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Chapter04:Stroke
RelatedQuestions
Previous:SeizuresandEpilepsy

Stroke

DefinitionofStroke
Strokeischaracterizedbythesuddenonsetafocalneurologicimpairmentthatcanbeascribed
toaspecificlocationinthebrain,retina,orspinalcord.Thefourthleadingcauseofdeathinthe
UnitedStatesandtheleadingcauseofsignificantdisability,strokecanbefurthersubdivided
intoischemicandhemorrhagicstroke,withtherelativeproportionofeachvaryingbyageand
geographiclocation.Hemorrhagicstrokehastwofurthersubtypes:subarachnoidhemorrhage
(SAH),whichisusuallycausedbyruptureofanintracranialaneurysm,andnontraumatic
intracerebralhemorrhage(ICH).Ischemicstrokecanbefurtherclassifiedaslacunar(asmall
subcorticalinfarct),largearteryatherosclerotic(eitherintraorextracranial),cardioembolic,or
cryptogenic.Oneoftheprincipalgoalsofhospitalizationforstrokeisthedeterminationof
strokesubtype,whichhasimportantimplicationsforacutetreatment,secondaryprevention
strategies,andprognosis.

KeyPoint
Aprincipalgoalofhospitalizationinpatientswithstrokeistodeterminethestroke
subtype,whichhasimportantimplicationsforacutetreatment,secondaryprevention
strategies,andprognosis.

DiagnosisofStroke
RelatedQuestions

Question10
Question12

Acompleteneurologicexaminationiswarrantedinallpatientswithsuspectedstroketolocalize
thedeficittothecentralnervoussystemandinformprognosis.Intheacutestrokesetting,when
timeisoftheessence,validatedscalesformeasuringneurologicimpairmentcanberapidly
performedbyanyhealthcareprovider.TheNationalInstitutesofHealthStrokeScale
(Table15)isthemostcommonlyusedscale,andtrainingisavailableonlinethroughseveral
organizationsforcertification.

Table15.OpeninNewWindowNationalInstitutesofHealthStrokeScale

Parameter(TestingMethod) Scoresa

0=normal
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1=notalertbutarousablebyminorstimulation

1a.LOC 2=notalertandrequiresconstantverbalor
painfulstimulitoremaininteractive

3=unresponsiveorrespondswithonlyreflexive
movements

0=answersbothcorrectly

1b.LOC,questions(statemonthandage) 1=answersonecorrectly

2=answersneithercorrectly

0=performsbothtaskscorrectly
1c.LOC,commands(closeandopeneyes
1=performsonetaskcorrectly
makefistorcloseonehand)
2=performsneithertaskcorrectly

0=normal

1=partialgazepalsyorisolatedcranialnerve
2.Gaze(trackafingerinahorizontalplane)
paresis

2=forcedgazedeviationortotalgazeparesis

0=novisualloss

3.Visualfields(eacheyetested 1=partialhemianopia
individually) 2=completehemianopia

3=bilateralhemianopia

0=normal

1=minorparalysis(flatteningofthenasolabial
4.Facialstrength(showteeth,raise foldorasymmetryonsmiling)
eyebrows,closeeyes)
2=partialparalysis(paralysisofthelowerface
only)

3=completeparalysis(upperandlowerface)

0=nodrift

5.Armstrength(holdarmwithpalmsdown 1=somedriftbutdoesnothitbed
orliftarmfor10seacharmscored 2=driftsdowntobed
separately)
3=noeffortagainstgravity

4=nomovement
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0=nodrift

1=somedriftbutdoesnothitbed
6.Legstrength(holdlegat30degreesfor5
2=driftsdowntobed
seachlegscoredseparately)
3=noeffortagainstgravity

4=nomovement

0=absent
7.Limbataxia(fingernosefingertest,heel
1=presentinonelimb
kneeshinslide)
2=presentintwolimbs

0=normal

8.Sensation(pinch/pinpricktestedinface, 1=mildtomoderatesensorylossorlossof
arm,andleg) sensationinonlyonelimb

2=completesensoryloss

0=noaphasia

9.Language(describeapicture,namesix
objects,andreadfivesentences)
1=mildtomoderateaphasia(difficultywith
fluencyandcomprehensionmeaningcanbe
identified)
2=severeaphasia(fragmentarylanguage
meaningcannotbeclearlyidentified)

3=globalaphasiaormute

0=normal

10.Dysarthria(repeatorreadwords) 1=mildtomoderate

2=severe(speechnotunderstandable)

0=normal

1=visualortactileextinctionormild
11.Extinction/inattention(visualandtactile
hemispatialneglect
stimuliappliedonrightandleftsides)
2=profoundhemiinattentionorextinctionto
morethanonemodality

LOC=levelofconsciousness.
aScoreinterpretation:0=nostoke14=minorstroke515=moderatestroke1620=
moderatetoseverestroke2142=severestroke(maximumscore,42).
Adaptedfromwww.ninds.nih.gov/doctors/NIH_Stroke_Scale.pdf.AccessedFebruary9,
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2015.Certificationavailableatwww.stroke.org/wecanhelp/healthcare
professionals/improveyourskills/toolstrainingandresources/training/nih?
gclid=CJWx_IDO08MCFcnm7AodZloACA.

Becausethepredictivevalueofanyspecificfindingfromthehistoryorphysicalexaminationis
insufficienttodistinguishischemicfromhemorrhagicstroke,promptneuroimagingalsois
required.AnoncontrastCTscanoftheheadwillreadilyidentifyICHandSAH(Figure10)and
istheinitialtestofchoice.AnypatientwithsuspectedSAHwhoseheadCTscanisnormal
shouldhavealumbarpuncturetoevaluateforbloodorxanthochromiainthecerebrospinalfluid
toruleoutaneurysmalbleeding.AnoncontrastCTscanoftheheadalsocanidentifytheearly
changesseenintheacutesettinginsomepatientswithcerebralinfarction(Figure11).Inmany
instances,theinitialnoncontrastCTwillnotshowanyappreciablechangesforaslongas24
hoursafterischemicstroke,andsmallinfarcts,particularlyinthethalamusandbrainstem,may
notbevisiblewithCTbeyondthattimewindow.Afteraninitialevaluationwithnoncontrast
headCT,otherneuroimagingstudiesmayprovideinformationregardingstrokelocationand
allowforevaluationofthecerebralvasculature.MRI(Figure12)canhelpdeterminethe
presenceofcerebralinfarctionwhentheCTscanisnotinformativeandprovideadditional
informationaboutpreviousstrokesorotherintracranialpathology.However,becauseofits
greatercost,lesswidespreadavailability,andgenerallylongerduration,MRIisrarelytheinitial
imagingtechniqueofchoicetoevaluateforhemorrhageorsuitabilityforsystemicthrombolysis.
Similarly,CToftheheadwithcontrastisrarelyhelpfulintheevaluationofbrainparenchymain
patientswithstrokeunlessitisbeingusedtoexcludeotherintracranialpathology(suchas
metastasis)thatmaymimicstrokeinapatientwhocannotreceiveanMRI.

