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VertebrobasilarStrokeOverviewof
VertebrobasilarStroke
Updated:Feb10,2017
Author:VladimirKaye,MDChiefEditor:StephenKishner,MD,MHAmore...

OVERVIEWOFVERTEBROBASILARSTROKE

OverviewofVertebrobasilarStroke
Thevertebrobasilararterialsystemperfusesthemedulla,cerebellum,pons,midbrain,thalamus,
andoccipitalcortex.Occlusionoflargevesselsinthissystemusuallyleadstomajordisabilityor
death.Vertebrobasilarstrokecarriesamortalityrateofmorethan85%.Becauseofinvolvementof
thebrainstemandcerebellum,mostsurvivorshavemultisystemdysfunction(eg,quadriplegiaor
hemiplegia,ataxia,dysphagia,dysarthria,gazeabnormalities,cranialneuropathies).

However,manyvertebrobasilarlesionsarisefromsmallvesseldiseaseandarecorrespondingly
smallanddiscrete.Theclinicalcorrelatesofthesesmallerlesionsconsistofavarietyoffocal
neurologicdeficits,dependingontheirlocationwithinthebrainstem.Patientswithsmalllesions
usuallyhaveabenignprognosiswithreasonablefunctionalrecovery.

Seetheimagesbelowregardingvertebrobasilarstroke.

Lesionofthemediallongitudinalfasciculus(MLF)resultingininternuclearophthalmoplegia(INO).(Courtesyof
BCDeckerInc.)
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Illustrationofafferent(CNV)andefferent(CNVII)limbsoftheblinkreflex.(CourtesyofBCDeckerInc.)
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VisceralmotorcomponentofCNIIIandpathwaysinvolvedinpupillaryconstriction.(CourtesyofBCDecker
Inc.)
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Notethehorizontaleyemovement.Alsonoteatopographicrelationshipofthecenterforverticalgaze.
(CourtesyofBCDeckerInc.)
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Vestibularnucleiandtheirconnections.(CourtesyofBCDeckerInc.)
ViewMediaGallery

Distinctionofvertebrobasilarandhemisphericstroke
Lesionsinthevertebrobasilarsystemhavesomecharacteristicclinicalfeaturesthatdistinguish
themfromlesionsinthehemispheres,includingthefollowing[1]:

Whencranialnervesortheirnucleiareinvolved,thecorrespondingclinicalsignsare
ipsilateraltothelesionandthecorticospinalsignsarecrossed,involvingtheoppositearm
andleg
 Cerebellarsigns(eg,dysmetria,ataxia)arefrequent
Involvementoftheascendingsensorypathwaysmayaffectthespinothalamicpathwayorthe
mediallemniscus(dorsalcolumns),resultingindissociatedsensoryloss(ie,lossof1sensory
modalityononesideandpreservationofothersensorymodalitiesintheoppositelimbs)
Dysarthriaanddysphagiatypicallyarepresent
Vertigo,nausea,andvomiting,alongwithnystagmus,representinvolvementofthevestibular
system
UnilateralHornersyndromeoccurswithbrainstemlesions
Occipitallobelesionsresultinvisualfieldlossorvisuospatialdeficits
Corticaldeficits,suchasaphasiaandcognitiveimpairments,areabsent

AnatomyoftheVertebralandBasilarArteries
Thevertebralarteriesarisefromthesubclavianarteries,andastheycoursecephaladintheneck,
theypassthroughthecostotransverseforaminaofC6toC2.Theyentertheskullthroughthe
foramenmagnumandmergeatthepontomedullaryjunctiontoformthebasilarartery.Each
vertebralarteryusuallygivesofftheposteriorinferiorcerebellarartery(PICA).Atthetopofthe
pons,thebasilararterydividesinto2posteriorcerebralarteries(PCAs).

Proximaltoitsbifurcationintotheterminalbranches(PCAs),thebasilararterygivesoffthe
superiorcerebellararteriesthatsupplythelateralaspectoftheponsandmidbrain,aswellasthe
superiorsurfaceofthecerebellum.Thecerebellumissuppliedbylongcircumferentialarteries,the
PICA,andtheanteriorinferiorandsuperiorcerebellararteriesfromthebasilarartery.

ThemedullaisperfusedbythePICAandbydirect,smallerbranchesfromthevertebralarteries.
Theponsisperfusedbysmall,penetratingbranchesfromthebasilararteryanditsmajor
branches.PenetratingarteriesfromthePCAsperfusethemidbrainandthalamus,andtheoccipital
cortexisperfusedbythePCAs.

Atthebaseofthebrain,thecarotidandbasilarsystemsjointoformacircleoflarge,
communicatingarteriesknownasthecircleofWillis.Becauseofthisarrangementofcollateral
vessels,evenwhenoneofthemainarteriesisoccluded,adequateperfusionofthebrainstillmay
bepossible.[2]

PathophysiologyofVertebrobasilarStroke
Themostcommonvascularconditionaffectingthevertebrobasilarsystemisatherosclerosis,in
whichplaquescausenarrowingandocclusionofthelargevessels.

Thepathologyofsmallvesseldisease(affectingarteries50200mindiameter)isdifferentfrom
thatofatherosclerosis,becausethesmallvesselsbecomeoccludedbyaprocesscalled
lipohyalinosis,whichfrequentlyoccursinassociationwithhypertension.Occlusionsofthesesmall
vesselsleadtosmall,roundinfarctionscalledlacunes,whichmayappearassinglelesionsormay
bedistributedasmultiplelesionsscatteredwidelythroughoutthesubcortexandbrainstem.

Lipohyalinosisweakensthevesselwall,andinhypertensiveindividuals,ruptureofthearterymay
occur,resultinginafocalhemorrhage.Almostallintracerebralhemorrhagesoriginatefromthe
ruptureofthesesmall,penetratingvessels.

Becauseofthecloseanatomicalrelationshipbetweenthevertebralarteriesandthecervicalspine,
chiropracticmanipulationorneckrotationmaytraumatizethevertebralarteriesintheneck.The
damagedarteriesmayoccludewiththrombusorundergodissection.However,aretrospective
studybyWhedonetalofpatientsaged6699yearssuggestedthatthereisverylittleriskof
vertebrobasilarstrokeinassociationwithchiropracticmanipulationofthecervicalspine.[3]

Embolicocclusionofthevertebrobasilarsystemisnotcommonandusuallyisarterytoarterywith
occlusionofthebasilarartery.Donorsitesfortheembolitypicallyaretheaorticarch,the
subclavianartery,andtheoriginofthevertebralarteries.

