Imaging of Traumatic Brain Injury

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Imaging of Traumatic Brain Injury
Rathachai Kaewlai, MD
Ramathibodi Hospital, Mahidol University, Bangkok
Emergency Radiology Minicourse 2013
Slides available at RiTradiology.com or Slideshare.net/rathachai


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patients. All case descriptions are fictional, similar to descriptions you can
find in a multiple choice questions textbook for examination preparation.


Outline
•  Background of traumatic
brain injury (TBI)
•  Imaging modalities
–  CT
–  X-ray
–  MRI
•  Clinical prediction rules
•  Primary lesions
–  Intraaxial hemorrhages
–  Extraaxial hemorrhages
•  Secondary lesions


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) score
Head injury classified by GCS
13-15 = mild HI
8-12 = moderate HI
7 or less = severe HI


•  Closed or open? It depends on dura integrity
Closed Open
More common Less common
Dura intact Dura disrupted
Violent accelerations of
brain tissue (coup-
contrecoup)
Fracture or FB penetrating
dura


•  Primary or secondary brain lesions? It’s “how”
closely lesions are linked to traumatic event
Primary Secondary
Caused by trauma itself Processes arising from 1) brain’s
responses to trauma 2)
compression of brain, CN, BV,
skull and dura
Less devastating More devastating
Skull fractures, extraaxial
hemorrhages, intraaxial lesions
(DAI, contusion, IVH)
Herniations, diffuse edema,
infarction and infarction
DAI = Diffuse axonal injury, IVH = intraventricular hemorrhage, CN = cranial nerves, BV = blood vessels


Goals of Imaging in TBI
Goals Answered by...
Rapid diagnosis of life-
threatening injuries
Explanation of neurological
abnormality
Prognosis information
CT
CT (if not  MRI)
Clinical findings, CT, MRI,
advanced MR techniques


CT in TBI: Why?
•  Widely available
•  Fast
•  Sensitive for detection and evaluation of
injuries requiring acute neurosurgical
intervention
  Deciding whether surgical or medical Rx
Image from salvationist.ca


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 injury
HI = head injury


CT in TBI: When?
•  Patients with mild HI with
one of 7 clinical findings
need CT:
–  Short-term memory deficit
–  Drug/alcohol intoxication
–  Physical evidence of trauma
above clavicles
–  Age > 60
–  Seizure
–  Headache
–  Vomiting
NEJM 2000
New Orleans Criteria
Using this scheme, CT
positivity rate was about
7-10%
Sensitivity = 100%


CT in TBI
•  Sensitivity for
predicting need for
neurosurgery
–  High risk 100%
–  Medium risk 98.4%
•  Reduced the need
for CT in mild HI to
54%
•  Positivity rate = 8%
(1% of cases
require
neurosurgical
intervention)
Stiell IG, et al. Lancet 2001;357:1391-96. | Diagram from ohri.ca


CT in TBI: How?
•  Non-contrast, axial scan with spiral technique
•  At our hospital, we use 3 mm slice thickness and
alway do bone algorithm, coronal/sagittal
reformations
•  If you see maxillary hemosinus  do facial CT
•  If you see skull base fracture  consider CTA
and skull base reformation (thin slices with small
FOV)
•  If suspect C-spine fracture  do C-spine CT


CT in TBI: Checklist
•  Look at all three windows
Brain Subdural Bone


CT in TBI: Checklist
•  Look for primary lesions
•  Don’t forget secondary lesions (they may
be more catastrophic)
•  If the study looks near-normal
–  Find coup injury  look for contrecoup (can be
subtle)
–  Check potential areas for contusions and DAI (esp if
low GCS)
•  Recheck interpeduncular fossa for small
SAH


Skull X-ray: Outdated Yet?
•  No!
•  Penetrating injury
•  Radiopaque foreign bodies e.g. GSW
•  Part of skeletal survey in cases suspecting
child abuse
•  Caveats: Skull fractures...
– About 1/3 of cases with severe TBI do not
have skull fracture!
– Negative skull x-ray does not mean no CT


Skull X-ray: How?
•  Skull trauma series in adults should
include at least 3 views given complex
skull bones
– Frontal
– Lateral
– Towne’s
•  Learn to find fractures and distinguish
them from mimics


MRI in TBI: Pros
•  More sensitive for 10 and 20 injuries than CT
•  Better differentiation of hemorrhagic and
non-hemorrhagic lesions in acute phase
Same-day MRI
Diffuse axonal injury