Figure10.OpeninNewWindow

NoncontrastCTscansofthehead.Toppanel,anacuteleftthalamicintracerebralhemorrhage
(arrows)withouthydrocephalusorintraventricularextensionisshown.Bottompanel,anacute
subarachnoidhemorrhageisshownthatinvolvesthebasalcisterns(thinnerarrows)with
associatedenlargementofthelateralhornofthelateralventricles,consistentwithobstructive
hydrocephalusandelevatedintracranialpressure(thickerarrows).

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Figure11.OpeninNewWindow

HeadCTfindingsinacuteischemicstroke.Topleft,sulcaleffacementandlossofthegray
whitedifferentiation(ovalcircle)inapatient1.5hoursafterthewitnessedonsetofglobal
aphasia.Topright,hyperdensity(arrow)intheproximalrightmiddlecerebralarteryinapatient
withlefthemiparesisandlefthemiinattention60minutesafterlastbeingseenwell.Bottomleft,
CTangiogramofthesamepatientthatshowsabsentcontrastintherightinternalcarotidand
proximalmiddlecerebralarteries(arrow),consistentwithathrombusintheartery.Bottom
right,lossofgraywhitematterdifferentiationintheinsula(lossoftheinsularribbon)onthe
right(arrow)comparedwiththeleftwherethegraywhitematterdifferentiationisclearlyseen
inapatient2hoursafteronsetoflefthemiparesis.

Figure12.OpeninNewWindow

DiffusionweightedMRIsfromapatientwithsymptomaticleftmiddlecerebralartery
atherosclerosisrevealanacuteinfarctionindeep(thinnerarrows)andsuperficial(thicker
arrows)structuresintheleftcerebralhemisphere.

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Theneurologicexaminationprovidesusefulinformationaboutthespecificneuroanatomic
localizationofstroke,whichinitselfcansuggestthestrokesubtype.Forexample,theabsence
ofcorticalfeatures,suchasaphasiaandvisuospatialneglect,canpointtoasmallsubcortical
infarct,whereasmonocularvisuallossandacarotidbruitcansuggestextracraniallargeartery
atheroscleroticdisease.Theexamination,however,isnotsufficientlysensitiveorspecificto
furtheridentifythesubtypeofischemicstroke,andvesselimagingandcardiacevaluationare
requiredinmostpatientswithischemicstroke.

KeyPoint
Inpatientswithstroke,neuroimaging(usuallyanoncontrastCTscanofthehead)is
requiredtodistinguishischemicfromhemorrhagicstrokewhensubarachnoid
hemorrhageissuspectedbutneuroimagingfindingsarenormal,lumbarpunctureis
necessarytoevaluateforbloodorxanthochromiainthecerebrospinalfluid.

StrokeSubtypes
TransientIschemicAttack

RelatedQuestion

Question4

Transientischemicattack(TIA)isdefinedbytransientfocalneurologicsymptomsresulting
frombrain,retinal,orspinalcordischemiaandwasinitiallydefinedaslastinglessthan24
hours.Amorerecentlyadopteddefinitionrecognizesthehighprevalenceofacuteinfarctson
neuroimagingandemphasizesthatTIAisdefinedbytheabsenceofinfarctiononneuroimaging,
independentofsymptomduration.TIAsymptomstypicallyareshortlasting,usually5minutes
to1hour,andincludesuddenonsethemiparesis,hemisensoryloss,changeinspeechfunction
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(eitheraphasiaordysarthria),lossofvision,orinabilitytowalk.PatientswithasuspectedTIA
shouldthusundergoneuroimagingwitheithernoncontrastMRIorCTwithin24hoursofthe
onsetofneurologicdeficits.

TIAisconsideredaneurologicemergencygiventhesubsequent48hourand90dayriskof
ischemicstroke.Severalclinicalscaleshavebeendevelopedforriskstratificationofpatients
withaTIA(orstroke)themostwidelyacceptedistheABCD2score,whichisbasedona
patient'sAge,Bloodpressure,Clinicalpresentation,Durationofsymptoms,andthepresenceof
Diabetesmellitus(Table16).TheriskofstrokeincreasesastheABCD2scoreincreases,and
hospitaladmissionisrecommendedforallpatientswithanABCD2scoreof3orgreatersothat
rapidevaluationandtreatmentcanoccur.AnoncontrastheadCTisrequiredtoruleout
hemorrhagicstroke.Hospitaladmissionalsocanbeconsideredinpatientswithascoreof0to2
ifsuspicionofinfarctionishighorifrapidoutpatientevaluationcannotbecompletedwithin48
hours.AllpatientswithsuspectedTIArequireanexpeditedevaluationwithin48hourswith
bothcerebrovascularimagingandcardiacexamination.Cerebrovascularimagingisnecessaryto
excludeextracranialinternalcarotidarterydisease,whichisassociatedwithahighriskof
subsequentstroke,andcanbeperformedwithcarotidultrasonographymagneticresonanceand
CTangiographyareotheroptions,butcostandriskfromcontrastandradiationshouldbe
considered.Thecardiacexaminationisprimarilyfocusedonidentifyingpatientswhocouldbe
candidatesforanticoagulationforstrokepreventionelectrocardiographyorcardiacevent
monitoringisperformedtodetectanyatrialfibrillation,andechocardiographyisneededto
evaluateforventricularthrombusorotherhighriskembolicsources(forfurtherdiscussion,see
MKSAP17CardiovascularMedicine).

Table16.OpeninNewWindowABCD
ScoringSystema

PatientCharacteristics Scoreb

Age60y 1

Bloodpressure140/90mmHg 1

Clinicalsymptoms

FocalweaknesswiththeTIA 2

Speechimpairmentwithoutweakness 1

DurationofTIA

60min 2

1059min 1

Diabetesmellituspresent 1
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TIA=transientischemicattack.
aBasedonAge,Bloodpressure,Clinicalpresentation,Durationofsymptoms,andthe
presenceofDiabetesmellitus.
bThe48hourstrokeriskbasedonscore:01=0%23=1.3%45=4.1%67=8.1%.

KeyPoint
Inpatientswhohavehadatransientischemicattack,theriskofstrokeincreasesasthe
ABCD2score(basedonapatient'sAge,Bloodpressure,Clinicalpresentation,Duration
ofsymptoms,andthepresenceofDiabetesmellitus)increaseshospitaladmissionis
recommendedforallpatientswithanABCD2scoreof3orgreatersothatrapid
evaluationandtreatmentcanoccur.

IschemicStroke

CardioembolicStroke

Themostcommoncauseofcardioembolicstrokeisatrialfibrillation.Otherpotential
cardioembolicsourcescanbeidentifiedduringthediagnosticevaluation,includingreducedleft
ventricularejectionfraction,severecalcificmitralstenosis,ventricularthrombusorapical
aneurysm,orcongenitalabnormalities(suchasapatentforamenovale[PFO]).Forfurther
detailsonriskstratificationwithcardioembolicsourcesandanticoagulationcriteria,see
MKSAP17CardiovascularMedicine.

