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- Dr.Neeraj Patange
INTRODUCTION
 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
CLASSIFICATION
It depends on dura integrity
Primary or secondary brain
lesions
 It’s “how” closely lesions are linked to
traumatic event.
According to Location of
Lesions
• Intra-axial: Cortical contusions,
intracerebral hematoma, axonal
shearing injuries, gray matter injury, and
vascular injury
• Extra-axial: Epidural, subdural,
subarachnoid, and intraventricular
hemorrhage.
Goals of Imaging
Skull X-ray
 Skull xray is still a primary modality for head
trauma without any neurological deficit.
 Penetrating injury
 Radiopaque foreign bodies.
 Part of skeletal survey in cases suspecting
child abuse
 Drawbacks: not 100% sensitive for 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
 Skull trauma series in adults should
include at least 3 views given complex
skull bones
– Frontal
– Lateral
– Towne’s
 The reader should be able to find
fractures and distinguish them from
mimics
CT IN CNS TRAUMA
 Widely available
 Fast.
 Sensitive for detection and evaluation of
injuries requiring acute neurosurgical
intervention
 Deciding whether surgical or medical
Rx
ROLE OF CT IN CNS
TRAUMA
 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.
INDICATION OF CT IN CNS
TRAUMA
 Patients with mild Head Injury with one of
7 clinical findings need CT:
1. Short-term memory deficit
2. Drug/alcohol intoxication
3. Physical evidence of trauma above
clavicles
4. Age > 60
5. Seizure
6. Headache
7. Vomiting
INDICATION OF CT IN CNS
TRAUMA
Approach to a CNS trauma
case
 Non-contrast, axial scan with spiral
technique
 Use 3 mm slice thickness and always do
bone algorithm, coronal/sagittal
reformations
 If you see maxillary hemosinus ,do facial
CT
 If you see skull base fracture consider 3D
reconstruction and skull base reformation
(thin slices with small FOV)
 If suspect C-spine fracture do C-spine CT.
All three windows
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
MRI IN CNS TRAUMA
PROS-
 More sensitive for 10 and 20 injuries than CT
 Better differentiation of hemorrhagic and non-
hemorrhagic lesions in acute phase.
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
SCALP INJURY
 Begin by looking at the extracranial
structures for evidence of soft-tissue injury
and/or radio-opaque foreign bodies.
 Scalp injury provides a reliable indication of
the site of impact.
 Types of Scalp Injury
 • Simple soft-tissue lacerations
 • Subgaleal hematoma
 • Cephalohematoma
 • Residual foreign bodies
SKULL FRACTURE
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
Cns trauma
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
Significance of Skull
Fracture
 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)
 Bone window with edge enhancement
algorithm.
Difficulty on XR
Cns trauma
Skull Fracture: Difficulty on
CT
TYPES
1. 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
Cns trauma
2. 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
3. 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)
Skull Base
• Thin slices, bone algorithms and coronal
images needed for Diagnosis
• Indirect CT signs:
– Pneumocephalus
– Air-fluid level or opacification of
mastoid or sinuses
Cns trauma
Temporal Bone Fractures
• Presence of pneumocephalus,
• Opacification of the mastoid air cells, and
• Fluid in the middle ear cavity should raise
the suspicion of a temporal bone
fracture.
Types of Temporal Bone
Fractures
1. Longitudinal
2. Transverse
3. Mixed
 Fractures are classified depending on the
orientation of fracture line relative to the
long axis of the petrous bone.
 Longitudinal fractures parallel the long axis
of the petrous pyramid, and transverse
fractures are perpendicular to the long axis
of the petrous bone.
