THE
NEUROPATHOLOGY
OF
CNS TRAUMA
Bennet I. Omalu, M.D.
OUTLINE: section 5
1.
Definitions
2.
Epidemiology
3.
Craniocerebral injuries:
Scalp, Skull, Intracranial cavity,
Brain, Spinal cord, diffuse axonal injury
4.
Sequelae of trauma
5.
Non-accidental trauma in childhood
DEFINITIONS
CNS trauma :
Injury or damage to living CNS tissue caused by an extrinsic
agent or force by either direct or indirect mechanisms
comprising:
a.
direct blunt force trauma
b.
direct penetrating force trauma
c.
indirect translational force trauma
d.
indirect asphyxiational trauma
Synonyms:
Traumatic brain injury, Craniocerebral injury, Head trauma
DEFINITIONS
CNS trauma can be subdivided into:
 Focal trauma:
focal distribution of trauma
Diffuse trauma:
diffuse distribution of trauma
Primary trauma:
Secondary trauma:
Closed CNS trauma :
Open CNS trauma :
immediate and direct CNS response to trauma
delayed physiologic CNS response to trauma
dura mater is not disrupted by trauma
dura mater is disrupted by trauma
DEFINITIONS
Direct blunt force trauma
CNS injuries that are due to the impact of a blunt object/
surface on the head/ body or vice versa
e.g. : blow on the head with a baseball bat
fall from a tenth floor balcony
DEFINITIONS
Direct penetrating force trauma
CNS injuries that are due to the impact of a sharp object
on the head/ body resulting in penetration/ perforation of
CNS tissue
e.g.:
gunshot wound of the head
stab wound of the orbital cavity
DEFINITIONS
Indirect translational force trauma
CNS injuries that are due to accelerating, decelerating
and rotational kinetic energy, which are translated into
shearing forces that disrupt CNS tissue and vessels.
e.g.:
‘whiplash’/ shaken baby syndrome
DEFINITIONS
Indirect asphyxiational trauma
CNS injuries that are due to agents or mechanisms of
trauma that will sufficiently reduce blood and/ or oxygen
supply to the brain to result in reversible or irreversible
neuronal metabolic deficits
e.g.:
suicidal hanging
smoke inhalation/ carbon monoxide intoxication
EPIDEMIOLOGY
500, 000 - 750, 000 cases of CNS trauma per year
10% are fatal
30 - 50% are moderate/ severe
5 - 10% result in residual deficits
150/ 100, 000 population exhibit sequelae of CNS trauma
EPIDEMIOLOGY
Leading cause of death in people under 45 years of age
Accounts for 1% of all deaths
Accounts for 30% of deaths from trauma
Accounts for 50% of deaths due to road traffic accidents
CRANIOCEREBRAL INJURIES: SCALP
Abrasions of the scalp
Contusions of the scalp
Scalp hemorrhages, subcutaneous
Scalp hemorrhages, subgaleal
Lacerations of the scalp
Incised wounds of the scalp
Gunshot wounds of entrance and exit
Abrasions of the scalp
Scraping and removal of
the superficial layers of the
skin (epidermis and/ or
upper dermis)
Commonly a product of
blunt force impacts
Eccentric and marginal
tags of epidermis on an
abrasion indicate direction
of impact
Patterned abrasions:
imprints of the surface of
impacting object on the skin
Contusions of the scalp
Hemorrhage into the skin or underlying soft tissue without breaching
the skin which can manifest as:
1. Subcutaneous or intra-galeal hemorrhage:
Hemorrhage into the fibro-adipose tissue of the scalp
2. Subgaleal hemorrhage:
Hemorrhage below the epicranial aponeurosis (galea aponeurotica)
Subcutaneous
scalp hemorrhage
Subgaleal
hemorrhage
Contusions of the scalp
Commonly a product of crushing impacts that rupture blood vessels
Rate of degeneration of extravasated red blood cells and heme can be
used to date scalp contusions
Contusions of the scalp
Laceration of the
scalp
A tear of the fibroadipose
and aponeurotic scalp due
to perpendicular or glancing
blunt force impact
Edges are usually