EtiologyofVertebrobasilarStroke
Vertebrobasilarinsufficiencyorstrokemaybecausedbyanumberofmechanisms,including
thrombus,embolism,andhemorrhage(secondarytoaneurysmortrauma).Ingeneral,strokes
occurbecauseofischemicevents(8085%ofpatients)orhemorrhage(1520%ofpatients).A
numberofriskfactorsareassociatedwithstroke,suchasthefollowing:

Increasingage
Familyhistory
Race
Priorhistoryofstroke
Hypertension
Coronaryarterydisease
Diabetesmellitus
Cigarettesmoking
Heartdisease
Obesity
Physicalinactivity
Drugoralcoholabuse

AprospectivestudybyAminHanjanietalindicatedthatinpatientswithsymptomatic
atheroscleroticvertebrobasilarocclusivedisease,angiographicevidenceoflowdistalflowstatus
signalsahigherlikelihoodofsubsequentvertebrobasilarstroke.Thestudyusedlargevessel
quantitativemagneticresonanceangiographytodistinguishlowfromnormalflowinpatientswho
hadsufferedarecentvertebrobasilartransientischemicattackorstrokeandinwhomatleast50%
atheroscleroticstenosisorocclusionwaspresentinvertebraland/orbasilararteries.Among
patientswithlowdistalflowstatus,the12and24montheventfreesurvivalrateswere78%and
70%,respectively,whileinpatientswithnormalflow,therateswere96%and87%,respectively.[4]

AnotherstudybyAminHanjanietalindicatedthatinpatientswithvertebrobasilardiseaseandlow
bloodflow,strictbloodpressurecontrolmayactuallyraisethestrokerisk.Again,thestudys
patientshadrecentlysufferedavertebrobasilartransientischemicattackorstrokeandhad50%or
moreatheroscleroticstenosisorocclusionofvertebralorbasilararteries.Theinvestigatorsfound
thegreatestriskofsubsequentstroketobeinthoseindividualswithacombinationoflowblood
flowandbloodpressurebelow140/90mmHg.[5]

EpidemiologyofVertebrobasilarStroke
Thefrequency,incidence,andprevalenceofthevertebrobasilarsyndromesvary,dependingonthe
specificareaandsyndromeinvolved.Approximately8085%ofallstrokesareischemic,and20%
ofthelesionsproducingischemicstrokesoccurinthevertebrobasilarsystem.

Overall,hemorrhagecauses1520%ofstrokes.Althoughmostintracerebralhemorrhagesoccurin
theregionoftheputamenandthalamus,about7%ofallhemorrhagiclesionsinvolvethe
cerebellumintheareaofthedentatenucleus,andapproximately6%ofhemorrhagiclesions
involvethepons.

Inmostofthereportedseries,mortalitypatientswithbasilararteryocclusionhasbeenconsistently
greaterthan7580%.[6]Mostsurvivorsofbasilararteryocclusionhavesevere,persistingdisability.

ClinicalPresentationinVertebrobasilarStroke
PatientHistory
Theonsetanddurationofsymptomsinvertebrobasilarstrokedepends,inlargepart,uponthe
etiology.Patientswithbasilararterythrombosistypicallyhaveawaxingandwaningcourseof
symptoms,withasmanyas50%ofpatientsexperiencingtransientischemicattacksforseveral
daystoweekspriortotheocclusion.

Incontrast,emboliceventsaresudden,withoutprodromeorwarning,withacuteanddramatic
presentation.Commonlyreportedsymptomsassociatedwithvertebrobasilarstrokesincludethe
following[1]:

Vertigo
Nauseaandvomiting
Headache
Abnormalitiesinthelevelofconsciousness
Abnormaloculomotorsigns(eg,nystagmus,lateralgazeabnormalities,diplopia,pupillary
changes)
Ipsilateralcranialnerveweakness(eg,dysarthria,dysphagia,dysphonia,weaknessoffacial
musclesandtongue)
Sensoryloss(inthefaceandscalp)
Ataxia
Contralateralmotorweakness(eg,hemiparesis,quadriparesis)
Painandtemperatureloss
Incontinence
Visualfielddefects
Presenceofcentralpain
Abnormalswelling
Sweatinginthefaceorextremities

PhysicalExamination
Commonclinicalfindingsobservedinmorethan70%ofpatientswithvertebrobasilarstroke
includeanabnormallevelofconsciousness,aswellashemiparesisorquadriparesis,which
usuallyisasymmetric.Pupillaryabnormalitiesandoculomotorsignsarecommon,andbulbar
manifestations,suchasfacialweakness,dysphonia,dysarthria,anddysphagia,occurinmorethan
40%ofpatients.

Oculomotorsignsusuallyreflecttheinvolvementoftheabducensnucleusthehorizontalgaze
centerlocatedinthepontineparamedianreticularformation(PPRF),contiguoustotheabducens
nucleusand/orthemediallongitudinalfasciculus(MLF).Lesionstothesestructuresresultin
ipsilaterallateralgazeorconjugategazepalsy.

Seetheimagesbelow.
Lesionofthemediallongitudinalfasciculus(MLF)resultingininternuclearophthalmoplegia(INO).(Courtesyof
BCDeckerInc.)
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Centerforverticalgazeandpathwaysinvolvedinverticaleyemovement(CourtesyofCranialNerves
AnatomyandClinicalComments.BCDeckerIncToronto.1988)
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Illustrationofafferent(CNV)andefferent(CNVII)limbsoftheblinkreflex.(CourtesyofBCDeckerInc.)
ViewMediaGallery

Vestibularreflexillustratinghorizontaleyemovementsonly.(CourtesyofBCDeckerInc.)
ViewMediaGallery

VisceralmotorcomponentofCNIIIandpathwaysinvolvedinpupillaryconstriction.(CourtesyofBCDecker
Inc.)
ViewMediaGallery

Ocularbobbingisdescribedasabrisk,downwardmovementoftheeyeballwithasubsequent
returntotheprimaryposition.Thisdeficitlocalizesthelesiontothepons.Otherreportedsignsof
pontineischemiaincludeataxiaandtremorassociatedwithmildhemiparesis.Thesignsdescribed
canoccurindifferentcombinations,presentingadiagnosticchallengeinlesionlocalization.
Certainconstellationsoffindingsmayserveascluestothelocationofthelesion,includingthe
followingexamples:

Midbrainsyndromescranialnerve(CN)IIIlesionandverticalgazepalsy
PontinesyndromesCNVIlesion,horizontalgazepalsy,andVIInervepalsy
Medullarysyndromesipsilateralfacialpainandtemperatureloss,Hornersyndrome,
ipsilateralataxia,contralaterallossofpainandtemperaturesensation,andipsilateral
paralysisofthetongue,softpalate,vocalcord,orsternocleidomastoid[SCM]muscle
Posteriorcerebralarterycontralateralhemianopiawithmacularsparing

Complications
Potentialcomplicationsofvertebrobasilarstrokeincludethefollowing:

Aspirationpneumonia
Deepvenousthrombosis
Pulmonaryembolism
Myocardialinfarction

AliteraturereviewbyYuanetalindicatedthatthetopriskfactorforlunginfectioninstrokepatients
ismultiplevertebrobasilarstrokes,followedby,amongtheothertop5riskfactors,aNational
InstitutesofHealthStrokeScalescoreofover15,theuseofmechanicalventilation,theuseof
nasogastrictubes,anddysphagia.[7]

VertebrobasilarArteryStrokeSyndromes
Avarietyofspecificneurologicsyndromes[8,9]havebeendescribedinvertebrobasilarartery
stroke,basedonconstellationsoffindings.Someexamplesareasfollows:

Lateralmedullary(Wallenberg)syndrome
Medialmedullary(Dejerine)syndrome
Cerebellarinfarction
Lockedinsyndrome
Topofthebasilarsyndrome
Internuclearophthalmoplegia
Oneandahalfsyndrome
Ventralpontine(MillardGubler)syndrome
Upperdorsalpontine(RaymondCestan)syndrome
Upperdorsalpontine(RaymondCestan)syndrome
Lowerdorsalpontine(Foville)syndrome
Ventralmidbrain(Weber)syndrome
Dorsalmidbrain(Benedikt)syndrome
PosteriorCerebralArteryocclusion

Lateralmedullary(Wallenberg)syndrome

Thissyndromeismostoftenduetovertebralarteryocclusionor,lesscommonly,toposterior
inferiorcerebellarartery(PICA)occlusion.Patientspresentwithnausea,vomiting,andvertigofrom
involvementofthevestibularsystem.

