Describes in simple words the radiological investigations available for neuro trauma with emphasis on CT imaging

1. BORNEO NEUROSURGERY CONFERENCE 2014 • “CRANIAL & SPINAL
EMERGENCIES” • 17-18 OCT • PALACE HOTEL, SABAH
Dr.Wan Najwa ZainiWan Mohamed
Radiologist, HQE 2

3. 1. INTRODUCTION
2. IMAGINGTECHNIQUES
3. TYPES OF HEAD INJURIES
A. PRIMARY HEAD INJURY
B. SECONDARY HEAD INJURY
4. SEQUELAE OF HEADTRAUMA
5. CONCLUSION

4.  Traumatic brain injury (TBI) – leading cause of
death in children and young adults.
 Peak age – 15 -24 yrs.
 Secondary peak > 50 years of age.
 Twice as often among males compared to
females.
 Generally caused by motor vehicle accidents,
fall, assaults, violence and sports & recreation

5.  Can be classified into primary and secondary
injuries.
 By location – Intra or extra-axial.
 By mechanism – penetrating/open or
blunt/closed.
 By severity – minor, mild, moderate, or
severe using Glasgow Coma Scale score.

6. 1. SKULL RADIOGRAPH
 Poor predictors.
 Normal SXR does not exclude major
intracranial injuries.

7. 2. CT SCAN
 Most important step in evaluation of head
trauma.
 Modality of choice – fast, widely available,
and highly accurate in the detection of skull
fractures and intracranial hemorrhage.
 Goal of imaging is to identify treatable
injuries to prevent secondary damage.

8.  Indications –
 severeTBI (GCS ≤8)
 persistent neurologic deficit
 antegrade amnesia
 unexplained asymmetric pupillary response
 LOC > 5 minutes
 depressed skull fracture
 penetrating injury
 bleeding diathesis or anticoagulation therapy.

9.  In a typicalTBI, CT images must be reviewed
using multiple windows and levels:
 1) Brain window (W: 80, L: 40)
 2) Intermediate window : to exaggerate contrast
between extra-axial blood and the adjacent skull
(W: 150, L: 75)
 3) Bone window : to evaluate the osseous
structures (W: 2500, L: 500).

11. 3. MRI
 Recommended for patients with acuteTBI
when the neurologic findings are unexplained
by CT.
 Valuable to show small/subtle extra-axial
blood collections, diffuse axonal injury,
brainstem injuries.
 Higher sensitivity in the sub-acute and
chronic stages of head trauma.

12. A. PRIMARY HEAD INJURY
1. Scalp injury, skull vault, base of skull
fracture.
2. Primary haemorrhages:
a) Extra-axial – epidural, subdural,
subarachnoid, intraventricular
b) Intra-axial – diffuse axonal injury (DAI),
cortical contusions, intracerebral
haematoma, deep/ brainstem injury

13. 3. Primary vascular injuries:
a) Traumatic arterio–venous fistula (AVF)
b) Carotid-cavernous fistula (CCF)
c) Arterial pseudo-aneurysm
d) Arterial dissection/ laceration/ transaction/
occlusion
e) Dural sinus laceration/thrombosis/occlusion
f) Cortical vein rupture/thrombosis
4. Other : cranial nerve injury.

14. B. SECONDARY INJURY
a) Cerebral herniation
b) Traumatic ischemia, infarction
c) Diffuse cerebral swelling
d) Diffuse hypoxic injury
e) Secondary “delayed’’ hemorrhage
f) Secondary brain stem injury or haemorrhage
g) Others e.g. fatty embolism , infection

15. 1. SCALP INJURY, SKULL FRACTURE
SCALP INJURY
 Soft-tissue lacerations
 Subgaleal hematoma
 most common manifestation
 focal soft-tissue swelling beneath subcutaneous
tissue and above the temporalis muscle and skull.
 Cephalohematoma
 Residual foreign bodies

