Stroke Ctscan

8/25/2016
www.medscape.com/viewarticle/452843_print
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NeuroimagingofStroke:AReview
AndrewR.Xavier,MDAdnanI.Qureshi,MDJawadF.Kirmani,MDAbutaherM.Yahia,M,Rohit
Bakshi,MD
SouthMedJ.200396(4)
AbstractandIntroduction
Advancesinneuroimagingtechnologyduringthepast30yearshaveresultedinavirtualexplosionintheamountofpathologic
informationthatcanbeobtainedintheclinicalstrokesetting.Thisneuroimagingrevolutionhasledtoamuchbetter
understandingofcerebrovascularandtissuepathology,creatingawidearrayofopportunitiesforacutetreatmentand
secondaryprevention.Advancesincludeearlyandaccuratedetectionofischemicandinfarctedtissueandtheabilitytoreveal
hypoperfusedtissueatrisk.Cliniciansareincreasinglyabletononinvasivelydetectembolicandatherothromboticintravascular
lesions.Vascularlesionsassociatedwithstrokecanbecharacterizedthroughendovascularneuroimagingtechniquesand
repairedbyvariousmeans.Inthisarticle,weprovideanoverviewandupdateonthevarioustechniquesusedinthe
neuroimagingofstrokeandintracranialhemorrhage,includingcomputedtomography,magneticresonanceimaging,
ultrasound,andcatheterangiography.Weoutlinethespecificroleofeachmodalityinclinicalpractice.
Strokeisaleadingcauseofdeathanddisabilityworldwide.Threedecadesago,thediagnosisofstrokewaslargelydependent
onbedsideclinicalmethods.Ourknowledgeofthelocalizationandthenatureoftheunderlyingpathologicprocesscouldonly
beverifiedindependentlypostmortemthisseriouslyhamperedinitialattemptsatdevelopingandimplementingappropriate
therapeuticinterventions.Advancesinneuroimagingtechnologyduringthepast30yearshaveresultedinavirtualexplosionin
theamountofpathologicinformationthatcanbeobtainedintheclinicalstrokesetting.Thisneuroimagingrevolutionhasledto
amuchbetterunderstandingofcerebrovascularandtissuepathology,creatingawidearrayofopportunitiesforacutetreatment
andsecondaryprevention.Advancesincludeearlyandaccuratedetectionofischemicandinfarctedtissueandalsotheability
torevealhypoperfusedtissueatrisk.Cliniciansareincreasinglyabletononinvasivelydetectembolicandatherothrombotic
intravascularlesions.Throughendovascularneuroimagingtechniques,vascularlesionsassociatedwithstrokecanbe
characterizedandrepairedbyvariousmeans.Inthisarticle,weprovideanoverviewandupdateonthevarioustechniquesused
intheneuroimagingofstrokeandintracranialhemorrhage,includingcomputedtomography,magneticresonanceimaging,
ultrasound,andcatheterangiography.Weoutlinethespecificroleofeachmodalityinclinicalpractice.
ComputedTomography
Computedtomographic(CT)imagesofthebrainareproducedbyscanningacollimatedbeamofxraysthroughthebrainin
thin,sequentialslices.Thexrayoutputiscounted,analyzed,andreconstructedforclinicalinterpretation.Thenewer
generationscansusespiraltechnology,wheretheimagingisperformedinacontinuoushelicalfashioninsteadofthe
conventionalslicebyslicemethod.CTscanningisstillthepreferredmethodforimaginghyperacutestroke.Itiswidely
available,canbeperformedonpatientswhohaveapacemakerorareonaventilator,andcanbeperformedquicklyon
confused,deliriouspatients.Inaddition,interpretationinthehyperacutestrokesettingisfairlystraightforwardwithouttheneed
forspecialtraining.
