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NeuroimagingNeuroimaging ofofvascularvascular//secondarysecondary effectseffects

and and sequelaesequelae ofof head trauma.head trauma.AndrAndrèèss Server AlonsoServer Alonso

DepartmentDepartment ofofNeuroradiologyNeuroradiology

DivisionDivision ofof RadiologyRadiologyUllevUllevåål l UniversityUniversity HospitalHospital

Oslo, Oslo, NorwayNorway..

Guidelines for Guidelines for identifyingidentifying trauma trauma patientspatientsat at highhigh risk for risk for bluntblunt cerebrovascularcerebrovascular

injuryinjuryCervicalCervical spinespine fracturefracture withwith–– ForamenForamen transversariumtransversarium involvementinvolvement, or, or–– 30% or more 30% or more subluxationsubluxation, or, or–– SignificantSignificant rotationrotation or or distractiondistraction mechanismmechanism

BasillarBasillar skullskull fracturefracture crossingcrossing carotidcarotid canalcanal, , foramenforamen lacerumlacerum, or , or cavernouscavernous sinussinusSevereSevere facialfacial fracturesfractures ((LeFortLeFort II or III; II or III; nasonaso--orbitalorbital ethmoidethmoid complexcomplex, , facialfacial smash).smash).CarotidCarotid or vertebral or vertebral arteryartery perivascularperivascular hematomahematomaHorner`sHorner`s syndromesyndromeGCS<6 at 24 h GCS<6 at 24 h afterafter initial initial assessmentassessmentNeurologicNeurologic examinationexamination incongruentincongruent withwith brainbrain imagingimagingStroke or TIAStroke or TIAHangingHanging atemptatempt withwith cervicalcervical hematomas or hematomas or cervicalcervical spinespine fracturesfractures

From Sliker CW, Mirvis SE. Eur J Radiol 2007, 64(1):3-14.

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PrimaryPrimary vascularvascular injuriesinjuries

TraumaticTraumatic arterialarterial dissectiondissection–– ExtracranialExtracranial carotidcarotid dissectionsdissections–– IntracranialIntracranial dissectionsdissections or or dissectingdissecting aneurysmsaneurysms–– Vertebral Vertebral arteryartery dissectiondissection

CarotidCarotid--cavernouscavernous fistulasfistulasTraumaticTraumatic intracranialintracranial aneurysmsaneurysmsTraumaticTraumatic venousvenous thrombosisthrombosis

TraumaticTraumatic carotidcarotid dissectionsdissections

70% 70% ofof carotidcarotid dissectionsdissections involveinvolve bothboth thethecervicalcervical and and petrouspetrous portionsportions ofof thethe arteryarteryDissectionsDissections shouldshould be be suspectedsuspected ifif::–– NeurologicNeurologic deficitsdeficits–– InfarctsInfarcts–– EvidenceEvidence ofof significantsignificant skullskull traumatrauma

AneurysmsAneurysms occuroccur in 58% in 58% ofof traumatictraumatic dissectionsdissectionsIntimalIntimal flapflap present in 20present in 20--35% 35% ofof casescasesCarotidCarotid occlusionocclusion occuroccur in 20% in 20% ofof dissectionsdissections

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IntracranialIntracranial dissectionsdissections or or dissectingdissectinganeurysmsaneurysms

AffectAffect thethe supraclinoidsupraclinoid carotidcarotid or middel or middel cerebral arteriescerebral arteriesTheThe location location ofof thethe intramuralintramural hematoma is hematoma is usuallyusually subintimalsubintimalDissectingDissecting aneurysmsaneurysms oftenoften present present withwith a a ””stringstring--ofof--beadsbeads”” appearanceappearance

Vertebral Vertebral arteryartery dissectiondissection

20% 20% ofof all all cervicalcervical vascularvascular injuriesinjuriesA 24% to 46% A 24% to 46% incidenceincidence ofof vertebral vertebral arteryarteryinjuryinjury associatedassociated withwith major major bluntblunt cervicalcervicalspinespine trauma trauma includingincluding fracturesfractures, , subluxationssubluxations or or severesevere hyperextensionhyperextension or or hyperflexionhyperflexion injuryinjury..TheThe angiographicangiographic findings: findings: stenosisstenosis, , aneurysmsaneurysms and and intimalintimal flaps.flaps.