Ipsilateralclinicalfeaturesincludethefollowing:

Ataxiaanddysmetria,duetodamagetotheinferiorcerebellarpeduncleandcerebellum
Hornersyndrome(eg,ptosis,miosis,hypohidrosisoranhidrosis,enophthalmos),dueto
damagetodescendingsympatheticfibers
Facialpainandtemperatureloss
Reducedcornealreflex,fromdamagetothedescendingspinaltractandnucleusofCNV
 Nystagmus
Hypoacusis(cochlearnucleus)
Dysarthria
Dysphagia
Paralysisofthepharynx,palate,andvocalcord
Lossoftastefromtheposteriorthirdofthetongue(nucleiorfibersofCNIXandX)

Contralateralfindingsincludethelossofpainandtemperaturesenseinthebodyandextremities,
indicatinginvolvementofthelateralspinothalamictract.Otherfindingsincludetachycardiaand
dyspnea(dorsalnucleusofCNX)andpalatalmyoclonus,arhythmicinvoluntaryjerkingmovement
ofthesoftpalate,pharyngealmuscles,anddiaphragm.Palatalmyoclonussometimesfollows
infarctionofthedentatenucleusofthecerebellumandinferioroliva.

Theprognosisofpatientswiththelateralmedullarysyndromeusuallyisquitegoodforfunctional
outcomehowever,patientsmaydieintheacutephasefromaspirationpneumonia,anddeathhas
beenreportedfromsleepapneainanumberofcases.

Medialmedullary(Dejerine)syndrome
Thissyndromeisanuncommonlesionresultingfromocclusionofavertebralarteryoritsbranchto
theanteriorspinalarteryitinvolvesthepyramid,themediallemniscus,and,sometimes,the
hypoglossalnerve.

Theclinicalfeaturesincludeipsilateralparesisofthetonguewithdeviationtowardthelesion(lower
motorneuronlesionofCNXII),contralateralhemiplegiawithsparingoftheface(corticospinal
tract),andlossofipsilateralvibrationandproprioception(mediallemniscus).(Seetheimage
below.)

LMNLesionofthehypoglossalnerveproducingtonguedeviationtothesideofthelesion.(CourtesyofBC
DeckerInc.)
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Cerebellarinfarction

Astrokeinvolvingthecerebellummayresultinalackofcoordination,clumsiness,intentiontremor,
ataxia,dysarthria,scanningspeech,andevendifficultieswithmemoryandmotorplanning.Early
diagnosisofcerebellarinfarctionsisimportant,becauseswellingmaycausebrainstem
compressionorhydrocephalus.

Lockedinsyndrome
Thisdramaticclinicalsyndromeoccurswhenthereisaninfarctionoftheupperventralpons.
Lockedinsyndromecanresultfromocclusionoftheproximalandmiddlesegmentsofthebasilar
arteryorfromhemorrhageinvolvingthatregion.Itcanalsobecausedbytrauma,centralpontine
myelinolysis,encephalitis,oratumor.

Bilateralventralpontinelesionsinvolvingcorticospinalandcorticobulbartractsleadtoquadriplegia.
Thepatientisunabletospeak,toproducefacialmovement(damagetothecorticobulbartracts),or
tolooktoeitherside(horizontaleyemovementisimpairedduetoalesionofbilateralCNVI
nuclei).Becausethetegmentumoftheponsisspared,thepatient'sconsciousnessispreserved,
withthepatientfullyawake,sensate,andaware.Theonlymovementspreservedareverticaleye
movementsandblinking.Thepatientisparalyzedcompletelyandcommunicatesonlybyblinking.
Somerecoveryoffacialmusclemovementandhorizontalgazemayoccurwithtimeorinan
incompleteformofthissyndrome.

Comamayoccurwithbilateralinvolvementofthepontinetegmentumorwithlesionsofthe
midbrainreticularformation.Comagenerallyisassociatedwithoculomotorabnormalities,and
motorabnormalitiesmaybepresent.Acomatosepatientisunresponsive,andthecomamaybe
prolongedwhenitisduetobasilararteryocclusion.Sleepwakecyclesareabsentinpatientswith
coma.

Topofthebasilarsyndrome

Thissyndromeisthemanifestationofupperbrainstemanddiencephalicischemiacausedby
occlusionoftherostralbasilararterytheocclusionusuallyresultsfromanembolism.[10]Varying
degreesofinvolvementofthemidbrain,thalamus,andportionsofthetemporalandoccipitallobes
mayoccurandcanproduceseveredisability.

Patientspresentwithsuddenchangesinthelevelofconsciousness,confusion,amnesia,and
visualsymptoms(eg,hemianopia,corticalblindness,abnormalcolorvision/colordysnomia).These
patientscanalsodemonstrateoculomotorabnormalities,mostcommonlyoftheverticalgaze,such
asgazepalsy,skewdeviation,convergencespasmresultinginpseudoabducenspalsy,or
convergenceretractionnystagmus.

CNIIIpalsyandpupillaryabnormalities,includingsmallpupilswithdecreasedlightreactivity
(diencephalic),large/midpositionandfixedpupils(midbrain),andectopicorovalpupils,alsoare
frequent.

Otherabnormalitiesincludevaryingdegreesofweakness,sensorydeficits,orposturing.

Internuclearophthalmoplegia
Clinically,internuclearophthalmoplegia(INO)isahorizontalgazepalsyitresultsfromabrainstem
lesionaffectingtheMLFbetweenthenucleiofCNVIandIII,mostcommonlyinthepons.(Seethe
imagebelow.)
Lesionofthemediallongitudinalfasciculus(MLF)resultingininternuclearophthalmoplegia(INO).(Courtesyof
BCDeckerInc.)
ViewMediaGallery

WhenapatientwithalesionintherightMLFattemptstolooktohis/herleft(ie,awayfromthe
involvedside),he/sheshowsnoadductionoftherighteyeandfullabductionofthelefteyewiththe
endpointabductionnystagmus.

Bythesamelogic,inthecaseofbilateralINO,thereisnoadductiontoeithersidewithnystagmus
oftheabductingeyeinbothdirections.Convergenceispreserved,becausethenucleiofCNIII
andperipheralinnervationofthemedialrectimusclesareintact.

BecausehorizontalgazerequirescoordinatedactivityoftheipsilateralCNIIIandcontralateralCN
VI(relativetothelesion),disruptionofthecommunicationpathway(ie,theMLF)betweenthe
nucleiofCNIII(inthemidbrain)andCNVI(inthepons)resultsintheinabilityoftheeyeipsilateral
tothelesiontoadductandthecontralateraleyetoexhibitabductionnystagmuswhenlookingaway
fromtheinvolvedside.

Inelderlypatients,INOiscausedmostoftenbyocclusionofthebasilararteryoritsparamedian
branches.Inyoungeradults,itmayoccurduetomultiplesclerosis(MS),commonlywithbilateral
involvement.

Oneandahalfsyndrome
ThissyndromeiscausedbyalesionaffectingthePPRFandMLFsimultaneously,resultingin
ipsilateralconjugategazepalsyandINO[11]Apatientwiththissyndromeiscompletelyunableto
movetheipsilateraleye,andisableonlytoabductthecontralateraleye,withresultingnystagmus
theoneinthesyndromenamereferstotheformer,andthehalftothelatter.

