Primary Effects of CNS Trauma The document summarizes various primary injuries that can occur to the central nervous system following traumatic brain injury. It describes direct injuries such as scalp lacerations, skull fractures, and epidural or subdural hematomas caused by blows to the head. It also discusses indirect injuries such as diffuse axonal injury caused by rapid acceleration/deceleration forces. Specific types of injuries are defined, including cortical contusions, subarachnoid hemorrhage, and deep brain injuries to structures like the brainstem and ventricles. Diagnostic imaging findings for the various injuries on CT and MRI are also summarized.

1. Primary Effects
of CNS Trauma
MODERATOR:DR.BHAGYALAKSHMI M.D
PRESENTOR: N.LAKSHMI CHAITANYA

2. • Primary head injuries are defined as those that occur at
the time of initial trauma even though they may not be
immediately apparent on initial evaluation.

3. • Head injury can be caused by direct or indirect trauma
• Direct trauma involves a blow to the head and is usually caused by
automobile collisions, falls, or injury inflicted by an object such as a
hammer or baseball bat. Scalp lacerations, hematomas, and skull
fractures are common. Associated intracranial damage ranges from
none to severe.
• Significant forces of acceleration/deceleration, linear translation,
and rotational loading can be applied to the brain without direct
head blows-indirect trauma. Here the brain undergoes rapid
deformation and distortion.

4. Scalp and Skull Injuries
• five layers of the scalp.
• Scalp injuries include lacerations and hematomas.
• Two different types of scalp hematomas: cephalohematomas and
subgaleal hematomas.

6. Cephalohematoma
• Cephalohematoma is
subperiosteal, limited by
sutures.
• typically unilateral.
• Mc in newborns following
instrumented delivery.
Subgaleal hematomas
• Subgaleal hematoma is under
the scalp aponeurosis, not
limited by sutures.
• usually bilateral
• Can be very large and life-
threatening.

8. Skull Fractures
linear,
depressed,
elevated,
diastatic fractures
Growing skull fractures

12. Extraaxial Hemorrhages

13. Extraaxial Hemorrhages
• Epidural hematomas arise between the inner table of the skull and
outer (periosteal) layer of the dura.
• Subdural hematomas are located between the inner (meningeal)
layer of the dura and the arachnoid.
• Traumatic subarachnoid hemorrhage is found within the sulci
and subarachnoid cisterns, between the arachnoid and the pia.

15. Arterial Epidural Hematoma
• 90% are caused by arterial injury, most commonly to the middle
meningeal artery.
• 10% of EDHs are venous
• unilateral and supratentorial.
• 90- 95% are found directly adjacent to a skull fracture. The
squamous portion of the temporal bone is the most common site.
• EDHs are biconvex in shape-classic lens-shaped hematoma

17. • EDHs in adults rarely cross suture lines.
• "lucid interval"
• Look for other comorbid lesions such as "contre-coup" injuries,
tSAH, and secondary brain herniations, all of which are
common findings in patients with EDHs.
• hyperdense (60-90 HU) biconvex extraaxial collection;
Presence of a hypodense component ("swirl" sign) is seen in
about one-third of cases and indicates active, rapid bleeding
with unretracted clot

18. • EDHs compress the underlying subarachnoid space and displace
the cortex medially, "buckling" the gray-white matter interface
inward.
• Adverse clinical outcomes are thickness > 1.5 cm,
volume > 30 mL,
Pterional
midline shift > 5 mm,
and presence of a
"swirlsign" within the hematoma on imaging.

19. • MR Findings. Acute EDHs are typically isointense with underlying
brain, especially on T1WI. The displaced dura can be identified
as a displaced "black line" between the hematoma and the brain.

20. Venous Epidural Hematoma
• Venous EDHs are often smaller, are under lower pressure, and
develop more slowly than their arterial counterparts.
• skull fracture that crosses a dural venous sinus.
• subtypes of venous EDHs: Vertex EDH
Anteriortemporal EDH
Clival EDH

21. Vertex EDH
• Skull fracture crosses superior sagittal sinus(SSS)
• SSS can be lacerated, compressed, thrombosed

22. Anterior temporal EDH
• Sphenoid wing or zygomatico maxillary fracture
• Injures sphenoparietal venous sinus
• Hematoma accumulates at anterior tip of middlecranialfossa

23. Clival EDH
• Usually develop after a hyperflexion or hyperextension injury to the
neck and are possibly caused by stripping of the tectorial
membrane from attachments to the clivus.
• most often occur in children and present with multiple cranial
neuropathies.
• The abducens nerve is the most commonly affected, followed by
the glossopharyngeal and hypoglossal nerves.
• Usually benign course, resolves spontaneously.

