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
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
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
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
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