Incasesofhyperacutestroke(06h),CTisusuallynotsensitiveintheidentificationofcerebralinfarction. [1]But,itisquite
sensitiveinidentifyingvariousformsofacuteintracranialhemorrhageandothergrosslesionsthatwouldprecludetheuseof
thrombolytictherapy(Fig.1). [2]Inthefirst24hours,CTsignsofinfarctionaresulcaleffacementwithlossofgraywhite
differentiationinsuperficialcorticalinfarction[3]andhypodensityofthebasalganglia[4,5]incasesofdeepcerebralinfarction
(Fig.2).Thepresenceoftheseearlychangesspreadoveralargearea(>1/3oftheparentarterialterritory)isoftenassociated
withlargeinfarctionsandarelativecontraindicationtotheuseofthrombolytictherapyinapatientwhowouldotherwisequalify
forthattherapy. [69]Ataminimum,thepresenceofextensiveCTabnormalitiesinapatientpresentinginthefirst3hoursfor
possiblethrombolysisshouldnecessitateacarefulreviewofthetimeofstrokeonset.Ahyperdenselargevessel,describedin
casesofmiddlecerebralartery(MCA)stroke[10]isoftensuggestiveofapersistentlargevesselocclusionwithpoorprognosis
("hyperdenseMCA"or"denseMCA"sign)(Fig.3). [11]Thepresenceofthissignisnotacontraindicationforintravenous
thrombolysis, [6]butisanindicatorthatalargeclotburdenmaybepresent,andsupplementalrecanalizationstrategiesmight
havetobeconsidered.RecentadvancesinCTtechnologyprovideadditionaldatathatarehelpfulinthemanagementofstroke
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patients.TwosuchpromisingtechniquesareCTangiographyandperfusionCT.CTangiography(CTA)isa3dimensional
reconstructionofthecerebralvasculaturefromsourceimagesshowingcontrastmaterialinthecerebralvesselsshortlyafteran
intravenouscontrastbolus.Itisafairlysensitivetechniqueinidentifyinglargevesselocclusions. [1216]Itcanbealsousedto
trackpatientswithlargevesselocclusions,whohaveundergonerecanalizationprocedures.AnormalCTAcanpotentiallybe
usedtoexcludepatientsfromfurtheraggressiverecanalizationprocedures.Thecontrastsaturationinasliceofbrainfollowing
arapidintravenousinjectionofhighvolumecontrastisusedtoconstructperfusionCTimages.Theperfusiondeficitgivesa
roughestimateoftheextentofmicrovasculaturehypoperfusionandhypometabolismandincludesthecerebralinfarctionand
thesurroundingischemicpenumbra. [1720]
AnoncontrastCTscan(left,middle)andfastFLAIRMRI(right)wasobtained3hoursaftertheonsetofapatient'ssevere
headache.TheCTshowshyperdensities(arrows)inthebasalcisternsandleftsylvianandfrontalcorticalsulci,consistentwith
acutesubarachnoidhemorrhage.FLAIRMRIshowsbilateralhyperintensefrontalandparietalsulci(arrow),consistentwith
acutesubarachnoidhemorrhage.TheMRIabnormalitiesaremoreconspicuousandmorewidespreadthanshownbyCT.
An89yearoldwomanpresentedwithslurredspeechandconfusion12hoursbeforetheperformanceoftheinitialnoncontrast
CTscan(left).Notethesubtleasymmetryoffindings.Thereisearlyhypodensityoftheleftposteriorputamen(arrowhead)and
periinsularcortex(arrow)ascomparedwiththecontralateralside.Twentyfourhoursaftertheinitialscan,repeatCT(right)
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showsclearhypodensityinvolvingtheentiremainstemmiddlecerebralarteryterritorywithmildassociatedmasseffect.The
findingsarediagnosticofanacutemiddlecerebralarterystroke.
NoncontrastCTscanisshownofapatientwhopresented8hoursafteronsetofleftsidedweaknessandaphasia.Notethe
tubularhyperdensity(arrow)suggestiveofacuteclotintheleftmiddlecerebralartery.Thisisaccompaniedbyhypodensityof
theipsilateraltemporallobeinthemiddlecerebralarteryterritory(arrowhead).Comparetheseabnormalitiestothe
contralateral(right)sideofthebrain.Takentogether,thesefindingsarehighlysuggestiveofacutestroke.
Intheacuteperiod(624h),thechangesofischemiabecomemoreapparentonthenoncontrastCTscan.Thelossofgray
whiteinterface,sulcaleffacement,hypodensityofbasalganglia,andhypodensityoftheinsularcortexbecomeprominent(Fig.
3).Thevasculardistributionoftheinfarctbecomesincreasinglyclearduringthisstage.Inseverecases,edemaandmass
effectcanappearatthisstage.
Duringthesubacuteperiod(17d),thereisincreasingedemaandmasseffectwithlateralandverticalshiftofinfarctedtissue
incasesofinfarctioninvolvinglargevesselterritories.Edemaandmasseffectpeakat1to2daysandthendecline.The
edemasurroundingtheinfarctscausedbyocclusionsofthedeep,perforatingbranchesaremuchmoremodest,withlittle,if
any,associatedmasseffect.Thefirst1to2daysarealsowhenhemorrhagictransformationpeaksthisisnotedinabout5to
40%ofallischemicstrokes. [2125]Whenhemorrhagictransformationoccurs,itisusuallyintheformofpetechialhemorrhages
andisclinicallynotsignificantbut,inaminority,particularlyinthosewhoreceivedthrombolyticoranticoagulantmedication,it
couldtaketheformofafrankparenchymalhematomawithclinicaldeterioration(Fig.4). [8,22,24]Contrastscansperformed
duringthisperiodhaveacharacteristic"gyralenhancement"pattern. [26]Chronicinfarctionsarecharacterizedbymarked
hypodensityandlackofmasseffectonCTscansthedensityissimilartocerebrospinalfluid(CSF)(Fig.5).
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Twopatientswithsubacutehemorrhagicstroke.Patient1receivedintraarterialurokinasetreatmentforahyperacutestroke
associatedwithinternalcarotidarteryocclusion.Afterurokinasetreatment,thepatientdevelopedincreasedfunctionoftheleft
side.Twodayslater,noncontrastCTwasperformedandisshown.Notethehematoma,seenasaroundhyperdensity,inthe
rightsubcorticalregion(arrowhead).Thereisacompletedsubacutemiddlecerebralarteryinfarction.Patient2(right)obtained
noncontrastCTscan36hoursafterstrokeonset.Notethesubtlelinearandpatchyhyperdensities(arrow)intheanteriorand
medialaspectsoftheoperculofrontalinfarction.Thehyperdensitiesareconsistentwithpetechialhemorrhagictransformationof
infarction.