Thin-CT sections (1 mm) in axial plane in bone
algorithm showing temporal bone fractures. (A) Transverse
fracture
(B) Longitudinal 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
• 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
• 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
• 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)
CEREBRAL CONTUSION
• Cerebral gyri impact inner table skull
• Characterizes coup and contrecoup
injuries
• Petechial hemorrhage of gyri leading to
small
hemorrhage followed by large hematoma
Cns trauma
• Anterior base frontal,
temporal lobes (esp
tip), cortex surrounding
Sylvian fissure
• Multiple, bilateral
• Can be normal early;
can be non-hemorrhagic
• Imaging worsened with
time,
most evident after 24 h
Cns trauma
Cerebral Contusion: MRI
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
Cns trauma
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)
• 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
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
• 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
• 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
Cns trauma
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)
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
• 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”
• Usually co-exist with other brain injuries
– Esp. contusion-typed injuries > skull fractures
• Acute: within 3 days from trauma
• Subacute: within 3 months
• Chronic: after 3 months
Cns trauma
Subdural Hematoma:
CT Appearance
• Crescentic hyperdense collection
• Can cross suture
• Can extend to interhemispheric fissure,
along tentorium cerebelli
Cns trauma
Cns trauma
“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
Cns trauma
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
TRAUMATIC SUBARACHNOID
HEMORRHAGE (TSAH)
• 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
• 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
Cns trauma
TRAUMATIC VASCULAR
LESIONS
• Rare
• Can be overlooked initially
• ICA injury (dissection, aneurysm,
occlusion)
– Base of skull fracture
• Traumatic carotid-cavernous fistula
(TCCF)
 MR findings of vascular injury include:
(a) presence of an intramural hematoma, which is
best seen on T1-weighted with fat suppression;
(b) intimal flap with dissection and
(c) absence of a normal vascular flow void secondary
to slow flow or occlusion.
 An associated parenchymal infarction supplied by
the injured vessel may also be seen.
 Conventional angiogram remains the gold standard
for confirmation and delineation of the vascular
dissection and may also show spasm or
pseudoaneurysm formation.
 However, magnetic resonance angiography and
MDCT angiography serve as important screening
tools in the evaluation of patients with suspected
vascular injury.
Traumatic ICA Injury
• Common cause of ischemic stroke in the
young
• Extracranial ICA much more common
(esp just proximal to petrous bone)
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.
Traumatic CCF
 • Most common traumatic AV fistula = CCF
– Clues on CT: proptosis, bulging cavernous sinus, enlarged arterialized
ophthalmic vein
 The injury leads to communication between the cavernous portion of the
internal carotid artery and the surrounding venous plexus, resulting in
venous engorgement of the cavernous sinus and its draining branches
namely the ipsilateral superior ophthalmic vein and inferiorpetrosal
sinus.
 Skull base fractures, especially those involving the sphenoid bone,
should alert the radiologist to search for associated cavernous carotid
injury.
 Another cause of CCF is the rupture of a cavernous carotid aneurysm.
On imaging, CCF can present as an enlarged superior ophthalmic vein,
cavernous sinus, and/or petrosal sinus.
 Other findings include proptosis, preseptal soft-tissue swelling, and
extraocular muscle enlargement.
 The findings may be bilateral because venous channels connect the
cavernous sinuses. Again, definitive diagnosis often requires selective
carotid angiography with rapid filming to demonstrate the site of
communication. Patients can present with findings weeks or even
months after the initial trauma.
Types of CCF
Type A: Direct shunt between ICA and
cavernous sinus
Type B: Fistula between meningeal
branches of ICA and cavernous sinus
Type C: Fistula between meningeal
branches of ECA and cavernous sinus
Type D: Fistula between meningeal
branches of both ICA and ECA and
cavernous sinus.
Cns trauma
SECONDARY LESIONS
Herniation
• Supra- and
infratentorial cranial
compartments by dura
and bones
• Expanding lesion causing
mechanical shift of
cerebral parenchyma,
CSF and attached BV
from one compartment
to another
TYPES
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
Cns trauma
Herniation: Subfalcine
 Subfalcine herniation is the most
common form of herniation.
 Imaging features include displacement of
the cingulate gyrus across the midline
under the falx cerebri, compression of the
ipsilateral ventricle due to mass effect and
enlargement of the contralateral ventricle
due to obstruction of the foramen of Monro.
 Due to such displacement, there will be
trapping of the callosomarginal branches of
the ACA, which may lead to ACA infarction.
Transtentorial herniation
 Can occur either in upward or downward direction.
 Upward herniation typically occurs with large
posterior fossa hematomas that displace portions
of the cerebellum and vermis through the tentorial
incisura.
 The mass effect of the hematoma can also cause
downward herniation of the cerebellar tonsils through
the foramen magnum.
 Downward herniation of the cerebrum manifests
as effacement of the suprasellar and
perimesencephalic cisterns. Inferior displacement of
the pineal calcification is an additional imaging clue
for the presence of downward herniation.
