Imaging of Traumatic Brain Injury


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Summary and illustrations of various traumatic brain injury including primary and secondary lesions as well as limited information on indications of brain imaging in trauma

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Imaging of Traumatic Brain Injury

  1. 1. Imaging of Traumatic Brain InjuryRathachai Kaewlai, MDRamathibodi Hospital, Mahidol University, BangkokEmergency Radiology Minicourse 2013Slides available at or
  2. 2. DisclaimerAll opinions expressed here are those of the authors and not of theiremployers.Information provided here is for medical education only. It is not intended asand does not substitute for medical advice. If you are a patient, please seeyour doctor for evaluation of your individual case. Under no circumstanceswill the authors be liable to you for any direct or indirect damages arising inconnecting with the use of this website.The presentation may contain links to third party web sites. This does notconstitute endorsement, guarantee, warrantee or recommendation by theauthors. We do not verify, endorse, or take responsibility for the accuracy,currency, completeness or quality of the content contained in these sites.There is no real life patient data on this presentation. We do not write aboutpatients. All case descriptions are fictional, similar to descriptions you canfind in a multiple choice questions textbook for examination preparation.
  3. 3. Outline•  Background of traumaticbrain injury (TBI)•  Imaging modalities–  CT–  X-ray–  MRI•  Clinical prediction rules•  Primary lesions–  Intraaxial hemorrhages–  Extraaxial hemorrhages•  Secondary lesions
  4. 4. Traumatic Brain Injury (TBI)•  Leading cause of death and disability•  Major risk factors: extreme age, male,low socioeconomic status•  Mortality related to Glasgow Coma Scale(GCS) scoreHead injury classified by GCS13-15 = mild HI8-12 = moderate HI7 or less = severe HI
  5. 5. Traumatic Brain Injury (TBI)•  Closed or open? It depends on dura integrityClosed OpenMore common Less commonDura intact Dura disruptedViolent accelerations ofbrain tissue (coup-contrecoup)Fracture or FB penetratingdura
  6. 6. Traumatic Brain Injury (TBI)•  Primary or secondary brain lesions? It’s “how”closely lesions are linked to traumatic eventPrimary SecondaryCaused by trauma itself Processes arising from 1) brain’sresponses to trauma 2)compression of brain, CN, BV,skull and duraLess devastating More devastatingSkull fractures, extraaxialhemorrhages, intraaxial lesions(DAI, contusion, IVH)Herniations, diffuse edema,infarction and infarctionDAI = Diffuse axonal injury, IVH = intraventricular hemorrhage, CN = cranial nerves, BV = blood vessels
  7. 7. Goals of Imaging in TBIGoals Answered by...Rapid diagnosis of life-threatening injuriesExplanation of neurologicalabnormalityPrognosis informationCTCT (if not  MRI)Clinical findings, CT, MRI,advanced MR techniques
  8. 8. CT in TBI: Why?•  Widely available•  Fast•  Sensitive for detection and evaluation ofinjuries requiring acute neurosurgicalintervention  Deciding whether surgical or medical RxImage from
  9. 9. CT in TBI: When?•  Moderate & severe acute closed HI•  Minor acute closed head injury with…– Risk factors* or– Neurological deficit present•  Children <2 years old•  Penetrating injury•  Skull fracture•  R/O carotid or vertebral artery injuryHI = head injury
  10. 10. CT in TBI: When?•  Patients with mild HI withone of 7 clinical findingsneed CT:–  Short-term memory deficit–  Drug/alcohol intoxication–  Physical evidence of traumaabove clavicles–  Age > 60–  Seizure–  Headache–  VomitingNEJM 2000New Orleans CriteriaUsing this scheme, CTpositivity rate was about7-10%Sensitivity = 100%