undermined and
accompanied by marginal
abrasions
Tissue bridges consisting
of nerves, connective tissue
and blood vessels connect
the margins of lacerations
Incised/ stab wounds of
the scalp
An incised wound is a cut that
is longer than it is deep
Produced by a sharp-edged
object drawn over the scalp
Wound edges are straight
without marginal abrasions or
tissue bridges
A stab wound is deeper than
its length on the skin
Produced by penetration of a
pointed object into the depth
of the scalp/ head
Gunshot wounds of entrance
Typically a circular perforating defect with loss of
tissue
+/- rim of marginal abrasions, +/-radiating marginal
lacerations
Contact wounds: +/- muzzle imprint, +/- soot deposits
(range: < 15cm)
Close range wounds: punctate abrasions (powder
stippling/ tattooing) around the wound due to particles
of propellant
(range: 30 - 45 cm)
Underlying perforating defect in skull shows inward
bevelling of margins
Gunshot wounds of exit
Typically an ellipsoid or stellate perforating defect without loss
of tissue
Marginal abrasions are usually absent
+/- radiating marginal lacerations
Soot deposits and powder stippling are absent
Underlying perforating defect in skull shows outward bevelling of
margins
Gunshot wounds of entrance
Gunshot wound of exit
CRANIOCEREBRAL INJURIES: SKULL
Fractures of the cranium
Non-depressed linear fractures
Depressed Circular and curvilinear fractures
Comminuted displaced fractures
Sutural diastasis
Fractures of base of skull
Longitudinal/ axial fractures
Transverse fractures
Ring fractures
Blow out fractures
Non-depressed linear
fractures of skull
Typically produced by blunt
force impacts
Multiple fracture lines radiate
from epicenter of point of
impact
Fracture lines are oriented in
direction of impacting force
Typically occurs when a
mobile head impacts a stationary
flat surface
Puppe’s rule for sequencing of
injuries: the course of a linear
fracture will be interrupted by
an antecedent fracture line
Depressed circular
and curvilinear
fractures
Typically produced by
focal blunt force
impacts of a mobile
object on stationary
head
Inward displacement
of outer and inner bone
plate fragments
May exhibit pattern of
concentric ripples of
fracture line
Comminuted
displaced fractures
Multiple fracture lines
and fragmentation of
bone typically
produced by severe
blunt force impacts and
shot gun wounds of the
head
 mosaic/ spider’s web
fracture pattern
or
Pond fracture pattern
Sutural diastasis
Separation of the
cranial sutures most
commonly the sagittal
suture
Typical due to severe
blunt force impacts
Occurs more
commonly in children
A marker of nonaccidental mechanisms
of trauma
Base of skull:
Longitudinal
fractures
Front to back linear
fractures
Can divide entire skull
base into two halves,
right and left
Produced by severe
blunt impacts on the
face, forehead or occiput
Base of skull:
Transverse fractures
Side to side linear
fractures
Can divide entire skull
base into two halves,
front and back
Hinge fracture:
complete transverse
fracture in middle cranial
fossa
Produced by severe
blunt impacts on either
side of the head or the
chin
Base of skull: Ring
fractures
Circumferential fracture
around foramen magnum
Separates rim of
foramen magnum from
remainder of skull base
Produced in a fall from
significant height
Severe blunt impacts on
the feet or buttocks on
landing
Vertebral column is
driven into the skull
Base of skull:
‘Blow-out’ fractures
Comminuted fractures
of the orbital plates of
frontal bone
Mechanism not well
established
May involve contre-coup
impacts of frontal lobes
on orbital plates
May involve violent
increases in intracranial
pressure as seen in
shotgun wounds i.e.
