分水岭区梗死及影像学表现

分水岭区梗死分水岭区梗死及影像学表现分水岭区梗死及影像学表现分水岭区梗死及影像学表现分水岭区梗死及影像学表现WatershedInfarcts

Watershedinfarctsoccurattheborderzonesbetweenmajorcerebralarterialterritoriesasaresultofhypoperfusion.

Therearetwopatternsofborderzoneinfarcts:

Corticalborderzoneinfarctions

InfarctionsofthecortexandadjacentsubcorticalwhitematterlocatedattheborderzoneofACA/MCAandMCA/PCA

Internalborderzoneinfarctions

InfarctionsofthedeepwhitematterofthecentrumsemiovaleandcoronaradiataattheborderzonebetweenlenticulostriateperforatorsandthedeeppenetratingcorticalbranchesoftheMCAorattheborderzoneofdeepwhitematterbranchesoftheMCAandtheACA.分水岭区梗死及影像学表现Corticawatershedstrokes(CWS),orouterbraininfarcts,arelocatedbetweenthecorticalterritoriesoftheanteriorcerebralartery(ACA),middlecerebralartery(MCA),andposteriorcerebralartery(PCA).Internalwatershedstrokes(IWS),orsubcorticalbraininfarcts,arelocatedinthewhitematter,alongandslightlyabovethelateralventricle,betweenthedeepandthesuperficialarterialsystemsoftheMCA,orbetweenthesuperficialsystemsoftheMCAandACA.分水岭区梗死及影像学表现分水岭区梗死及影像学表现分水岭区梗死及影像学表现

Watershedsorborderzonesareareasthatlieatthejunctionoftwodifferentdrainage

areas.Thevascularsupplyofthecerebralparenchymacanbeenvisionedinasimilarmanner,withdefinedboundariesbetweendifferentarterialsystems.Cerebralinfarctsinborderzoneswerefirstdiscussedin1883andweredefinedasischemiclesionsinanareabetweentwo

neighboringvascularterritories.Theseterritoriescanbefurtherclassifiedintwobroadcategoriesas(a)external(cortical)or(b)internal(subcortical)borderzones.Borderzoneinfarctsconstituteapproximately10%ofallcerebralinfarcts.Varioustheorieshavebeenproposedtoexplaintheirpathogenesis.Itisbelievedthatrepeatedepisodesofseveresystemichypotensionarethemostfrequentcause.Susceptibilityofborderzonestoischemiawasprovedinanautopsystudyofpatientswithborderzoneinfarcts.Variousneuropathologicstudieshaveshownneuronalnecrosisfromhypotensionintheseregionsandhaveadvancedourunderstandingofthepreferentialdistributionofborderzoneinfarcts.分水岭区梗死及影像学表现

Theappearancesofborderzoneinfarctsdepictedbystandardimagingmodalitiesarewelldescribed.Advancedimagingtechniquescanhelpidentifyareasofmiseryperfusionassociatedwiththeseinfarcts.Miseryperfusion(低灌注)representsachronicfailureofcerebralautoregulationassociatedwithdecreased

cerebralperfusionpressuresinthepresenceofextracranialandintracranialatheromatousdisease.Theimportantinformationderivedfromimagingcanbeusefulforpatientmanagementanddiseaseprognosis分水岭区梗死及影像学表现

Theexternalorcorticalborderzonesarelocatedatthejunctionsoftheanterior,middle,andposteriorcerebralarteryterritories.Infarctsintheanteriorexternalborderzonesandparamedianwhitematterarefoundatthejunctionoftheterritoriessuppliedbytheanteriorandmiddlecerebralarteries,andthoseintheparieto-occipitalareas(posteriorexternalborderzones)arefoundatthejunctionoftheterritoriessuppliedbythemiddleandposteriorcerebralarteries.分水岭区梗死及影像学表现Theinternalorsubcorticalborderzonesarelocatedatthejunctionsoftheanterior,middle,andposteriorcerebralarteryterritorieswiththeHeubner,lenticulostriate,andanteriorchoroidalarteryterritories.Internalborderzoneinfarctsthusmaybedesignatedasinfarctsofthelenticulostriate–middlecerebralartery,lenticulostriate–anterior

cerebralartery,Heubner–anteriorcerebralartery,anteriorchoroidal–middlecerebralartery,andanteriorchoroidal–posteriorcerebralarteryterritories.Infarctsofthelenticulostriate–middlecerebralarteryborderzone,whichissuppliedbytheendbranchesofdeepperforatinglenticulostriatearteriesandmedullarypenetratorsfromthepial–middlecerebralartery,arethemostcommonlyseenatimagingandaredescribedindetailinthisarticle.分水岭区梗死及影像学表现

