分水嶺區(qū)梗死及影像學(xué)表現(xiàn)2

優(yōu)選分水嶺區(qū)梗死及影像學(xué)表現(xiàn)目前一頁(yè)\總數(shù)三十四頁(yè)\編于二十點(diǎn)目前二頁(yè)\總數(shù)三十四頁(yè)\編于二十點(diǎn)目前三頁(yè)\總數(shù)三十四頁(yè)\編于二十點(diǎn)目前四頁(yè)\總數(shù)三十四頁(yè)\編于二十點(diǎn)WatershedInfarcts

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

Therearetwopatternsofborderzoneinfarcts:

Corticalborderzoneinfarctions

InfarctionsofthecortexandadjacentsubcorticalwhitematterlocatedattheborderzoneofACA/MCAandMCA/PCA

Internalborderzoneinfarctions

InfarctionsofthedeepwhitematterofthecentrumsemiovaleandcoronaradiataattheborderzonebetweenlenticulostriateperforatorsandthedeeppenetratingcorticalbranchesoftheMCAorattheborderzoneofdeepwhitematterbranchesoftheMCAandtheACA.目前五頁(yè)\總數(shù)三十四頁(yè)\編于二十點(diǎn)Corticawatershedstrokes(CWS),orouterbraininfarcts,arelocatedbetweenthecorticalterritoriesoftheanteriorcerebralartery(ACA),middlecerebralartery(MCA),andposteriorcerebralartery(PCA).Internalwatershedstrokes(IWS),orsubcorticalbraininfarcts,arelocatedinthewhitematter,alongandslightlyabovethelateralventricle,betweenthedeepandthesuperficialarterialsystemsoftheMCA,orbetweenthesuperficialsystemsoftheMCAandACA.目前六頁(yè)\總數(shù)三十四頁(yè)\編于二十點(diǎn)目前七頁(yè)\總數(shù)三十四頁(yè)\編于二十點(diǎn)目前八頁(yè)\總數(shù)三十四頁(yè)\編于二十點(diǎn)

Watershedsorborderzonesareareasthatlieatthejunctionoftwodifferentdrainage

areas.Thevascularsupplyofthecerebralparenchymacanbeenvisionedinasimilarmanner,withdefinedboundariesbetweendifferentarterialsystems.Cerebralinfarctsinborderzoneswerefirstdiscussedin1883andweredefinedasischemiclesionsinanareabetweentwo

neighboringvascularterritories.Theseterritoriescanbefurtherclassifiedintwobroadcategoriesas(a)external(cortical)or(b)internal(subcortical)borderzones.Borderzoneinfarctsconstituteapproximately10%ofallcerebralinfarcts.Varioustheorieshavebeenproposedtoexplaintheirpathogenesis.Itisbelievedthatrepeatedepisodesofseveresystemichypotensionarethemostfrequentcause.Susceptibilityofborderzonestoischemiawasprovedinanautopsystudyofpatientswithborderzoneinfarcts.Variousneuropathologicstudieshaveshownneuronalnecrosisfromhypotensionintheseregionsandhaveadvancedourunderstandingofthepreferentialdistributionofborderzoneinfarcts.目前九頁(yè)\總數(shù)三十四頁(yè)\編于二十點(diǎn)

Theappearancesofborderzoneinfarctsdepictedbystandardimagingmodalitiesarewelldescribed.Advancedimagingtechniquescanhelpidentifyareasofmiseryperfusionassociatedwiththeseinfarcts.Miseryperfusion(低灌注)representsachronicfailureofcerebralautoregulationassociatedwithdecreased

cerebralperfusionpressuresinthepresenceofextracranialandintracranialatheromatousdisease.Theimportantinformationderivedfromimagingcanbeusefulforpatientmanagementanddiseaseprognosis目前十頁(yè)\總數(shù)三十四頁(yè)\編于二十點(diǎn)

Theexternalorcorticalborderzonesarelocatedatthejunctionsoftheanterior,middle,andposteriorcerebralarteryterritories.Infarctsintheanteriorexternalborderzonesandparamedianwhitematterarefoundatthejunctionoftheterritoriessuppliedbytheanteriorandmiddlecerebralarteries,andthoseintheparieto-occipitalareas(posteriorexternalborderzones)arefoundatthejunctionoftheterritoriessuppliedbythemiddleandposteriorcerebralarteries.目前十一頁(yè)\總數(shù)三十四頁(yè)\編于二十點(diǎn)Theinternalorsubcorticalborderzonesarelocatedatthejunctionsoftheanterior,middle,andposteriorcerebralarteryterritorieswiththeHeubner,lenticulostriate,andanteriorchoroidalarteryterritories.Internalborderzoneinfarctsthusmaybedesignatedasinfarctsofthelenticulostriate–middlecerebralartery,lenticulostriate–anterior