CTscanswereobtainedfortwopatientswithchronicinfarctions.Notethemarkedhypodensityofeachlesionwithsimilar
densitysimilartocerebrospinalfluidandhoweachconformstoaknownvasculardistributioncentralsulcalmiddlecerebral
arterystrokeandposteriorcerebralarteryoccipitalstroke.
ImagingofintracranialhemorrhageisfairlystraightforwardwithCT,
[27]whereimagecontrastisdeterminedbytissuedensity.
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ImagingofintracranialhemorrhageisfairlystraightforwardwithCT, [27]whereimagecontrastisdeterminedbytissuedensity.
Acutebloodclotshaveahighdensityandappearhyperdense, [28]oftenstrikinglyso,whencomparedwiththesurroundingbrain
tissue.(Figure1,Figure4,Figure6)Acutesubarachnoidhemorrhage(SAH)appearsasahighdensityinthesubarachnoid
spaces(Fig.1). [29,30]TheseverityofSAHonCTisusuallygradedusingthesystemdescribedbyFisher, [31]andtheCT
findingsareimportantpredictorsofclinicaloutcome. [32,33]TheCTfindingsofSAHmaybesubtle(Fig.1),particularlyinthe
subacutestage. [34,35]Findingsmayonlyincludeamildhydrocephalus,diffusesulcaleffacement,andsubtlehyperdensitiesin
theCSFspaces.AcuteandsubacuteintraparenchymalhemorrhageiscomparativelymucheasiertoidentifyonCTasithas
excellentcontrastascomparedwiththesurroundingbraintissue(Figure4,Figure6).Thelocationofthehemorrhageoften
givesacluetotheunderlyingpathophysiology. [36]Hemorrhagesduetochronichypertensionarecommonlysituatedinthe
putamen, [37]thalamus,pons,cerebellum, [38]caudate, [39]andthesubcorticalwhitematter/graywhitejunction. [40]Itis
controversialwhetherCharcotBouchardaneurysmsaretheprimaryunderlyingpathologyinthesecases.Thelocation,size,
andintraventricularextensioncorrelatewellwithclinicalseverityandcanpredictclinicaloutcome. [32,41]Incasesofamyloid
angiopathy,thehemorrhagesareusuallylarge,superficial,lobar,andpronetorecur(Fig.6). [4244]Inthesettingof
anticoagulation,thrombolysis,orsystemiccoagulopathy,hemorrhagesareoftenmultiple,large,andassociatedwithfluidfluid
levelsduetoimpairedclottingability. [35,45,46]Anothercommoncauseofnontraumaticintracranialhemorrhageishemorrhagic
transformationofcerebralinfarction(describedabove)(Fig.4).Inpatientswhoreceivedintraarterialthrombolysistreatment,
extravasations(focalintraparenchymalextravasations)oftheangiographicdyecommonlyoccurduringtheprocedureandmay
beconfusedwithhemorrhagictransformation. [47,48]
Patient1isa97yearoldwomanwhopresentedwithacuteonsetcoma.ThenoncontrastCTscan(left)showsalargeacute
intraparenchymalfrontallobarhemorrhagewithseveremasseffect.Patient2isa75yearoldmanwhopresentedwith
lethargy.ThenoncontrastCTscan(right)showsanacuteintraparenchymaloccipitallobarhemorrhage(arrowhead)withmildto
moderatemasseffect.Autopsyofbothpatientsshowedwidespreadcerebralamyloidangiopathy.
MagneticResonanceImaging
Magneticresonanceimaging(MRI)hasnowbecometheprimarynoninvasivemodalityforstrokeimagingFigure7,Figure8,
Figure9,Figure10). [35,49]Thelatestmagneticresonancetechniquesprovideexcellentanatomicdetailhavetheabilityto
differentiatebetweenischemicandinfarctedbraintissueexcludeintracranialhemorrhageandprovideangiographic,
spectroscopic,andperfusioninformationofthecerebralvesselsandtissuebed. [35]MRIalsohashighersensitivityand
specificitythanCTinthedetectionofotherbraindiseasesthatcanmimicstrokeclinicallysuchascerebraledema,vascular
malformations,neoplasms,infections,inflammatorydiseases,andtoxicometabolicdisorders. [35,50]Furthermore,withthe
adventofechoplanarmethodology,MRIcanbeperformedmuchfasterthanCTwithsequencesthatcancovertheentirebrain
inafewseconds. [35]MRIhastheaddedadvantageoflackofexposuretoionizingradiationbutthedisadvantageofhigher
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cost.WhiletheavailabilityofMRIisincreasing,therearemanyacutecarecentersthatcontinuetolackaccesstoanonsite
24houradayMRI.TherearealsoabsoluteandrelativecontraindicationstoMRI,limitingitsavailability,suchascardiac
pacemakersandcertainmetallicimplantedsubstances.ClaustrophobiaismorecommonwithMRIthanwithCT.However,with
fasterscanningtimeandcontinuingimprovementinshortboreandopenMRItechnology,claustrophobiaisadecreasing
concern.