 Axial CT images showing various types of brain
herniations. (A) Subfalcine heraniation, (B)
Uncal Herniation, (C) Downward transtentorial
and (D) Ascending transtentorial herniation
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
• 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 with transtentorial
herniation
Posttraumatic
Ischemia/Infarct
• m/c cause = herniation
• m/c location = occipital (PCA infarct from
descending transtentorial)
• 2nd m/c location = frontal(ACA infarct
from
subfalcine hemorrhage)
• Rare = basal ganglia
(perforator/choroidal
infarct against base skull)
Cns trauma
Hydrocephalus
• Acute hydrocephalus can occur
secondary to brain herniation or IVH
• Delayed hydrocephalus usually
secondary 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
Cerebrospinal fluid (CSF)
leak
 Occurs when there is an osseous and dural
defect at the skull base, with direct
communication of the subarachnoid space
to the extracranial space, usually a
paranasal sinus.
 Recognition of the leak site and sourceand
appropriate treatment are necessary to
avoid rhinorrhea or otorrhea, low-pressure
headaches, and meningitis, known
complications of CSF leak.
• CSF otorrhea occurs when there is
communication between
the subarachnoid space and middle ear in association
with a
ruptured tympanic membrane.
• CSF rhinorrhea occurs when there is
communication between
the subarachnoid space and the paranasal sinuses.
Eighty percent of posttraumatic CSF leaks occur
within the
first 48 hours after injury, and 95 percent will manifest
within the
first 3 months. A small subset of patients will present
with rhinorrhea
or meningitis decades after the trauma.
CT Cisternography
 CT cisternography is being used widely for evaluating a possible
CSF fistula.
 This technique traditionally involves obtaining thin section coronal
and axial CT images in both prone and supine positions through the
region of interest (maxillofacial or temporal region) both before and
after intrathecal contrast material.
 Approximately 3–10 mL of an iodinated nonionic low-osmolar
contrast agent is administered by means of lumbar puncture, and
the patient is placed in a Trendelenburg position to opacify the
basal cisterns, followed by CT imaging after administration of
contrast material.
 Manoeuvres that provoke an active leak, such as sneezing or head
hanging, are performed prior to the CT portion of cisternography.
Postcontrast images are then compared with the precontrast
images.
 A positive result involves the presence of a skull base defect and
contrast opacification within the sinus, nasal cavity, or middle ear.
 MR cisternography typically involves heavily T2-
weighted fast spin-echo sequences with fat
suppression and subtraction of the adjacent
background tissue signal to enhance conspicuity of
the fistulous tract, or CSF column.
 The fast spin-echo sequences have decreased
susceptibility artifacts at the air-bone interface of
the skull base, compared with conventional T2-
weighted imaging.
 Images are generally obtained in coronal, axial, and
sagittal planes, and, similar to conventional MR, the
finding of a contiguous CSF column communicating
from the subarachnoid space to the extracranial
space and/or the herniation of brain parenchyma
and/ or meninges, extracranially heralds a positive
examination.
 MR images in multiple planes showing herniation of brain
parenchyma through the bone defect in anterior cranial fossa (arrow)
and air-cerebrospinal fluid level suggestive of communication with
paranasal sinuses
The leptomeningeal cyst or
“growing fracture”
 Leptomeningeal cysts are usually delayed complications of skull
fractures, although they occasionally occur within weeks of trauma.
 Since the infant skull is highly malleable, the margins of pediatric
skull fractures are often inwardly displaced at the time of trauma.
 The pia-arachnoid membrane (and occasionally swollen, edematous
cortex) can herniate through the dural tear and prevent apposition
and healing of the dura. CSF pulsations subsequently fill and enlarge
the subarachnoid pouch that extends through the fracture line.
 The pulsations eventually widen the dural defect and expand the
fracture margins. This results in a leptomeningeal cyst that extends
from the subarachnoid space into the subgaleal space.
 CSF pulsations tend to erode the inner table more than the outer one,
giving rise to “beveled” edges.
 The margins of the fracture often show marked resorption and
saucerization.
 The term “growing fracture” refers to interval widening of the space
between the fracture margins on successive skull radiographs or CT
scans.
 CT images showing features of leptomeningeal cyst (growing fracture) as
evidenced by herniation of subarachanoid space though the fracture line
into subcutaneous tissue with underlying encephalomalacia, focal
ventricular enlargement.
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
Thank you!!

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Cns trauma

  • 2. INTRODUCTION  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
  • 4. Primary or secondary brain lesions  It’s “how” closely lesions are linked to traumatic event.
  • 5. According to Location of Lesions • Intra-axial: Cortical contusions, intracerebral hematoma, axonal shearing injuries, gray matter injury, and vascular injury • Extra-axial: Epidural, subdural, subarachnoid, and intraventricular hemorrhage.