25. Acute Subdural Hematoma
• More common.
• collection of acute blood products that lies in or between the
inner border cell layer of the dura and the arachnoid.
• Tearing of bridging cortical veins as they cross the subdural
space to enter a dural venous sinus (usually the superior sagittal
sinus) is the most common etiology.
• More than 95% are supratentorial.
• typically crescent-shaped.

28. • An aSDH that is thicker than 2 centimeters correlates with poor
outcome.
• An aSDH that occupies more than 10% of the total available
intracranial volume is usually lethal.
• SDHs are typically more extensive than EDHs
• SDHs may cross suture lines but generally do not cross dural
attachments.

29. • The classic finding of an aSDH is a supratentorial crescent-
shaped extraaxial collection that displaces the gray-white matter
interface medially.
• Pockets of hypodensity within a larger hyperdense aSDH usually
indicate rapid bleeding
• Mass effect with an aSDH is common
• Subfalcine herniation should be proportionate to the size of the
subdural collection. However, if the difference between the midline
shift and thickness of the hematoma is 3 mm or more, then
mortality is very high.

30. • MR Findings- aSDHs appear isointense on T1WI and
hypointense on T2WI.
• Signal intensity on FLAIR scans is usually iso- to hyperintense
compared with CSF but hypointense compared with the adjacent
brain. aSDHs are hypointense on T2* scans.
• DWI shows heterogeneous signal within the hematoma but may
show patchy foci of restricted diffusion in the cortex underlying the
aSDH.

31. Subacute Subdural Hematoma
• Density of an extraaxial hematoma decreases approximately 1-2
HU each day.
• Therefore, an SDH will become nearly isodense with the
underlying cerebral cortex within a few days following trauma.
• sSDHs are typically crescent-shaped fluid collections that are
iso- to slightly hypodense compared with the underlying cortex
on NECT.
• Medial displacement of the gray-white interface ("buckling") is
often present, along with "dot-like" foci of CSF in the trapped,
partially effaced sulci underlying the sSDH

35. • MR can be very helpful in identifying sSDHs.
• early subacute SDHs are isointense with cortex on T1WI
• hypointense on T2WI but gradually become more hyperintense
as extracellular methemoglobin increases.
• Most late-stage sSDHs are T1/T2 "bright-bright."
• FLAIR is the most sensitive standard sequence for detecting
sSDH, as the collection is typically hyperintense

36. Chronic/Mixed Subdural Hematoma
• cSDH is an encapsulated collection of sanguineous or
serosanguineous fluid confined within the subdural space.
• Recurrent hemorrhage(s) into a preexisting cSDH are common
and produce a mixed-age or "acute on chronic" SDH
• In the absence of repeated hemorrhages, cSDHs gradually resorb
and largely resolve, leaving a residue of thickened dura-arachnoid
that may persist for months or even years

40. • A hypodense crescentic fluid collection extending over the surface
of one or both cerebral hemispheres is the classic finding in cSDH.
• Uncomplicated cSDHs approach CSF in density.
• The hematocrit effect creates a slight gradation in density that
increases from top to bottom.
• With age, the encapsulating membranes surrounding the cSDH
become thickened and may appear moderately hyperdense.

41. • Eventually, some cSDHs show peripheral calcifications that
persist for many years. In rare cases, a cSDH may densely calcify
or even ossify, a condition aptly termed "armored brain"
• The encapsulating membranes show strong enhancement
following contrast administration.
• On T1 scans, uncomplicated cSDHs are typically iso- to slightly
hyperintense compared with CSF
• Depending on the stage of evolution, cSDHs are iso- to
hypointense compared with CSF on T2 scans.

42. • Most cSDHs are hyperintense on FLAIR and may show "blooming"
on T2* scans if subacute-chronic blood clots are still present.

43. Traumatic Subarachnoid Hemorrhage
• Most common traumatic extra axial hemorrhage.
• tSAHs are predominantly found in the perisylvian regions, in the
anteroinferior frontal and temporal sulci, and over the hemispheric
convexities.
• Rarely, Terson syndrome (intraocular hemorrhage) is associated
with tSAH.

46. • CT Findings. Acute tSAH is typically peripheral, appearing as linear
hyperdensities in sulci adjacent to cortical contusions or under epi- or
subdural hematomas.
• Posttraumatic interpeduncular or ambient cistern hemorrhage is a good
marker for possible brainstem lesions in patients with otherwise unexplained
coma.
• MR Findings. As acute blood is isointense with brain, it may be difficult to
detect on T1WI. "Dirty" sulci with "smudging" of the perisylvian cisterns is
typical.
• Subarachnoid blood is hyperintense to brain on T2WI and FLAIR.