MRIofhyperacutestrokeat2hourspostictus.TheT2weightedimageisnormal.TheFLAIRimageshowshyperintense
vessels(HVSseetext)intheterritoryofthemiddlecarotidartery(MCA)(arrow),consistentwithslowarterialflow,butthe
FLAIRshowsnotissueabnormality.Diffusionweightedimaging(DWI)showshyperintensityinthedeepmiddlecerebralartery
territoryconsistentwithcytotoxicedemainanacutestroke(arrow),butthereisnoevidenceofcorticalischemia.Perfusion
weightedimaging(PWI)(timetopeakimage)showsreducedperfusioninthefull(corticalandsubcortical)MCAterritory.This
suggestsamuchlargerareaoftissueatriskthanshownbyDWIorconventionalimages.Thisisknownasadiffusionperfusion
mismatch(seetext).SomeareasofreducedperfusionshowHVSonFLAIRwhereasothersdonot.Threedimensionaltimeof
flightmagneticresonanceangiography(MRA)confirmsaproximalMCAocclusionorseverestenosis. [35]
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MRIofacutemiddlecarotidartery(MCA)strokeonMRIat12hourspostictus.T2weightedimageshowsmildhyperintensityof
themiddlecarotidarteryterritory(arrows).NoncontrastT1weightedimagedemonstratesearlystrokechangeswitheffacement
ofcorticalsulciintheMCAterritoryassociatedwithswellingandmildhypointensityofthecorticalribbon(arrows).After
contrast(gadolinium)administration,intravascularenhancementispresent,indicatingsluggishflowintheischemiczone
(arrows). [35]
Tendayspostictus,MRIisconsistentwithsubacuteinfarction.T2weighted(protondensity[PD])MRIshowsamarkedly
hyperintensewelldemarcatedlesionconformingtoalateraltemporalbranchterritoryofthemiddlecerebralartery.
Postgadoliniumcontrastimagesshowenhancementofthetemporalcortexthatconformstoagyralpattern.
Twopatientsareshown.Theleftandmiddleimagesshowachronicoccipitalinfarction.Notethemarkedhypointensityincore
ofthelesion(fluidity)ontheFLAIRimagesurroundedbyarimofhyperintensity(chronicgliosis).Thereisnomasseffect
instead,theadjacentCSFspacesareexpandedinanexvacuomanner.Thediffusionweightedimage(DWI)shows
hypointensityofthelesion,consistentwithincreaseddiffusion.Asecondpatient(rightimage)hadastroke3yearspreviously
involvingtheleftmotorcortex(notshown).Ipsilaterally,thecerebralpeduncleisshrunken(arrow),consistentwithwallerian
degenerationofthedescendingcorticospinaltract.
MRIissuperiortoCTscanninginthedetectionofacutestroke.However,conventionalMRIdoesnotdemonstrateacute
cerebralischemiasensitivelyinatimeperiodwhentherapymayreverseorlimitthepermanentbraininjury(thefirstfewhours).
NewMRItechniquesarebeingusedincreasinglyinevaluatingpatientsinthehyperacutesettingtohelpdecisionmaking. [35,49,
5161]Inthefirstfewminutesaftervascularocclusion,cytotoxicedemadevelopsintheischemictissue,resultinginanetshift
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5161]Inthefirstfewminutesaftervascularocclusion,cytotoxicedemadevelopsintheischemictissue,resultinginanetshift
ofwatermoleculesintotheintracellularcompartment.Thisshiftdecreasesthediffusioncharacteristicsofthehydrogenionsin
theischemicbrainandresultsinaprecipitousdropintheapparentdiffusioncoefficient(ADC)inthatregion. [35,62,63]
DiffusionweightedMRI(DWI)isrelatedinparttothenegativeconstructionoftheADCmap,andhenceregionswithlowADC
appearbrightanddistinctfromregionswithnormalADC. [64]DWIishighlysensitiveinidentifyinghyperacuteandacute
cerebralinfarction,showingischemiawithinminutesofvascularocclusion,whileconventionalMRItypicallydoesnotshow
ischemicchangesuntilseveralhoursafterictus(seebelow)(Fig.7). [35,51,60,6567]WhethertheareaidentifiedonDWI
includesischemicbutstillsalvageablebraintissueinadditiontocompletelyinfarctedtissue,orifitincludesonlyinfarcted
tissuebeyondrepair,isstillunderdebate. [6870]Astheinfarctevolves,thecellsdisintegrate,releasingthetrappedwater
moleculesintotheextracellularcompartment.Inaddition,thereisincreasedvascularpermeabilityduetobreakdowninthe
bloodbrainbarrier.Thisresultsinamixtureofcytotoxicandvasogenicedema,whichcausesasteadyincreaseinthe
extracellularrandommovementofwatermolecules,therebyraisingADC.ThestrokeremainsbrightonDWIscansintheacute