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Day 1

Day 0

Day 3

Day 0

Day 8

Day 3

5

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TraumaticTraumatic intracranialintracranial aneurysmsaneurysmsclassificationclassification

ProximalProximal to to thethe circlecircle ofof WillisWillis–– InfraclinoidInfraclinoid carotidcarotid arteryartery–– SupraclinoidSupraclinoid carotidcarotid arteryartery–– VertebrobasilarVertebrobasilar

DistalDistal to to thethe circlecircle ofof WillisWillis–– SubcorticalSubcortical–– corticalcortical

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TIATIAmechanismsmechanisms ofof injuryinjury

InfraclinoidInfraclinoid carotidcarotid and and basilarbasilar arteryartery aneurysmsaneurysms areareassociatedassociated withwith::–– BasilarBasilar skullskull fracturesfractures

SupraclinoidSupraclinoid carotidcarotid arteryartery aneurysmsaneurysms cancan be be thethe resultresult ofof ::–– EitherEither movementmovement ofof thethe supraclinoidsupraclinoid segment segment againstagainst thethe anterioranterior

clinoidclinoid processprocess–– Or Or stretchingstretching ofof thethe carotidcarotid arteryartery

DistalDistal subcorticalsubcortical aneurysmsaneurysms occursoccurs alongalong::–– TheThe anterioranterior cerebral cerebral arteryartery and and itsits branchesbranches–– TraumaticTraumatic movementmovement ofof thethe brainbrain and and vesselsvessels againstagainst thethe fixedfixed falxfalx

cerebricerebriPosteriorPosterior cerebral cerebral arteryartery aneurysmsaneurysms–– ResultResult ofof trauma trauma ofof thethe vesselvessel againstagainst thethe tentoriumtentorium

TIA TIA diagnosisdiagnosis

PatientsPatients withwith historyhistory ofof trauma and trauma and recurrentrecurrentepistaxisepistaxis, , visualvisual loss, progressive loss, progressive cranialcranialnerve nerve palsypalsy or an or an enlargingenlarging skullskull fracturefractureMRI/MRA/CTA MRI/MRA/CTA ArteriographyArteriography

DelayedDelayed formationformation ofof aneurysmsaneurysms

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29,7%21,6%

ICA just below theskull base

Petrous internalcarotid artery

Anterior aspect ofthe cavernous ICA

Pericallosal and callosomarginalarteries

Peripheral MCA

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SecondarySecondary lesionslesions

TheThe secondarysecondary effectseffects ofof craniocerebralcraniocerebral trauma trauma maymay be more be more devastatingdevastating thanthan thethe primaryprimary injuries.injuries.SecondarySecondary lesionslesions areare thosethose thatthat developdevelopsubsequentsubsequent to initial to initial impactimpact..TheyThey arisearise fromfrom–– EitherEither sequelaesequelae ofof primaryprimary lesionslesions–– Or Or thethe neurologicneurologic effectseffects ofof systemicsystemic injuriesinjuries

SecondarySecondary lesionslesions, , areare potentiallypotentially preventablepreventable, , providedprovided thatthat causativecausative factorsfactors areare quicklyquicklyrecognizedrecognized and and appropiateappropiate treatmenttreatment promptlypromptlyinstitutedinstituted..

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BRAIN INJURYBRAIN INJURY

Tissue damage

Cerebral swelling/edema

•Cell lesion

•Ruptured BBB

•Cerebral vasoplegia

Cytotoxic edema

Vasogenic edema

Brain swelling

ICPCPPCBF

Ischemia

Loss of autoregulation

vasoparalysis

hypoxia

hypercapnia

ischemia

hypotension

EvaluationEvaluation ofof relevant CT relevant CT scanscanfindingsfindings

Status Status ofof thethe basal basal cisternscisternsMidlineMidline shiftshiftSubarachnoidSubarachnoidhemorrhagehemorrhage in in thethebasal basal cisternscisterns

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Status Status ofof thethe basal basal cisternscisternsCompressedCompressed or absent basal or absent basal cisternscisterns indicateindicate a a threefoldthreefold risk risk ofof raisedraised intracranialintracranial pressurepressureand and thethe status status ofof thethe basal basal cisternscisterns is is relatedrelated to to outcomeoutcome..TheThe degreedegree ofof massmass effecteffect is is evaluatedevaluated at at thethe levellevel ofofmidbrainmidbrain::–– OpenOpen (all (all limbslimbs openopen))–– PartiallyPartially closedclosed ((oneone or or twotwo

limbslimbs obliteratedobliterated))–– CompletelyCompletely closedclosed (all (all limbslimbs

obliteratedobliterated))

MidlineMidline shiftshift

TheThe presencepresence ofof midlinemidlineshiftshift is is inverselyinversely relatedrelated to to prognosisprognosis..MidlineMidline shiftshift at at thethe levellevel ofofforamenforamen ofof MonroMonro shouldshouldbe be determineddetermined by first by first measuringmeasuring thethe widthwidth ofof thetheintracranialintracranial spacespace (A); (A); nextnextthethe distancedistance from from thethe bone bone to to thethe septumseptum pellucidumpellucidumis is measuredmeasured (B).(B).

