudiesalsosupportthehypothesisthatborderzoneinfarctsdistaltointernalcarotidarterydiseasearemorelikelytooccurinthepresenceofanoncompetentcircleofWillis.

PathophysiologyofBorderZoneInfarcts本文檔共34頁；當(dāng)前第15頁；編輯于星期五\23點49分

Insharpcontrastwiththiswidelyprevalentinterpretation,severalpathologicinvestigationshaveemphasizedanassociationbetweenborderzoneinfarctionandmicroemboli,andembolicmaterialhasbeenfoundwithinareasofborderzoneinfarctioninautopsyseries.Preferentialpropagationofemboliintheborderzoneregionsalsohasbeenfoundinexperimentalstudies.

Borderzoneinfarctionmaybebetterexplainedbyinvokingacombinationoftwoofteninterrelatedprocesses:hypoperfusionandembolization.Hypoperfusion,ordecreasedbloodflow,islikelytoimpedetheclearance(washout)ofemboli.Becauseperfusionismostlikelytobeimpairedinborderzoneregions,clearanceofemboliwillbemostimpairedintheseregionsofleastbloodflow.Severeocclusivediseaseoftheinternalcarotidarterycausesbothembolizationanddecreasedperfusion.Similarly,cardiacdiseaseisoftenassociatedwithmicroembolizationfromtheheartandaortawithperiodsofdiminishedsystemicandbrainperfusion.Thistheory,althoughitseemsreasonable,remainsunprovedandhasbeenchallengedonmanyaccounts.本文檔共34頁；當(dāng)前第16頁；編輯于星期五\23點49分ImagingAppearance

Theexternal,corticalborderzonesarelocatedbetweentheanterior,middle,andposteriorcerebralarteriesandareusuallywedge-shapedorovoid.However,theirlocationmayvarywithdifferencesinthearterialsupply.ItissometimesdifficulttodeterminewhetherapersonhassustainedaborderzoneinfarctonthebasisofthelocationoftheinfarctinrelationtothevesselsonaCTorMRimag.Becauseofthisextensiveanatomicvariation,minimumandmaximumdistributionterritoriesofeachvesselhavebeendefined.Itisnotuncommontodescribeacorticalinfarctasa“territorial”infarctifitliescompletelywithintheexpectedorpossiblemaximumareaofavascularterritoryorasa“potential”infarctifitisoutsidethesemaxima.Furthermore,thelocationofcorticalborderzonesmayvarybecauseofthedevelopmentofleptomeningealcollaterals.Theanatomyofcorticalborderzonescanbecomplex,withmarkedvariabilityduetoindividualdifferencesintheterritoriessuppliedbythemajorarteriesofthebrain.本文檔共34頁；當(dāng)前第17頁；編輯于星期五\23點49分

(a,b)Coronalfluid-attenuatedinversionrecoveryMRimagesshowthedistributionofexternal(cortical)borderzoneinfarctsatthejunctionsoftheanteriorcerebralarteryandmiddlecerebralarteryterritories(a)andthemiddlecerebralarteryandposteriorcerebralarteryterritories(b).(c)Diffusion-weightedMRimagesshowacorticalborderzoneinfarctatthejunctionoftheanteriorcerebralarteryandmiddlecerebralarteryterritories.Angiographyoftheright-sidedcommoncarotidandinternalcarotidarteriesinthesamepatientshowednormalvesselswithnoocclusionorstenosis.本文檔共34頁；當(dāng)前第18頁；編輯于星期五\23點49分CausalMechanisms

Themechanismofexternalborderzoneinfarctionhasbeenwidelydebated.Manystudieshavedocumentedhemodynamicabnormalitiesintheanteriorwatershedorfrontalcorticalborderzone.However,inmanyrecentstudies,noevidenceofsuchhemodynamicimpairmentwasfound.Inotherstudies,substantiallyfewerseverestenosesorocclusionsofmajorvesselsthanborderzoneinfarctswerefound.Thecerebralorcarotidvesselsmayappearentirelynormalorshowmildormoderatenarrowingwithouthemodynamiccompromise.Isolatedcorticalborderzoneinfarctsmaybeembolicinnatureandarelessfrequentlyassociatedwithhemodynamiccompromise.Microembolifromtheheartoratheroscleroticplaques

inmajorarteriesmaypreferentiallypropagatetocorticalborderzones,whichhavelowerperfusionthanotherareasofthevasculature,and,thus,alimitedabilitytowashouttheseemboli.Manypatientswithcorticalborderzoneinfarctshaveconcomitantsmallercorticalinfarcts.Thesefindingssupportthehypothesisthatanembolicmechanismplaysacrucialroleinthepathogenesisofexternalborderzoneinfarcts本文檔共34頁；當(dāng)前第19頁；編輯于星期五\23點49分ClinicalCourse