‘blow-out’
CRANIOCEREBRAL INJURIES: TRAUMATIC
INTRACRANIAL HEMORRHAGES
Epidural (extra-dural, subperiosteal) hemorrhage
Subdural hemorrhage
Subarachnoid hemorrhage
Intraventricular hemorrhage
Epidural hemorrhage
Occurs in 10 - 15% of severe CNS trauma
Usually occurs in the presence of skull fracture accompanied by
dural separation and tearing of dural vessels
Rare in the elderly because of markedly adherent dura to cranium
Commonly occurs in children without skull fracture
Epidural hemorrhage
Most common scenario:
lateral hemispheric location
fracture of squamous temporal bone
Laceration of middle meningeal artery
Associated with a lucid interval due delayed onset of bleeding
caused by spasm of lacerated artery
Subdural hemorrhage (SDH)
Usually occurs without a skull fracture
Commonly occurs as a result of translational shearing forces on the
bridging subdural veins
May occur without significant blunt force impact
 proclivity in the elderly due to cerebral atrophy and accentuated
subdural space
Subdural hemorrhage (SDH)
Acute SDH:
symptom onset
< 24 hrs
Subacute SDH:
symptom onset
24 hrs - 7 days
Chronic SDH:
symptom onset
> 7 days
SDH become organized with time
Age of SDH can be estimated with sequence of histologic changes
Subdural hemorrhage
Histologic dating of Subdural hemorrhage
Time
24 hrs
2-3 days
Dural surface (outer membrane)
Arachnoid surface (Inner membrane)
Thin fibrin layer
Sparse mononuclear cells in fibrin
Thin fibrin layer
Rare mononuclear cells in fibrin
Rare fibroblast
4-5 days
Sparse fibroblasts
Rare fibroblasts
Rare hemosiderophage
5-10 days
3 - 5 fibroblast layers
Rare hemosiderophages
neovascularization: capillaries
Sparse fibroblasts
Sparse hemosiderophages
10-20 days
10 - 20 fibroblast layers
Prominent capillaries
14-28 days:
2-4 fibroblast layers
No capillaries
Some hemosiderophages
21-28 days
Collagenization and fibrous membrane formation
mths. - yrs: fibrous membrane: inner is less than half thickness of outer membrane
Subarachnoid hemorrhage (SAH)
Traumatic SAH commonly occurs around the cerebral fissures and
basal cisterns of the brain
May accompany cerebral contusions
Acute ethanol intoxication and heavy use of alcohol carry an
increased risk of SAH following trivial blunt impact
Subarachnoid hemorrhage (SAH)
Fatal basal SAH can follow severe blunt impacts on the face and
forehead; and severe hyperextension of the head and neck
The basilar and/ or vertebral arteries are lacerated in such a scenario
Remote SAH is associated with xanthochromia (hemosiderin deposits)
of the leptomeninges
Subarachnoid hemorrhage
Intraventricular hemorrhage (IVH)
Traumatic IVH as a sole finding is due to blunt impacts of the head
on a hard surface during a fall
Usually arterial in origin
Usually accompanies SAH, extensive contusions of the brain and
penetrating injuries of the brain
Traumatic porencephaly: extensive contusions and lacerations of
the cerebrum leading to a free communication between lateral
ventricle and subarachnoid space
CRANIOCEREBRAL INJURIES: BRAIN
Contusions
Lacerations
Transections
Pulpefaction
Diffuse axonal injury
Diffuse vascular injury
Contusions of brain
Causes
Blunt impacts of the brain on the inner skull plate due to
unidirectional inertia of the brain to violent motion of the skull
Tissue shearing forces at the moment of severe blunt impacts
Intra-cranial expansile cavitation of gunshot wounds
Contusions of brain
Location and gross morphology:
Contusions are typically located on the crests of the gyri
Parallel, Streak-like or columnar hemorrhages and necrosis
Perpendicular to the leptomeningeal surface
May be cone shaped with the base at the surface and apex pointing
or extending into white matter
+/- overlying focal subarachnoid hemorrhage
Contusions of brain
Contusions of brain
Microscopy: extravasation of erythrocytes
Contusions of brain
Histomorphology (<24 hours old)
Distinct margins of parenchymal extravasation of erythrocytes