andsubacutestagesduetoacombinationoflowADCandT2effects. [35]Inthechronicstage,therearenocellsleftinthe
coreoftheinfarct,andthewatermoleculesarealmostexclusivelyextracellular.Hence,chronicinfarctsarecharacterizedby
highADCvaluesandappeardarkonDWI(Fig.10). [35,7173]
Anothermagneticresonancesequencethatisbeingincreasinglyusedinacutestrokemanagementisperfusionweighted
imaging(PWI).Theimagingprincipleistodetectthesusceptibilityeffectsofarapidlyadministeredintravenouscontrast
(gadolinium)bolusasitpassesthroughthecerebralmicrovasculature. [35]UsingPWI,avarietyofperfusionpropertiesofthe
contrastboluscanbecalculatedsuchascerebralbloodvolume,cerebralbloodflow,meantransittime,timetopeak,andtime
ofarrival.PWImayshowhypoperfusioninamuchlargerareaoftissuethanshownbytheDWI(Fig.7).Thisindicatesamuch
largerareaoftissueisatriskforinfarction,a"diffusionperfusionmismatch",indicatingathreatenedportionofthebrainthatis
stillsalvageable. [69,70]Fluidattenuatedinversionrecovery(FLAIR)MRIhashadimportantapplicationsintheimagingof
strokepatients.FLAIRdepictsareasoftissueT2prolongationwhilesuppressingCSFsignal,offeringasensitivemethodto
detectlesions. [35,74,75]HyperintensityoftheischemicbraininacutestrokesisseenonFLAIRasearlyas4to6hoursafter
ictusatatimewhenT1weightedimages(T1WI)andT2weightedimages(T2WI)areusuallynormal.FLAIRmaydetectslow
flowinthearterialbedinthehyperacutephaseofstroke. [35,75]TheseslowflowingarteriesaredepictedbyFLAIRas
hyperintensitiesagainstdarkerbraintissue,leadingtothe"hyperintensevesselssign"(HVS)(Fig.7). [35,75]HVSisareversible
signmostcommonlyassociatedwithhypoperfusionwithoutinfarction. [35,75]Noninvasiveimagingofthecerebralvasculatureis
nowpossibleusingMRIangiography(MRA).MRAcanbeusedinthehyperacutephaseofstroketodemonstrateocclusionof
aparentartery(Fig.7).Traditionalphasecontrastand3dimensionaltimeofflighttechniqueshavebeenimprovedrecently
withtheuseofcontrastenhancement. [76,77]TheseadvancementshavemadeMRAafairlysensitivetoolinassessingthe
presenceandseverityofvasculardiseaseinboththeintracranialandtheextracranialportions.Butthesensitivityislimitedto
largeandmediumsizedvessels,whiledistalcorticalbranchesandsmallperforatingbranchesareoftennotvisualizedbyMRA.
[7678]
Atthistimepoint(624h),tissueischemia/infarctioniswelldevelopedonFLAIRimagesandbeginstoshowonT2WI
(hyperintensity)andT1WI(hypointensity)(Fig.8). [79]HyperintensitydevelopsonT2WIasearlyas8hoursafterinfarctiondue
tocytotoxicandvasogenicedema.HypointensityonnoncontrastT1WIisusuallyseen16to24hoursafterictusand,again,is
relatedtobothcytotoxicandvasogenicedema.Theintravascularenhancementsignpeaksatthisstageduetosluggish
intravascularflow.ThisisthecounterpartofHVSbutisnotspecificforstroke[75,80](Fig.8).
Afterthefirst24hours,T1W1,T2W1,FLAIR,andcontrastenhancedimagesaremostusefulinsubacuteandchronicstroke,
wherethefocusshiftsfromidentifyingthepresenceandextentofinfarctandischemicpenumbratoidentifyingtheunderlying
pathophysiology.Astheinfarctevolvesduringthefirstweek,theedemaandmasseffectincreases,andboththemorphologic
andsignalchangesseeninthemagneticresonancesequencesbecomemoreprominentandwelldemarcated(Fig.9).
InfarctionscontinuetoappearasareasofhypointensityonT1WIandhyperintensityonT2WI.Edemaisgenerallymaximalat
48to72hoursbeyondictus,althoughthereisconsiderablevariability.Ingeneral,masseffectisbestappreciatedonT1WI.
Theintravascularenhancementsignmaypersistwellintothesubacutestagebutistypicallyabsentafter1week.Gyriform
parenchymalenhancement,similartotheenhancementseeninpostcontrastCTscans,istypicallyseenapproximately5to7
daysbeyondstrokeonsetandremainsforafewweeksincasesofcompleteinfarction(Fig.9).Asreperfusionofinfarcted
tissueoccurs,bothpetechialhemorrhageandfrankhematomasmaybeseen,especiallyat24to48hoursafterstrokeonset
(Fig.4).Petechialhemorrhagewithininfarctionsmaygiverisetoa"fogging"phenomenoninwhichhemoglobindegradation
products,extravasatedproteins,orbothgeneratesignalchangeswithininfarctedtissue,whichmasktheinfarctiononT1WI
andT2WI.