cerebralartery,Heubner–anteriorcerebralartery,anteriorchoroidal–middlecerebralartery,andanteriorchoroidal–posteriorcerebralarteryterritories.Infarctsofthelenticulostriate–middlecerebralarteryborderzone,whichissuppliedbytheendbranchesofdeepperforatinglenticulostriatearteriesandmedullarypenetratorsfromthepial–middlecerebralartery,arethemostcommonlyseenatimagingandaredescribedindetailinthisarticle.目前十二頁(yè)\總數(shù)三十四頁(yè)\編于二十點(diǎn)

ColoroverlaysonaxialT2-weightedmagneticresonance(MR)imagesofnormalcerebrumshowprobablelocationsofexternal(blue)andinternal(red)borderzoneinfarcts.目前十三頁(yè)\總數(shù)三十四頁(yè)\編于二十點(diǎn)

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

PathophysiologyofBorderZoneInfarcts目前十四頁(yè)\總數(shù)三十四頁(yè)\編于二十點(diǎn)

Insharpcontrastwiththiswidelyprevalentinterpretation,severalpathologicinvestigationshaveemphasizedanassociationbetweenborderzoneinfarctionandmicroemboli,andembolicmaterialhasbeenfoundwithinareasofborderzoneinfarctioninautopsyseries.Preferentialpropagationofemboliintheborderzoneregionsalsohasbeenfoundinexperimentalstudies.Borderzoneinfarctionmaybebetterexplainedbyinvokingacombinationoftwoofteninterrelatedprocesses:hypoperfusionandembolization.Hypoperfusion,ordecreasedbloodflow,islikelytoimpedetheclearance(washout)ofemboli.Becauseperfusionismostlikelytobeimpairedinborderzoneregions,clearanceofemboliwillbemostimpairedintheseregionsofleastbloodflow.Severeocclusivediseaseoftheinternalcarotidarterycausesbothembolizationanddecreasedperfusion.Similarly,cardiacdiseaseisoftenassociatedwithmicroembolizationfromtheheartandaortawithperiodsofdiminishedsystemicandbrainperfusion.Thistheory,althoughitseemsreasonable,remainsunprovedandhasbeenchallengedonmanyaccounts.目前十五頁(yè)\總數(shù)三十四頁(yè)\編于二十點(diǎn)ImagingAppearanceTheexternal,corticalborderzonesarelocatedbetweentheanterior,middle,andposteriorcerebralarteriesandareusuallywedge-shapedorovoid.However,theirlocationmayvarywithdifferencesinthearterialsupply.ItissometimesdifficulttodeterminewhetherapersonhassustainedaborderzoneinfarctonthebasisofthelocationoftheinfarctinrelationtothevesselsonaCTorMRimag.Becauseofthisextensiveanatomicvariation,minimumandmaximumdistributionterritoriesofeachvesselhavebeendefined.Itisnotuncommontodescribeacorticalinfarctasa“territorial”infarctifitliescompletelywithintheexpectedorpossiblemaximumareaofavascularterritoryorasa“potential”infarctifitisoutsidethesemaxima.Furthermore,thelocationofcorticalborderzonesmayvarybecauseofthedevelopmentofleptomeningealcollaterals.Theanatomyofcorticalborderzonescanbecomplex,withmarkedvariabilityduetoindividualdifferencesintheterritoriessuppliedbythemajorarteriesofthebrain.目前十六頁(yè)\總數(shù)三十四頁(yè)\編于二十點(diǎn)

(a,b)Coronalfluid-attenuatedinversionrecoveryMRimagesshowthedistributionofexternal(cortical)borderzoneinfarctsatthejunctionsoftheanteriorcerebralarteryandmiddlecerebralarteryterritories(a)andthemiddlecerebralarteryandposteriorcerebralarteryterritories(b).(c)Diffusion-weightedMRimagesshowacorticalborderzoneinfarctatthejunctionoftheanteriorcerebralarteryandmiddlecerebralarteryterritories.Angiographyoftheright-sidedcommoncarotidandinternalcarotidarteriesinthesamepatientshowednormalvesselswithnoocclusionorstenosis.目前十七頁(yè)\總數(shù)三十四頁(yè)\編于二十點(diǎn)CausalMechanisms

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

inmajorarteriesmaypreferentiallypropagatetocorticalborderzones,whichhavelowerperfusionthanotherareasofthevasculature,and,thus,alimitedabilitytowashouttheseemboli.Manypatientswithcorticalborderzoneinfarctshaveconcomitantsmallercorticalinfarcts.Thesefindingssupportthehypothesisthatanembolicmechanismplaysacrucialroleinthepathogenesisofexternalborderzoneinfarcts目前十八頁(yè)\總數(shù)三十四頁(yè)\編于二十點(diǎn)ClinicalCourse