47. • "Blooming" with hypointensity can be identified on T2* scans, typically
adjacent to areas of cortical contusion. tSAH is recognized on GRE or SWI
sequences as hypointense signal intensity surrounded by hyperintense CSF.
• Emergent CTA is usually unnecessary in cases with typical peripheral tSAH
on NECT.
• Patients with suprasellar ("central") SAH may harbor a ruptured aneurysm
and should be screened with CTA regardless of mechanism of injury.

48. Parenchymal Injuries

49. 1) cortical contusions and lacerations,
2) diffuse axonal injury (DAI),
3) subcortical injuries, and intraventricular hemorrhages
The deeper the abnormalities, the more serious the injury.

50. Cerebral Contusions and Lacerations
• Cerebral contusions are the most common of the intraaxial
injuries.
• Cerebral contusions are basically "brain bruises." They evolve
with time and often are more apparent on delayed scans than
at the time of initial imaging.
• Contusions are injuries of the brain surface that involve the
gray matter and contiguous subcortical white matter

52. • The temporal tips, as well as the lateral and inferior surfaces
and the perisylvian gyri, are most commonly affected.
• Contusions that occur at 180° opposite the site of direct impact
(the "coup") are common and are called "contre-coup" lesions.
• CT Findings: . A mixture of petechial hemorrhages surrounded
by patchy ill-defined hypodense areas of edema is common

53. • MR Findings: MR is much more sensitive than CT in detecting
cerebral contusions
• T1 scans may show only mild inhomogeneous isointensities and
mass effect.
• T2 scans show patchy hyperintense areas (edema) surrounding
hypointense foci of hemorrhage
• FLAIR scans are most sensitive for detecting cortical edema and
associated tSAH, both of which appear as hyperintense foci on
FLAIR.

54. • T2* (GRE, SWI) is the most sensitive sequence for imaging
parenchymal hemorrhages. Significant "blooming" is typical in
acute lesions.
• The major differential diagnosis of cortical contusion is diffuse
axonal injury
• Contusions tend to be superficial, located along gyral crests. DAI is
most commonly found in the corona radiata and along compact
white matter tracts such as the internal capsule and corpus
callosum.

55. • Brain laceration occurs when severe trauma disrupts the pia and
literally tears the underlying brain apart.
• A "burst lobe" is the most severe manifestation of frank brain
laceration.

56. Diffuse Axonal Injury
• DAI is the second most common parenchymal lesion.
• traumatic axonal stretch injury
• Most DAIs are caused by high-velocity motor vehicle collisions.
• sudden changes in acceleration/deceleration.
• The cortex moves at a different speed relative to underlying
deep brain structures (white matter, deep gray nuclei).
• axonal stretching, especially where brain tissues of different
density intersect, i.e., the gray-white matter interface

58. • The cortex is typically spared; it is the subcortical and deep white
matter that is most commonly affected.
• The vast majority of DAIs are microscopic and nonhemorrhagic.
• Microscopic Features axonal swellings or "retraction balls"
• Mild TBI, lesions are seen in the frontotemporal gray-white matter
interfaces.
• Moderate TBI, lobar white matter and corpus callosum are
affected
• severe TBI, dorsolateral midbrain and upper pons.

59. • When to suspect DAI ?
• CT
• MR Findings. T1 scans are often normal, especially in the early
stages of TBI.
• T2WI and FLAIR may show hyperintense foci in the subcortical
white matter and corpus callosum.
• T2* scans are very sensitive to the microbleeds of DAI and
typically show multifocal ovoid and linear hypointensities
• MRS shows widespread decrease of NAA with increased Cho.

60. Subcortical (Deep Brain) Injury
• traumatic lesions of deep brain structures such as the brainstem,
basal ganglia, thalami, and ventricles.
• SCI include deep hemorrhagic contusions, nonhemorrhagic
lacerations, intraventricular bleeds, and traumatic subarachnoid
hemorrhage (tSAH).
• NECT scans often show diffuse brain swelling with punctate
and/or gross hemorrhage in the deep gray nuclei and midbrain

62. • Intraventricular and choroid plexus hemorrhages are common
and may form a "cast" of the lateral ventricles.
• MR is much more sensitive than CT even though acute
hemorrhage is isointense with brain on T1 scans.
• FLAIR and T2* are the most sensitive sequences. DWI may
show foci of restricted diffusion.

63. Miscellaneous: Pneumocephalus

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