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Bythechronicstage,edemahasresolvedandvolumelossoccursintheareaofinfarction,beginning1monthpostictus.Tissue
lossleadstoipsilateralexvacuoventricularenlargementandwideningofcorticalgyriandfissuresintheareaoftheinfarct
(Fig.10).ParenchymalsignalintheareaofchronicinfarctioncontinuestoshowCSFlikehypointensityonT1WIand
hyperintensityonT2WI.ThecoreofthechronicinfarctionisalsoCSFlikeonFLAIRimages,butsurroundinggliosisappears
hyperintense(Fig.10).Afterseveralmonths,walleriandegenerationoccurs(Fig.10).Afterseveralyears,dystrophic
calcificationmayappearbrightonT1WI. [35]
AcompletediscussionoftheMRIfindingsinintracranialhemorrhageisbeyondthescopeofthisreviewinwhichwefocuson
ischemicstroke.Abookchapterreviewofthiscomplexsubjecthasbeenpublishedrecently[35]andseveralexcellentsource
articlesarerecommended. [8190]ThereisagrowingbodyofevidenceindicatingthatMRIiscomparabletoorperhapsmore
sensitivethanCTinthedetectionofvariousformsofintracranialhemorrhage,especiallysubdural,subarachnoid,and
intraventricularhemorrhage(IVH). [35,49,88,9194]FLAIRhasshownespeciallyhighsensitivityinthedetectionofSAHand
IVH[35,49,9194]withutilitycomparableorsuperiortoCT(Fig.1).MRIissuperiortoCTinidentifyinganunderlyingcausefor
cerebralhemorrhagesuchasprimaryormetastatictumor,arteriovenousmalformations(AVM),venoussinusthrombosis,septic
emboli,abscess,orischemicinfarct. [35,95,96]
CerebralAngiography
Cerebralangiographyremainsthegoldstandardforvisualizingcerebrovascularanatomy.However,withtheincreasing
availabilityandreliabilityofCTAandMRA,itisbeingusedlessoftenforpurelydiagnosticpurposesandmoreoftenfor
possibleinterventions.
Inthehyperacutestrokesetting,cerebralangiographyisusuallyperformedwhenintraarterialthrombolysistreatmentor
mechanicalinterventionsareplanned.Theobjectiveoftheinitialpartofanangiographicevaluationinpatientswithischemic
strokeistodocumentthesiteoftheocclusionandthepresenceofcollateralizationtotheaffectedarea.Themajorityof
patientswithacuteischemicstrokearefoundtohavepersistentarterialocclusions. [97]Whenstudiedinthefirst6hoursafter
strokeonset,upto80%ofpatientshaveanocclusion. [98,99]Patientswithsevereneurologicdeficitsalsohaveahigher
frequencyofpersistentarterialocclusions. [100]Themajority(5060%)ofarterialocclusionsarefoundintheMCA(Fig.11)and
theinternalcarotidartery(1525%).About10%ofindividualshaveocclusionsinthevertebrobasilarsystem(Fig.12). [101]The
arterialocclusionintheacutestrokesettingisgradedusingtheQureshi[102]system().Thescoreonthegradingschemeis
predictiveofposttreatmentrecanalizationandthelevelofneurologicrecoveryanddeathat7daysaftertreatment. [102]In
additiontooccludedvessels,abnormalvascularfillingpatterns,suchasslowanterogradeflowwithprolongedcontraststasis,
retrogradefillingthroughcollateralchannels,arteriovenousshunting,andvascularblushsecondarytoluxuryperfusion,alsoaid
inthecharacterizationofcerebralinfarction. [103]
Table1.GradingArterialOcclusionUsingQureshiSystema
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Thecerebralangiogramofan87yearoldmanwithacuteonsetlefthemiplegia.Therightinternalcarotidartery(shortarrow)
injectionsareshownintheanteroposteriorprojection.Themiddle(longarrow)andanterior(arrowhead)cerebralarteriescanbe
visualized.Theimageontheleft(A)obtainedpreoperativelyshowsamiddlecerebralartery(MCA)occlusionatthelevelof
M1.ThewholeMCAdistributionterritory,includingthelenticulostriatesystem,isaffectedwithnocollateralsupply(Grade3b).
Theimageontheright(B)wasobtainedafterintraarterialthrombolysis.TheM1segmenthasrecanalizedwithrestorationof
bloodflowtothesuperiordivision.Apersistentocclusionisnotedintheinferiordivision(Grade2).
Thecerebralangiogramofa67yearoldwomanpresentingwithacuteonsetunresponsivenessandquadriparesis.Theleft
vertebralartery(shortarrow)injectionsareshowninthelateralview.Thebasilarartery(longarrow)andtheposteriorinferior
cerebellararteries(arrowhead)arevisualized.Theimageontheleft(A)showsanocclusionatthemidbasilarlevelwithabsent
flowtothedistalbasilararteryaswellasthedistalbranchesofthebasilarartery.Carotidinjections(notshown)showedno
collateralflowtotheposteriorcirculationthroughtheposteriorcommunicatingarteries(Grade5occlusion).Postthrombolysis
images(B)showedcompleterecanalizationofthebasilarartery.Thesuperiorcerebellararteries(whitearrowhead)andthe
posteriorcerebralarteries(whitearrow)canbevisualizedwell(Grade0postthrombolysis).