MRI in TBI: Cons
•  Intrinsic limits:
–  Absolute C/I: cardiac pacemaker, ferromagnetic foreign
bodies
–  Lower sensitivity for bone fractures and hyperacute blood
•  Difficult managing trauma patients in MRI suite:
metallic life support, monitoring device, time
T1 T2 FLAIR
CT
Images from Scarabino, et al. Emergency Neuroradiology, 2006


SKULL FRACTURE


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


Quick Anatomy
(c) 2003 Encyclopedia Brittanica


Quick Anatomy


Types of Skull Fracture
•  Linear fracture
–  a/w EDH, SDH
•  Depressed fracture
–  a/w focal parenchymal
lesions
•  Skull base fracture
•  Open head injuries
–  Knife, firearm
–  Laceration of dura www.uchospitals.edu


Significance of Skull Fracture
•  Indicator of brain injuries?...Not quite
– Present in the majority of cases with severe
HI
– 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


Skull Fracture: Imaging
•  Best = Helical CT scan with multiplanar
reformation (MPR)
In-plane fracture easier to see on reformats


Skull Fracture: Imaging
•  Bone window with edge enhancement algorithm
Soft tissue algorithm Bone algorithm


Skull Fracture: Difficulty on XR
Window level adjustedRoutine window


Skull Fracture vs. Suture
FRACTURE SUTURE
Smooth or jagged edge Serrated edge
Straight line Curvilinear line
Angular turn Curvilinear turn
Greater in width Lesser in width
(X-ray) darker (X-ray) lighter
Any locations Specific anatomic location


Skull Fracture: Difficulty on CT
Use subgaleal hematoma as a clue


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


Skull Fracture: Depressed
•  In adults, criteria to elevate:
–  >8-10 mm depression or >1
thickness of skull
–  Deficit related to underlying brain
–  CSF leak
•  In children, two types:
–  Simple depressed: usually
remodelling occurs with growth,
surgery if dura penetrated or
persistent cosmetic defect
–  Ping-pong ball fractures: Rx if
underlying brain injury or dura
penetrated


Skull Fracture: Skull Base
•  Most are extensions of
fracture of cranial vault
•  Clinical clues:
–  CSF otorrhea or rhinorrhea
–  Hemotympanum or laceration of
EAC
–  Postauricular ecchymoses
–  Periorbital ecchymoses in
absence of direct orbital trauma
esp if bilateral
–  Cranial nerve injury (I, VI, VII,
VIII)
Longitudinal


Skull Fracture: Skull Base
•  Thin slices, bone
algorithms and
coronal images
needed for Dx
•  Indirect CT signs:
–  Pneumocephalus
–  Air-fluid level or
opacification of
mastoid or sinuses
Longitudinal Oblique


Skull Fracture:
Missile Injuries
Depressed Penetrating Perforating
Missile not
penetrate skull
but produces
depressed fx
or brain
contusion
Missile enters
cranial cavity
but does not
leave it
Missile enters
and exits
cranial cavity
Focal brain
damage
Injury depends
on damage to
vital structures
Most severe
injury due to
shockwaves
generated by
missiles
Foreign body,
meningitis,
abscesses
Foreign body,
meningitis,
abscesses


Skull Fracture: Pneumocephalus
•  Gas within cranial cavity
•  In acute trauma setting, this is
commonly due to fractures of
PNS and temporal bones (open
skull fracture is another cause)
•  Most do not cause immediate
danger but rapid expansion can
lead to brain compression
(tension pneumocephalus)
–  Mount Fuji sign
•  Usually decreases by 10-15 days
and almost never present by 3
weeks


DIFFUSE AXONAL INJURY


Diffuse Axonal Injury (DAI)
•  Traumatic acceleration/deceleration or violent
rotation
•  LOC immediately at the time of trauma  coma
•  Most severe of all primary brain lesions
Images from http://www.pathguy.com/bryanlee/dai.htm


Diffuse Axonal Injury (DAI)
•  Frequent cause of
persistent vegetative
state / morbidity in
trauma patients
•  Clinical symptoms
worse than CT findings
•  Can be isolated with no
or little association with
SAH, SDH, fracture


Diffuse Axonal Injury
•  Non-hemorrhagic 80% of cases
•  Common locations:
–  Grey-white matter interface (m/c)
–  Corpus callosum
–  Dorsolateral midbrain
•  Number and location of lesions
predict prognosis (worse if
multiple & supratentorial)
•  MRI most sensitive imaging but
still underestimates real extent
Susceptibility-weighted MRI
CT


