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


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


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


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


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


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


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


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


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


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


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


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


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

Documents

THE NEUROPATHOLOGY OF CNS TRAUMA