ThepatientwithalesionintheipsilateralPPRForabducensnucleusandMLFconnectingtothe
contralateralCNVIexhibitshorizontalgazepalsywhenlookingtowardthesideofthelesionand
exhibitsINOwhenlookingawayfromthesideofthelesion.Associatedfeaturesmayinclude
verticalnystagmus,exotropiaofthecontralateraleye,andskewdeviation.Verticalgazeand
convergencegenerallyarepreserved.

Ventralpontine(MillardGubler)syndrome
Thissyndromeoccursafterparamedianinfarctionintheponsandresultsinipsilaterallateral
rectuspalsy(CNVI)withdiplopia,completefacialparesis(unilateralCNVIIpalsy),and
contralateralhemiparesis/hemiplegia(corticospinaltractinvolvement)withsparingoftheface.

Upperdorsalpontine(RaymondCestan)syndrome
Thissyndromeisduetoobstructionofflowinthelongcircumferentialbranchesofthebasilar
artery.Thisocclusionresultsinipsilateralataxiaandcoarseintentiontremor(indicating
involvementofthesuperiorandmiddlecerebellarpeduncles),weaknessofmasticationand
sensorylossintheface(suggestingsensoryandmotortrigeminalnucleiandtracts),and
contralaterallossofallsensorymodalities(duetodamagetomediallemniscusandspinothalamic
tract)withorwithoutfacialweaknessandhemiparesis(corticospinaltract).

Horizontalgazepalsyalsomayoccur.

Lowerdorsalpontine(Foville)syndrome

Thissyndromemayresultfromlesionstothedorsaltegmentumofthelowerpons.Thepatient
exhibitsipsilateralparesisofthewholeface(nucleusandfibersofCNVII),horizontalgazepalsy
ontheipsilateralside(ie,PPRFwithorwithoutCNVInucleus),andcontralateralhemiplegia
(corticospinaltract)withsparingoftheface.

Ventralmidbrain(Weber)syndrome
Webersyndromeoccurswithanocclusionofthemedianand/orparamedianperforatingbranches
ofthebasilarartery.TypicalclinicalfindingsincludeipsilateralCNIIIpalsy,ptosis,andmydriasis
(ie,damagetoparasympatheticfibersofCNIII)withcontralateralhemiplegia.Weaknessofthe
lowerface(corticospinalandcorticobulbartracts)maybenoted.

Dorsalmidbrain(Benedikt)syndrome

Thissyndromeisduetoalesioninthemidbraintegmentumresultingfromocclusionof
paramedianbranchesofthebasilarartery,thePCA,orboth.

Thepatientdemonstratesipsilateraloculomotorpalsy,ptosis,andmydriasis(asinWeber
syndrome),alongwiththecontralateralinvoluntarymovements,suchasthoseofintentiontremor,
ataxia,orchorea(duetotheinvolvementoftherednucleus).

Posteriorcerebralarteryocclusion

Themostcommonfindingisoccipitallobeinfarctionleadingtocontralateralhemianopiawith
macularsparing.ClinicalsymptomsassociatedwithocclusionofthePCAvarydependingonthe
locationoftheocclusionandmayincludethethalamicsyndrome,thalamicperforatesyndrome,
Webersyndrome,corticalblindness,colorblindness,failuretoseetoandfromovements,verbal
dyslexia,andhallucinations.

DiagnosticConsiderations
Thedifferentialdiagnosisofvertebrobasilarstrokeincludesthefollowing:

Centralpontinemyelinolysis
Metastaticdiseaseofthebrain
Subarachnoidhemorrhage
Basilarmeningitis
Basilarmigraine
Cerebellopontineangletumors
 Supratentorialhemisphericmasslesionswithmasseffect,herniation,andbrainstem
compression

LaboratoryStudiesforVertebrobasilarArteryStroke
Thelaboratoryworkupshouldincludethefollowing:

Completebloodcount(CBC)
Electrolytes
Bloodureanitrogen(BUN)andcreatinine
Prothrombintimeandactivatedpartialthromboplastintime(aPTT)
Cholesterollevel
Lipidprofile

Patientswhoareyoungerthan45yearsorwhohavenoevidenceofatherosclerosisshouldbe
investigatedforthepresenceofhypercoagulablestates,suchasthefollowing:

Lupusanticoagulantandanticardiolipinantibodies
ProteinC,proteinS,andantithrombinIIIdeficiencies
FactorVLeidenmutation

Creatinekinase,cardiacisoenzymes,andtroponinlevelshouldbetestedinthefollowingpersons:

Allpatientswithsuggestivesymptoms(eg,chestpain)
Patientswithevidenceofischemicchangesintheelectrocardiogram(ECGbecauseofthe
highincidenceofconcomitantcoronaryarterydisease)[12]

ComputedTomography
CTscanningusuallyisthefirstimagingstudyperformed,becauseithasasensitivityofmorethan
95%whenusedintheidentificationintraaxialorextraaxialhemorrhagewithinthefirst24hoursof
onset.[13,14]Otherhelpfulfindingsincludeevidenceofinfarctsinthethalamusoroccipitallobes
(implicatinginvolvementoftherostralbasilarartery)andevidencethatahyperdensebasilarartery
ispresent(suggestingaprobableocclusion).[15,16]

SpiralCTangiographyisusedfurthertoidentifyoccludedanddolichoectaticvessels.[17,18]

ThedisadvantagesofCTscanningincludealowsensitivityforearlyischemiaandthepresenceof
significantartifactscausedbythebonystructuressurroundingthebrainstemandcerebellum.

MagneticResonanceImaging
MRIismoresensitivethanCTintheidentificationofischemia(sincebonedoesnotdegradethe
image).Newertechniques,includingflowsuppressionandtheproductionofdiffusionweightedand
perfusionweightedimages,makeMRIaverypowerfultoolfortheexclusionofintraparenchymal
hemorrhageoredemaandfortheidentificationofearlyandpotentiallyreversibleischemia.[13,14,
19,20,21]

MRIandmagneticresonanceangiography(MRA)areveryhelpfulinfindingoccultlesions,suchas
demyelinatingplaques,tumors,vertebrobasilardolichoectasia,ordissection.[22,23,24]MRAhasa
sensitivityofupto97%andaspecificityofupto98%whenusedtoidentifyvertebrobasilar
occlusion.

AlimitationofMRAisitstendencytooverestimatethedegreeofstenosis.Thisoverestimation
occursbecausetheproductionofavessel'simageinMRAisabasedonaflowrelated
phenomenonhence,thepresenceofseverestenosiswithsignificantflowcompromisemayresult
inpoorvisualizationofavesselandcausetheMRAimagetoresemblevascularocclusion.

Angiography
Whiletheroleofcerebral(catheter)angiographyhaschangedduetotheavailabilityofnoninvasive
imagingmodalities(eg,MRI,MRA,TCD),itstillisconsideredthecriterionstandardforimaging.
Cathetercerebralangiographyisperformedinthefollowingcircumstances:

ThepatienthasanabsolutecontraindicationtoMRA(eg,apacemaker,metallicimplant)
Thequalityofnoninvasivestudiesisnotsatisfactory
Theresultsofnoninvasivestudiesdonotexplaintheclinicalfindings

AngiographyshouldbeconsideredafirstlinediagnostictestafteraCTscan,onceithasbeen
decidedthatrecanalizationwiththrombolysisshouldbecompleted.Themostimportantgoalofthe
workupistoestablishthetypeofvascularlesionandthemechanismofthestroke.

