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| 20190808杨迎迎strock.ppt |
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MagneticResonanceImagingofStrokeYangYingying2019_08_08Preview
Thrombolysis/θrɑm''bɑl?s?s/Plasminogen/pl?z''m?n?d??n/Opercu
lum/?(?)''p??kj?l?m/?Sodium/''s??d??m/?Potassium/p?''t?s??m/?L
ysis/''la?s?s/?Penumbra?/p?''n?mbr?/Endothelial/,end??''θi?l?
?l/?leptomeningealMacrophagesEncephalomalacia/?n,s?f?lom?''l
e???/?Peduncle/p?''d??k(?)l/Ictus/''?kt?s/1.Thegoalof
imagingofstrokeThegoalofstrokeimagingistodeterminewho
wouldbenefitfromtherapy.Thegoalofstroketherapyistores
toreperfusiontothebrain.2.Determinepotentialcandidatefor
therapyIntheappropriatepatients,intravenousorintra-arter
ialthrombolysisperformedwithtissueplasminogenactivatorcan
havenear-miraculousresults.However,thereisgraveriskoffa
talhemorrhageifpatientsareinappropriatelyselectedforthera
py.Theexactexclusioncriteriaforadministrationofthromboly
tictherapyvariesamonginstitutions.3.Acutestroke:MRimagi
ngFortheinitialevaluation,diffusionsequencescandetectacu
teinfarctionwithhighsensitivitywithinminutesofsymptomons
et.DWIismoresensitivethanFLAIRinthedetectionofhyperacu
testroke.FLAIRAxialFLAIRMRIshowsgeographicT2prolongatio
nintherightMCAterritoryinvolvingtherightfrontalandtemp
orallobesandrightbasalganglia.ThesizeoftheT2signalab
normalityislessextensivethantheinfarctsizeapparentonDWI
.DWIDWIshowsalargeregionofhyperintensityintherightMCA
territoryinvolvingtherightfrontaloperculum,therightinsul
a,therighttemporaloperculum,therightputamen,andtheright
caudate.MRAAxialobliqueMIPfromatimeofflightMRangiogra
mshowscompleteocclusionoftherightMCA.4.Evolutionofi
nfarction4.1Hyperacuteinfarct(0–6hours)Withinminutesofc
riticalischemia,thesodiumpotassiumATPpumpthatmaintainsth
enormallowintracellularsodiumconcentrationfails.Sodiumand
waterdiffuseintocells,leadingtocellswellingandcytotoxic
edema.Calciumalsodiffusesintocells,whichtriggerscascades
thatcontributetocelllysis.Diffusionisreducedinanacute
infarctbytwofactors:Shiftfromextracellulartointracel
lularwaterduetoNa/KATPpumpfailure.Increasedviscosit
yofinfarctedbrainduetocelllysisandincreasedextracellula
rprotein.4.1Hyperacuteinfarct(0–6hours)DWIhyperinten
sityandADCmaphypointensityreflectreduceddiffusivity,which
canbeseenwithinminutesoftheictus.FLAIRmaybenormal.S
ubtlehyperintensitymaybeseenonFLAIRimagesinthehyperacut
estage.Thesechangesareseenlessthantwothirdsofthetime
withinthefirstsixhours.Perfusionshowsdecreasedcerebralb
loodvolumeoftheinfarctcore,withorwithoutasurroundingre
gionofdecreasedcerebralbloodflow,whichrepresentsthepenum
bra.4.2Acuteinfarct(6hours–72hours)Theacuteinfarctphase
ischaracterizedbyincreaseinvasogenicedemaandmasseffect.
Damagedvascularendothelialcellscauseleakageofextracellul
arfluidandincreasetheriskofhemorrhage.Thereisincreased
sulcaleffacementandmasseffect.Themasseffectpeaksat3-4
days,whichisanoverlaptimebetweentheacuteandearlysubacu
tephases.4.2Acuteinfarct(6hours–72hours)MRIshowshyperin
tensityoftheinfarctcoreonT2WI,bestseenonFLAIR.TheFLAI
Rabnormalityisusuallyconfinedtothegraymater.DWIcontinue
stoshowrestricteddiffusion.Theremaybesomearterialenhan
cementduetoincreasedcollateralflow.Perfusionimagesmostco
mmonlyshowincreaseinsizeoftheinfarctcorewithresultantd
ecreaseinsizeofthepenumbra.4.3Earlysubacuteinfarct(1.5
days–5days)Intheearlysubacutephase,bloodflowtotheaffe
ctedbrainisre-establishedbyleptomeningealcollateralsandin
growthofnewvesselsintotheregionofinfarction.Thenewves
selshaveanincompletebloodbrainbarrier,causingacontinued
increaseinvasogenicedemaandmasseffect,whichpeaksat3-4d
ays.4.3Earlysubacuteinfarct(1.5days–5days)MRimagingsh
owsmarkedhyperintensityonT2WIinvolvingbothgrayandwhitem
ater.TheADCmapbecomeslessdarkorevenresolvesifthereis
extensiveedema;however,theDWIimagestypicallyremainbright
duetounderlyingT2shinethrough.Perfusionimagingshowscon
tinuedexpansionoftheinfarctcoreandfurtherreductioninthe
ischemicpenumbra.4.4Latesubacuteinfarct(5days–2weeks)T
hesubacutephaseischaracterizedbyresolutionofvasogenicede
maandreductioninmasseffect.DWImayremainbrightduetoT2
shinethrough,althoughtheADCmapwilleitherreturntonormal
orshowincreaseddiffusivity.4.4Latesubacuteinfarct(5day
s–2weeks)Akeyimagingfindingisgyriformenhancement,whichm
ayoccasionallybeconfusedforaneoplasm.Unlikeatumor,asub
acuteinfarctionwillnottypicallydemonstratebothmasseffect
andenhancementsimultaneously.Enhancementcanbeseenfromappr
oximately6daysto6weeksaftertheinitialinfarct.Theenhan
cementofasubacuteinfarcthasalsobeendescribedbythe“2-2-
2”rule,whichstatesthatenhancementbeginsat2days,peaksat
2weeks,anddisappearsby2months.4.5ChronicinfarctInth
echronicstageofinfarction,cellulardebrisanddeadbraintis
sueareremovedbymacrophagesandreplacedbycysticencephaloma
laciaandgliosis.Infarctinvolvementofthecorticospinaltrac
tmaycausemasseffect,mildhyperintensityonT2WI,andeventua
latrophyoftheipsilateralcerebralpeduncleandventralponsd
uetoWalleriandegeneration.Thesechangescanfirstbeseenin
thesubacutephase,withatrophybeingthepredominantfeaturein
thechronicstage.4.5ChronicinfarctDWIhasusuallyreturne
dtonormalinthechronicstage.Occasionally,corticallaminarnecrosiscandevelopinsteadofencephalomalacia.CorticallaminarnecrosisisahistologicfindingcharacterizedbydepositionoflipidladenmacrophagesafterischemiathatmanifestsonimagingashyperintensityonbothT1WIandT2WI.5.SummaryDetailedMRimagingofthemultipletemporalstagesofstrokeThanksforyourattention! |
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