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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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