MidlineMidline shiftshift = (A/2)= (A/2)--B.B.

AB

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DifferentDifferent types types ofof cerebral cerebral herniationsherniations

SubfalcineSubfalcine h.h.TranstentorialTranstentorial h.h.–– LateralLateral

Anterior=uncalAnterior=uncalPosterior=parahyppocampalPosterior=parahyppocampal

–– CentralCentralAscendingAscendingDescendingDescending

TranssphenoidalTranssphenoidal h.h.–– DescendingDescending–– AscendingAscending

Tonsillar h.Tonsillar h.ExternalExternal h.h.

Johnson PL et al. Neuroimag Clin N Am 12(2002):217-228.

SubfalcineSubfalcine herniationherniation

It is It is causedcaused by unilateral frontal, by unilateral frontal, parietalparietal or or temporal temporal lobelobe massmass effecteffect or or edemaedemaTheThe ipsilateralipsilateral cingulatedcingulated gyrusgyrus is is pushedpusheddowndown and under and under thethe rigid rigid midlinemidline falxfalxOwingOwing to to arterialarterial compressioncompression::–– FocalFocal necrosisnecrosis ofof thethe cingulatedcingulated gyrusgyrus–– InfarctionInfarction involvinginvolving thethe ACA ACA territoryterritory

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TranstentorialTranstentorial herniationherniation

Symptoms Symptoms maymay resultresult from from displacementdisplacement, , compressioncompression and and stretchingstretching ofof thethe brainstembrainstem and and cranialcranial nervesnervesHemorrhageHemorrhage and and infarctioninfarction causedcaused by by compressioncompression and and tearingtearing ofof arteries and arteries and veinsveinsIncreasingIncreasing edemaedema and and intracranialintracranial pressurepressurecausedcaused by by venousvenous obstructionobstructionHydrocephalusHydrocephalus causedcaused by by obstructionobstruction ofof thetheaqueductaqueduct..

Rhoton AJ . Neurosurgery 2000, 47:S 131-53.

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Day 2Day 2 Day 2

Day 2Day 0

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PostPost--traumatictraumatic cerebral cerebral infarctioninfarction

MechanismsMechanisms–– DirectDirect vascularvascular compressioncompression by by massmass effecteffect(81(81--88%)88%)

–– Cerebral Cerebral vasospasmvasospasm–– VascularVascular injuryinjury–– SystemicSystemic hypoperfusionhypoperfusion

PTCIPTCI

PTCI is most PTCI is most commoncommon in in thethe PCA PCA distributiondistribution

PTCI is an PTCI is an indicationindication ofof a a poorpoor clinicalclinicaloutcomeoutcome, , especiallyespecially amongamong patientspatients withwith::–– AssociatedAssociated subduralsubdural hematomahematoma–– BrainBrain swellingswelling//edemaedema–– tSAHtSAH

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DISTRIBUTION OF POSTTRAUMATIC CEREBRAL DISTRIBUTION OF POSTTRAUMATIC CEREBRAL INFARCTION IN 16 PATIENTSINFARCTION IN 16 PATIENTS

0

5

10

15

20

25

30

35

40

vascular territory

PCA 37,5%MCA 20,8%ACA 12,5%L-TT 8,3%VBT 12,5%CI 8,3

Server A et al. Acta radiologica 2001 (42):254-260.

Day 0 Day 1

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Outcome Outcome in in patients with patients with PTCIPTCI

good recoverymoderate disabilitysevere disabilityvegetative statedeath

43.8%

6.2%

25%

12.5%

12,.5%

Server A et al. Acta radiologica 2001 (42):254-260.