Severalfindingsonneuroimagingsuggestacardioemboliccause,suchasinvolvementofthe
corticalsurfaceintheabsenceofcerebralarteryatherosclerosispresenceofmorethanone
infarct,especiallyifbilateralorinvolvingtheterritoryofboththeinternalcarotidand
vertebrobasilararteriesandinvolvementoftheentireterritoryofalargeintracranialartery.
Cardiacrhythmevaluationisadvisableforallpatientswithischemicstroke,including
electrocardiographyandinhospitaltelemetry,toevaluateforatrialfibrillation.Transthoracic
echocardiographyshouldbeconsideredinpatientswithstrokewhohaveasuspectedembolic
strokeorunderlyingheartdiseasewithoutanotheridentifiedcausetoidentifycandidatesfor
anticoagulation.Transesophagealechocardiographycanbeconsideredonacasebycasebasis
toidentifyrarecausesofstroke,suchasvalvularendocarditisorintracardiactumors.

LargeArteryAtherosclerosis

Strokeduetolargearteryatherosclerosiscommonlyoccursafterlocalthrombusformationin
theareaofplaquerupturewithsubsequentdistalembolization.Ofthecommoncausesofstroke,
extracranialinternalcarotidarteryatherosclerosishasthehighestriskofrecurrentstrokeinthe
first2weeks.Suggestiveclinicalhistoryandexaminationfindingsincluderecentmonocular
visuallossandthepresenceofacarotidbruit,bothonthesideoftheaffectedhemisphere.The
riskofrecurrentstrokeishighestwhenthestenosisisgreaterthan70%stenosisinthe50%to
70%rangehasamoremodestriskofrecurrence.Promptvascularimagingistherefore
recommendedforpatientswithaTIAoracarotidterritoryinfarctionseenonneuroimaging.
Severalimagingmodalitiesareavailableforquantifyingthedegreeofstenosis,including
ultrasonography,magneticresonanceangiography(MRA),andCTorcatheterdigital
subtractionangiography.Carotidultrasonographyisausefulinitial,noninvasivetest,
particularlybecauseofitshighsensitivityforhemodynamicallysignificantstenosisanditslow
risk.Ifthecarotidultrasoundshowssignificantstenosis,thepercentageofnarrowingandthe
anatomiclocationshouldbeconfirmedwitheitherCTangiographyorMRAwithoutcontrast
beforerecommendingstentingproceduresorothersurgery(seeFigure13foracomparisonof
differentimagingmodalities).Unlesscarotidarteryangioplastywithstentingisplanned,
catheterangiographyisnotroutinelynecessary.
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Figure13.OpeninNewWindow

Diagnosticimagingmodalitiesinapatientwithasymptomaticextracranialinternalcarotid
arteryatheroscleroticplaqueandassociated90%stenosis.Toppanels:aCTangiogram(A),a
digitalsubtractionangiogram(B),andamagneticresonanceangiogram(C)allshowhighgrade
stenosisattheareaoftheoriginoftheinternalcarotidartery(arrows).Bottompanel:
ultrasounds(D)oftheextracranialproximalinternalcarotidarteryshowalargeplaqueatthe
origin(arrow)oftheartery,withassociatedelevatedsystolic(394.8cm/s)anddiastolic
(176.7cm/s)velocitiesconsistentwith80%to99%stenosis.PICA=proximalinternalcarotid
artery.

Strokearisingfromatherosclerosisoftheintracranialarteriestypicallyoccurswithstenosis
greaterthan70%inthevertebrobasilar,intracranialinternalcarotid,andmiddlecerebral
arteries.Intracranialatherosclerosisalsoisassociatedwithahighlongtermriskofrecurrent
strokeitspresencecanbedetectedwitheitherCTorMRA.TranscranialDoppler
ultrasonographycandetectacceleratedvelocitiesconsistentwithsignificantstenosisandcanbe
usedinpatientsunabletoundergoCTorMRAdiagnosticcerebralangiographyisrarely
necessaryinthesepatients.

SmallSubcorticalInfarcts(Lacunes)

Smallsubcorticalinfarcts(lacunes)arecommonlylessthan1.5cminsizeandarisefrom
occlusionofsmallperforatingarteriesemanatingfromthelargeintracranialvessels.Thisstroke
subtypetypicallypresentswithonlymotororsensoryfindingsonexaminationcortical
hemisphericsymptoms,suchasvisualfieldcuts,aphasia,orhemispatialneglect,arelacking.
Themainriskfactorforlacunarstrokeishypertension,leadingtoassociatedpathologicchanges
attheoriginoftheperforatingarteries.Becausetheseinfarctsmaystillarisefrom
atherothromboticlesionsinlargecerebralarteries,vascularimagingisrequiredinaffected
patientstoinitiateappropriatesecondarystrokeprevention.

CryptogenicandRareCausesofStroke
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RelatedQuestion

Question59

Asizeableproportionofpatientswillhaveacerebralinfarctionwithnodefinitivecause
identifiedoncardiacorvasculardiagnostictesting.Inthesepatients,prolongedcardiacrhythm
monitoringorinterrogationofapacemaker,ifpresent,mayrevealundiagnosedparoxysmal
atrialfibrillationthatcouldchangesecondarypreventionstrategies.Otherdiagnostictestingcan
beconsideredonacasebycasebasis,dependingonthespecificcircumstances.Headache
precedingstrokeinyoungerpatientswithoutcardiovasculardiseaseriskfactors,particularly
thosewithrecenthead/necktrauma,suggestscervicocephalicarterialdissectionandcanbe
ruledoutwithheadandneckvascularimaging.Testingforautoimmuneandhypercoagulable
disorderscanbeconsideredinyoungpatientswithotherwiseunexplainedstroke.
EchocardiographymayrevealaPFO,whichispresentinupto25%ofthegeneralpopulation.
Inyoungerpatients,aPFOislikelytobecausallyrelatedtothestroke,althoughthesepatients
generallyareatalowriskofsubsequentstrokeintheabsenceofahypercoagulabledisorder.
Recentlycompletedclinicaltrials,however,havefailedtoshowthebenefitofpercutaneous
closurecomparedwithbestmedicaltherapy.ForfurtherdetailsseeMKSAP17Cardiovascular
Medicine.

KeyPoints
Cardiacrhythmevaluation,includingelectrocardiographyandinhospitaltelemetry,is
advisableforallpatientswithischemicstroketoevaluateforatrialfibrillation.
Strokeiscommonlycausedbylargearteryatherosclerosis,andtheriskofstroke
recurrenceishighestwhenanyassociatedstenosisisgreaterthan70%.