Parenchymal edema and focal eosinophilic necrosis of neurons
Sparse marginal infiltration by neutrophils
Involvement of entire thickness of neocortical lamina I
(molecular layer)
In non-traumatic infarction of the brain the superficial aspects of the
molecular layer are intact
Contusions of brain
Histomorphology (<24 hours old)
Distinct margins of parenchymal extravasation of erythrocytes
Parenchymal edema and focal eosinophilic necrosis of neurons
Sparse marginal infiltration by neutrophils
Involvement of entire thickness of neocortical lamina I
(molecular layer)
In non-traumatic infarction of the brain the superficial aspects of the
molecular layer are usually spared
Contusions of brain
Classification according to causative mechanism
Coup contusions:
contusions located beneath point of impact and caused by direct
impact
Contre-coup contusions:
contusions located in an area opposite to side of impact
Intermediary contusions:
contusions along the trajectory of impact between coup and contrecoup contusions
Contusions of brain
Classification according to causative mechanism
Fracture contusions:
contusions caused by fractures of the skull
Gliding contusions:
contusions of the dorsal cerebral hemispheres in the region of the
pacchionian granulations away from trajectory of impact due to gliding
of the brain
Herniation contusions:
contusions due to transient herniations caused by expansile cavitatory
effect of gunshot wounds of the head
Contusions of brain:
mechanisms of coup and contre-coup
contusions: brain inertia and deformation forces
Fall from height
Laceration of brain
Classification according to causative mechanism
A slit-like or irregular tear of brain tissue involving gray and white
matter
Commonly occurs with open head injuries due to penetrating forces
and gunshot wounds
Can be associated with comminuted or depressed fractures of skull
Can occur in severe blunt force impacts in infants with intact dura
due to severe shearing forces
Transection of the brain
Can be partial or complete transection
Usually occurs at the level of :
Upper cervical spinal medulla and medulla oblongata
Ponto-medullary junction
Midbrain-pons junction
Cerebral peduncles
Causative scenario: violent hyperextension and perforating gunshot
wounds.
Pulpefaction of the brain
Total or near total pulverization of brain tissue
Loss of anatomic detail
Causative scenario: crush injuries and close range shotgun wounds
DAI: Diffuse Axonal Injury
Global disruption of axons due to severe shearing forces
Immediate primary axotomy
Delayed secondary axotomy principally due to ischemia
Causative scenario: severe blunt force impacts in any direction
 immediate loss of consciousness following impact
no lucid interval
sustained unconsciousness and vegetative state until
death
Focal axonal injury may occur in milder forms with recovery of
consciousness
DAI: Diffuse Axonal Injury
Gross Pathology
Acute
White matter petechial hemorrhages:
Chronic
Atrophy
centrum semiovale
Cerebral white matter
corpus callosum
Corpus callosum
dorsolateral brainstem
Cerebral peduncles
cerebellar peduncles
Base of pons
Medullary pyramids
Petechial hemorrhages in corpus
Hydrocephalus
+/- intraventricular hemorrhage
Dusky gray centrum semiovale
Gliding contusions
Normal cortical ribbon
DAI: Diffuse Axonal Injury
Histology
Histologic sequencing/ dating
4-5 hours:
focal accumulations of -amyloid precursor protein (APP)
12-24 Hours
axonal varicosities
24 hrs - 2 mths
axonal swellings
2 wks - 5 mths
micro-gliosis
2 mths - years
Loss of myelinated fibers
DAI: Diffuse Axonal Injury
Accumulation of Amyloid
Precursor Protein
Hemorrhages in Corpus
Callosum
DVI: Diffuse Vascular Injury
Sudden death following severe blunt force impacts
Gross pathology:
Petechial hemorrhages in white matter of frontal and temporal
lobes
Histology:
acute perivascular hemorrhages: arteries, veins, capillaries
Causative scenario: shearing translational forces
SEQUELAE OF TRAUMA: Definition
Secondary brain injury resulting from