Diffuse Axonal Injury
•  When initial head CT is normal but the
patient is in vegetative state
– Do MRI with susceptibility sequence OR
– Follow up CT in 24 hours (1/6 of DAI will
evolve)
Small interpeduncular SAH and petechial hemorrhage in dorsolateral midbrain on CT and susceptibility-weighted MRI


CEREBRAL CONTUSION


Cerebral Contusion
•  Cerebral gyri impact inner table skull
•  Characterizes coup and contrecoup
injuries
•  Petechial hemorrhage of gyri  small
hemorrhage  large hematoma
Images from Wikipedia.org


Cerebral Contusion
•  Anterior base frontal,
temporal lobes (esp
tip), cortex surrounding
Sylvian fissure
•  Multiple, bilateral


Cerebral Contusion
•  Can be normal early; can be non-hemorrhagic
•  Imaging worsened with time, most evident after 24 h
Day 0 Day 1


Cerebral Contusion: MRI
FLAIR T2W
MRI 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


OTHER INTRAAXIAL LESIONS
Traumatic intraparenchymal hematoma
Intraventricular hemorrhage
Traumatic lesions of deep grey structures and brainstem


Intraparenchymal Hematoma
•  Parenchymal vessel
rupture from blunt or
penetrating forces
•  May not lose
consciousness (unlike
DAI, contusion)
•  Hematoma at primary
trauma site (usually
frontal and temporal)


Intraparenchymal Hematoma
•  Well-circumscribed
hyperdense lesion w/wo
perilesional edema
•  Up to 60% a/w SDH, EDH
•  Not always easy to
distinguish IPH from DAI or
contusion
Traumatic intraparenchymal hemorrhage with IVH


Intraventricular Hemorrhage
•  Uncommon
•  Consequence of severe trauma. a/w DAI and
trauma of deep grey and brainstem
•  Poor prognosis


Trauma of Deep Grey &
Brainstem
•  Stretch and torsion causing ruptured perforators,
or direct impact on dorsolateral brainstem
against tentorial incisura
•  Severe trauma, poor prognosis
•  CT:
–  Small hemorrhages in brainstem surrounding
aqueduct, basal grey nuclei
–  Can be normal


EPIDURAL HEMATOMA


Epidural Hematoma (EDH)
•  Hematoma between inner
table of the skull and dura
•  Source of bleeding
–  Most common = middle
meningeal artery (90%)
(squamous temporal bone)
–  Venous EDH from dural
venous sinus
www.practicalhospital.com


•  Most urgent of all cases of cranial trauma
–  Requiring prompt Rx to relieve compression of
brainstem, 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


•  Delayed development in 10-25% of cases
(within 36 hrs)
– Arterial EDH: blood can flow into epidural
space only after resolution of arterial spasm
– Venous EDH bleeds slowly


Epidural Hematoma:
CT Appearance
•  Biconvex or lens shape
hyperdense lesion (rare to be
isodense)
•  May cross midline and dural
attachment
•  Do not cross suture (except
diastatic fracture, large EDH)


Epidural Hematoma:
Potential Indications for Surgery
•  Size > 2 cm
•  Active bleeding
•  Impending herniation
•  Corresponding
neurologic deficit


Epidural Hematoma: Swirl Sign
•  First described by
Zimmerman in 1982
•  Small rounded lesion
isodense to the brain,
representing active
extravasation of
unclotted blood
•  Clotted component is
hyperdense (50-70
HU)


Venous EDH
•  Tear of venous sinus
(high flow, low pressure
system)
•  More benign course,
subacute presentation,
usually not require
surgery
•  Posterior fossa venous
sinus > sagittal sinus


SUBDURAL HEMATOMA


Subdural Hematoma (SDH)
•  Blood collects between
dura and arachnoid
•  Torn cortical bridging veins
•  10-20% of all cranial
trauma cases
•  Demographics:
–  Elderly (60-80y) with brain
atrophy,
–  Large intracranial
subarachnoid spaces
–  “Shaken baby syndrome”
www.nucleusinc.com


Subdural Hematoma (SDH)
•  Usually co-exist with
other brain injuries
–  Esp. contusion-typed
injuries > skull fractures
•  Acute: within 3 days
from trauma
•  Subacute: within 3 mo
•  Chronic: after 3 months
Layer of acute blood on pre-existing CSF-like subdural
collection in the right cerebral convexity


Subdural Hematoma:
CT Appearance
•  Crescentic hyperdense
collection
•  Can cross suture
•  Can extend to
interhemispheric
fissure, along tentorium
cerebelli
Note coup (Rt.) and contrecoup (Lt.) pattern.
This SDH is a contrecoup injury.