HemorrhagicStroke

SubarachnoidHemorrhage

NontraumaticSAHpresentswiththesuddenonsetofasevereheadache,describedbypatients
astheworstheadacheoftheirlifeorthunderclapinorigin(seeHeadacheandFacialPain).
ThemostcommonexaminationfindinginpatientswithSAHisimpairmentinconsciousness
duetoelevatedintracranialpressurethatmanifestsasaspectrumrangingfrommildsomnolence
tocomaorbraindeath.Theinitialclinicalexaminationisoftensummarizedbyusingclinical
scalesthatcorrelatewellwithmortality(Table17).Otherearlylocalizingfindingsinclude
subhyaloidhemorrhagesonfunduscopy(Figure14)andoculomotornervepalsieswith
pupillarydilationfromdirectcompression.Inpatientswithelevatedintracranialpressurefrom
eithercerebraledemaorobstructivehydrocephalus,lossofbrainstemreflexes,posturingin
responsetopainfulstimuli,andimpairmentsinconsciousnesscanoccur.Anypatientwith
suddenunexplainedcomarequiresneuroimagingtoexcludeSAHandhydrocephalus.The
principalcauseofSAHisarupturedcerebralsaccularaneurysm,whichoftencanbeidentified
byCTangiography.Catheterangiographystillisrequiredinallpatientstoconfirmthepresence
ofasymptomaticaneurysmandtodetectotherpathologythatmaybebeyondtheresolutionof
CTangiography,suchasintracranialarterialdissection,intracranialvascularmalformation,or
smalldistalaneurysms.Catheterangiographyhastheadditionalbenefitofbeingatreatment
modalityforrupturedintracranialaneurysms(Figure15).Besidesintracranialarterial
dissectionsandintracranialvascularmalformations,otherconditionsthatcanleadtoSAH
includereversiblecerebralvasoconstrictionsyndromeandduralsinusthrombosis.

Figure15.OpeninNewWindow

Angiogramsshowinganinternalcarotidarteryaneurysminapatientwithasubarachnoid
hemorrhage(SAH).Topleft,noncontrastheadCTscanshowinganextensiveSAHwith
intraventricularextension.Topright,CTangiogramshowingalargerightinternalcarotidartery
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aneurysm.Bottomleft,anteroposteriorviewofadigitalsubtractionangiogramoftheright
intracranialinternalcarotidarteryshowingthesamelargeaneurysm.Bottomright,lateralview
ofthedigitalsubtractionangiogramshowingthesamelargeaneurysm.

Figure14.OpeninNewWindow

Subhyaloidhemorrhagesonfunduscopicexaminationsuggestingananeurysmalsubarachnoid
hemorrhage.

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AdaptedwithpermissionfromLaforestC,SelvaD,CromptonJ,LeibovitchI.Entopic
phenomenonasinitialpresentationofacutemyelogenousleukemia.AnnInternMed.
2005Dec6143(11):847.PMID:16330805

IntracerebralHemorrhage

ICHshouldbesuspectedinanypatientwithfocalneurologicsymptomswithassociated
headache,nausea,orimpairmentinconsciousness.OtherpredictivefeaturesofICHinclude
hypertensionatonset,useoforalanticoagulants,andsuddenunexplainedlossofconsciousness.
However,noreliablehistoryorexaminationfindingscanreliablyconfirmorruleout
hemorrhagicstroke,andthediagnosisofICHrequiresapromptCTscanoftheheadwithout
contrast,whichcanreadilyidentifythepresenceofblood.Thisprocedurecanbecompleted
quicklyandallowsfortheidentificationofassociatedpathologythatcanhaveasignificant
negativeeffectonprognosis,includingcerebraledemaandhydrocephalus.Repeat
neuroimagingoftenisrequiredinpatientswithICHtodetecthematomaexpansion,worsening
cerebraledema,orothercausesofchangesinneurologicstatus.

ThelocationoftheICHcorrelateswithdifferentunderlyingpathologies,whichcanfurther
dictatelongtermprognosisandsecondarypreventionstrategies.ICHoriginatingfromdeep
structuresofthebrain,suchasthebasalganglia,pons,andcerebellum,istypicallydueto
hypertension.Withadequatecontrolofthebloodpressure,patientswithdeephemorrhagesmay
stillbecandidatesforanticoagulation,ifneeded,inthefuture.Lobarhemorrhagesinolder
patientswithouthypertensionthatoriginatenearthecorticalsurfacecanbecausedbyamyloid
angiopathystemmingfromamyloiddepositsindistalcerebralarteriolesthisprocessis
similartowhatoccursinAlzheimerdisease,inwhichamyloiddepositsarefoundinthe
parenchyma.Amyloidangiopathyisassociatedwithahighriskofrecurrentlobarhemorrhage,
andanticoagulationandstatinsshouldbeavoidedinthesepatients.VascularimagingorMRI
mayberequiredinpatientswithatypicalpresentationsorotherwiseunexplainedICH.

KeyPoints
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Theprincipalcauseofsubarachnoidhemorrhageisarupturedcerebralsaccularaneurysm,
whichcanbeidentifiedbyCTangiographycatheterangiographyisrequiredfor
confirmationofthediagnosisandpotentialtreatmentoftheaneurysm.
Repeatneuroimagingoftenisrequiredinpatientswithintracerebralhemorrhagesto
detecthematomaexpansion,worseningcerebraledema,orothercausesofchangesin
neurologicstatus.

AcuteStrokeTherapy
Theinitialtherapyinacutestrokedependsonwhetherthestrokeisischemicorhemorrhagic.
Regardlessofstrokeetiology,aprimarygoalofhospitalizingallaffectedpatientsisthe
preventionandtreatmentofassociatedmedicalandneurologiccomplications.

IschemicStrokeTreatment

Thrombolysis

RelatedQuestions

Question78
Question86
Question94

Theinitialgoalintheevaluationofapatientwithacuteischemicstrokeistoestablisheligibility
forintravenousthrombolysis.Theprimarydeterminantofeligibilityisthetimesincestroke
onset,whichisdeterminedbyeitherselfreportorthetimewhenthepatientwaslastwitnessed
ataprestrokebaseline.Thrombolysisinstrokeaimstorestorecerebralbloodflowtothe
ischemicpenumbrawherecerebraltissuehassustainedischemicinjurybuthasnotyet
progressedtoinfarction.Intravenousthrombolysisinischemicstrokeisindicatedwithin3hours
ofonsetinpatientswithameasurabledeficitwhodonotmeetanyoftheexclusioncriteriaand
ismosteffectivetheearlieritisadministered.Afocusedhistoryandphysicalexaminationanda
fingerstickmeasurementofbloodglucoselevelcandetermineanyoftheexclusioncriteria
rapidimagingwithnoncontrastheadCTisrequiredtoexcludeICH.Laboratorytesting,
includingacompletebloodcount,coagulationprofile,andbasicmetabolicprofile,alsoshould
beobtainedinallpatientswithacuteischemicstroke,althoughtheresultsarenotnecessaryto
initiatethrombolysisunlessasuspicionofcoagulopathyorthrombocytopeniaexists.The
optimaltimefromhospitalarrivaltotreatmentwiththrombolysisis60minutesorless,whichis
consideredamarkerofhighqualitycare.Additionaltestingisnotindicatedinmostpatients
becauseitleadstounnecessarydelaysintreatment.Vascularimagingintheacuteischemic
strokesettingalsoisnotnecessaryandcanleadtotreatmenttimedelays.

Treatmentwithintravenousthrombolysisbetween3to4.5hoursfromstrokeonsetcanbe
consideredinaselectgroupofpatientswhomeetstrictinclusion/exclusioncriteria,although
thistherapylacksFDAapproval.Theefficacyofendovascularstroketherapyinlieuof,orafter,
intravenousthrombolysishasnotbeenestablishedbyseveralrecentlycompletedclinicaltrials.
Endovascularacutestroketherapywithintraarterialthrombolyticorthrombectomydevicescan
beconsideredonacasebycasebasisforpatientswithin6hoursofstrokeonsetwhoare
otherwiseineligibleforintravenousthrombolysis.Aproposedpathwayfortheevaluationand
treatmentofacuteischemicstrokeisprovidedinFigure16.