  11. 11. CT in TBI•  Sensitivity forpredicting need forneurosurgery–  High risk 100%–  Medium risk 98.4%•  Reduced the needfor CT in mild HI to54%•  Positivity rate = 8%(1% of casesrequireneurosurgicalintervention)Stiell IG, et al. Lancet 2001;357:1391-96. | Diagram from
  12. 12. CT in TBI: How?•  Non-contrast, axial scan with spiral technique•  At our hospital, we use 3 mm slice thickness andalway do bone algorithm, coronal/sagittalreformations•  If you see maxillary hemosinus  do facial CT•  If you see skull base fracture  consider CTAand skull base reformation (thin slices with smallFOV)•  If suspect C-spine fracture  do C-spine CT
  13. 13. CT in TBI: Checklist•  Look at all three windowsBrain Subdural Bone
  14. 14. CT in TBI: Checklist•  Look for primary lesions•  Don’t forget secondary lesions (they maybe more catastrophic)•  If the study looks near-normal–  Find coup injury  look for contrecoup (can besubtle)–  Check potential areas for contusions and DAI (esp iflow GCS)•  Recheck interpeduncular fossa for smallSAH
  15. 15. Skull X-ray: Outdated Yet?•  No!•  Penetrating injury•  Radiopaque foreign bodies e.g. GSW•  Part of skeletal survey in cases suspectingchild abuse•  Caveats: Skull fractures...– About 1/3 of cases with severe TBI do nothave skull fracture!– Negative skull x-ray does not mean no CT
  16. 16. Skull X-ray: How?•  Skull trauma series in adults shouldinclude at least 3 views given complexskull bones– Frontal– Lateral– Towne’s•  Learn to find fractures and distinguishthem from mimics
  17. 17. MRI in TBI: Pros•  More sensitive for 10 and 20 injuries than CT•  Better differentiation of hemorrhagic andnon-hemorrhagic lesions in acute phaseSame-day MRIDiffuse axonal injury
  18. 18. MRI in TBI: Cons•  Intrinsic limits:–  Absolute C/I: cardiac pacemaker, ferromagnetic foreignbodies–  Lower sensitivity for bone fractures and hyperacute blood•  Difficult managing trauma patients in MRI suite:metallic life support, monitoring device, timeT1 T2 FLAIRCTImages from Scarabino, et al. Emergency Neuroradiology, 2006
  20. 20. Quick Anatomy•  3 layers–  Outer table–  Diploe–  Inner table•  Parts without diploe prone to fracture–  Squamous temporal bone / Parietal bone–  Foramen magnum, skull bases, cribiform plates,orbital roofs
  21. 21. Quick Anatomy(c) 2003 Encyclopedia Brittanica
  22. 22. Quick Anatomy
  23. 23. Types of Skull Fracture•  Linear fracture–  a/w EDH, SDH•  Depressed fracture–  a/w focal parenchymallesions•  Skull base fracture•  Open head injuries–  Knife, firearm–  Laceration of dura
  24. 24. Significance of Skull Fracture•  Indicator of brain injuries?...Not quite– Present in the majority of cases with severeHI– Absent in 1/4 of fatal injuries at autopsy– Absent in 1/3 of severe brain injury cases•  Injuries to underlying brain structures•  Association– 15% concomitant C-spine injury– 10-15% concomitant facial injury
  25. 25. Skull Fracture: Imaging•  Best = Helical CT scan with multiplanarreformation (MPR)In-plane fracture easier to see on reformats
  26. 26. Skull Fracture: Imaging•  Bone window with edge enhancement algorithmSoft tissue algorithm Bone algorithm
  27. 27. Skull Fracture: Difficulty on XRWindow level adjustedRoutine window
  28. 28. Skull Fracture vs. SutureFRACTURE SUTURESmooth or jagged edge Serrated edgeStraight line Curvilinear lineAngular turn Curvilinear turnGreater in width Lesser in width(X-ray) darker (X-ray) lighterAny locations Specific anatomic location
  29. 29. Skull Fracture: Difficulty on CTUse subgaleal hematoma as a clue