Subdural Hematoma:
Value of Coronal Reformats


Bilateral Subdural Hematomas
Don’t feel “enough” with trauma findings. There’re almost always more to be discovered.


“Isodense” Subdural Hematoma
•  Usually takes 2-6
weeks for acute SDH
to become isodense
•  At Hb 8-10 g/dL, blood
will be isodense to
grey matter
•  Anemic patients can
present with acute
isodense SDH


Acute On Chronic SDH
•  New hemorrhage
superimposed on
chronic SDH
•  Recurrent trauma
•  Can be spontaneous
•  Blood-fluid level , blood
clot organization,
membranes


Comparison of EDH and SDH
EDH SDH
Incidence 1-4% of trauma cases;
10% of fatal trauma cases
10-20% of all trauma cases;
30% of fatal trauma cases
Etiology a/w fractures in 90% of cases
Laceration of MMA/venous sinus
Tearing of cortical veins
Site Between skull and dura
95% supratentorial
Between dura and arachnoid
95% supratentorial
Crosses dura but not sutures Crosses suture but not dura
CT findings Biconvex (lens) shape
Shift grey-white matter interface
Crescentic shape
Diagram from Kumar et al. Basic Pathology 7E


Subdural Hygroma
•  Extraaxial collection of
CSF caused by
extravasation of CSF
from SA space
through a traumatic
tear in arachnoid
mater
•  Acute: Children >> adults
•  Subacute and chronic:
Following surgery for head
injuries in operative bed or
opposite site
1 week after injury
Day of injury


TRAUMATIC SUBARACHNOID
HEMORRHAGE (TSAH)


Subarachnoid Hemorrhage
(SAH)
•  Blood collects beneath
arachnoid
•  Tear of veins in SA space
•  Usually associated with
other brain injuries
(common with contusions)
•  ‘Nearly all cases of
traumatic SAH have other
lesions to suggest
traumatic cause’
–  Isolated SAH in trauma
patients – possible ruptured
aneurysm causing trauma
SAH with SDH


•  Site
–  Next to brain contusion,
under SDH/fracture/
scalp lac
–  Can be distant because
blood diffuses in SA
space
•  IVH may co-exist due to
retrograde flow through
foramen of Luschka
and Magendie
SAH with contusion


•  Subtle SAH –
interpeduncular fossa


TRAUMATIC VASCULAR
LESIONS
ICA dissection
Carotid-cavernous fistula (CCF)


Traumatic Vascular Lesions
•  Rare
•  Can be overlooked initially
•  ICA injury (dissection, aneurysm, occlusion)
–  Base of skull fracture
•  Traumatic carotid-cavernous fistula (TCCF)


Traumatic ICA Injury
•  Common cause of
ischemic stroke in the
young
•  Extracranial ICA much
more common (esp
just proximal to
petrous bone)
•  Dissection 
occlusion or
thromboembolism
At initial trauma, there were diffuse subarachnoid hemorrhage, pneumocephalus, facial fractures
and C-spine injury. Days after the injury (image C) , the patient developed left ICA territory
infarction. Angiiography (D) confirmed occlusion of the cervical ICA.
Images from Yang S, et al. J Clin Neurosci 2006;13:123


Traumatic CCF
•  Most common traumatic AV fistula = CCF
–  Clues on CT: proptosis, bulging cavernous sinus, enlarged-
arterialized ophthalmic vein
A vividly enhancing structure in the right cavernous sinus with a dilated superior ophthalmic vein.
Note right proptosis


SECONDARY LESIONS
Herniation
Cerebral edema
Ischemia and infarction
Secondary hemorrhage
Hydrocephalus
Brain death


Herniation
•  Supra- and
infratentorial cranial
compartments by dura
and bones
•  Expanding lesion 
mechanical shift of
cerebral parenchyma,
CSF and attached BV
from one compartment
to another Wikipedia.org