ColoroverlaysonaxialT2-weightedmagneticresonance(MR)imagesofnormalcerebrumshowprobablelocationsofexternal(blue)andinternal(red)borderzoneinfarcts.分水岭区梗死及影像学表现

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

PathophysiologyofBorderZoneInfarcts分水岭区梗死及影像学表现

Insharpcontrastwiththiswidelyprevalentinterpretation,severalpathologicinvestigationshaveemphasizedanassociationbetweenborderzoneinfarctionandmicroemboli,andembolicmaterialhasbeenfoundwithinareasofborderzoneinfarctioninautopsyseries.Preferentialpropagationofemboliintheborderzoneregionsalsohasbeenfoundinexperimentalstudies.Borderzoneinfarctionmaybebetterexplainedbyinvokingacombinationoftwoofteninterrelatedprocesses:hypoperfusionandembolization.Hypoperfusion,ordecreasedbloodflow,islikelytoimpedetheclearance(washout)ofemboli.Becauseperfusionismostlikelytobeimpairedinborderzoneregions,clearanceofemboliwillbemostimpairedintheseregionsofleastbloodflow.Severeocclusivediseaseoftheinternalcarotidarterycausesbothembolizationanddecreasedperfusion.Similarly,cardiacdiseaseisoftenassociatedwithmicroembolizationfromtheheartandaortawithperiodsofdiminishedsystemicandbrainperfusion.Thistheory,althoughitseemsreasonable,remainsunprovedandhasbeenchallengedonmanyaccounts.分水岭区梗死及影像学表现ImagingAppearanceTheexternal,corticalborderzonesarelocatedbetweentheanterior,middle,andposteriorcerebralarteriesandareusuallywedge-shapedorovoid.However,theirlocationmayvarywithdifferencesinthearterialsupply.ItissometimesdifficulttodeterminewhetherapersonhassustainedaborderzoneinfarctonthebasisofthelocationoftheinfarctinrelationtothevesselsonaCTorMRimag.Becauseofthisextensiveanatomicvariation,minimumandmaximumdistributionterritoriesofeachvesselhavebeendefined.Itisnotuncommontodescribeacorticalinfarctasa“territorial”infarctifitliescompletelywithintheexpectedorpossiblemaximumareaofavascularterritoryorasa“potential”infarctifitisoutsidethesemaxima.Furthermore,thelocationofcorticalborderzonesmayvarybecauseofthedevelopmentofleptomeningealcollaterals.Theanatomyofcorticalborderzonescanbecomplex,withmarkedvariabilityduetoindividualdifferencesintheterritoriessuppliedbythemajorarteriesofthebrain.分水岭区梗死及影像学表现

(a,b)Coronalfluid-attenuatedinversionrecoveryMRimagesshowthedistributionofexternal(cortical)borderzoneinfarctsatthejunctionsoftheanteriorcerebralarteryandmiddlecerebralarteryterritories(a)andthemiddlecerebralarteryandposteriorcerebralarteryterritories(b).(c)Diffusion-weightedMRimagesshowacorticalborderzoneinfarctatthejunctionoftheanteriorcerebralarteryandmiddlecerebralarteryterritories.Angiographyoftheright-sidedcommoncarotidandinternalcarotidarteriesinthesamepatientshowednormalvesselswithnoocclusionorstenosis.分水岭区梗死及影像学表现CausalMechanisms

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

inmajorarteriesmaypreferentiallypropagatetocorticalborderzones,whichhavelowerperfusionthanotherareasofthevasculature,and,thus,alimitedabilitytowashouttheseemboli.Manypatientswithcorticalborderzoneinfarctshaveconcomitantsmallercorticalinfarcts.Thesefindingssupportthehypothesisthatanembolicmechanismplaysacrucialroleinthepathogenesisofexternalborderzoneinfarcts分水岭区梗死及影像学表现ClinicalCourse

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

internalborderzoneinfarcts,thereisahigherprobabilityofhemodynamicimpairment,andtheprognosismaynotbegood.分水岭区梗死及影像学表现InternalBorderZoneInfarctsImagingAppearance