Ultrasonography
TranscranialDoppler(TCD)isusedintheevaluationofcerebrovasculardisease,butitoftenis
inaccurate.Absenceofsignalinaninitialexaminationdoesnotnecessarilymeanocclusion.

TCDishelpfulforpurposesoffollowuponceaninitialevaluationhasdemonstratedthelesion.
TCDhasasensitivityof72%andaspecificityof94%inpatientswithbasilararterydisease.[25]

Electrocardiography
Electrocardiographyshouldbeperformedinallpatientsoninitialevaluation.Allpatientsshouldbe
monitoredcontinuouslyforthefirstfewdays.IschemicchangesintheECGshouldbeinvestigated
furtherwithassaysofserumcreatinekinase,cardiacisoenzymes,andtroponin,forreasonsthat
includethefollowing:

Upto20%ofpatientswithacutestrokehaveanarrhythmia
Myocardialinfarctionoccursin23%ofpatients
Thepresenceofarrhythmias(eg,atrialfibrillation)hasanimpactonlongtermpatient
managementrelatedtostrokeprevention

Echocardiography
Echocardiography[26]shouldbeconsideredinthefollowingpatients:

Thoseyoungerthan45years
Thosewithexplainedbasilararteryocclusion

Findingsthatmayaffectmanagementincludevalvulardisorders,vegetations,intramuralor
extramuralthrombi,ventricularaneurisms,cardiactumors(myxoma),righttoleftshunts,andpoor
ejectionfraction.

TreatmentofAcuteVertebrobasilarArteryStroke
Ideally,allpatientswhohavesufferedavertebrobasilarstrokeshouldbeadmittedtoaunit
specializinginthecareofstrokepatients.Admissiontoaneurologicintensivecareunit(ICU)is
indicatedforpatientswhoarecandidatesforinterventionaltherapies(eg,thrombolysis)orwho
haveanyofthefollowing[27]:
 Unstableorfluctuatingneurologicsymptoms
Decreasedlevelofconsciousness
Hemodynamicinstability
Activecardiacorrespiratoryproblems

Hemodynamicmanagement
Hemodynamicmanagementshouldbeaimedatminimizingtheischemicinjury.Cerebralischemia
impairsthebrainsabilitytoautoregulateitscirculationthroughvasoconstrictionandvasodilatation.
Therefore,underischemicconditions,thecerebralbloodflowbecomesbloodpressuredependent.
[28] Anincreaseinthemeanarterialpressure(MAP)resultsinvasoconstriction.Thisresponse
limitstheperfusionpressureandthebloodvolume.AdecreaseintheMAPresultsin
vasodilatation.

Innormotensivepatients,thelimitsofautoregulationarewithintherangeof50150mmHgofthe
MAP.Inchronichypertensivepatients,thecurveofautoregulationisshiftedupward.Inthepatients
withseverecerebralvascularocclusivedisease,theMAPandthecerebralperfusionpressure
(CPP)becomecriticalinmaintainingthecerebralbloodflow.CPPisequaltoMAPlessintracranial
pressure(ICP)(ie,CPP=MAPICP).Therefore,overzealoustreatmentofhypertensionshouldbe
avoided,becauseitcandecreasethecerebralperfusionpressureandexacerbatetheongoing
ischemia.

Noexistinginformationfromrandomizedtrialsindicateswhethertreatinghypertensionisbetter
thannottreatingit.Basedonevidencefromexperimentalmodelsandondatafromclinical
experience,hypertensionshouldnotbetreatedunlessthereisevidenceofendorgandamage,
suchashypertensiveencephalopathy,unstableangina,acutemyocardialinfarction,heartfailure,
oracuterenalfailure.

Hypertensionshouldbetreatedwhenthediastolicbloodpressureisgreaterthan120mmHgor
whenthesystolicbloodpressureisover200mmHg.Otherwise,whenthrombolysisisastrong
consideration,thetreatmentparametersbecome110mmHgormorefordiastolicbloodpressure
orgreaterthan180mmHgforsystolicbloodpressure.

Commonlyusedantihypertensivesarelabetalolandnitroprusside.Whendiastolicbloodpressure
isgreaterthan140mmHg,nitroprussideisthepreferreddrug,providedthatnocontraindications
exist.

PatientswithhypotensionneedtobetreatedtooptimizetheMAPand,consequently,theblood
pressuredependentcerebralbloodflow.Maximaleffortshouldbemadetomaintainanormal
intravascularvolumeusingisotonicsolutions.IftheMAPcontinuestobelowdespitefluid
management,vasopressors,suchasdopamine,dobutamine,andphenylephrine,shouldbeused.

Inpatientswithunknownintravascularvolumestatusorthosewithcomplications,suchas
congestiveheartfailureandpulmonaryedema,apulmonaryarterycathetershouldbeplacedto
monitorthecentralvenouspressureandthepulmonarycapillarywedgepressure.Thisapproach
wouldimprovemonitoringoftheintravascularvolumetoavoidoverload.

Respiratorymanagement

Earlyassessmentandmanagementoftheairwayarecriticalduetothefrequentinvolvementof
lowercranialnervesandtheimpairmentofconsciousnessinpatientswithbrainstemischemia.
Assessmentoftherespiratorydrive,gagreflex,andabilitytohandlesecretionswithaforceful
coughalsoisofgreatimportance.

Endotrachealintubationmaybeconsideredinpatientswithadecreasedlevelofconsciousness
andaGlasgowcomascoreoflessthan8.Ofthemechanicalventilationmodes,pressuresupport
ventilation(PSV)andsynchronizedintermittentmandatoryventilationareusedmostoften.For
patientswithgoodrespiratorydrive,themostcomfortablemodeisPSV.Inthismode,theventilator
doesnotdeliverasetofbreathsbutprovidesenoughpressuresupporttomaintainthedesired
tidalvolume,usuallyintherangeof58mL/kg.Mostpatientswithnopulmonarycomorbidities
reachthisgoalwithaPSVof510.

Forpatientswithpoorrespiratorydrive,synchronizedintermittentmandatoryventilationmaybea
bettermode.Thisformofventilationdeliversasetnumberofbreathswithasettidalvolume,which
issynchronizedwiththepatient'sinspiratoryeffortwhileallowingthepatienttotakeextrabreaths.
AddingPSVduringtheextrabreathscanminimizethepatient'srespiratoryeffortwhentaking
them.

Sedationandparalysisshouldbeavoided,becausetheymayobscuretheneurologicassessment.
Circumstancesmayexistthatrequiretheuseofsedationandparalysis(eg,neurogenic
hyperventilation)toavoidhypocarbiaandworseningoftheischemicprocess.

Thrombolysis
In1996,TheUSFoodandDrugAdministration(FDA)approvedtissueplasminogenactivator(tPA)
forthetreatmentofacuteischemicstrokewithinthefirst3hoursofonset.[13]Approvalwasbased
ondatafromtheNationalInstituteofNeurologicalDisordersandStroketrial,whichshowedthata
highernumberoftreatedversusuntreatedpatientshadminimaldeficitandminimalornodisability.

However,thistrialdidnotincludepatientsinstupororcoma,andthatcriterionprobablyexcluded
patientswhosufferedabasilararteryocclusion.Moreover,thetrialdidnotstudythevascular
anatomysystematicallyinallpatients.Fromexperimentalevidenceandthrombolytictrials,itis
apparentthatrecanalizationimprovesoutcome.[6,29,30]

In2009,theAmericanHeartAssociation/AmericanStrokeAssociation(AHA/ASA)publisheda
scienceadvisoryrecommendingthatthetimewindowfortPAadministrationbeincreasedto4.5
hoursafterastroke,althoughthischangehasnotbeenapprovedbytheFDA.[31]Research
indicatesthattPAiseffectiveinpatientsevenwhenadministeredwithinthe3to4.5hourwindow,
[32,33,34] buttheAHA/ASAstatedthat,despiteitsrecommendation,theeffectivenessoftPA
administrationincomparisonwithothertreatmentsforthrombosis,withinthattimeperiod,isnotyet
known.