18. SKULLVAULT FRACTURE
 Could be linear, depressed or diastatic
 Depressed fracture usually associated with
intracranial injury
 Diastatic fracture/ sutural diastasis
 Seperation of cranial bones at suture site
 Width of the suture > 3 mm (normal < 2 mm)
 In adults, most common site is lambdoid suture

19. BASE OF SKULL FRACTURE
 Should be sought when blood behind
tympanic membrane, otorrhoea, rinorrhoea,
echymosis surrounds the orbits without
direct orbital trauma, intracranial air, air
fluid level in PNS or mastoid air cells.
 Basilar fracture cause compression or
entrapment of cranial nerves.
 Fracture of optic canal cause loss of vision.

20.  Sphenoidal fractures can cause disruption of
intra- cavernous internal carotid artery,
leading to pseudo- aneurysm or a carotid
cavernous fistula.
 Petrous temporal bone fracture
 Transverse or longitudinal (relative to long axis of
bone)
 Longitudinal – direct temporal impact, 70%
 Transverse – occiput or frontal impact
 Can cause hearing loss from ossicular bone fracture/
dislocation, otorhinorrhoea from CSF leak, facial
nerve palsy, vascular injury, perilymphatic fistula

22. 2. PRIMARY HEMORRHAGES
a) EXTRA-AXIAL HEMORRHAGES
EXTRA/EPIDURAL HEMATOMA (EDH)
 Usually within first 24-48 H.
 Occurs between the inner table of the skull and
the dura with a biconvex configuration.
 Etiology – disruption of middle meningeal
artery, laceration of diploic veins or dural sinus.

23.  May cross dural attachments but not sutures.
 Usually associated with overlying skull fracture
and secondary intracranial mass effect/ injuries.
 Can be acute, subacute and chronic.
 Hypodense area within indicates active bleed.
 Imaging criteria where EDH may be treated
conservatively:
(1) Diameter less than 1.5 cm
(2) Minimal mid line shift < 2 mm
(3) Neurologically intact without focal deficit.

26. SUBDURAL HEMATOMA (SDH)
 Interposed between the dura and arachnoid.
 Typically crescent shaped with concave
medial and convex lateral border.
 May cross suture lines but not dural (falx or
tentorial) attachments.
 Common sites: over the fronto-parietal
convexities, middle cranial fossa, para- falcial
area, inter- hemispheric fissure.

27.  Acute SDH – homogenously hyperdense, up to
40% mixed hyper/ hypodense due to unclotted
blood - serum extruded during clot retraction.
 Subacute SDH – isodense within a few days to a
few weeks, may be difficult to diagnose, wider
window helpful.
 Chronic SDH – typically low attenuation, mixed
density in 5% due to recurrent haemorrhage,
enhancement in post contrast, calcification in
0.3 to 2.7% cases.

31. SUBARACHNOID HAEMORRHAGE (SAH)
 Can result from the disruption of small pial
vessels, extension into the subarachnoid
space by a contusion or hematoma or
diffusion of intraventricular hemorrhage.
 Very common, but rarely causes mass effect.
 Typically appears as linear or serpentine area
of hypendensity in the basal cisterns, the
sulci, the Sylvian fissure and inter-
hemispheric fissure.

32.  Normal calcified or ossified falx may be
mistaken for parafalcine SAH in older
adolescents.
 “Pseudo sub-arachnoid haemorrhage” is seen
in cases of severe diffuse cerebral oedema.
 Posterior parafalcine or inter-hemispheric
SAH can mimic the “Empty delta sign’’ of
superior sagittal sinus thrombosis.
 Rapidly cleared within 1 week.

35. INTRAVENTRICULAR HEMORRHAGE (IVH)
 Can result from rotationally induced tearing
of subependymal veins along the surface of
the ventricles, by direct extension of a
parenchymal hematoma into the ventricular
system or from retrograde flow of SAH into
the ventricular system via the fourth
ventricular outflow foramina.