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

internalborderzoneinfarcts,thereisahigherprobabilityofhemodynamicimpairment,andtheprognosismaynotbegood.目前十九頁(yè)\總數(shù)三十四頁(yè)\編于二十點(diǎn)InternalBorderZoneInfarctsImagingAppearance

Internalborderzoneinfarctsappearinmultiples,inarosarylikepattern.Inonereport,thispatternwasdescribedasaseriesofthreeormorelesions,eachwithadiameterof3mmormore,arrangedinalinearfashionparalleltothelateralventricleinthecentrum

semiovaleorcoronaradiata.Internalborderzoneinfarctsareclassifiedonthebasisoftheirradiologicappearanceaseitherconfluentorpartial

Partialinfarctsareusuallylarge,cigarshaped,andarrangedinapatternresemblingthebeadsofarosary,parallelandadjacenttothelateralventricle.Thedurationofhemodynamiccompromisehasbeenpostulatedasthecauseofthevariedradiologicappearances,withabriefepisodeofcompromiseleadingtoapartialinfarct,andalongerperiodofcompromise,toconfluentinfarcts.Confluentinternalborderzoneinfarctsmaybemanifestedbyastepwiseonsetofcontralateralhemiplegia.Theyalsomaybeassociatedwithapoorerrecoverythanistypicalforpartialinfarcts目前二十頁(yè)\總數(shù)三十四頁(yè)\編于二十點(diǎn)

Internalborderzoneinfarctsmustbedifferentiatedfromsuperficialperforator(medullary)infarcts,whichmayhaveasimilarappearanceonMRimages.Superficialperforatorinfarcts,whicharecausedbytheocclusionofmedullaryarteriesfrompialplexuses,aresmaller,superficiallylocated,andwidelyscattered,whereasinternalborderzoneinfarctstendtolocalizeinparaventricularregions.Superficialperforatorinfarctsareassociatedwithlessseverevascularstenosesandabetterprognosisthaninternalborderzoneinfarcts.Becauseofthedifficultyofdifferentiatingbetweenthetwotypesofinfarctsonradiologicimages,theyhavesometimesbeencollectivelydescribedassubcorticalwhitematterinfarcts,butthattermisdiagnosticallynonspecific.目前二十一頁(yè)\總數(shù)三十四頁(yè)\編于二十點(diǎn)CausalMechanismsIncontrasttoexternalborderzoneinfarcts,internalborderzoneinfarctsarecausedmainlybyarterialstenosisorocclusion,orhemodynamiccompromise.Thegreatervulnerabilityofinternalborderzonestohemodynamiccompromisehasbeenexplainedonthebasisofanatomiccharacteristicsofthecerebralarterioleswithinthesezones.theinternalborderzonesaresuppliedbymedullarypenetratingvesselsofthemiddleandanteriorcerebralarteriesandbydeepperforatinglenticulostriatebranches.Themedullarypenetratingarteriesarethemostdistalbranchesoftheinternalcarotidarteryandhavethelowestperfusionpressure.Thedeepperforatinglenticulostriatearterieshavelittlecollateralsupply,andtherearenoanastomosesbetweenthedeepperforatorsandthewhitemattermedullaryarterioles.Therefore,thecentrumsemiovaleandcoronaradiataaremoresusceptiblethanotherregionstoischemicinsultsinthesettingofhemodynamiccompromise.目前二十二頁(yè)\總數(shù)三十四頁(yè)\編于二十點(diǎn)ClinicalCourse

Internalborderzoneinfarctsareassociatedwithapoorprognosisandclinicaldeterioration.Patientsmayundergoprolongedhospitalization,andtheyhaveanincreasedlikelihoodofremaininginadisabledstateduringclinicalfollow-up.Theresultsofdiffusion-weightedimagingstudiessuggestthatpatientswithinternalborderzoneinfarctshaveanincreasedriskforstroke

duringthefirstfewdays

afterinfarction.Perfusionstudiesinpatientswithsuchinfarctshaveshownafargreaterareaofmiseryperfusionthanisreflectedondiffusion-weightedimages.Involvementoftheadjacentcortexalsohasbeenfoundonperfusionimages.Thus,thetypicallysmallinternalborderzoneinfarctsrepresentthe“tipoftheiceberg”ofdecreasedperfusionreserveandmaybepredictiveofimpendingstroke.Thishypothesiswastestedfurtherwithquantitativecarbon11–flumazenilpositronemissiontomography(PET),whichshowedadecreaseinbenzodiazepinereceptors,afindingsuggestiveofneuronaldamagebeyondtheregionofinfarctionseenonMRimages.目前二十三頁(yè)\總數(shù)三十四頁(yè)\編于二十點(diǎn)