Theeligibilitycriteriafortreatmentbetween3and4.5hoursaresimilartothoseemployedfor
treatmentpriorto3hours,asestablishedintheAHA/ASA's2007guidelines,[35]butwiththe
exclusioncriteriaexpandedtoincludeanyofthefollowingpatientcharacteristics:

Agegreaterthan80years
Useoforalanticoagulants
BaselineNationalInstitutesofHealth(NIH)StrokeScalescore>25
Ahistoryofbothstrokeanddiabetes

Intheearly1980s,Nenciandcolleaguesreportedthefirst4casesoflocalthrombolysisfor
vertebrobasilarocclusion,establishingatrendtotreatpatientswithintraarterialthrombolysis.[13,
36] Todate,severalcaseserieshavebeenpublished.Theaveragetimetotreatmenthasranged
from848hours.Overallmortalityhasdecreasedfrom4675%to2660%.Thepatient'scondition
atpresentationappearstobethemajorprognosticfactorpatientswithquadriplegiaand/orcoma
havedemonstratedtheleastfavorableoutcomes.Despitetheaboveefforts,intraarterial
thrombolysisforvertebrobasilarocclusionhasnotbeenstudiedsystematicallyinrandomized,
controlledtrials.

Ofthedifferentagentscurrentlyusedforthrombolysis(urokinase,prourokinase,streptokinase,
tPA),prourokinaseandtPAseemtohavemoreselectivityforthrombi.Streptokinasehasnotbeen
usedforstrokesincethemulticenterEuropeanandAustraliantrialsdocumentedagreater
mortalityinthetreatedpatients.Becauseofconcernswithitsproduction,urokinaseisnotcurrently
availableintheUnitedStates.
Prourokinasewastestedinaprospective,randomizedfashion,includingonlypatientswithmiddle
cerebralarterystemocclusion.Resultsshowedabetteroutcomeintreatedpatients,but
prourokinasehasnotbeenapprovedforuseinacutestroke.

Atthistime,theonlyviableoptionforthrombolysisintheUnitedStatescontinuestobetPA.This
drughasbeenstudiedprospectivelyintrialsinvolvingcombinedintravenousandintraarterial
therapy,indosesof0.3mg/kg,withamaximumof1020mg.Limitedexperiencewiththeuseof
GPIIb/IIIainhibitors,suchasabciximab,toblocktheplateletfunctionandrethrombosishasshown
anoverallreocclusionrateofapproximately30%.

Anticoagulation
Anticoagulationtherapywithheparinhasbeenused,butthereisnoevidencethatithasanimpact
onoutcome.Resultsfromatrialusinglowmolecularweightheparinintravenouslyinpatientswith
acutestroke,althoughnegativeoverall,didshowabetteroutcomeat7daysforpatientswithlarge
vesseldisease.

Angioplasty

Angioplastyhasbeenperformedtotreatpatientswithatheroscleroticbasilararterystenosis.The
useofangioplastyisbasedonthetendencyofthrombosistooccurinstenosedarterialsegments.
Reportsdescribeangioplastyperformedinpatientswithacutevertebrobasilarocclusion,aswellas
electively.Thepublishedcaseseriesreportamorbidityrateof016%andamortalityrateofupto
33%however,theroleofangioplastyinthetreatmentofvertebrobasilarocclusionisnotwell
defined.

AstudybyHatanoandTsukaharaindicatedthatendovasculartreatmentwithballoonangioplasty
canbesafeandeffectiveinselectedpatientswithintracranialvertebrobasilararterystenosis.In
thereport,44patientswiththeconditionwhofitcertaincriteriaie,thosewhoweremedically
refractoryandsymptomatic,withlesionsbelow15mminlengthand,asrevealedonangiography,
greaterthan60%stenosisunderwentballoonangioplastyunderlocalanesthesia.Stent
placementwasalsoused,ifdilationwasinsufficientorifdissectionorrestenosisoccurred.By30
daysaftertreatment,thestrokeanddeathratewasjust2.3%.[37]

Withinsixmonthsfollowingtreatment,restenosishadoccurredinninepatients,withfourofthem
beingsymptomatic,butsubsequentballoonangioplastyorstentingsuccessfullyrelievedthe
probleminthesymptomaticpatients.HatanoandTsukaharacautionedthatalthoughtheirstudy
indicatesthatendovasculartherapycaneffectivelytreatintracranialvertebrobasilararterystenosis,
clinicalandradiologicfollowupisnecessaryowingtothepossibilityofrestenosis.[37]

OtherTreatment
Otheraspectsoftreatmentforvertebrobasilarstrokeshouldincludethefollowing:

Aggressivepulmonarytoilettopreventmucouscongestionandpneumonia
Preventionofaspirationpneumonitis
Earlyestablishmentofbowelandbladderprograms
Monitoringofskinandallindwellingcathetersforsignsofinfection
Controlofbodytemperature(fevermayworsentheoutcomeinstrokepatients)
Tightbloodglucosecontrol
HeelprotectorsorL'NardMultiPodusbootswithregularskininspectionfor
breakdown/decubitus
Deepveinthrombosisprophylaxiswithsequentialcompressiondevicesorarteriovenous
pumpsand/oranticoagulants(eg,lowmolecularweightheparinadjusteddose,
subcutaneousheparinwarfarin),providedthattherearenocontraindications
AstudybyAlexanderetalindicatedthatsymptomaticvertebrobasilaratherosclerosiscanbesafely
andeffectivelytreatedwithendovasculartherapy.Thestudyinvolvedinterventionsfor136lesions
(122patients),including13treatmentsforacutestroke.Theinvestigatorsfoundthattreatmentwas
technicallysuccessfulfor123ofthelesions(90.4%),withbettertechnicalresultsachievedincases
ofextracranialdisease.Patientswithnonprogressivesymptomsinthesubacuteperiodand
individualswhounderwentstatintreatmenthadbetterclinicalresults.[38]

Furtherinpatientcare
Mostpatientswithvertebrobasilarstrokehaveasignificantdegreeofdisability,duetoinvolvement
ofthebrainstemandcerebellum,withresultantmultisystemdysfunction(eg,quadriplegiaor
hemiplegia,ataxia,dysphagia,dysarthria,gazeabnormalities,cranialneuropathies).Theyoften
requireongoing,acuterehabilitation,withattentionpaidtospecificpatientissuesandthe
formulationofshorttermandlongtermcareplans.Therehabilitationandplanningareperformed
bestinamultidisciplinaryandinterdisciplinarysetting.

RehabilitationAfterVertebrobasilarArteryStroke
Rehabilitationserviceshavebeenshowntoplayacriticalroleinrecoveryfromacutestroke.
Physiciansandnursesplaycrucialrolesontherehabilitationteamnursesoftenarethefirstto
suggestinitiationoftherapyservices,becausetheyhavethemostextensiveinvolvementwiththe
patient.Priortoadiscussionofthespecifictherapydisciplines,addressnursingissuesinthecare
ofpatientswithvertebrobasilarstroke.