  30. 30. Skull Fracture: Diastatic• Fracture along suture lines “traumatic sutural separation”• Usually affected newborns and infants (unfused sutures)• Commonly unilateral• Most common location = lambdoid and sagittal sutures• >2 mm separation that is asymmetric
  31. 31. Skull Fracture: Depressed•  In adults, criteria to elevate:–  >8-10 mm depression or >1thickness of skull–  Deficit related to underlying brain–  CSF leak•  In children, two types:–  Simple depressed: usuallyremodelling occurs with growth,surgery if dura penetrated orpersistent cosmetic defect–  Ping-pong ball fractures: Rx ifunderlying brain injury or durapenetrated
  32. 32. Skull Fracture: Skull Base•  Most are extensions offracture of cranial vault•  Clinical clues:–  CSF otorrhea or rhinorrhea–  Hemotympanum or laceration ofEAC–  Postauricular ecchymoses–  Periorbital ecchymoses inabsence of direct orbital traumaesp if bilateral–  Cranial nerve injury (I, VI, VII,VIII)Longitudinal
  33. 33. Skull Fracture: Skull Base•  Thin slices, bonealgorithms andcoronal imagesneeded for Dx•  Indirect CT signs:–  Pneumocephalus–  Air-fluid level oropacification ofmastoid or sinusesLongitudinal Oblique
  34. 34. Skull Fracture:Missile InjuriesDepressed Penetrating PerforatingMissile notpenetrate skullbut producesdepressed fxor braincontusionMissile enterscranial cavitybut does notleave itMissile entersand exitscranial cavityFocal braindamageInjury dependson damage tovital structuresMost severeinjury due toshockwavesgenerated bymissilesForeign body,meningitis,abscessesForeign body,meningitis,abscesses
  35. 35. Skull Fracture: Pneumocephalus•  Gas within cranial cavity•  In acute trauma setting, this iscommonly due to fractures ofPNS and temporal bones (openskull fracture is another cause)•  Most do not cause immediatedanger but rapid expansion canlead to brain compression(tension pneumocephalus)–  Mount Fuji sign•  Usually decreases by 10-15 daysand almost never present by 3weeks
  37. 37. Diffuse Axonal Injury (DAI)•  Traumatic acceleration/deceleration or violentrotation•  LOC immediately at the time of trauma  coma•  Most severe of all primary brain lesionsImages from
  38. 38. Diffuse Axonal Injury (DAI)•  Frequent cause ofpersistent vegetativestate / morbidity intrauma patients•  Clinical symptomsworse than CT findings•  Can be isolated with noor little association withSAH, SDH, fracture
  39. 39. Diffuse Axonal Injury•  Non-hemorrhagic 80% of cases•  Common locations:–  Grey-white matter interface (m/c)–  Corpus callosum–  Dorsolateral midbrain•  Number and location of lesionspredict prognosis (worse ifmultiple & supratentorial)•  MRI most sensitive imaging butstill underestimates real extentSusceptibility-weighted MRICT
  40. 40. Diffuse Axonal Injury•  When initial head CT is normal but thepatient is in vegetative state– Do MRI with susceptibility sequence OR– Follow up CT in 24 hours (1/6 of DAI willevolve)Small interpeduncular SAH and petechial hemorrhage in dorsolateral midbrain on CT and susceptibility-weighted MRI
  42. 42. Cerebral Contusion•  Cerebral gyri impact inner table skull•  Characterizes coup and contrecoupinjuries•  Petechial hemorrhage of gyri  smallhemorrhage  large hematomaImages from
  43. 43. Cerebral Contusion•  Anterior base frontal,temporal lobes (esptip), cortex surroundingSylvian fissure•  Multiple, bilateral
  44. 44. Cerebral Contusion•  Can be normal early; can be non-hemorrhagic•  Imaging worsened with time, most evident after 24 hDay 0 Day 1
  45. 45. Cerebral Contusion: MRIFLAIR T2WMRI is the study of choice in patients with• Acute TBI when neurological findins are unexplained by CT• Subacute or chronic phases when there are TBI-related symptoms