a)ColoroverlayonacoronalMIPimagefromCTangiographyinahealthyvolunteershowstheprobablelocationoftheinternalborderzone(bluedots).目前二十四頁(yè)\總數(shù)三十四頁(yè)\編于二十點(diǎn)(b)Diffusion-weightedMRimages,obtainedina52-year-oldwomanwithprogressiveweaknessandnumbnessfor6monthsandacompletefootdrop,showmultipleinternalborderzoneinfarctsinarosarylikepatternalongtheleftcentrumsemiovale.(c)LeftinternalcarotidangiograminthesamepatientdemonstratesseverestenosisoftheM1segmentoftheleftmiddlecerebralartery.目前二十五頁(yè)\總數(shù)三十四頁(yè)\編于二十點(diǎn)PosteriorExternal(Cortical)BorderZoneInfarctsAnteriorexternalborderzoneinfarctsaremorecommonthanposterioronesbecauseofthehighprevalenceofinternalcarotidarterydisease.Vertebrobasilarsystem

diseasewithsuperimposedfetalcirculation(ie,afetal-typeposteriorcerebralartery)mayleadtoposteriorexternalborderzoneinfarcts.Unilateralposteriorexternalborderzoneinfarctshavebeenrelatedtocerebralembolieitherofcardiacoriginorfromthecommoncarotidartery,whereasbilateralinfarctsaremorelikelytobecausedbyunderlyinghemodynamicimpairment(vascularstenosis).目前二十六頁(yè)\總數(shù)三十四頁(yè)\編于二十點(diǎn)

Axialdiffusion-weightedMRimageandapparentdiffusioncoefficientmapshowbilateralposteriorcorticalborderzoneinfarcts.目前二十七頁(yè)\總數(shù)三十四頁(yè)\編于二十點(diǎn)VascularBorderZoneChangesThelesionsproducedbyneurotoxiceffectsofcyclosporinetherapyhaveadistinctdistributioninvascularanastomoticborderzonesbutdonotleadtoinfarction.Reversiblevasculopathyhasbeensuggestedasthemechanismforreversibleposteriorencephalopathyinpatientswiththiscondition.Decreasedcorticalbloodflowhasbeenfoundintheborderzonesinthesepatients.目前二十八頁(yè)\總數(shù)三十四頁(yè)\編于二十點(diǎn)

AxialT2-weightedfluid-attenuatedinversionrecoveryMRimagesshowabnormalregionsofhyperintensesignalinvascularwatershedterritoriesinapatientwithtoxiceffectsofcyclosporinetherapy.目前二十九頁(yè)\總數(shù)三十四頁(yè)\編于二十點(diǎn)Hypereosinophilia（紅細(xì)胞增多癥）andBorderZoneInfarctsMultipleischemicstrokeshavebeenreportedasararecomplicationofhypereosinophilia,whichcouldbeduetoidiopathichypereosinophilicsyndromeoraparasiticinfection(eg,filariasis,trichinosis,orschistosomiasis).Theresultantinfarctscanbeseeninthecortexaswellastheborderzoneregionsofthedeepandsuperficialmiddlecerebralarteryperforators.Theborderzoneinfarctscouldbeduetoeitherthromboembolismfromendomyocardialfibrosisortovascularendothelialtoxiceffectsofeosinophiliccells;thromboembolicanoccurinconjunctionwithcardiacinvolvementthroughoutthecourseofthedisease.Inafewcases,theinfarctshavebeenattributedtolocalthrombusformationinsteadofathromboemboliccause.目前三十頁(yè)\總數(shù)三十四頁(yè)\編于二十點(diǎn)

Axialdiffusion-weightedMRimagesobtainedina26-year-oldmanwithasuddenonsetofencephalopathyshowmultiplesmallabnormalregionswithhyperintensesignaldistributedinvascularwatershedterritories.Idiopathichypereosinophilicsyndromewassubsequentlydiagnosed目前三十一頁(yè)\總數(shù)三十四頁(yè)\編于二十點(diǎn)BorderZoneInfarctsintheCerebellumBorderzoneinfarctsinthecerebellumareusuallylessthan2cminsizeandareseenatthebordersoftheanteriorinferiorcerebellarartery,superiorcerebellarartery,posteriorinferiorcerebellarartery,andtheirbranches.Theoriginoftheseborderzoneinfarctsissimilartothatofterrito