Patientswithexternalborderzoneinfarctshaveamorebenignclinicalcourseandabetterprognosisthanthosewithinternalborderzoneinfarcts,althoughtheseverityofclinicalsignsandsymptomsandthescoreontheNationalInstitutesofHealthStrokeScaleatthetimeofadmissionmightnotdiffersubstantiallybetweenthetwopatientgroups.Theexternalborderzoneisclosertothecorticalsurface,wherepenetratingarteriesoriginate,andthusithasabetterchanceofdevelopingacollateralsupplythroughleptomeningealorduralanastomoses.However,whenexternalborderzoneinfarctsoccurinassociationwith

internalborderzoneinfarcts,thereisahigherprobabilityofhemodynamicimpairment,andtheprognosismaynotbegood.本文檔共34頁；當(dāng)前第20頁；編輯于星期五\23點49分InternalBorderZoneInfarctsImagingAppearance

Internalborderzoneinfarctsappearinmultiples,inarosarylikepattern.Inonereport,thispatternwasdescribedasaseriesofthreeormorelesions,eachwithadiameterof3mmormore,arrangedinalinearfashionparalleltothelateralventricleinthecentrum

semiovaleorcoronaradiata.Internalborderzoneinfarctsareclassifiedonthebasisoftheirradiologicappearanceaseitherconfluentorpartial

Partialinfarctsareusuallylarge,cigarshaped,andarrangedinapatternresemblingthebeadsofarosary,parallelandadjacenttothelateralventricle.Thedurationofhemodynamiccompromisehasbeenpostulatedasthecauseofthevariedradiologicappearances,withabriefepisodeofcompromiseleadingtoapartialinfarct,andalongerperiodofcompromise,toconfluentinfarcts.Confluentinternalborderzoneinfarctsmaybemanifestedbyastepwiseonsetofcontralateralhemiplegia.Theyalsomaybeassociatedwithapoorerrecoverythanistypicalforpartialinfarcts本文檔共34頁；當(dāng)前第21頁；編輯于星期五\23點49分

Internalborderzoneinfarctsmustbedifferentiatedfromsuperficialperforator(medullary)infarcts,whichmayhaveasimilarappearanceonMRimages.Superficialperforatorinfarcts,whicharecausedbytheocclusionofmedullaryarteriesfrompialplexuses,aresmaller,superficiallylocated,andwidelyscattered,whereasinternalborderzoneinfarctstendtolocalizeinparaventricularregions.Superficialperforatorinfarctsareassociatedwithlessseverevascularstenosesandabetterprognosisthaninternalborderzoneinfarcts.Becauseofthedifficultyofdifferentiatingbetweenthetwotypesofinfarctsonradiologicimages,theyhavesometimesbeencollectivelydescribedassubcorticalwhitematterinfarcts,butthattermisdiagnosticallynonspecific.本文檔共34頁；當(dāng)前第22頁；編輯于星期五\23點49分CausalMechanismsIncontrasttoexternalborderzoneinfarcts,internalborderzoneinfarctsarecausedmainlybyarterialstenosisorocclusion,orhemodynamiccompromise.Thegreatervulnerabilityofinternalborderzonestohemodynamiccompromisehasbeenexplainedonthebasisofanatomiccharacteristicsofthecerebralarterioleswithinthesezones.theinternalborderzonesaresuppliedbymedullarypenetratingvesselsofthemiddleandanteriorcerebralarteriesandbydeepperforatinglenticulostriatebranches.Themedullarypenetratingarteriesarethemostdistalbranchesoftheinternalcarotidarteryandhavethelowestperfusionpressure.Thedeepperforatinglenticulostriatearterieshavelittlecollateralsupply,andtherearenoanastomosesbetweenthedeepperforatorsandthewhitemattermedullaryarterioles.Therefore,thecentrumsemiovaleandcoronaradiataaremoresusceptiblethanotherregionstoischemicinsultsinthesettingofhemodynamiccompromise.本文檔共34頁；當(dāng)前第23頁；編輯于星期五\23點49分ClinicalCourse