Figure16.OpeninNewWindow

Proposedpathwayfortheevaluationandtreatmentofanacutestrokewithin6hoursofonset.
aPTT=partialthromboplastintime,activatedNIHSS=NationalInstitutesofHealthStroke
ScalePT=prothrombintimertPA=recombinanttissueplasminogenactivator.

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artPAcanbeconsideredinpatientswithoneormorerelativeexclusioncriteriaafter
considerationofneurologicdeficitsandrisksversusbenefits.
bAvailableevidenceforthebenefitofmechanicalintraarterialtherapyislimited,andits
appropriateuseremainstobedefined.

ThemaincomplicationfromintravenousthrombolysisissymptomaticICH,definedas
intracranialbleedingwithanassociateddeclineinneurologicfunctiondetectedonneurologic
examinationthatcannotbeascribedtoothercauses.Itoccursinapproximately6%oftreated
patientsandhasanassociated50%mortality.Headache,nausea,orworseningofneurologic
examinationfindingsaresignsofintracranialbleedingandshouldpromptstoppingtheinfusion
andrepeatingtheheadCT.ThemainriskfactorsforsymptomaticICHareprotocolviolations,
notablytreatmentbeyondthetimewindowandbloodpressureaboverecommendedtargets.
Bloodpressureshouldbelessthan185/110mmHgbeforethrombolysis,whichcanbeachieved
withintravenouslabetalolornicardipine,accordingtoAmericanHeartAssociationguidelines.
Aftertheinitiationofintravenousthrombolysisusingrecombinanttissueplasminogenactivator,
adherencetostrictmonitoringprotocolsregardingvitalsignsandneurologicexamination
findingsisrequiredtoachieveatargetbloodpressurelessthan180/105mmHgandtodetect
signsofsymptomaticICH.Otherprecautionsafterintravenousthrombolysisinclude
withholdingallantithromboticagentsuntilarepeatheadCTorMRIperformed24hoursafter
theprocedureexcludesICHandmonitoringforangioedema.

Antiplatelet,Anticoagulant,andOtherAgentsforAcuteIschemicStrokeTreatment

RelatedQuestion

Question45

Mostpatientswithischemicstrokewillarrivebeyondthestatedwindowsforintravenous
thrombolysis.Formostofthesepatients,aspirinisappropriate,butonlyafteradysphagia
evaluationdocumentingtheabilitytosafelyswallow.Inthoseunabletoswallow,arectal
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formulationofaspirinisavailable.Aspirintakenwithin48hoursofischemicstrokeonset
modestlyreducestheriskofrecurrentischemicstrokeat2weekswithoutsignificantly
increasingtheriskofintracerebralhemorrhage.Noacuteischemicstroketrialshavetested
monotherapywithclopidogrelorthecombinationofaspirinanddipyridamole.However,in
patientswithahighriskTIA(ABCD2score4)orminorischemicstroke(NationalInstituteof
HealthStrokeScalescore3),a21daycourseofcombinationaspirinandclopidogrelfollowed
byclopidogrelmonotherapyforatotalof90daysreducedtheriskofsubsequentstrokewhen
administeredwithin24hoursofonsetcomparedwithaspirinmonotherapy.Noincreaseinthe
riskofICHordifferencesinefficacybysubgroupswasreported.Heparinoidsdonotreducethe
riskofrecurrentstrokeintheacutesettingforeithercardioembolicornoncardioembolicstroke.
Acuteintravenousheparinoccasionallyisusedinpatientswithrarecausesofstroke,suchas
dissectionorahypercoagulablestate,orinpatientswithmechanicalcardiacvalvesiftheriskof
hemorrhageintotheinfarctislow.

Othermedicationclasseshavenotbeenextensivelystudiedintheacutesetting.Todate,no
studieshavebeenpublishedaboutstatinsadministeredintheacutestrokesetting.Arecenttrial
ofacutebloodpressureloweringwithcandesartanwithin36hoursshowednoreductionin
cardiaceventsormortalitybutatrendtowardworseningofneurologicdeficits.Bloodpressure
loweringinpatientswhodonotreceiveintravenousthrombolysisisonlyrecommendedifthe
bloodpressureisgreaterthan220/120mmHgorifahighriskorevidenceofotherendorgan
damageexists.

AntithromboticTherapyAfterIschemicStroke

RelatedQuestions

Question16
Question38

ThemanagementofantithromboticagentsafterischemicstrokeandTIAdiffersfromthatin
otherischemicatheroscleroticdiseasesbecauseoftheriskofhemorrhagicstroke.Inpatients
withstrokeandatrialfibrillation,anticoagulationcanbestartedbeforehospitaldischargeifthe
riskofhemorrhageintothebedoftheinfarctislow,suchasinpatientswithinfarctsbutno
petechialhemorrhage,asdeterminedbyneuroimaging,orwithinvolvementoflessthanone
thirdofthemiddlecerebralarterydistribution.Forfurtherdiscussionofanticoagulationinatrial
fibrillation,seeMKSAP17CardiovascularMedicine.Warfarinisnotrecommendedforpatients
withsymptomaticintracranialatherosclerosisunlessanotherhighriskconditionalsois
identifiedbecausethisdrugisassociatedwithincreasedmortalitycomparedwithantiplatelet
agents.Inallothernoncardioembolicischemicstrokes,warfarinandantiplateletagentsare
equivalentintermsofefficacy,althoughantiplateletagentsoftenareconsideredfirstlineagents
becauseofeaseofuse.

Inthenonacutesetting,thecombinationofaspirinandclopidogrelfornoncardioembolicstroke
increasestheriskofmortalityandhemorrhagicstrokewithoutsignificantlyreducingtheriskof
ischemicstroke,comparedwithsingleagenttherapy.Thecombinationofaspirinand
dipyridamoletwicedailymodestlyreducestheriskofrecurrentischemicstrokewhencompared
withaspirinmonotherapy,butinalargeischemicstrokesecondarypreventiontrial,the
combinationofaspirinanddipyridamolewasequivalenttoclopidogrelmonotherapy.The
choiceofantiplateletagentsforsecondarystrokepreventionisoftendrivenbypatient
preference,includingcost,andbyriskforothermedicalcomorbidities,giventhesmallabsolute
riskdifferencesbetweeneachagent.Fornoncardioembolicstroke,lowdose(81mg/d)aspirin
monotherapyisoftenfirstlinetherapyforpatientsnotpreviouslytakingantiplateletagents.
Clopidogreloraspirinplusdipyridamolecanbeconsideredinpatientswhohavearecurrent
ischemicstroke,despiteadequatecontrolofotherstrokeriskfactors,whiletakingaspirin
monotherapy.Theeffectivenessofnewerantiplateletagentsorplateletresistanceassayshasnot
beenestablishedforstroke.