  46. 46. OTHER INTRAAXIAL LESIONSTraumatic intraparenchymal hematomaIntraventricular hemorrhageTraumatic lesions of deep grey structures and brainstem
  47. 47. Intraparenchymal Hematoma•  Parenchymal vesselrupture from blunt orpenetrating forces•  May not loseconsciousness (unlikeDAI, contusion)•  Hematoma at primarytrauma site (usuallyfrontal and temporal)
  48. 48. Intraparenchymal Hematoma•  Well-circumscribedhyperdense lesion w/woperilesional edema•  Up to 60% a/w SDH, EDH•  Not always easy todistinguish IPH from DAI orcontusionTraumatic intraparenchymal hemorrhage with IVH
  49. 49. Intraventricular Hemorrhage•  Uncommon•  Consequence of severe trauma. a/w DAI andtrauma of deep grey and brainstem•  Poor prognosis
  50. 50. Trauma of Deep Grey &Brainstem•  Stretch and torsion causing ruptured perforators,or direct impact on dorsolateral brainstemagainst tentorial incisura•  Severe trauma, poor prognosis•  CT:–  Small hemorrhages in brainstem surroundingaqueduct, basal grey nuclei–  Can be normal
  52. 52. Epidural Hematoma (EDH)•  Hematoma between innertable of the skull and dura•  Source of bleeding–  Most common = middlemeningeal artery (90%)(squamous temporal bone)–  Venous EDH from duralvenous
  53. 53. Epidural Hematoma (EDH)•  Most urgent of all cases of cranial trauma–  Requiring prompt Rx to relieve compression ofbrainstem, tentorial herniation, acute hydrocephalus–  EDH in posterior fossa very worrisome•  1-4% of head injury cases, 10% of fatal cases•  Young men (20s – 40s). Rare in patients >60 y•  Almost always with skull fracture•  Lucid interval in 40% of cases
  54. 54. Epidural Hematoma (EDH)•  Delayed development in 10-25% of cases(within 36 hrs)– Arterial EDH: blood can flow into epiduralspace only after resolution of arterial spasm– Venous EDH bleeds slowly
  55. 55. Epidural Hematoma:CT Appearance•  Biconvex or lens shapehyperdense lesion (rare to beisodense)•  May cross midline and duralattachment•  Do not cross suture (exceptdiastatic fracture, large EDH)
  56. 56. Epidural Hematoma:Potential Indications for Surgery•  Size > 2 cm•  Active bleeding•  Impending herniation•  Correspondingneurologic deficit
  57. 57. Epidural Hematoma: Swirl Sign•  First described byZimmerman in 1982•  Small rounded lesionisodense to the brain,representing activeextravasation ofunclotted blood•  Clotted component ishyperdense (50-70HU)
  58. 58. Venous EDH•  Tear of venous sinus(high flow, low pressuresystem)•  More benign course,subacute presentation,usually not requiresurgery•  Posterior fossa venoussinus > sagittal sinus
  60. 60. Subdural Hematoma (SDH)•  Blood collects betweendura and arachnoid•  Torn cortical bridging veins•  10-20% of all cranialtrauma cases•  Demographics:–  Elderly (60-80y) with brainatrophy,–  Large intracranialsubarachnoid spaces–  “Shaken baby syndrome”
  61. 61. Subdural Hematoma (SDH)•  Usually co-exist withother brain injuries–  Esp. contusion-typedinjuries > skull fractures•  Acute: within 3 daysfrom trauma•  Subacute: within 3 mo•  Chronic: after 3 monthsLayer of acute blood on pre-existing CSF-like subduralcollection in the right cerebral convexity
  62. 62. Subdural Hematoma:CT Appearance•  Crescentic hyperdensecollection•  Can cross suture•  Can extend tointerhemisphericfissure, along tentoriumcerebelliNote coup (Rt.) and contrecoup (Lt.) pattern.This SDH is a contrecoup injury.
  63. 63. Subdural Hematoma:Value of Coronal Reformats
  64. 64. Bilateral Subdural HematomasDon’t feel “enough” with trauma findings. There’re almost always more to be discovered.