Inthesubacutesetting,cerebralangiographyisusedtoconfirmthenatureandseverityofcerebrovascularpathology. [104]The
noninvasivemodalitiessuchasCTA,MRA,andultrasoundare,inthemajorityofcases,capableofidentifyingthepresenceof
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vascularpathology.However,whenquantificationofthestenosisisneeded(forexample,whenapatientisfoundtohave
carotidarterydiseaseandisbeingreferredforsurgeryorendovascularprocedures)angiographyisthepreferredmodality.In
addition,angiographyismoresensitivethannoninvasivemethodsinidentifyingarterialnarrowinginspecificsites,eg,vertebral
arteryorigin,carotidsiphon,etc.Angiographyalsoisbetterinidentifyingnonatheroscleroticconditionssuchasvasculitis, [105]
dissection, [106108]fibromusculardysplasia, [109111]andmoyamoyadisease. [112]
Themajorityofintraparenchymalhemorrhagesarerelatedtohypertensionandamyloidangiopathy(Fig.6),andtheunderlying
lesionsintheseconditionsareusuallyangiographicallysilent.HemorrhagesmightobliteratetheunderlyingAVM(occultAVM),
andarepeatangiogramafewweeksafterthehemorrhagemightbehelpfulinidentifyingtheabnormality.Venoussinus
thrombosisandvasculitisareothereasilyidentifiedcauses. [113]Cerebralangiographyisanessentialcomponentintheworkup
ofpatientswithnontraumaticSAH.Inabout90%ofthesecases,theprimarypathologyisasaccularaneurysm.Thecommon
locationsareanteriorcommunicatingartery,posteriorcommunicatingartery,MCA,basilararterytip,anteriorcerebralartery,
basilarartery,vertebralarteries,andposteriorcerebralartery.Serialtranscranialultrasoundmeasurementscanusuallyidentify
theonsetofvasospasmafterSAH. [114,115]Cerebralangiographycanconfirmthepresenceofvasospasmandbeusedto
deliverinterventionstorelievevasospasm. [116,117]Inadditiontoaneurysms,AVMsandduralarteriovenousfistulascanalso
causeSAH.EveninpatientswhohaveaneurysmalSAH,theinitialangiogramcouldbenegativebecauseofvasospasmor
thrombus.Hence,angiographicallynegativeSAHpatientsshouldhaveacerebralangiogramrepeatedafterthefirstweek. [118,
119]
Ultrasonography
Ultrasonographic(ie,neurosonologic)investigationsplayanimportantroleinidentifyingarterialnarrowingandocclusioninthe
settingofcerebrovasculardisease.Twoprinciplesareusedinultrasounddiagnosis:theechoimpulsetechniqueandthe
Dopplertechnique.Bmodeimagesarebuiltontheechoimpulseprincipleandprovideinformationaboutmorphologic
structureswithinthevascularlumenandthesurroundingtissues.Thismoderequirestheuseofhigherfrequencyultrasound
waveshence,theyareusedintheevaluationofcervicalcarotidandvertebralarteriesaswellastheevaluationoftheaortic
archandheartthroughechocardiography.Bmodeimagingdoesnotprovidesufficientmorphologicdetailstostudydeeply
situatedintracranialvessels.TheDopplertechniquecancalculatebloodflowvelocities,andarterialvelocitiesare(inturn)used
toindirectlycalculatethedegreeofstenosisinthevesselstudied.Dopplerultrasonographyistheonlymethodavailableto
studyICvessels.Modernduplexmachinescombinethetwotechniquesandareabletoprovidebothmorphologicandblood
flowinformation. [120]
DopplerexaminationoftheICvessels(transcranialDoppler[TCD])isplayinganincreasinglyimportantroleinthenoninvasive
evaluationofacutestrokepatients. [121123]TCDcanbeusedtoidentifylargevesselocclusionsintheacutestrokesettingand
tomonitortheresponsetothrombolytictherapy. [124126]Patientsreceivingintravenousthrombolysiswhodonotshow
improvementclinicallyandwhoappeartohavepersistentlargevesselocclusiononTCDcanbeselectedforinterventional
procedures.
DuplexDopplerscanplaysanimportantroleintheworkupofcarotiddisease.UnlikeCTA,MRA,andcerebralangiogram,
duplexDopplerscanhastheabilitytodirectlyvisualizethevesselwallandtodefinethecharacteristicsoftheatherosclerotic
plaque:hemorrhage, [127]ulceration, [128,129]calcification,etc.Whethertheseplaquecharacteristicsshouldalterthe
managementstrategyisstillamatterofdebate. [130133]Thedegreeofcarotidarterialstenosishasbeenthebestpredictorfor
futurecerebralischemicevents. [132,134]Thedegreeofstenosiscanbeestimateddirectlybymorphologicmethodsand
indirectlyfromincreasedbloodflowvelocities(Fig.13). [120]Arterialocclusionisdiagnosedbyabsentarterialpulsations,lumen
occlusionbyechogenicmaterial,absentDopplerflowsignal(Fig.14),and(incasesofchronicocclusion)decreasedvesselsize.