Internalborderzoneinfarctsappearinmultiples,inarosarylikepattern.Inonereport,thispatternwasdescribedasaseriesofthreeormorelesions,eachwithadiameterof3mmormore,arrangedinalinearfashionparalleltothelateralventricleinthecentrum

semiovaleorcoronaradiata.Internalborderzoneinfarctsareclassifiedonthebasisoftheirradiologicappearanceaseitherconfluentorpartial

Partialinfarctsareusuallylarge,cigarshaped,andarrangedinapatternresemblingthebeadsofarosary,parallelandadjacenttothelateralventricle.Thedurationofhemodynamiccompromisehasbeenpostulatedasthecauseofthevariedradiologicappearances,withabriefepisodeofcompromiseleadingtoapartialinfarct,andalongerperiodofcompromise,toconfluentinfarcts.Confluentinternalborderzoneinfarctsmaybemanifestedbyastepwiseonsetofcontralateralhemiplegia.Theyalsomaybeassociatedwithapoorerrecoverythanistypicalforpartialinfarcts分水岭区梗死及影像学表现

Internalborderzoneinfarctsmustbedifferentiatedfromsuperficialperforator(medullary)infarcts,whichmayhaveasimilarappearanceonMRimages.Superficialperforatorinfarcts,whicharecausedbytheocclusionofmedullaryarteriesfrompialplexuses,aresmaller,superficiallylocated,andwidelyscattered,whereasinternalborderzoneinfarctstendtolocalizeinparaventricularregions.Superficialperforatorinfarctsareassociatedwithlessseverevascularstenosesandabetterprognosisthaninternalborderzoneinfarcts.Becauseofthedifficultyofdifferentiatingbetweenthetwotypesofinfarctsonradiologicimages,theyhavesometimesbeencollectivelydescribedassubcorticalwhitematterinfarcts,butthattermisdiagnosticallynonspecific.分水岭区梗死及影像学表现CausalMechanismsIncontrasttoexternalborderzoneinfarcts,internalborderzoneinfarctsarecausedmainlybyarterialstenosisorocclusion,orhemodynamiccompromise.Thegreatervulnerabilityofinternalborderzonestohemodynamiccompromisehasbeenexplainedonthebasisofanatomiccharacteristicsofthecerebralarterioleswithinthesezones.theinternalborderzonesaresuppliedbymedullarypenetratingvesselsofthemiddleandanteriorcerebralarteriesandbydeepperforatinglenticulostriatebranches.Themedullarypenetratingarteriesarethemostdistalbranchesoftheinternalcarotidarteryandhavethelowestperfusionpressure.Thedeepperforatinglenticulostriatearterieshavelittlecollateralsupply,andtherearenoanastomosesbetweenthedeepperforatorsandthewhitemattermedullaryarterioles.Therefore,thecentrumsemiovaleandcoronaradiataaremoresusceptiblethanotherregionstoischemicinsultsinthesettingofhemodynamiccompromise.分水岭区梗死及影像学表现ClinicalCourse

Internalborderzoneinfarctsareassociatedwithapoorprognosisandclinicaldeterioration.Patientsmayundergoprolongedhospitalization,andtheyhaveanincreasedlikelihoodofremaininginadisabledstateduringclinicalfollow-up.Theresultsofdiffusion-weightedimagingstudiessuggestthatpatientswithinternalborderzoneinfarctshaveanincreasedriskforstroke

duringthefirstfewdays

afterinfarction.Perfusionstudiesinpatientswithsuchinfarctshaveshownafargreaterareaofmiseryperfusionthanisreflectedondiffusion-weightedimages.Involvementoftheadjacentcortexalsohasbeenfoundonperfusionimages.Thus,thetypicallysmallinternalborderzoneinfarctsrepresentthe“tipoftheiceberg”ofdecreasedperfusionreserveandmaybepredictiveofimpendingstroke.Thishypothesiswastestedfurtherwithquantitativecarbon11–flumazenilpositronemissiontomography(PET),whichshowedadecreaseinbenzodiazepinereceptors,afindingsuggestiveofneuronaldamagebeyondtheregionofinfarctionseenonMRimages.分水岭区梗死及影像学表现