  65. 65. “Isodense” Subdural Hematoma•  Usually takes 2-6weeks for acute SDHto become isodense•  At Hb 8-10 g/dL, bloodwill be isodense togrey matter•  Anemic patients canpresent with acuteisodense SDH
  66. 66. Acute On Chronic SDH•  New hemorrhagesuperimposed onchronic SDH•  Recurrent trauma•  Can be spontaneous•  Blood-fluid level , bloodclot organization,membranes
  67. 67. Comparison of EDH and SDHEDH SDHIncidence 1-4% of trauma cases;10% of fatal trauma cases10-20% of all trauma cases;30% of fatal trauma casesEtiology a/w fractures in 90% of casesLaceration of MMA/venous sinusTearing of cortical veinsSite Between skull and dura95% supratentorialBetween dura and arachnoid95% supratentorialCrosses dura but not sutures Crosses suture but not duraCT findings Biconvex (lens) shapeShift grey-white matter interfaceCrescentic shapeDiagram from Kumar et al. Basic Pathology 7E
  68. 68. Subdural Hygroma•  Extraaxial collection ofCSF caused byextravasation of CSFfrom SA spacethrough a traumatictear in arachnoidmater•  Acute: Children >> adults•  Subacute and chronic:Following surgery for headinjuries in operative bed oropposite site1 week after injuryDay of injury
  70. 70. Subarachnoid Hemorrhage(SAH)•  Blood collects beneatharachnoid•  Tear of veins in SA space•  Usually associated withother brain injuries(common with contusions)•  ‘Nearly all cases oftraumatic SAH have otherlesions to suggesttraumatic cause’–  Isolated SAH in traumapatients – possible rupturedaneurysm causing traumaSAH with SDH
  71. 71. Subarachnoid Hemorrhage•  Site–  Next to brain contusion,under SDH/fracture/scalp lac–  Can be distant becauseblood diffuses in SAspace•  IVH may co-exist due toretrograde flow throughforamen of Luschkaand MagendieSAH with contusion
  72. 72. Subarachnoid Hemorrhage•  Subtle SAH –interpeduncular fossa
  73. 73. TRAUMATIC VASCULARLESIONSICA dissectionCarotid-cavernous fistula (CCF)
  74. 74. Traumatic Vascular Lesions•  Rare•  Can be overlooked initially•  ICA injury (dissection, aneurysm, occlusion)–  Base of skull fracture•  Traumatic carotid-cavernous fistula (TCCF)
  75. 75. Traumatic ICA Injury•  Common cause ofischemic stroke in theyoung•  Extracranial ICA muchmore common (espjust proximal topetrous bone)•  Dissection occlusion orthromboembolismAt initial trauma, there were diffuse subarachnoid hemorrhage, pneumocephalus, facial fracturesand C-spine injury. Days after the injury (image C) , the patient developed left ICA territoryinfarction. Angiiography (D) confirmed occlusion of the cervical ICA.Images from Yang S, et al. J Clin Neurosci 2006;13:123
  76. 76. Traumatic CCF•  Most common traumatic AV fistula = CCF–  Clues on CT: proptosis, bulging cavernous sinus, enlarged-arterialized ophthalmic veinA vividly enhancing structure in the right cavernous sinus with a dilated superior ophthalmic vein.Note right proptosis
  77. 77. SECONDARY LESIONSHerniationCerebral edemaIschemia and infarctionSecondary hemorrhageHydrocephalusBrain death
  78. 78. Herniation•  Supra- andinfratentorial cranialcompartments by duraand bones•  Expanding lesion mechanical shift ofcerebral parenchyma,CSF and attached BVfrom one compartmentto another
  79. 79. HerniationHerniation Clinical Findings Imaging Findings Where toLook?ComplicationsDescendingtranstentorial• Ipsilated dilated pupil• Contralateral hemiparesis• Ipsilateral hemiparesis (ifKernohan notch is present)• Uncus extending into suprasellarcistern• Widening of ipsilateral ambient andprepontine cisterns• Widening of contralateral temporalhornMidbrain Occipital infarctfrom PCAcompressionAscendingtranstentorial• Nausea• Vomitting• Obtundation• Spinning top appearance of midbrain• Narrow bilateral ambient cisterns• Filling of quadrigeminal plate cisternMidbrain andassociatedcisternsHydrocephalusRapid onsetobtundation andpossible deathAlar(sphenoid)• None • Displacement of MCA on axial views• Distorted insular cortex on sagittalviewsMCA NoneSubfalcine • Headache• Contralateral leg weakness• Asymmetric anterior falx• Obliterated ipsilateral frontal hornand atrium of lateral ventricle• Septum pellucidum shiftSeptumpellucidum atlevel of foramenof MonroIpsilateral ACAinfarctionTonsillar • Bilateral arm dysesthesia• Obtundation• Tonsils at level of dens on axial• Tonsils on sagittal 5mm belowforamen magnum (adult); 7mm below(children)Foramenmagnum onaxials andsagittalsObtundationDeath
