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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
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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.