Nursingissues

Awidevariationinsymptomsmaybeseenwithstroke,dependingontheseverityofthebrain
damage.Initialnursinginterventioninvolvesmaintainingskinintegrity,establishingaboweland
bladderprogram,maintainingnutrition,andensuringtheperson'ssafetyfrominjury.

Otherimportantnursingissuesincludecommunicationwiththetreatingclinicianinordertoinitiate
therapyservicesfortheassessmentofambulation,transfers,swallowingfunction,andthe
performanceofactivitiesofdailyliving(ADL).Insomepatients,theseverityofthedeficitsmakes
ambulationimpossiblehowever,patientsshouldbemobilizedoutofbedandshouldbeactively
involvedinphysicalandoccupationaltherapy.

Positioninginbedandinachairassuresthepatient'scomfortandpreventscomplicationsfrom
skinbreakdown.Iftheupperextremityisflaccidorparetic,positioningiscriticaltothepreventionof
shouldersubluxationandpainfromshoulderhandsyndrome.

Nursingstaffalwaysshouldinvolvefamilymembersinthecareofapersonwhohassustaineda
stroke.Thepatientandfamilymembersmaybeunfamiliarwithstrokeanditseffects.Education
mustbeprovidedtomakethepatientandhis/herfamilymembersawareoftheimportanceof
continuingwithactivities,ofappropriateprecautions,andofcontinuingtherapyupondischargeto
home.

Somepatientshavefluctuatingsymptomsandsigns,whichoftenarerelatedtoposition.Because
ofthispossibility,precautionsarenecessarywithactivitiesthatcanbeundertakenuntilthe
symptomshavestabilized.

Physicaltherapy(PT)andoccupationaltherapy(OT)shouldbeinitiatedsoonafteradmission,
dependingontheconditionofthepatient.Oncethesymptomshavestabilized,patientsshouldbe
mobilizedoutofbed,whichwillallowthemtoparticipateinfullPTandOTactivities.

Physicaltherapy
Thephysicaltherapistisresponsibleforretrainingofgrossmotorskills,suchasgait,balance,
transfers,bedmobility,andwheelchairmobility.Thephysicaloroccupationaltherapistmaybe
involvedwithassessingthepatientfortheproperwheelchairandseatingsystem.

ThephysicaltherapistalsodevelopsaPTprogramandinstructsthepatientingeneral
strengtheningandrangeofmotion.Trainingofthepatientandfamilymembersintheuseoflower
extremityorthoticsmaybenecessarytoprovideforfunctionalmobility.

Vestibularevaluationandtrainingareveryimportant,duetoahighprevalenceofvestibularand
cerebellarinvolvementinvertebrobasilarstrokes.Patientsoftenneedextensivebalanceandgait
training.Evaluationalwaysshouldbeginwithadetailedandfocusedhistory.Apremorbid
vestibularstatusdeterminationisofgreatimportance,becausedizzinessisthethirdmostfrequent
complaintduringphysicianvisitsfrompatientsaged65yearsandthemostfrequentcomplaintfrom
patientsaged75yearsandolder.

Furtherclinicaltestingmayincludethefollowing:

OculomotorexaminationVisualtracking,convergence/divergence,saccadesandsmooth
pursuitmovement,spontaneousandgazeevokednystagmus,static/dynamicvisualacuity,
andvestibuloocularreflex(VOR)
PositionaltestingHallpikeDixmaneuver
StaticbalanceRomberg,sharpenedRomberg,andsinglelegstance(eachtestis
performedonevenandunevensurfaces,witheyesopenandclosed)
DynamicbalanceThoroughgaitassessment,includingheadturning,tandemgait,retro
walking,negotiatingobstacles,andturning

Anexercisebasedapproachhasbeensuccessfulinthetreatmentofvestibulardisorders,dueto
severalpossiblemechanisms.Theseincludeadaptation,substitution,habituation,and
repositioning.

Withadaptationbythecentralvestibularsystem,thebrainmodulatesthegainofthevestibular
response,attemptingtocorrectforaretinalslip(errorsignal)causedbythedecreasedgainofthe
VOR.TheVORtrainingstrategyincludesfocusingonastationaryormovingtargetwhilerotating
thehead,resultinginaretinalslipthatfacilitatesadaptation.

Substitutionforthelossoffunctionbytheremainingintactvisualandsomatosensorysystemsis
usedintreatingpatientswithbilateralvestibularlesions(completeorpartiallossofbothlabyrinths).

Habituationforposturalvertigoresultsindecreasedresponsetorepeatedprovokingstimuli.
Patientsmoveintotheprovokingposition23timesduringeachsession,andrepeatthese
sessions35timesperday.

Repositioningmaneuvers(eg,Epleymaneuver)areusedforpositionalvertigo,basedonthe
mechanicaldisplacementofthedebrisfromtheaffectedcanal(s)byaseriesofheadmovements.
Alternatingeyepatchesorprismscanhelpdiplopia.

Generalconditioningalsoisincorporatedintotheoverallrehabilitationplan,encouragingan
increaseintheperformanceofADLastolerated.

Occupationaltherapy
OTisusedforretrainingfinemotorskillsthatareneededtoperformADL(eg,dressing,bathing,
grooming),aswellasforimprovinghandandarmfunction.OTalsoisinvolvedingeneral
strengthening,wheelchairmobility,upperextremityorthotics,andtheevaluationofneedsfor
adaptiveequipment,aswellasinfamilytrainingandcognitiveretrainingforsafetyandADL.

Speechtherapy
Speechtherapy(ST)isusedforcognitiveretraining,speechandlanguageskills,safetyskills,
swallowingassessment,andfamilytraining.Inpatientswithdysphagiafrombrainstemlesions,the
cricopharyngeusmusclemayfailtoopensufficiently,resultinginanimpairedpassageofthebolus
fromthepharynxtotheesophagus.Increasedpoolingofabolusinthevalleculaand/orpyriform
sinuses,whichspillsintotheairway,posesasignificantriskforaspirationandpneumonia.

Evaluationofthesepatientsshouldbethoroughandshouldincludeavideofluoroscopywitha
modifiedbariumswallowtoassessforsilentaspiration.Thespeechandlanguagetherapistoften
performstheinitialswallowingevaluationanddeterminestheriskforaspirationandthe
consistencyofthepatient'sdiet.

Thepatient'svocalizationandpossiblereading,writing,andprocessingdeficitsalsoare
addressed.Interventionsforthepreventionofaspirationincludecompensatorystrategies,suchas
oromotorexercisesandposturalchangeswhileswallowing,aswellasfacilitativestrategies(eg,
modificationofbolusconsistency,volume,delivery).

Surfaceelectromyographybiofeedbackfordysphagiahasshownpromisingresults.Surface
electromyographyisusedintrainingapatienttoperformmaneuversthatcompensatefortheweak
swallow.

TheMendelsohnmaneuver,forexample,requiresvoluntarymaintenanceofthethyroidcartilagein
anelevatedpositionforafewseconds,resultinginfurtherwideningoftheopeningofthe
cricopharyngeusmuscleandeasierpassageofthefoodbolusthroughtotheesophagus.The
patientobservestheplateau(asopposedtothepeak)ofthegeneratedwaveformonthescreen,
reinforcingtheconceptofmuscleactivationinthedesiredposition(thyroidcartilageelevation).