  80. 80. Herniation: Tonsillar•  Downward displacement of tonsils throughforamen magnum•  Seen with–  Up to ½ of all descending transtentorial herniation–  Up to 2/3 of ascending transtentorial herniation
  81. 81. Herniation: Subfalcine andMidline Shift•  Shift of cingulate gyrus across midline below falx•  Thinner ipsilateral ventricle, dilated oppositeventricle (CSF obstruction at foramen of Monro)
  82. 82. Herniation: Subfalcine andMidline Shift•  Measured at level of foramen of Monro•  Distal ACA may be compressed against falx
  83. 83. Herniation:Descending Transtentorial•  Medial and caudal shiftof uncus andparahippocampal gyrusof temporal lobe beyondtentorium cerebelli•  Asymmetric prepontinecisterns and CP angle(wider on side of lesion)•  AchA, PCoA, PCA maybe compressed againsttentorium
  84. 84. Herniation:Descending TranstentorialBefore surgery After surgery
  85. 85. Herniation:Ascending Transtentorial•  Cranial shift of vermis andparts of superomedialcerebellar hemispherethrough tentorium incisura•  Compressed superiorcerebellar, vermiancisterns and forth ventricle
  86. 86. Posttraumatic Cerebral Edema•  Increased water content of brain and/orincreased intravascular blood volume•  Severe condition. Can be fatal•  Can be unilateral or bilateral•  Vasogenic and cytotoxic edema coexist(vasogenic immediately, then cytotoxic)•  Evolves over 24-48 hours•  Generally resolved in 2 weeks
  87. 87. Posttraumatic Cerebral Edema•  Generalized obliteration ofcortical sulci and SAspaces of suprasellar,perimesencephalic andcompressed/thin ventricles•  Diffuse hypodensity, loss ofgrey-white matter interface•  Hyperdense cerebellum•  Often w/ transtentorialherniation
  88. 88. Posttraumatic Ischemia/Infarct•  m/c cause = herniation•  m/c location = occipital(PCA infarct fromdescending transten)•  2nd m/c location = frontal(ACA infarct fromsubfalcine h)•  Rare = basal ganglia(perforator/choroidalinfarct against base skull)3 months laterAt time of trauma
  89. 89. PosttraumaticSecondary Hemorrhages•  Small hemorrhagic foci integmen = Duret hemorrhage–  Classic in midline ofpontomesencephalic junction–  May be multiple or extendinginto cerebellar peduncles•  Necrosis/hemorrhage ofcontralateral cerebralpeduncle = Kernohan’s notch“false localizing sign”Hemorrhage in the midline nearpontomesencephalic junction. Also noteintraventricular hemorrhage in the 4thventricle
  90. 90. Hydrocephalus•  Acute hydrocephalus canoccur 2/2 brain herniationor IVH•  Delayed hydrocephalususually 2/2 adherence ofmeninges over cerebralconvexity, basal cisternsor aqueduct resulting inobstruction at level ofventricles and arachnoidgranulationsLook for “early sign” of hydrocephalus at temporal horns of lateral ventricles.When acute with high ICP, there may be hypodensity around the frontal horns of lateral ventricles
  91. 91. Brain Death•  Severe increased ICPdecreases cerebral bloodflow, then irreversible lossof brain function•  Clinical criteria: coma +absent brainstem reflexes+ apnea test•  No flow in intracranialarteries/venous sinuses•  Diffuse cerebral edema,hyperdense cerebellumPseudo-SAH with non-visualization of contrast enhancement of intracranial vessels.Only external carotid arterial branches are enhanced
  92. 92. Conclusions•  CT = primary modality for head trauma,enough for most parts– Skull x-rays still used in penetrating trauma,suspected child abuse– MR to help predicting prognosis by detectionof subtle injuries i.e., contusion and DAI•  Primary vs secondary lesion. Often,secondary lesion more important
  93. 93. Conclusions•  While checking the scan, make sure tothink if the patient needs CTA or other CTs(C-spine, facial bones, etc)•  Coup-contrecoup mechanism helpsconfirm acute trauma nature and searchfor subtle lesions
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