THE NEUROPATHOLOGY OF CNS TRAUMA
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Transcript of THE NEUROPATHOLOGY OF CNS TRAUMA
THE THE NEUROPATHOLOGY NEUROPATHOLOGY
OF OF
CNS TRAUMACNS TRAUMA
Bennet I. Omalu, M.D.Bennet I. Omalu, M.D.
1.1. 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
OUTLINE: section 5
DEFINITIONSDEFINITIONSCNS 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
DEFINITIONSDEFINITIONS
CNS trauma can be subdivided into:
Focal trauma: focal distribution of trauma
Diffuse trauma: diffuse distribution of trauma
Primary trauma: immediate and direct CNS response
to trauma
Secondary trauma: delayed physiologic CNS
response to trauma
Closed CNS trauma : dura mater is not disrupted by
trauma
Open CNS trauma : dura mater is disrupted
by trauma
DEFINITIONSDEFINITIONS
Direct blunt force traumaDirect 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
DEFINITIONSDEFINITIONS
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
DEFINITIONSDEFINITIONS
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
DEFINITIONSDEFINITIONS
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
EPIDEMIOLOGYEPIDEMIOLOGY
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
EPIDEMIOLOGYEPIDEMIOLOGY
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: SCALPCRANIOCEREBRAL 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: SKULLCRANIOCEREBRAL 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 non-accidental
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 Circumferential
fracture around fracture around
foramen magnumforamen magnum
Separates rim of Separates rim of
foramen magnum foramen magnum
from remainder of from remainder of
skull baseskull base
Produced in a fall Produced in a fall
from significant from significant
heightheight
Severe blunt Severe blunt
impacts on the feet impacts on the feet
or buttocks on or buttocks on
landinglanding
Vertebral column is Vertebral column is
driven into the skulldriven 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 Dural surface (outer membrane) Arachnoid surface (Inner
membrane)
24 hrs Thin fibrin layer Thin fibrin layer
2-3 days Sparse mononuclear cells in fibrin 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 14-28 days: 2-4 fibroblast layers
Prominent capillaries 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 contre-coup 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 heightFall 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
AcuteAcute
White matter petechial hemorrhages:
centrum semiovale
corpus callosum
dorsolateral brainstem
cerebellar peduncles
Petechial hemorrhages in corpus
+/- intraventricular hemorrhage
Gliding contusions
ChronicChronic
Atrophy
Cerebral white matter
Corpus callosum
Cerebral peduncles
Base of pons
Medullary pyramids
Hydrocephalus
Dusky gray centrum semiovale
Normal cortical ribbon
DAI: Diffuse Axonal Injury
Histology
Histologic sequencing/ datingHistologic 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
Hemorrhages in Corpus Callosum
Accumulation of Amyloid Precursor Protein
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: SEQUELAE OF CNS TRAUMA:
CT scan- cerebral atrophy and hydrocephalusCT scan- cerebral atrophy and hydrocephalus
Mechanisms of trauma induced cytotoxic neuronal injury and necrosis
Release of excitatory neurotrasmitters
Wide spread neuronal
depolarization
Arachidonic acid cascade
Massive influx of calcium
Coupled/ receptor channel
Receptor mediated channels
Voltage dependent channels
Traumatic membrane defect
Proteases and lipases
Activation
Activ
atio
n
Phospholipase A2
Lipo-oxygenase
Cyclo-oxygenase
Thromboxane A2
Prostaglandins
Leukotrienes
Activation
calpain
Neuronal injury
Cytoskeletal degradation
Generation of free radicals
Lipid peroxidation
Lysis of cell membranesLysis of cell membranes
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 non-
accidental 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: NON-ACCIDENTAL TRAUMA IN CHILDHOOD:
CT scan: Posterior interhemispheric subdural hemorrhageCT scan: Posterior interhemispheric subdural hemorrhage
NON-ACCIDENTAL TRAUMA IN CHILDHOOD: NON-ACCIDENTAL TRAUMA IN CHILDHOOD:
Ophthalmoscopy: bilateral retinal hemorrhagesOphthalmoscopy: 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