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KeyPoints
Intravenousthrombolysisisindicatedwithin3hours(andcanbeconsideredwithin3to
4.5hours)ofonsetofischemicstrokeinpatientswithameasurabledeficitwhomeet
inclusion/exclusioncriteria.
Afterinitiationofintravenousthrombolysis,adherencetostrictmonitoringprotocols
regardingvitalsignsandneurologicexaminationfindingsisrequiredtoachieveatarget
bloodpressurelessthan180/105mmHgandtodetectsignsofsymptomaticintracranial
hemorrhage.
Formostpatientswithischemicstrokewhoarriveatthehospitalbeyondthetreatment
windowforintravenousthrombolysis,oralorrectalaspirinisusuallyappropriate
treatmentaspirintakenwithin48hoursofischemicstrokeonsetmodestlyreducesthe
riskofrecurrentstrokeat2weekswithoutsignificantlyincreasingtheriskofhemorrhage.

HemorrhagicStrokeTreatment

IntracerebralHemorrhageTreatment

RelatedQuestion

Question55

ThemainstayoftherapyforacuteICHistreatmentofhematomaassociatedneurologic
complications.Antiplateletandantithromboticagentsshouldbediscontinued.Giventhesmall
riskofhemorrhagewithselectiveserotoninreuptakeinhibitors,discontinuationoftheseagents
shouldalsobeconsidered.Inpatientswithhydrocephalus,externalshuntingofcerebrospinal
fluidmayberequiredwhenclinicalevidenceofelevatedintracranialpressureisdetected
osmotherapywithmannitolorhypertonicsalinecanbeconsideredinpatientswithelevated
intracranialpressureassalvagetherapy.Surgicalevacuationofthehematomashouldbe
consideredinpatientswithacerebellarICHwithasizegreaterthan3cm,particularlyif
evidenceofneurologicworseningorbrainstemcompressionispresent.Surgicaldecompression
forotherlocationscanbeconsideredonacasebycasebasis.

AnadditionalgoaloftherapyinpatientswithICHhasbeentopreventexpansionofthe
hematomabyloweringbloodpressureorusinghemostaticagents.RecombinantfactorVIIa
therapy,however,wasnotassociatedwithimprovedclinicaloutcomesinarandomizedclinical
trialofspontaneousICH.InpatientswithavitaminKantagonistassociatedICH,freshfrozen
plasmaorprothrombincomplexconcentratesarerecommended,asisadministrationof
intravenousvitaminK.TheappropriatetreatmentofICHrelatedtodirectthrombininhibitorsor
factorXainhibitorsandtheeffectivenessofusingplatelettransfusionsinantiplateletassociated
ICHhavenotbeenwellestablished.ForfurtherdetailsseeMKSAP17Hematologyand
Oncology.Inpatientswithoutelevatedintracranialpressurewhosesystolicbloodpressureis
greaterthan180mmHgormeanarterialpressureisgreaterthan130mmHgatthetimeoftheir
ICH,treatmentwithintravenousmedicationscanbeinitiated,withatargetbloodpressureof
160/90mmHgormeanarterialpressureof110mmHg.Furtherreductionsinbloodpressure
alsomaybesafe.Arecenttrialshowedthatacuteloweringofsystolicbloodpressuretoless
than140mmHg(comparedwith<180mmHg)within6hourswasassociatedwithatrendto
reductionofdisability,withoutanychangeinadverseeventsormortality.Medicationsthatcan
betitratedeasily,suchasnicardipineorlabetalol,arepreferrednitratesshouldbeavoided
becauseofthepotentialforincreasingintracranialpressure.

SubarachnoidHemorrhageTreatment

RelatedQuestions

Question67
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Question75

NeurologiccomplicationsinaneurysmalSAHdifferaccordingtowhethertheyoccurearly
(within48hours)orlater(typically,510days)intheclinicalcourseofthehemorrhage.Inthe
earlyphase,patientsoftenhaveimpairmentsinconsciousnessduetohydrocephalusandrequire
externalcerebrospinalfluidshuntingtoalleviateandsubsequentlymonitorintracranialpressure.
Asignificantcauseofmorbidityandmortalityduringthisphaseisaneurysmalrebleeding,and
thusearlyvascularimagingisrequiredinallpatientswithSAHtodiagnoseanyruptured
cerebralarteryaneurysm.Treatmentwitheitherendovascularcoilingorclipping(performed
duringacraniotomy)shouldbeginearlyuntiltheaneurysmissecured,thebloodpressure
shouldbelessthan140/80mmHgtopreventrebleeding.Othersourcesofearlyneurologic
complicationsincludeglobalcerebraledemaandseizuresseizureprophylaxisiscommonin
patientswithSAH.Delayedcerebralischemiaduetoarterialvasospasmisasignificantsource
oflaterneurologicmorbidityandcanpresentwithnonspecificexaminationfindings.The
patientsathighestriskfordevelopingvasospasmwithsubsequentdelayedcerebralischemiaare
thosewiththelargestburdenofbloodinthebasalcisternsonneuroimaging.Thesesame
patientsgenerallyhaveimpairmentsinconsciousness,whichmakesdetectionofsubtle
examinationfindingschallenging.Althoughserialdailyscreeningtoidentifyvasospasm
typicallyisperformedwithnoninvasivetranscranialultrasonographyduringthefirst2weeks
afterSAHonset,CTangiographyismoresensitiveindetectingsubtlevasospasmsthatmaybe
treatedwitheithertheinitiationofvasopressorstoaugmentthebloodpressureorultimately
endovasculartreatmentinmorerefractorydisease.CTangiographyhastheadditionalbenefitof
imagingtheventricles,whichwillallowfordetectingachangeinventricularsize.Oral
nimodipineimprovesneurologicoutcomesinpatientswithaneurysmalSAHandis
recommendedinallpatientswithSAHforthefirst21daysoruntilhospitaldischarge,
whichevercomesfirst.Cerebralvasospasmisoftenmanagedinitiallybyinducinghypertension
topreventprogressiontocerebralischemia,butonlyaftertheaneurysmhasfirstbeentreated.
However,clinicaltrialdatasupportingaparticulartargetbloodpressurearescant,andthe
AmericanHeartAssociationhasmadenospecificrecommendation.Inpatientswithclinically
significantcerebralvasospasm,angiographymaybenecessarytoconfirmitsseverityandallow
forpotentialtherapeuticintervention.

AssociatedmedicalcomplicationsareasignificantsourceofmorbidityandmortalityinSAH.
Acutemyocardialinfarctionduetocontractilebandnecrosisinthesettingofasignificant
sympatheticsurgecanoccurearlyinthecourseofhighgradeSAH(seeTable17)andcanlead
tosignificantreductionsinsystolicfunction,hypotension,andpulmonaryedema.Respiratory
failurerequiringmechanicalventilationbecauseofimpairedconsciousnessorhypoxemiafrom
eitherpneumoniaorpulmonaryedemaisalsocommon.Othermedicalcomplicationsinclude
cerebralsaltwastingsyndrome,thesyndromeofinappropriateantidiuretichormonesecretion,
cardiacarrhythmias,andinfectionsfrompulmonary,urinary,andcentralvenouscathetersor
fromcerebrospinalfluidshuntingsources.Giventheassociatedlevelofmonitoringand
supportivecarerequiredforneurologicandmedicalcomplicationsofSAH,affectedpatients
shouldbecaredforinaneurologicICU,ifavailable.