36.  Shows high density intraventricular blood
with or without a fluid level.
 Occasionally focal choroid plexus hematoma
noted.
 At risk for developing both communicating
and non communicating hydrocephalus
secondary to obstruction and ependymitis
from the irritant effects of the blood.

38. 2. PRIMARY HEMORRHAGES
b) INTRA-AXIAL HEMORRHAGES
DIFFUSEAXONAL INJURY (DAI)
 Most common type of primary traumatic
injury.
 Results from rotational acceleration and
deceleration forces that produce shearing
deformations of brain tissue.

39.  Disruption of accompanying blood vessels
show numerous small hemorrhage foci.
 Diffuse & bilateral.
 Clinically, characterized by loss or severe
impairment of consciousness beginning at
the moment of direct impact.
 In chronic stage can result in overwhelming
cognitive and psychiatric problems.
 MRI more superior to CT to detect DAI.

40.  CT findings:
Early imaging may be subtle or normal.
Foci of decreased density.
May show some degrees of cerebral swelling.
May show small focal hemorrhage or small
petechial haemorrhage particularly at the
gray-white junction and corpus callosum.
May show extensive injury.

41.  Locations ( according to severity of trauma):
 Peripheral lobar white matter at cortico-
medullary junction.
 Common at the parasagital regions of frontal
lobe, periventricular regions of temporal lobe.
 Internal & external capsules, corona radiata,
cerebral peduncles.
 Corpus callosum.
 Brain stem – posterolateral quadrants of mid
brain and upper pons.

44. CORTICAL CONTUSION
 Common type, in 21% ofTBI patients.
 Mechanism: linear acceleration-deceleration
forces /penetrating trauma /direct impaction.
 Tissue necrosis, capillary disruption, petechial
hemorrhage followed by liquefaction and
oedema after 4 to 7 days.
 May be hemorrhagic or non-hemorrhagic.

45.  Coup: Direct impact to stationary brain. Injury
at the site of impaction.
 Counter coup: Impact of moving brain on
stationary clavarium opposite to the site of
the coup and produced injury.
 Focal lesion primarily involving superficial
gray matter, with relative sparing of the
underlying white matter.

46.  Location – orbitofrontal and temporal lobes
most frequently involved.
 Beneath an acute subdural hematoma or a
depressed skull fracture.
 Associated with a better prognosis than DAI,
unless accompanied by brainstem injury or
significant mass effect.

47.  CT findings:
 Initially may be subtle or absent.
 Early findings –characteristic “salt and pepper”
pattern of focal /multiple poorly defined mixed
areas of hypodensity and hyperdensity
(petechial hemorrhage).
 Diffuse oedema and mass effect in immediate
post-traumatic period, then gradually diminish
over time.
 Some degree of contrast enhancement.
 Isodense to brain after 2 – 3 weeks.

51. INTRACEREBRAL HEMATOMA
 Frequently associated with other primary
extra- and intra-axial injuries.
 May be delayed with 48 hours (lucid) interval.
 Due to shear-induced hemorrhage from
rupture of small intraparenchymal vessels.
 Differentiated from hemorrhagic contusion
by sharply marginated margin, perifocal
hypodensity and mass effect.

52.  Mostly located in the frontotemporal white
matter, other site basal ganglia
 Acute hematoma (< 3 days):
CT: Homogenous high density lesion (50 -70
HU) with irregular well-defined margins.
Usually surrounded by low attenuation area
(oedema, contusion) with mass effect.

53.  Subcute Hematoma (3 – 14 Days):
NCCT: Gradual decrease in density from
periphery inward and becomes isodense to
brain parenchyma.
CECT: Peripheral rim enhancement at inner
border of perilesional lucency.