  • 7. Skull X-ray  Skull xray is still a primary modality for head trauma without any neurological deficit.  Penetrating injury  Radiopaque foreign bodies.  Part of skeletal survey in cases suspecting child abuse  Drawbacks: not 100% sensitive for Skull fractures. – About 1/3 of cases with severe TBI do not have skull fracture. – Negative skull x-ray does not mean no CT
  • 8. Skull X-ray  Skull trauma series in adults should include at least 3 views given complex skull bones – Frontal – Lateral – Towne’s  The reader should be able to find fractures and distinguish them from mimics
  • 9. CT IN CNS TRAUMA  Widely available  Fast.  Sensitive for detection and evaluation of injuries requiring acute neurosurgical intervention  Deciding whether surgical or medical Rx
  • 10. ROLE OF CT IN CNS TRAUMA  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.
  • 11. INDICATION OF CT IN CNS TRAUMA  Patients with mild Head Injury with one of 7 clinical findings need CT: 1. Short-term memory deficit 2. Drug/alcohol intoxication 3. Physical evidence of trauma above clavicles 4. Age > 60 5. Seizure 6. Headache 7. Vomiting
  • 12. INDICATION OF CT IN CNS TRAUMA
  • 13. Approach to a CNS trauma case  Non-contrast, axial scan with spiral technique  Use 3 mm slice thickness and always do bone algorithm, coronal/sagittal reformations  If you see maxillary hemosinus ,do facial CT  If you see skull base fracture consider 3D reconstruction and skull base reformation (thin slices with small FOV)  If suspect C-spine fracture do C-spine CT.
  • 15. 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
  • 16. MRI IN CNS TRAUMA PROS-  More sensitive for 10 and 20 injuries than CT  Better differentiation of hemorrhagic and non- hemorrhagic lesions in acute phase. 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
  • 17. SCALP INJURY  Begin by looking at the extracranial structures for evidence of soft-tissue injury and/or radio-opaque foreign bodies.  Scalp injury provides a reliable indication of the site of impact.  Types of Scalp Injury  • Simple soft-tissue lacerations  • Subgaleal hematoma  • Cephalohematoma  • Residual foreign bodies
  • 18. SKULL FRACTURE 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
  • 20. 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
  • 21. Significance of Skull Fracture  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
  • 22. Skull Fracture: Imaging  Best = Helical CT scan with multiplanar reformation (MPR)  Bone window with edge enhancement algorithm.
  • 26. TYPES 1. 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
  • 28. 2. 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
  • 29. 3. 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)
  • 30. Skull Base • Thin slices, bone algorithms and coronal images needed for Diagnosis • Indirect CT signs: – Pneumocephalus – Air-fluid level or opacification of mastoid or sinuses
  • 32. Temporal Bone Fractures • Presence of pneumocephalus, • Opacification of the mastoid air cells, and • Fluid in the middle ear cavity should raise the suspicion of a temporal bone fracture.
  • 33. Types of Temporal Bone Fractures 1. Longitudinal 2. Transverse 3. Mixed  Fractures are classified depending on the orientation of fracture line relative to the long axis of the petrous bone.  Longitudinal fractures parallel the long axis of the petrous pyramid, and transverse fractures are perpendicular to the long axis of the petrous bone.