Thepatientshouldbeonanothingbymouthrestrictionuntiltheswallowingmechanismhasbeen
assessedandclearedandtheairwayhasbeenprotected.Ifthereisahighriskofaspiration,a
nasogastricornasoduodenaltubeshouldbeplaced,althoughneithercompletelyeliminatesthe
aspirationrisk.Iftheswallowingabnormalitiesaresoseverethatrecoveryisexpectedtotake
weeksormonths,thenagastrostomytubeshouldbeplacedeithersurgicallyorpercutaneously.

Recreationaltherapy
Therecreationaltherapistshouldconcentrateonfindingalternativerecreationalactivitiesfor
patientswhoareunabletoperformattheirpremorbidlevel.Engagingintheseactivitiesprovidesa
creativeoutletandapositiveemotionalgainthatpotentiallyenhancethepatient'spsychological
recovery.

Otherconsultations

Inadditiontoconsultationswithphysical,occupational,andspeechtherapists,consultationwitha
neuropsychologistandasocialservicesworkermayalsoberequiredinthemanagementof
patientswithvertebrobasilarstroke.

Evaluationbyaneuropsychologistisrecommendedtoscreenfordepression,familydysfunction,
copingskills,andsubtlecognitive,memory,orprocessingdeficits.Allofthesemayaffectfuture
participationinandcompliancewithrehabilitation.

Thesocialservicesdepartmentisresponsibleforcoordinatingintakeandplanningdischarge.
Dependingonthesetting,thesocialservicesrepresentativemaybealicensedsocialworkeror
mayinsteadbesomeonewithamorelimitedbackground.Homehealthagenciestypicallyemploy
licensedsocialworkers,butinnursinghomes,thesocialworkerusuallyisnotlicensedorcertified.

FollowupAfterVertebrobasilarStroke
Patientsshouldfollowupwiththeprimarycareprovider,neurologist,andotherspecialists,
includingthephysiatrist,andcontinuewiththeoutpatientrehabilitationprogram.Thepatient
requirescontinuedreassessmentofvariousfactors(eg,functionalgains,psychologicalstatus,
mood,theneedforfurtherequipment,homeandothermodifications,skincare,bowelandbladder
function,spasticitymanagement,pain,vocationalneeds,andsocialissues).

Preventionofrecurrentstroke

Strictriskfactorcontrolisimportanttodecreasetheriskofstrokerecurrence.[39]Prevention
strategiesdependontheprimarycauseofthestroke.Patientswithadefinitecardioembolic
source,suchasatrialfibrillation,shouldbetreatedwithwarfarintomaintainaninternational
normalizedratioof23.

Treatmentofpatientswithbasilararterystenosisand,forthatmatter,vertebralarterystenosisis
lessclear.Retrospectiveevidencesuggeststhatwarfarinisbetterthanaspirinforthepreventionof
strokerecurrenceinpatientswithgreaterthan50%basilararterystenosis.Theongoingwarfarin
aspirintrialforsymptomaticintracranialdiseasewillprovidevaluableinformationinthatregard.

Severaloralanticoagulantmedicationsareinvariousstagesofclinicaltrialsfortheprophylaxisof
ischemicthromboembolicstroke.[40]Ifapprovedforuse,thepotentialofsuchdrugsinthearenaof
stroketreatmentissignificant.

Prognosis
Patientswithacutebasilararteryocclusionhaveamortalityrateofmorethan85%.Survivors
usuallyareleftwithsignificantneurologicdeficit.Forsymptomaticpatientswhosurvive,theriskof
recurrentstrokeis1015%.

AstudybyKimetalindicatedthatinpatientswhoreceiveendovasculartreatmentforacute
vertebrobasilarstroke,outcomesareworseinthosewhoseocclusioniscausedbyintracranial
atheroscleroticdisease(IAD)ratherthanbyembolism.Theinvestigatorsfoundthatamong
patientsintheIADgroup,theNationalInstitutesofHealthStrokeScalescorewashigherthanthat
fortheembolicgroupat7dayspostprocedure(21vs8,respectively).[41]

PatientEducation
Forpatienteducationinformation,seetheStrokeCenter,aswellasStroke.

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ContributorInformationandDisclosures

Author

VladimirKaye,MDConsultingStaff,DepartmentsofNeurologyandPsychiatry,HoagHospital

VladimirKaye,MDisamemberofthefollowingmedicalsocieties:AmericanAcademyofPhysical
MedicineandRehabilitation,NorthAmericanSpineSociety,AmericanAcademyofAntiAging
Medicine

Disclosure:Nothingtodisclose.

Coauthor(s)

MurrayEBrandstater,MBBSChairmanandProgramDirector,Professor,DepartmentofPhysical
MedicineandRehabilitation,LomaLindaUniversitySchoolofMedicine

MurrayEBrandstater,MBBSisamemberofthefollowingmedicalsocieties:AmericanAcademyof
PhysicalMedicineandRehabilitation,AmericanAssociationofNeuromuscularand
ElectrodiagnosticMedicine,AmericanCongressofRehabilitationMedicine,AmericanMedical
Association,AssociationforAcademicPsychiatry,CaliforniaSocietyofPhysicalMedicineand
Rehabilitation,CanadianAssociationofPhysicalMedicineandRehabilitation,CanadianMedical
Association,CanadianSocietyofClinicalNeurophysiologists,CatholicMedicalAssociation,
NationalStrokeAssociation,OntarioMedicalAssociation,RoyalCollegeofPhysiciansand
SurgeonsofCanada,RoyalCollegeofPhysiciansandSurgeonsoftheUnitedStates

Disclosure:Nothingtodisclose.

SpecialtyEditorBoard

FranciscoTalavera,PharmD,PhDAdjunctAssistantProfessor,UniversityofNebraskaMedical
CenterCollegeofPharmacyEditorinChief,MedscapeDrugReference

Disclosure:ReceivedsalaryfromMedscapeforemployment.for:Medscape.

RichardSalcido,MDChairman,ErdmanProfessorofRehabilitation,DepartmentofPhysical
MedicineandRehabilitation,UniversityofPennsylvaniaSchoolofMedicine

RichardSalcido,MDisamemberofthefollowingmedicalsocieties:AmericanAcademyofPain
Medicine,AmericanAcademyofPhysicalMedicineandRehabilitation,AmericanAssociationfor
PhysicianLeadership,AmericanMedicalAssociation,AcademyofSpinalCordInjuryProfessionals

Disclosure:Nothingtodisclose.

ChiefEditor

StephenKishner,MD,MHAProfessorofClinicalMedicine,PhysicalMedicineandRehabilitation
ResidencyProgramDirector,LouisianaStateUniversitySchoolofMedicineinNewOrleans

StephenKishner,MD,MHAisamemberofthefollowingmedicalsocieties:AmericanAcademyof
PhysicalMedicineandRehabilitation,AmericanAssociationofNeuromuscularand
ElectrodiagnosticMedicine

Disclosure:Nothingtodisclose.

AdditionalContributors

MiltonJKlein,DO,MBAConsultingPhysiatrist,HeritageValleyHealthSystemSewickley
HospitalandOhioValleyGeneralHospital

MiltonJKlein,DO,MBAisamemberofthefollowingmedicalsocieties:AmericanAcademyof
DisabilityEvaluatingPhysicians,AmericanAcademyofMedicalAcupuncture,AmericanAcademy
ofOsteopathy,AmericanAcademyofPhysicalMedicineandRehabilitation,AmericanMedical
Association,AmericanOsteopathicAssociation,AmericanOsteopathicCollegeofPhysical
MedicineandRehabilitation,AmericanPainSociety,PennsylvaniaMedicalSociety

Disclosure:Nothingtodisclose.