Herniation
Herniation Clinical Findings Imaging Findings Where to
Look?
Complications
Descending
transtentorial
• Ipsilated dilated pupil
• Contralateral hemiparesis
• Ipsilateral hemiparesis (if
Kernohan notch is present)
• Uncus extending into suprasellar
cistern
• Widening of ipsilateral ambient and
prepontine cisterns
• Widening of contralateral temporal
horn
Midbrain Occipital infarct
from PCA
compression
Ascending
transtentorial
• Nausea
• Vomitting
• Obtundation
• Spinning top appearance of midbrain
• Narrow bilateral ambient cisterns
• Filling of quadrigeminal plate cistern
Midbrain and
associated
cisterns
Hydrocephalus
Rapid onset
obtundation and
possible death
Alar
(sphenoid)
• None • Displacement of MCA on axial views
• Distorted insular cortex on sagittal
views
MCA None
Subfalcine • Headache
• Contralateral leg weakness
• Asymmetric anterior falx
• Obliterated ipsilateral frontal horn
and atrium of lateral ventricle
• Septum pellucidum shift
Septum
pellucidum at
level of foramen
of Monro
Ipsilateral ACA
infarction
Tonsillar • Bilateral arm dysesthesia
• Obtundation
• Tonsils at level of dens on axial
• Tonsils on sagittal 5mm below
foramen magnum (adult); 7mm below
(children)
Foramen
magnum on
axials and
sagittals
Obtundation
Death


Herniation: Tonsillar
•  Downward displacement of tonsils through
foramen magnum
•  Seen with
–  Up to ½ of all descending transtentorial herniation
–  Up to 2/3 of ascending transtentorial herniation


Herniation: Subfalcine and
Midline Shift
•  Shift of cingulate gyrus across midline below falx
•  Thinner ipsilateral ventricle, dilated opposite
ventricle (CSF obstruction at foramen of Monro)


Herniation: Subfalcine and
Midline Shift
•  Measured at level of foramen of Monro
•  Distal ACA may be compressed against falx


Herniation:
Descending Transtentorial
•  Medial and caudal shift
of uncus and
parahippocampal gyrus
of temporal lobe beyond
tentorium cerebelli
•  Asymmetric prepontine
cisterns and CP angle
(wider on side of lesion)
•  AchA, PCoA, PCA may
be compressed against
tentorium


Herniation:
Descending Transtentorial
Before surgery After surgery


Herniation:
Ascending Transtentorial
•  Cranial shift of vermis and
parts of superomedial
cerebellar hemisphere
through tentorium incisura
•  Compressed superior
cerebellar, vermian
cisterns and forth ventricle


Posttraumatic Cerebral Edema
•  Increased water content of brain and/or
increased 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


Posttraumatic Cerebral Edema
•  Generalized obliteration of
cortical sulci and SA
spaces of suprasellar,
perimesencephalic and
compressed/thin ventricles
•  Diffuse hypodensity, loss of
grey-white matter interface
•  Hyperdense cerebellum
•  Often w/ transtentorial
herniation


Posttraumatic Ischemia/Infarct
•  m/c cause = herniation
•  m/c location = occipital
(PCA infarct from
descending transten)
•  2nd m/c location = frontal
(ACA infarct from
subfalcine h)
•  Rare = basal ganglia
(perforator/choroidal
infarct against base skull)
3 months later
At time of trauma


Posttraumatic
Secondary Hemorrhages
•  Small hemorrhagic foci in
tegmen = Duret hemorrhage
–  Classic in midline of
pontomesencephalic junction
–  May be multiple or extending
into cerebellar peduncles
•  Necrosis/hemorrhage of
contralateral cerebral
peduncle = Kernohan’s notch
“false localizing sign”
Hemorrhage in the midline near
pontomesencephalic junction. Also note
intraventricular hemorrhage in the 4th
ventricle


Hydrocephalus
•  Acute hydrocephalus can
occur 2/2 brain herniation
or IVH
•  Delayed hydrocephalus
usually 2/2 adherence of
meninges over cerebral
convexity, basal cisterns
or aqueduct resulting in
obstruction at level of
ventricles and arachnoid
granulations
Look 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


Brain Death
•  Severe increased ICP
decreases cerebral blood
flow, then irreversible loss
of brain function
•  Clinical criteria: coma +
absent brainstem reflexes
+ apnea test
•  No flow in intracranial
arteries/venous sinuses
•  Diffuse cerebral edema,
hyperdense cerebellum
Pseudo-SAH with non-visualization of contrast enhancement of intracranial vessels.
Only external carotid arterial branches are enhanced


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 detection
of subtle injuries i.e., contusion and DAI
•  Primary vs secondary lesion. Often,
secondary lesion more important


Conclusions
•  While checking the scan, make sure to
think if the patient needs CTA or other CTs
(C-spine, facial bones, etc)
•  Coup-contrecoup mechanism helps
confirm acute trauma nature and search
for subtle lesions

Imaging of Traumatic Brain Injury

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