a)ColoroverlayonacoronalMIPimagefromCTangiographyinahealthyvolunteershowstheprobablelocationoftheinternalborderzone(bluedots).分水岭区梗死及影像学表现(b)Diffusion-weightedMRimages,obtainedina52-year-oldwomanwithprogressiveweaknessandnumbnessfor6monthsandacompletefootdrop,showmultipleinternalborderzoneinfarctsinarosarylikepatternalongtheleftcentrumsemiovale.(c)LeftinternalcarotidangiograminthesamepatientdemonstratesseverestenosisoftheM1segmentoftheleftmiddlecerebralartery.分水岭区梗死及影像学表现PosteriorExternal(Cortical)BorderZoneInfarctsAnteriorexternalborderzoneinfarctsaremorecommonthanposterioronesbecauseofthehighprevalenceofinternalcarotidarterydisease.Vertebrobasilarsystem

diseasewithsuperimposedfetalcirculation(ie,afetal-typeposteriorcerebralartery)mayleadtoposteriorexternalborderzoneinfarcts.Unilateralposteriorexternalborderzoneinfarctshavebeenrelatedtocerebralembolieitherofcardiacoriginorfromthecommoncarotidartery,whereasbilateralinfarctsaremorelikelytobecausedbyunderlyinghemodynamicimpairment(vascularstenosis).分水岭区梗死及影像学表现

Axialdiffusion-weightedMRimageandapparentdiffusioncoefficientmapshowbilateralposteriorcorticalborderzoneinfarcts.分水岭区梗死及影像学表现VascularBorderZoneChangesThelesionsproducedbyneurotoxiceffectsofcyclosporinetherapyhaveadistinctdistributioninvascularanastomoticborderzonesbutdonotleadtoinfarction.Reversiblevasculopathyhasbeensuggestedasthemechanismforreversibleposteriorencephalopathyinpatientswiththiscondition.Decreasedcorticalbloodflowhasbeenfoundintheborderzonesinthesepatients.分水岭区梗死及影像学表现

AxialT2-weightedfluid-attenuatedinversionrecoveryMRimagesshowabnormalregionsofhyperintensesignalinvascularwatershedterritoriesinapatientwithtoxiceffectsofcyclosporinetherapy.分水岭区梗死及影像学表现Hypereosinophilia（红细胞增多症）andBorderZoneInfarctsMultipleischemicstrokeshavebeenreportedasararecomplicationofhypereosinophilia,whichcouldbeduetoidiopathichypereosinophilicsyndromeoraparasiticinfection(eg,filariasis,trichinosis,orschistosomiasis).Theresultantinfarctscanbeseeninthecortexaswellastheborderzoneregionsofthedeepandsuperficialmiddlecerebralarteryperforators.Theborderzoneinfarctscouldbeduetoeitherthromboembolismfromendomyocardialfibrosisortovascularendothelialtoxiceffectsofeosinophiliccells;thromboembolicanoccurinconjunctionwithcardiacinvolvementthroughoutthecourseofthedisease.Inafewcases,theinfarctshavebeenattributedtolocalthrombusformationinsteadofathromboemboliccause.分水岭区梗死及影像学表现

Axialdiffusion-weightedMRimagesobtainedina26-year-oldmanwithasuddenonsetofencephalopathyshowmultiplesmallabnormalregionswithhyperintensesignaldistributedinvascularwatershedterritories.Idiopathichypereosinophilicsyndromewassubsequentlydiagnosed分水岭区梗死及影像学表现BorderZoneInfarctsintheCerebellumBorderzoneinfarctsinthecerebellumareusuallylessthan2cminsizeandareseenatthebordersoftheanteriorinferiorcerebellarartery,superiorcerebellarartery,posteriorinferiorcerebellarartery,andtheirbranches.Theoriginoftheseborderzoneinfarctsissimilartothatofterritorialinfarctsinthecerebellum:Theinfarctionisduetostenosisorembolismofthevessels.Thesourceofembolismcouldbeatheroscleroticdiseaseordissectioninavertebrobasilararteryoracardiaccondition(eg,rightheartthrombusinparadoxicalembolism).Often,thesesmallborderzonelesionscoexistwithlargeterritoriallesions.ThemanagementofborderzoneinfarctsinthecerebellumissimilartothatofterritorialcerebellarinfarctsInpopulation-basedstudiesofmigrainepatients,silentborderzoneinfarctswerefoundintheposteriorcerebellum.分水岭区梗死及影像学表现

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