Table17.OpeninNewWindowClinicalGradingScaleforSubarachnoidHemorrhage

HuntHess
ClinicalDescription
Grade

1 Asymptomaticormildheadache

2 Moderatetosevereheadache,cranialnervepalsies

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3 Somnolence,confusion,orminorfocalneurologicdeficits

Significantimpairmentinconsciousness,significantfocalneurologic
4
deficits

5 Coma,posturing

KeyPoints
Surgicalevacuationofthehematomashouldbeconsideredinpatientswithacerebellar
intracerebralhemorrhagewhosesizeisgreaterthan3cm,particularlyifevidenceof
neurologicworseningorbrainstemcompressionispresent.
Earlyvascularimagingisrequiredinallpatientswithsubarachnoidhemorrhageto
evaluateforanyrupturedcerebralarteryaneurysmtreatmentoftheaneurysmwitheither
endovascularcoilingorclippingshouldbeginearly,withthebloodpressuremaintainedat
lessthan140/80mmHgtopreventrebleeding.

StrokePrevention
Table18liststheriskfactorsforstroke.

Table18.OpeninNewWindowCommonRiskFactorsforIschemicandHemorrhagicStroke

Subarachnoid
IschemicStroke/TIA IntracerebralHemorrhage
Hemorrhage

SharedRiskFactors

Hypertension
Hypertension
Hypertension Cocaineabuse
Cocaineabuse
Cocaineabuse
Tobaccouse
Tobaccouse
Tobaccouse
Arteriovenous
Arteriovenousmalformation
malformation

OtherRiskFactors

Diabetesmellitus Amyloidangiopathy

Atrialfibrillation DecreasedLDLcholesterol
level
Lowleftventricularejectionfractionand
Intracranialartery
intracardiacthrombus ElevatedHDLcholesterol
dissection
level
Cervicocephalicarterialdissection
Polycystickidney
Anticoagulantagentuse
Aorticarchatheromatousdisease disease
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Aorticarchatheromatousdisease
Antiplateletagentuse
Cardiacvalvevegetations
Selectiveserotoninreuptake
Patentforamenovale inhibitoruse

TIA=transientischemicattack.

PrimaryStrokePrevention

RelatedQuestions

Question35
Question72

Foradiscussionofmanagementofvasculardiseaseriskfactorsandantiplateletagentsusedin
primarypreventionofstroke,seeMKSAP17CardiovascularMedicine.

Theapproachtoasymptomaticextracranialinternalcarotidarterystenosishaschangedbecause
ofimprovementsinoptimalmedicaltherapythathaveresultedinstrokeratescloseto1%per
year(comparedwiththepreviousrateof2%peryear).Thislowerrateseemsdrivenbylipid
loweringtherapywithstatins.Aggressiveriskfactorcontrol,withoptimalmedicaltherapyand
comprehensivelifestylemodificationsindiet,exercisehabits,andtobaccouse(amongothers),
isrequiredforallpatients.Revascularizationwitheitherstentingorendarterectomycanbe
consideredinpatientswithagreaterthan80%stenosisandlowcardiovascularrisk,aslongas
theoperativecomplicationrateislessthan3%.

Unrupturedcerebralarteryaneurysmsarecommonlyfoundinasymptomaticpatients.Afraction
ofthesepatientshavesymptomsfromcompressionofadjacentstructures,suchaspupillary
enlargementfromcompressionoftheoculomotornervebyaposteriorcommunicatingartery
aneurysmorvisuallossfromcompressionoftheopticnervebyacavernouscarotidartery
aneurysm.Size,location,andahistoryofrupturedcerebralarteryaneurysmsinotherlocations
aretheprincipaldeterminantsoftreatment.Ruptureratesfromasymptomaticaneurysms
withoutapriorhistoryofSAHareoutlinedinTable19.Surgicaltreatmentwithclippingor
endovascularcoilingcanbeconsideredinpatientswithaneurysmsof7mmorgreaterinthe
posteriorcirculation(posteriorcommunicatingandbasilararteries)or12mmorgreaterinthe
anteriorcirculation.Regardlessofaneurysmalsizeandlocation,allpatientswithunruptured
cerebralarteryaneurysmsbenefitfromtobaccocessationandbloodpressurecontrol.

Table19.OpeninNewWindowRuptureRatesOver5YearsofUnrupturedIntracranialArtery
Aneurysms

Size Rupture
Position
(mm) Rate(%)

<7 0

712 2.6
Anteriorcirculationaneurysm(internalcarotid,anterior
communicating,middlecerebralarteries) 1324 14.5

>25 40

<7 2.5
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712 14.5
Posteriorcirculationaneurysm(posteriorcommunicating,basilar
arteries) 1324 18.4

>25 50

KeyPoints
Mostpatientswithasymptomaticextracranialinternalcarotidarterystenosisshouldbe
treatedwithaggressiveriskfactorcontrolandnotstentingorelectiveendarterectomy,
whichshouldonlybeconsideredinpatientswithagreaterthan80%stenosisandlow
cardiovascularrisk(aslongastheoperativecomplicationrateislessthan3%).
Inprimarystrokeprevention,allpatientswithunrupturedcerebralarteryaneurysms
benefitfromtobaccocessationandbloodpressurecontrol.

SecondaryStrokePrevention

LifestyleandMedicalManagement

Thetreatmentofmodifiablevasculardiseaseriskfactorscanleadtoasignificantdecreaseinthe
riskofrecurrentstroke.Hypertensionisacommonriskfactorforrecurrenceofallstroke
subtypes,andloweringofbloodpressureinpatientswithstrokeisassociatedwithasignificant
reductionintheriskforrecurrence.However,theoptimalgoalforsecondarypreventionof
strokeislessclear.TheEighthJointNationalCommittee(JNC8)recommendationsand
treatmentguidelinesforthepreventionofsecondarystrokerecommendantihypertensive
therapyforstablepatientswithasustainedbloodpressureof140/90mmHgorgreater,
includingthoseolderthan60yearswithpreexistingcardiovasculardisease.However,the
benefitofinitiatingantihypertensivetherapyinpatientswithstrokewhohaveabloodpressure
lessthan140/90mmHgisuncertain.Thereisevidence,however,thatpatientswitharecent
lacunarinfarctmaybenefitfromasystolicbloodpressuregoaloflessthan130mmHg.No
specificrecommendationsexistregardingpreferredpharmacologicagentsforsecondarystroke
prevention.Therefore,thechoiceofthemostappropriateantihypertensiveagentisoftendriven
byaconsiderationofcomorbidmedicalconditions.