  • 34. Thin-CT sections (1 mm) in axial plane in bone algorithm showing temporal bone fractures. (A) Transverse fracture (B) Longitudinal fracture
  • 35. 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
  • 36. DIFFUSE AXONAL INJURY • 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
  • 37. • 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
  • 38. • 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)
  • 39. CEREBRAL CONTUSION • Cerebral gyri impact inner table skull • Characterizes coup and contrecoup injuries • Petechial hemorrhage of gyri leading to small hemorrhage followed by large hematoma
  • 41. • Anterior base frontal, temporal lobes (esp tip), cortex surrounding Sylvian fissure • Multiple, bilateral • Can be normal early; can be non-hemorrhagic • Imaging worsened with time, most evident after 24 h
  • 43. Cerebral Contusion: MRI 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
  • 45. 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)
  • 46. • 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
  • 47. Intraventricular Hemorrhage • Uncommon • Consequence of severe trauma. a/w DAI and trauma of deep grey and brainstem • Poor prognosis
  • 48. 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
  • 49. EPIDURAL HEMATOMA • 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
  • 50. • 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
  • 52. 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)
  • 53. 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)
  • 54. 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
  • 55. SUBDURAL HEMATOMA • 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” • Usually co-exist with other brain injuries – Esp. contusion-typed injuries > skull fractures • Acute: within 3 days from trauma • Subacute: within 3 months • Chronic: after 3 months
  • 57. Subdural Hematoma: CT Appearance • Crescentic hyperdense collection • Can cross suture • Can extend to interhemispheric fissure, along tentorium cerebelli
  • 60. “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
  • 61. Acute On Chronic SDH • New hemorrhage superimposed on chronic SDH • Recurrent trauma • Can be spontaneous • Blood-fluid level , blood clot organization, membranes
  • 63. 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
  • 64. TRAUMATIC SUBARACHNOID HEMORRHAGE (TSAH) • 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 • 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
  • 66. TRAUMATIC VASCULAR LESIONS • Rare • Can be overlooked initially • ICA injury (dissection, aneurysm, occlusion) – Base of skull fracture • Traumatic carotid-cavernous fistula (TCCF)
  • 67.  MR findings of vascular injury include: (a) presence of an intramural hematoma, which is best seen on T1-weighted with fat suppression; (b) intimal flap with dissection and (c) absence of a normal vascular flow void secondary to slow flow or occlusion.  An associated parenchymal infarction supplied by the injured vessel may also be seen.  Conventional angiogram remains the gold standard for confirmation and delineation of the vascular dissection and may also show spasm or pseudoaneurysm formation.  However, magnetic resonance angiography and MDCT angiography serve as important screening tools in the evaluation of patients with suspected vascular injury.
  • 68. Traumatic ICA Injury • Common cause of ischemic stroke in the young • Extracranial ICA much more common (esp just proximal to petrous bone)
  • 69. 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.
  • 70. Traumatic CCF  • Most common traumatic AV fistula = CCF – Clues on CT: proptosis, bulging cavernous sinus, enlarged arterialized ophthalmic vein  The injury leads to communication between the cavernous portion of the internal carotid artery and the surrounding venous plexus, resulting in venous engorgement of the cavernous sinus and its draining branches namely the ipsilateral superior ophthalmic vein and inferiorpetrosal sinus.  Skull base fractures, especially those involving the sphenoid bone, should alert the radiologist to search for associated cavernous carotid injury.  Another cause of CCF is the rupture of a cavernous carotid aneurysm. On imaging, CCF can present as an enlarged superior ophthalmic vein, cavernous sinus, and/or petrosal sinus.  Other findings include proptosis, preseptal soft-tissue swelling, and extraocular muscle enlargement.  The findings may be bilateral because venous channels connect the cavernous sinuses. Again, definitive diagnosis often requires selective carotid angiography with rapid filming to demonstrate the site of communication. Patients can present with findings weeks or even months after the initial trauma.
  • 71. Types of CCF Type A: Direct shunt between ICA and cavernous sinus Type B: Fistula between meningeal branches of ICA and cavernous sinus Type C: Fistula between meningeal branches of ECA and cavernous sinus Type D: Fistula between meningeal branches of both ICA and ECA and cavernous sinus.
  • 74. Herniation • Supra- and infratentorial cranial compartments by dura and bones • Expanding lesion causing mechanical shift of cerebral parenchyma, CSF and attached BV from one compartment to another
  • 75. TYPES
  • 76. 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
  • 78. Herniation: Subfalcine  Subfalcine herniation is the most common form of herniation.  Imaging features include displacement of the cingulate gyrus across the midline under the falx cerebri, compression of the ipsilateral ventricle due to mass effect and enlargement of the contralateral ventricle due to obstruction of the foramen of Monro.  Due to such displacement, there will be trapping of the callosomarginal branches of the ACA, which may lead to ACA infarction.
  • 79. Transtentorial herniation  Can occur either in upward or downward direction.  Upward herniation typically occurs with large posterior fossa hematomas that displace portions of the cerebellum and vermis through the tentorial incisura.  The mass effect of the hematoma can also cause downward herniation of the cerebellar tonsils through the foramen magnum.  Downward herniation of the cerebrum manifests as effacement of the suprasellar and perimesencephalic cisterns. Inferior displacement of the pineal calcification is an additional imaging clue for the presence of downward herniation.