Multiplestudieshaveconfirmedthereliabilityofultrasoundasascreeningtoolforthedetectionofcarotidstenosis [132,135,
136]andnonatheroscleroticdiseasesofthecarotidartery,suchasvasculitis, [137]radiationinducedstenosis, [138]dissection
(Fig.15), [139,140]andtumors. [141]UltrasoundisbeingreplacedbyCTAandMRAintheevaluationofvertebralarterydisease
aswellastheevaluationofintracranialvesselsinthesubacutesetting.TCDisusedtomonitorforcerebralvasospasminthe
settingofSAH. [114,115]
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A76yearoldmanpresentedwithanepisodeofblurredvisionontherightsideassociatedwithheadache.Colorflowimaging
oftherightcarotidsystem(shownhere)identifiedalarge,heterogeneous,calcifiedplaque(arrow)intheinternalcarotidartery
(ICA)closetoitsoriginatthecarotidbifurcation,causingarterialnarrowing.Calcifiedplaquesappearbrightandhaveadark
sonolucentzone(arrowhead)beneaththesurface.Thelaminarbloodflowinthecommoncarotidartery(CCA)becomes
turbulentbeyondthesiteofarterialstenosis.Thebloodflowvelocitywas354/112cm/s,whichcorrelateswithahighgrade(80
99%)carotidstenosis.Thepatientunderwentarightcarotidendarterectomy.
A75yearoldmanpresentedwithrecurrentrightsidednumbness,clumsiness,andspeechdifficulties.DuplexDoppler
examinationoftheleftcarotidsystem(shownhere)revealedahomogenousechogenicmaterialfillingupthecommoncarotid
artery(arrow)andtheinternalcarotidartery(notshown).NoDopplersignalscouldbeidentified(arrowhead).Cerebral
angiogram(notshown)confirmedleftcommonandinternalcarotidocclusion.Theexternalcarotidartery,middlecerebral
artery,andanteriorcerebralarteryontheleftsidefilledfromcollaterals.
12/21
8/25/2016
A58yearoldwomanhadanepisodeofnearsyncopefollowedbyrightsidedneckpain.DuplexDopplerimagingoftheright
commoncarotid(shownhere)identifiedafalselumenandintimalflap(smallarrows),whichsuggestanarterialdissection.The
bloodblowvelocitieswerealsoelevated(202/37cm/s).
RoleofIndividualModalitiesinStrokeManagement
Variousneuroimagingmodalitiesareplayinganincreasingroleintheevaluationofpatientswithhyperacutestroke(presenting
within0to6hours)whenthereisapossibilityofclinicalbenefitfromreperfusion.Theprimarymodalityinthissettingisa
noncontrastCTscantoruleoutcerebralhemorrhageandrecentcerebralinfarctions.IfCTperfusionisavailable,itcouldhelp
definethetissueatriskforinfarction.IfTCDisavailable,thepresenceandpersistenceoflargevesselarterialocclusioncanbe
assessednoninvasivelyatthebedside.Inthefuture,MRIislikelytobecomethemodalityofchoiceinevaluatinghyperacute
stroke.MRIcanhelpdefinetheacutelyischemicregion(DWI),thetissueatriskforfurtherischemia(PWI),vascularanatomy
(MRA),andthepresenceofhemorrhage(FLAIRandgradientechomethods).Patientsshouldreceivecatheterangiography
whenacuteendovascularinterventionsareplanned(eg,intraarterialthrombolysis,angioplasty).Afterthehyperacuteperiod,
strokemanagementshiftstoidentifyingandtreatinghemorrhagictransformation,cerebraledema,andsecondarystroke
prevention.MRIiscurrentlythemodalityofchoiceinthissetting.MRAcombinedwithultrasoundissensitiveandspecificin
identifyingarterialocclusionsandstenosis.InpatientsunabletohaveMRIperformed,CTAcanbeused.
Sidebar:KeyPoints
Neuroimagingadvanceshaveledtoamuchbetterunderstandingofvascularandtissuepathology,creatingawidearray
ofopportunitiesforacutetreatmentandsecondarypreventionofstroke.
Neuroimagingadvancesincludeearlyandaccuratedetectionofischemicandinfarctedtissueandalsoidentifyingtissue
atrisk.
Asitsavailabilityincreases,magneticresonanceimagingislikelytobecometheprimarymodalityofchoiceinevaluating
strokeinacuteandsubacutecases.
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Fundinginformation
SupportedinpartbyaresearchgrantfromtheNationalInstituteofNeurologicalDisordersandStroke,NationalInstitutesof
Health(NIHNINDS1K23NS4237901).
ReprintAddress
ReprintrequeststoRohitBakshi,MD,BuffaloNeuroimagingAnalysisCenter,TheJacobsNeurologicalInstitute,100High
Street,Buffalo,NY14203.Email:rbakshi@buffalo.edu
SouthMedJ.200396(4)2003LippincottWilliams&Wilkins
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