54.  Chronic Hematoma (> 14 Days):
CT: Gradual decreased attenuation/
hypodensity.
Later – lucent hematoma (cephalomalacia
due to proteolysis and phagocytosis &
surrounding atrophy) with adjacent sulcal
enlargement and ventricular dilation with
ring blush ( DDX : tumor )

56. 3. PRIMARYVASCULAR INJURIES
 Traumatic arterio–venous fistula (AVF).
 Carotid cavernous fistula (CCF).
 Arterial pseudo-aneurysm. Location: branches
of ACA+MCA, Cavernous portion of ICA.
 Arterial dissection/laceration/ transection/
occlusion.
 Dural sinus laceration/ thrombosis / occlusion.
 Cortical vein rupture / thrombosis.

57.  Most often injured artery is the internal
carotid artery (ICA) especially at sites of
fixation – in the carotid canal at the base of
the petrous bone, and at its exit from the
cavernous sinus beneath the anterior clinoid
process.
 Conventional angiograms is the gold
standard for confirmation and delineation of
the vascular injuries.
 MRA, CTA serve as important screening tools.

58.  CCF:
Results from full-thickness arterial injury.
Leads to communication between the
cavernous portion of ICA and the surrounding
venous plexus.
Resulting in venous engorgement of the
cavernous sinus and its draining branches:
the ipsilateral superior ophthalmic vein and
inferior petrosal sinus.

60.  Diffuse cerebral swelling
 Brain herniation
 Traumatic ischemia , infarction
 Diffuse hypoxic injury
 Secondary “delayed’’ hemorrhage
 Secondary brain stem injury or haemorrhage
 Others --e.g. fatty embolism , infection

61. DIFFUSE CEREBRAL SWELLING
 Due to an increase in cerebral blood volume
(hyperemia), vasogenic edema, or increase in
tissue fluid (cerebral or cytotoxic edema).
 CT – effacement of the cerebral sulci and
cisterns and compression of the ventricles.
 In cerebral edema, the gray–white matter
differentiation is lost.
 In cerebral hyperemia, the gray–white matter
differentiation is preserved.

64. BRAIN HERNIATION
 Occurs secondary to mass effect produced by
other causes.
 Subfalcine herniation: most common form, the
cingulate gyrus displaced across midline under
the falx cerebri.
 Uncal herniation: the medial temporal lobe is
displaced over the free margin of tentorium.
Important clue - effacement of ambient and
lateral suprasellar cisterns.

65.  Transtentorial herniation – downward or
upward herniation in cerebellum/cerebrum.
 Translar ( trans sphenoidal ) herniation –
downward or upward herniation.
 Tonsilar herniation.
 Miscellaneous - trans dural / trans cranial
herniation.

67. ISCHAEMIA OR INFARCTION
 Occurs as a result of increased intracranial
pressure or mass effect on cerebral
vasculature by herniation or hematoma.
 ACA infarction – secondary to subfalcine
herniation which displaces the ACA to the
contralateral side, trapping the
callosomarginal branches of theACA.

68.  Uncal herniation can cause ischaemia in the
posterior cerebral artery territory.
 Tonsillar herniation can cause ischemia in the
posterior inferior cerebellar artery territory.

70.  Encephalomalacia and atrophy.
 Pneumocephalus, pneumatocele formation.
 CSF leaks and fistula.
 Acquired encephalocoele or leptomeningeal
cyst.
 Cranial nerve injuries.
 Diabetes incipidus.
 Hydrocephalus.
 Subdural hygroma.
 Post traumatic abscess.

72.  The goal of imaging in the management of
head trauma is to identify treatable injuries to
prevent secondary damage.
 CT continues to be the modality of choice in
the evaluation of acute head injury.
 CT is preferred in the acute setting because it
is accurate, fast, widely available and can
easily accommodate life-support and
monitoring equipment.

73.  MRI is indicated for patients with acuteTBI
when the neurologic findings are unexplained
by CT.
 MRI is also the modality of choice for
subacute or chronic injury.