Allpatientswithstrokerequirecomprehensivelifestylechanges,includingimprovingphysical
activityanddietandstoppingtobaccouse.SeeMKSAP17Nephrologyforfurtherdiscussionof
managementofhypertension,MKSAP17EndocrinologyandMetabolismformanagementof
type2diabetesmellitus,andMKSAP17GeneralInternalMedicineformanagementof
dyslipidemia.Forsecondarystrokeprevention,statinsarerecommendedforpatientswitha
plasmaLDLcholesterollevelof100mg/dL(2.59mmol/L)orhigheroncetheabilitytosafely
swallowhasbeenestablished.Statinshavebeenassociatedwithanincreasedriskof
hemorrhagicstrokeandmaybecontraindicatedinpatientswithalobarICHduetoamyloid
angiopathy.However,theymostlikelyaresafeinthosewithadeepICH.RegardlessofICH
subtype,statinsareindicatedforpatientsathighriskforischemicevents.

SurgeryforSecondaryIschemicStrokePrevention

Thestrokecausewiththehighestriskofrecurrenceissymptomaticextracranialinternalcarotid
arterystenosis,witha26%riskofrecurrentstrokeat2yearsandacloseto1%perday
increasedriskofrecurrentstrokeinthefirst2weeks.Carotidrevascularization,preferably
within14daysfromtheindexevent,isindicatedfornondisablingstrokesorTIAsinpatients
withsymptomaticextracranialinternalcarotidarterystenosisintherangeof70%to99%and
canbeperformedwithendarterectomyorangioplastystenting.Thechoiceofonesurgical
approachisoftendictatedbytheriskofperioperativecomplicationsoranatomicconsiderations.

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Angioplastystentingisoftenperformedinpatientsathighriskforperiprocedural
cardiopulmonarycomplicationsandinthosewithrestenosisandpreviousradiationtherapy.In
clinicaltrials,periproceduralstrokeisreportedtobehigherwithangioplastystentingthanwith
endarterectomy,butmyocardialinfarctionismorelikelywithendarterectomy.Inpatientswith
completeocclusion,noneofthesurgicaloptions(carotidstenting,endarterectomy,orexternal
carotidtointernalcarotidbypass)reducestheriskofrecurrentstroke,andbestmedicaltherapy
(includingantiplateletagentsandstatins)isadvised.Usingangioplastystentingalsoisnot
recommendedforpatientswithsymptomaticintracranialarterystenosisbecauseofthehighrisk
ofperiproceduralstrokeandthehighefficacyofoptimalmedicaltherapy.

Usingsurgicalapproachestotreatcausesofcardioembolicstrokeisanevolvingfield.For
furtherdiscussionofsurgicalapproachestocardiacdiseaseforstrokeprevention,see
MKSAP17CardiovascularMedicine.

KeyPoints
Forsecondarystrokeprevention,statinsarerecommendedforpatientswithaplasmaLDL
cholesterollevelof100mg/dL(2.59mmol/L)orhigheroncetheabilitytosafelyswallow
hasbeenestablished.
Inpatientswithnondisablingstrokesortransientischemicattackswhohavesymptomatic
extracranialinternalcarotidarterystenosis,carotidrevascularization,preferablywithin14
daysfromtheindexevent,isindicatedforsecondarystrokeprevention.

PrognosisandRecovery
NeurologicComplications
Neurologicworseningcanoccurinpatientswithischemicstrokeduringhospitalizationasa
resultofstrokerecurrence,hemorrhageintotheareaofinfarction,seizures,orcerebraledema.
Medicalcomplications,particularlyinfections,cancauseworseningoftheneurologicdeficit.
Anypatientwithachangenotedduringneurologicexaminationrequiresrepeatneuroimagingto
establishanynewstructurallesions.Patientswithamiddlecerebralarteryinfarctioninvolving
greaterthan50%ofthearterialterritoryareathighriskformalignantcerebralinfarctionwith
associatededemaandcerebralherniation.Hemicraniectomyisassociatedwithasignificant
reductioninmortalityandseveredisability(from76%to25%inpooleddatafromthreeclinical
trials)comparedwithbestmedicaltherapyandalsoshouldbeconsideredearlyinpatientswith
malignantcerebralinfarctioniftheyexhibitimpairedalertnessorhaveatleastonepupil
reactivetolight.

KeyPoint
Patientswithamiddlecerebralarteryinfarctioninvolvinggreaterthan50%ofthearterial
territoryareathighriskformalignantcerebralinfarctionwithassociatededemaand
cerebralherniationhemicraniectomy,whichisassociatedwithasignificantreductionin
mortalityandseveredisabilitycomparedwithbestmedicaltherapy,canbeconsideredin
thesepatients.

MedicalComplicationsandStrokeUnits

RelatedQuestion

Question18

Earlymobilizationandrehabilitationtoalevelthepatientcantolerateareindicatedforall
survivorsofstroketoimproverecoveryandmitigatemedicalcomplications.Thesepatientsare
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pronetourinarytractinfectionsfromindwellingcatheters,aspirationpneumoniafrom
dysphagia,anddeepvenousthrombosis(DVT).Theprincipalcauseofstrokerelatedmortality,
thesecomplicationscanbeamelioratedbyadmissiontoastrokeunit,definedas(ideally)a
discretewardwhereamultidisciplinaryteamwithexpertiseinstrokecaresforthesepatients.
Earlymobilizationappearstobeasignificantdeterminantofthesuccessofstrokeunits,
althoughadherencetoclinicalcareprotocolsfordysphagia,DVT,andindwellingurinary
cathetersalsoareinstrumental.Severalbedsidedysphagiascreeningprotocolsareavailableand
shouldbeperformedbeforeanyoralintakeaformalevaluationwithaspeechtherapistisoften
required.Aspirationpneumoniacanbefurtherpreventedbymaintainingtheheadofthebedat
30degreesandinstitutingoralhygieneprotocols.DVTpreventionisrequiredforall
hospitalizedstrokepatientsunlesstheyarefullyambulatory.Subcutaneousunfractionatedor
lowmolecularweightheparinshouldbestartedinallpatientswithimpairedmobilityby
hospitalday1forischemicstrokeandbyhospitalday4(ifnoactivebleedingisdocumented)in
hemorrhagicstroke.Forthosepatientsathighriskforhemorrhagiccomplicationsfrom
pharmacologictherapy,pneumaticcompressionstockingsshouldbeused.Forfurtherdetails,
seeMKSAP17HematologyandOncology.Unlessrequiredforotherreasons,indwelling
urinarycathetersshouldberemoved.

KeyPoint
Earlymobilizationisasignificantdeterminantofthesuccessofstrokeunits,although
adherencetoclinicalcareprotocolsfordysphagia,deepvenousthrombosis,and
indwellingurinarycathetersalsoisinstrumental.

LongTermPrognosisandRecovery

RelatedQuestion

Question49

Themainpredictorofstrokerecoveryistheseverityoftheneurologicdeficit.Longterm
followupevaluationshowsthatpatientswithstrokeareathighriskforadditional
complications,includingfatigue,depression,andrecurrentcardiovasculardisease.Survivorsof
strokealsoareathighriskforhavingordevelopingundiagnosedobstructivesleepapnea,which
canfurthercomplicatehypertensionmanagementandisacommoncauseoffatigue
polysomnographyishelpfulindiagnosis.Depressionishighlyprevalentintheacuteand
chronicsettingafterstrokeandisoneofthestrongestmodifiablepredictorsofstrokerecovery.

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