Internalborderzoneinfarctsareassociatedwithapoorprognosisandclinicaldeterioration.Patientsmayundergoprolongedhospitalization,andtheyhaveanincreasedlikelihoodofremaininginadisabledstateduringclinicalfollow-up.Theresultsofdiffusion-weightedimagingstudiessuggestthatpatientswithinternalborderzoneinfarctshaveanincreasedriskforstroke

duringthefirstfewdays

afterinfarction.Perfusionstudiesinpatientswithsuchinfarctshaveshownafargreaterareaofmiseryperfusionthanisreflectedondiffusion-weightedimages.Involvementoftheadjacentcortexalsohasbeenfoundonperfusionimages.Thus,thetypicallysmallinternalborderzoneinfarctsrepresentthe“tipoftheiceberg”ofdecreasedperfusionreserveandmaybepredictiveofimpendingstroke.Thishypothesiswastestedfurtherwithquantitativecarbon11–flumazenilpositronemissiontomography(PET),whichshowedadecreaseinbenzodiazepinereceptors,afindingsuggestiveofneuronaldamagebeyondtheregionofinfarctionseenonMRimages.本文檔共34頁；當(dāng)前第24頁；編輯于星期五\23點49分

a)ColoroverlayonacoronalMIPimagefromCTangiographyinahealthyvolunteershowstheprobablelocationoftheinternalborderzone(bluedots).本文檔共34頁；當(dāng)前第25頁；編輯于星期五\23點49分

(b)Diffusion-weightedMRimages,obtainedina52-year-oldwomanwithprogressiveweaknessandnumbnessfor6monthsandacompletefootdrop,showmultipleinternalborderzoneinfarctsinarosarylikepatternalongtheleftcentrumsemiovale.(c)LeftinternalcarotidangiograminthesamepatientdemonstratesseverestenosisoftheM1segmentoftheleftmiddlecerebralartery.本文檔共34頁；當(dāng)前第26頁；編輯于星期五\23點49分PosteriorExternal(Cortical)BorderZoneInfarcts

Anteriorexternalborderzoneinfarctsaremorecommonthanposterioronesbecauseofthehighprevalenceofinternalcarotidarterydisease.Vertebrobasilarsystem

diseasewithsuperimposedfetalcirculation(ie,afetal-typeposteriorcerebralartery)mayleadtoposteriorexternalborderzoneinfarcts.Unilateralposteriorexternalborderzoneinfarctshavebeenrelatedtocerebralembolieitherofcardiacoriginorfromthecommoncarotidartery,whereasbilateralinfarctsaremorelikelytobecausedbyunderlyinghemodynamicimpairment(vascularstenosis).本文檔共34頁；當(dāng)前第27頁；編輯于星期五\23點49分

Axialdiffusion-weightedMRimageandapparentdiffusioncoefficientmapshowbilateralposteriorcorticalborderzoneinfarcts.本文檔共34頁；當(dāng)前第28頁；編輯于星期五\23點49分VascularBorderZoneChanges

Thelesionsproducedbyneurotoxiceffectsofcyclosporinetherapyhaveadistinctdistributioninvascularanastomoticborderzonesbutdonotleadtoinfarction.Reversiblevasculopathyhasbeensuggestedasthemechanismforreversibleposteriorencephalopathyinpatientswiththiscondition.Decreasedcorticalbloodflowhasbeenfoundintheborderzonesinthesepatients.本文檔共34頁；當(dāng)前第29頁；編輯于星期五\23點49分

AxialT2-weightedfluid-attenuatedinversionrecoveryMRimagesshowabnormalregionsofhyperintensesignalinvascularwatershedterritoriesinapatientwithtoxiceffectsofcyclosporinetherapy.本文檔共34頁；當(dāng)前第30頁；編輯于星期五\23點49分Hypereosinophilia（紅細胞增多癥）andBorderZoneInfarctsMultipleischemicstrokeshavebeenreportedasararecomplicationofhypereosinophilia,whichcouldbeduetoidiopathichypereosinophilicsyndromeoraparasiticinfection(eg,filariasis,trichinosis,orschistosomiasis).Theresultantinfarctscanbeseeninthecortexaswellastheborderzoneregionsofthedeepandsuperficialmiddlecerebralarteryperforators.Theborderzoneinfarctscouldbeduetoeitherthromboembolismfromendomyocardialfibrosisortovascularendothelialtoxiceffectsofeosinophiliccell