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THE NEUROPATHOLOGY OF CNS TRAUMA

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Presentation on theme: "THE NEUROPATHOLOGY OF CNS TRAUMA"— Presentation transcript:

1 THE NEUROPATHOLOGY OF CNS TRAUMA
Bennet I. Omalu, M.D.

2 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

3 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

4 DEFINITIONS 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

5 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

6 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

7 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

8 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

9 EPIDEMIOLOGY 500, 000 - 750, 000 cases of CNS trauma per year
10% are fatal % are moderate/ severe 5 - 10% result in residual deficits 150/ 100, 000 population exhibit sequelae of CNS trauma

10 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

11 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

12 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

13 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)

14 Subcutaneous scalp hemorrhage
Subgaleal hemorrhage Subcutaneous scalp hemorrhage

15 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

16 Contusions of the scalp

17 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

18 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

19 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: cm) Underlying perforating defect in skull shows inward bevelling of margins

20 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

21 Gunshot wounds of entrance
Gunshot wound of exit

22 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

23 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

24 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

25 Comminuted displaced fractures mosaic/ spider’s web fracture pattern
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

26 Separation of the cranial sutures most commonly the sagittal suture
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

27 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

28 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

29 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

30 Comminuted fractures of the orbital plates of frontal bone
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’

31 CRANIOCEREBRAL INJURIES: TRAUMATIC INTRACRANIAL HEMORRHAGES
Epidural (extra-dural, subperiosteal) hemorrhage Subdural hemorrhage Subarachnoid hemorrhage Intraventricular hemorrhage

32 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

33 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

34 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

35 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

36 Subdural hemorrhage

37 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 fibroblast layers Rare hemosiderophages neovascularization: capillaries Sparse fibroblasts Sparse hemosiderophages 10-20 days fibroblast layers 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

38 Subarachnoid hemorrhage (SAH) May accompany cerebral contusions
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

39 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

40 Subarachnoid hemorrhage

41 Intraventricular hemorrhage (IVH) Usually arterial in origin
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

42 CRANIOCEREBRAL INJURIES: BRAIN
Contusions Lacerations Transections Pulpefaction Diffuse axonal injury Diffuse vascular injury

43 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

44 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

45 Contusions of brain

46 Microscopy: extravasation of erythrocytes
Contusions of brain Microscopy: extravasation of erythrocytes

47 Involvement of entire thickness of neocortical lamina I
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

48 Involvement of entire thickness of neocortical lamina I
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

49 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

50 contusions caused by fractures of the skull
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

51 Contusions of brain: mechanisms of coup and contre-coup contusions: brain inertia and deformation forces Fall from height

52 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

53 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.

54 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

55 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

56 DAI: Diffuse Axonal Injury
Gross Pathology Acute White matter petechial hemorrhages: centrum semiovale corpus callosum dorsolateral brainstem cerebellar peduncles Petechial hemorrhages in corpus +/- intraventricular hemorrhage Gliding contusions Chronic Atrophy Cerebral white matter Corpus callosum Cerebral peduncles Base of pons Medullary pyramids Hydrocephalus Dusky gray centrum semiovale Normal cortical ribbon

57 DAI: Diffuse Axonal Injury Histologic sequencing/ dating
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

58 DAI: Diffuse Axonal Injury
Accumulation of Amyloid Precursor Protein Hemorrhages in Corpus Callosum

59 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

60 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

61 SEQUELAE OF CNS TRAUMA:
Sub-acute/ delayed sequelae Brain swelling and edema Raised intracranial pressure Brain herniation Hypoxic/ ischemic injury Cerebral fat embolism Infections

62 SEQUELAE OF CNS TRAUMA:
Chronic sequelae Brain atrophy Hydrocephalus Progressive neurodegeneration Post traumatic epilepsy

63 SEQUELAE OF CNS TRAUMA: CT scan- cerebral atrophy and hydrocephalus

64 Mechanisms of trauma induced cytotoxic neuronal injury and necrosis
Lysis of cell membranes Cytoskeletal degradation Lipid peroxidation Release of excitatory neurotrasmitters Generation of free radicals calpain Activation Wide spread neuronal depolarization Activation Massive influx of calcium Proteases and lipases Activation Traumatic membrane defect Voltage dependent channels  Thromboxane A2  Prostaglandins  Leukotrienes Arachidonic acid cascade Receptor mediated channels Phospholipase A2 Lipo-oxygenase Cyclo-oxygenase Coupled/ receptor channel

65 Raised Intracranial Pressure
Causes: Traumatic Intracranial hemorrhages Brain edema surrounding contusions Diffuse unilateral or bilateral cerebral swelling/ edema Can be: mild: 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

66 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

67 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

68 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

69 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

70 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

71 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

72 NON-ACCIDENTAL TRAUMA IN CHILDHOOD:
CT scan: Posterior interhemispheric subdural hemorrhage

73 NON-ACCIDENTAL TRAUMA IN CHILDHOOD:
Ophthalmoscopy: bilateral retinal hemorrhages

74 Injuries of the spinal medulla
Similar to brain injuries with: Lacerations Transections Contusions Axonal and vascular injuries Commonly accompanies fractures of spinal vetebrae


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