physiological processes and neurochemical
cascades, either triggered by or associated with
the primary injury, that continue after the initial
traumatic event
SEQUELAE OF CNS TRAUMA:
Sub-acute/ delayed sequelae
Brain swelling and edema
Raised intracranial pressure
Brain herniation
Hypoxic/ ischemic injury
Cerebral fat embolism
Infections
SEQUELAE OF CNS TRAUMA:
Chronic sequelae
Brain atrophy
Hydrocephalus
Progressive neurodegeneration
Post traumatic epilepsy
SEQUELAE OF CNS TRAUMA:
CT scan- cerebral atrophy and hydrocephalus
Mechanisms of trauma induced cytotoxic neuronal injury and necrosis
Neuronal
injury
Lysis of cell membranes
Cytoskeletal
degradation
Lipid peroxidation
Release of excitatory
neurotrasmitters
Generation of free
radicals
Activation
Wide spread neuronal
depolarization
calpain
Massive influx
of calcium
Activation
Proteases and lipases
Traumatic membrane defect
 Thromboxane A2
Voltage dependent channels
Arachidonic acid cascade
Receptor mediated channels
 Leukotrienes
Phospholipase A2
Coupled/ receptor channel
 Prostaglandins
Lipo-oxygenase
Cyclo-oxygenase
Raised Intracranial Pressure
Causes:
Traumatic Intracranial hemorrhages
Brain edema surrounding contusions
Diffuse unilateral or bilateral cerebral swelling/ edema
Can be:
mild:
15-22 mmHg
reasonably tolerated
Moderate:
30 mmHg
requires intervention
Severe:
> 37.5 mmHg associated with ischemic brain damage
Terminal:
> 60 mmHg
When ICP = arterial pressure = global hypoxic/ ischemic injury
Brain Herniation
Displacement of brain tissue due to raised intracranial pressure
1. Downward herniation
Subfalcine herniation of cingulate gyrus and midline shift
Transtentorial herniation of mesial temporal lobe and uncus
Transforaminal herniation of cerebellar tonsils
2. Upward herniation
External herniation through craniotomy or fracture site
Transtentorial herniation of brainstem
Brain Herniation
Complications:
Transtentorial herniation of mesial temporal lobe and uncus
Necrosis and hemorrhage of uncus (Kernohan’s hemorrhages)
Compression of occulomotor nerve and brainstem
Midbrain and pontine hemorrhages (Duret hemorrhages)
Compression of cerebral vessels and cerebral infarction
Transforaminal herniation of cerebellar tonsils
Necrosis and hemorrhage of cerebellar tonsils
Hypoxic/ Ischemic Injury
Likely in patients with:
Clinically evident hypoxia
Systolic blood pressure less than 80 mmHg for at least 15 minutes
Episodes of  ICP (> 30 mmHg)
Eosinophilic necrosis of neurons may be confined to CA-1 region of
hippocampus and/ or deep gray matter
Neuronal necrosis accentuated in border zones between cerebral
arteries
NON-ACCIDENTAL TRAUMA IN
CHILDHOOD: definition
Refers to specific constellations of patterns of
craniocerebral injuries that are highly suggestive
if not pathognomonic of adult-induced nonaccidental injuries in a child
NON-ACCIDENTAL TRAUMA IN CHILDHOOD:
constellations of injuries
Extracranial manifestations:
Bilateral retinal hemorrhages
Multiplicity of scalp abrasions/ contusions/ hemorrhages
Scalp contusions of differing ages
Multiple skull fractures
Bilateral complex fractures of both sides of the skull
Depressed skull fractures especially of the occiput
Diastatic fractures
Complex fractures involving both sides of the skull
Skull fractures of differing ages
NON-ACCIDENTAL TRAUMA IN CHILDHOOD: constellations of
injuries
Intracranial manifestations:
Subdural hematoma without a skull fracture
Bilateral subdural hematoma
Posterior interhemispheric subdural hematoma
Intracranial complications of brain trauma:
Ischemic/ hypoxic injury
Cerebral atrophy
Hydrocephalus
Multicystic encephalomalacia
NON-ACCIDENTAL TRAUMA IN CHILDHOOD:
CT scan: Posterior interhemispheric subdural hemorrhage
NON-ACCIDENTAL TRAUMA IN CHILDHOOD:
Ophthalmoscopy: bilateral retinal hemorrhages
Injuries of the spinal medulla
Similar to brain injuries with:
Lacerations
Transections
Contusions
Axonal and vascular injuries
Commonly accompanies fractures of spinal vetebrae