  • 80.  Axial CT images showing various types of brain herniations. (A) Subfalcine heraniation, (B) Uncal Herniation, (C) Downward transtentorial and (D) Ascending transtentorial herniation
  • 81. 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
  • 82. • 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 with transtentorial herniation
  • 83. Posttraumatic Ischemia/Infarct • m/c cause = herniation • m/c location = occipital (PCA infarct from descending transtentorial) • 2nd m/c location = frontal(ACA infarct from subfalcine hemorrhage) • Rare = basal ganglia (perforator/choroidal infarct against base skull)
  • 85. Hydrocephalus • Acute hydrocephalus can occur secondary to brain herniation or IVH • Delayed hydrocephalus usually secondary adherence of meninges over cerebral convexity, basal cisterns or aqueduct resulting in obstruction at level of ventricles and arachnoid granulations
  • 86.  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
  • 87. Cerebrospinal fluid (CSF) leak  Occurs when there is an osseous and dural defect at the skull base, with direct communication of the subarachnoid space to the extracranial space, usually a paranasal sinus.  Recognition of the leak site and sourceand appropriate treatment are necessary to avoid rhinorrhea or otorrhea, low-pressure headaches, and meningitis, known complications of CSF leak.
  • 88. • CSF otorrhea occurs when there is communication between the subarachnoid space and middle ear in association with a ruptured tympanic membrane. • CSF rhinorrhea occurs when there is communication between the subarachnoid space and the paranasal sinuses. Eighty percent of posttraumatic CSF leaks occur within the first 48 hours after injury, and 95 percent will manifest within the first 3 months. A small subset of patients will present with rhinorrhea or meningitis decades after the trauma.
  • 89. CT Cisternography  CT cisternography is being used widely for evaluating a possible CSF fistula.  This technique traditionally involves obtaining thin section coronal and axial CT images in both prone and supine positions through the region of interest (maxillofacial or temporal region) both before and after intrathecal contrast material.  Approximately 3–10 mL of an iodinated nonionic low-osmolar contrast agent is administered by means of lumbar puncture, and the patient is placed in a Trendelenburg position to opacify the basal cisterns, followed by CT imaging after administration of contrast material.  Manoeuvres that provoke an active leak, such as sneezing or head hanging, are performed prior to the CT portion of cisternography. Postcontrast images are then compared with the precontrast images.  A positive result involves the presence of a skull base defect and contrast opacification within the sinus, nasal cavity, or middle ear.
  • 90.  MR cisternography typically involves heavily T2- weighted fast spin-echo sequences with fat suppression and subtraction of the adjacent background tissue signal to enhance conspicuity of the fistulous tract, or CSF column.  The fast spin-echo sequences have decreased susceptibility artifacts at the air-bone interface of the skull base, compared with conventional T2- weighted imaging.  Images are generally obtained in coronal, axial, and sagittal planes, and, similar to conventional MR, the finding of a contiguous CSF column communicating from the subarachnoid space to the extracranial space and/or the herniation of brain parenchyma and/ or meninges, extracranially heralds a positive examination.
  • 91.  MR images in multiple planes showing herniation of brain parenchyma through the bone defect in anterior cranial fossa (arrow) and air-cerebrospinal fluid level suggestive of communication with paranasal sinuses
  • 92. The leptomeningeal cyst or “growing fracture”  Leptomeningeal cysts are usually delayed complications of skull fractures, although they occasionally occur within weeks of trauma.  Since the infant skull is highly malleable, the margins of pediatric skull fractures are often inwardly displaced at the time of trauma.  The pia-arachnoid membrane (and occasionally swollen, edematous cortex) can herniate through the dural tear and prevent apposition and healing of the dura. CSF pulsations subsequently fill and enlarge the subarachnoid pouch that extends through the fracture line.  The pulsations eventually widen the dural defect and expand the fracture margins. This results in a leptomeningeal cyst that extends from the subarachnoid space into the subgaleal space.  CSF pulsations tend to erode the inner table more than the outer one, giving rise to “beveled” edges.  The margins of the fracture often show marked resorption and saucerization.  The term “growing fracture” refers to interval widening of the space between the fracture margins on successive skull radiographs or CT scans.
  • 93.  CT images showing features of leptomeningeal cyst (growing fracture) as evidenced by herniation of subarachanoid space though the fracture line into subcutaneous tissue with underlying encephalomalacia, focal ventricular enlargement.
  • 94. 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
  • 95.  Pseudo-SAH with non-visualization of contrast enhancement of intracranial vessels.  Only external carotid arterial branches are enhanced