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TraumaticTraumatic cerebral cerebral edemaedema//swellingswelling

VasogenicVasogenic due to bloddue to blod--brainbrain barrierbarrierdisruption extracellulardisruption extracellular water water accumulationaccumulationCytotoxicCytotoxic/cellular/cellular due to due to sustainedsustainedintracellularintracellular water water accumulationaccumulationOsmoticOsmotic causedcaused by by osmoticosmotic inbalancesinbalancesbetweenbetween brainbrain and and tissuetissueHydrocephalicHydrocephalic edemaedema//interstitialinterstitial from from edemaedema relatedrelated to an to an obstructionobstruction ofof CSF CSF outflow outflow

TraumaticTraumatic diffuse cerebral diffuse cerebral edemaedema//swellingswelling

EarlyEarly–– GyralGyral swellingswelling, , sulcalsulcal effacementeffacement, loss , loss ofof graygray--

whitewhite matter matter interfaceinterfaceLateLate–– Diffuse Diffuse lowlow attenuationattenuation ofof thethe brainbrain, , generalizedgeneralized

effacementeffacement ofof subarachnoidsubarachnoid cisternscisterns–– ””PseudosubarachnoidPseudosubarachnoid hemorrhagehemorrhage””–– ””White White cerebellumcerebellum signsign””–– ””TheThe reversalreversal signsign””

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Day 1 Day 2

Day 3

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4 months later

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SequelaeSequelae ofof head traumahead trauma

EarlyEarly–– DelayedDelayed intracerebralintracerebral

hematomahematoma–– DelayedDelayed subduralsubdural

hematomahematoma–– DelayedDelayed epidural epidural

hematomahematoma–– CSF CSF leakleak or or fistulafistula

LateLate–– Cerebral Cerebral atrophyatrophy–– CerebellarCerebellar atrophyatrophy–– AtrophyAtrophy ofof thethe corpus corpus

callosumcallosum–– AcquiredAcquired cephalocelecephalocele–– LeptomeningealLeptomeningeal cystcyst–– hypopituitarismhypopituitarism

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LeptomeningealLeptomeningeal cystcyst

WhenWhen a a skullskull fracturefracture is is accompaniedaccompanied by a by a teartear ofof thethe dura, dura, meningesmeninges and and brainbrain tissuetissuemaymay herniateherniate intointo thethe fracturefracture, , preventingpreventinghealing healing ofof thethe fracturesfractures and and permitingpermitingcerebrospinal fluid cerebrospinal fluid pulsationpulsation to to enlargeenlarge thethefracturefracture and and extentextent intointo thethe subgalealsubgaleal spacespace..90%< 3 90%< 3 yearsyears..TheThe averageaverage time time ofof diagnosisdiagnosis is 14 is 14 monthsmonthsafterafter thethe initial initial fracturefracture..

1 year later

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PostPost--traumatictraumatic hydrocephalushydrocephalus

PTH as PTH as lowlow as 0,7% or as as 0,7% or as highhigh as 20%as 20%PTH PTH cancan present present acutelyacutely, , subacutelysubacutely and and syndromesyndrome ofof NPHNPHPTH is to be PTH is to be distinguisheddistinguished from from posttraumaticposttraumaticventriculomegalyventriculomegaly due to cerebral due to cerebral atrophyatrophyTheThe appropiateappropiate managementmanagement ofof thesethese patientspatientsincludeinclude::–– StudyStudy ofof CSF CSF dynamicsdynamics–– And/or ICP And/or ICP monitoringmonitoring

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Day-0 Day-3 Day-18

Day-21 Day-30 Day-42

TraumaticTraumatic cerebrospinal fluid cerebrospinal fluid leakleak

AcuteAcute CSF CSF fistulasfistulas occuroccur in 2 to 11% in 2 to 11% ofof all all patientspatients withwith closedclosed head traumahead trauma70% 70% occursoccurs withinwithin 1 1 weekweekCTCT--cisternographycisternographyHighHigh--definitiondefinition CT CT alonealoneMRIMRI--CISSCISS

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conclusionconclusionCTA has CTA has beenbeen shownshown to be a to be a goodgood nonnon--invasiveinvasivealternative alternative tecniquetecnique to to cathetercatheter angiographyangiography for for thethe initial initial assessmentassessment ofof cerebrovascularcerebrovascular traumatraumaand and vascularvascular injuriesinjuries ofof thethe neckneck..NeuroimagingNeuroimaging is is playingplaying a a crucialcrucial rolerole in in definingdefiningthethe mechanismsmechanisms ofof secondarysecondary injuryinjury in in traumatictraumaticbrainbrain injuryinjury and, in turn, and, in turn, potentiallypotentially identifyingidentifyingtargets targets ofof newnew therapytherapy..CT is CT is adequateadequate in in thethe evaluationevaluation for for earlyearly onsetonset ofofsequelaesequelae ofof head traumahead trauma. MRI is . MRI is thethe modalitymodality ofofchoicechoice for for evaluationevaluation ofof subacutesubacute and later and later onsetonsetofof delayeddelayed sequelaesequelae ofof head trauma.head trauma.

Radiology in traumatic brain injury has a bright future.