NEUROPATHOLOGY- TRAUMA TO THE CNS

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I. CLASSIFICATION
II. CLOSED HEAD INJURIES
III. MASS LESIONS FROM CLOSED HEAD INJURIES
IV. DIFFUSE AXONAL INJURY (DAI) FROM CLOSED HEAD INJURIES V. SECONDARY EFFECTS OF HEAD INJURIES
VI. DELAYED EFFECTS OF CLOSED HEAD INJURY
VII. CERVICAL SPINE TRAUMA

VOCABULARY
Terms you should be familiar with:

Closed head injury
Penetrating head injury
Compressive head injury
Concussion
Epidural Hematoma
Subdural hematoma
Subdural hygroma
Contusion
Coup and contrecoup
Laceration
Diffuse axonal injury
Hypoxia
Edema
Transtentorial herniation
Cerebellar herniation
Post-traumatic epilepsy
Hangman's fracture
Cervical spondylosis

OBJECTIVES: The objectives of this hour are to distinguish between closed and open head injuries, to understand the mechanisms of craniocerebral trauma, to be familiar with some of the pathologic lesions produced by trauma to the head, and to realize that a head injury is always a neck injury until proven otherwise.

I. CLASSIFICATION

• Penetrating Head Injuries: The dura is pierced. Bullet or knife wounds to the head are examples. Not further discussed.
  
  
• Compressive Head Injuries- The Skull is compressed between two forces. Massive injury that usually results in instantaneous death. Not further discussed.
  
  
• Closed or blunt head injuries present the major problem in civilian life. Head is either suddenly accelerated or decelerated as a result of a non-penetrating blow. The dura remains intact.

II. CLOSED HEAD INJURIES

• Brain sometimes damaged without external evidence of injury. Most of the injuries described below can be produced by motion without impact.
  
  
• Physical factors influencing type and severity of injury to brain include energy load per unit area, duration, velocity and direction of the force, configuration of various parts of skull, rate of acceleration or deceleration, and diffusion of forces resulting in agitation of entire cerebrum. The bottom line is: The amount of brain damage is directly proportional to the rotational acceleration achieved and the mass of the brain.
  
  
• Concussion
  
  
  • May come as the only result of a head injury, but practically always an accompanying phenomenon of more severe head injuries.
  • Experimental work has demonstrated that sudden acceleration or deceleration of more than 28 ft per second is necessary to produce concussion in cats.
  • Although experimental data suggest that slight morphologic nerve cell changes can be demonstrated, significant structural changes in humans have not been discovered with present techniques. Experiments in cats and monkeys have shown loss of consciousness, loss of autonomic and somatic reflexes, and focal loss of normal histochemical staining reactions in RAS neurons in severe concussion.
  • Clinically, concussion is usually defined as a transient, self-limited disorder in which brain function is abolished, and unassociated with evidence of structural damage. Amnesia is important in assessing severity of brain injury.
  • Theories of mechanism of concussion. At present it is thought by some to be a manifestation of widespread altered nerve cell metabolism affecting neuronal excitability, resulting from diffuse agitation of nerve cells ("molecular commotion"). Other experiments implicate the reticular formation as the major system whose function is abolished in concussion.
  • Sudden death from severe head injury is probably due to extremely severe concussion rather than accompanying contusion or laceration.

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III. MASS LESIONS FROM CLOSED HEAD INJURIES

• Epidural Hematoma (Transverse Forces)
  
  
  • Usually results from fracture over middle meningeal artery, tearing this vessel.
  • Bleeding is brisk, creating a rapidly expanding mass over the dura (25-75 cc).
  • Brain is compressed causing distortion and displacement of midline structures, uncal or cerebellar herniation, and brain stem compression.
    
    
• Subdural Hematoma (Axial Forces)
  
  
  • Much more common than epidural hemorrhages
  • Consists of accumulation of blood between dura and arachnoid and due to tear of bridging vein between arachnoid and dura. Usually located over dorsolateral surface of frontal and parietal lobes. Rarely in other locations.
  • Large ones may occur from minor head injuries and even without external evidence of trauma.
  • May be bilateral (15-20%)
  • Acute subdural hematoma
    • Blood accumulates moderately rapidly, though rarely as rapidly as with epidural hematomas. May result from tear of venous sinus.
    • Sometimes the arachnoid is torn. CSF contributes to the expanding mass in this case.
    • Steadily expanding mass compresses brain with same secondary effects as from an epidural hematoma.
  • Chronic subdural hematoma
    • Slower expanding subdural hematoma usually ceases bleeding spontaneously.
    • Small ones occasionally are gradually absorbed, but this is minimal. More often they are organized leaving thin, permanent membranes.
    • Gradual enlargement of the blood clot over a few to several weeks may occur, even though bleeding has stopped, and is due to: increased osmotic tension resulting from products of blood breakdown; rupture of large capillaries in the granulation tissue that organizes the clot.
    • Thus a hematoma may gradually compress the brain, in the manner of an extrinsic tumor, producing similar pathologic effects upon the brain.
    • Body's local response to subdural hematoma is organization. Takes place entirely from inner surface of dura. Capillaries and fibroblasts invade clot along its dural surface, and grow out over its arachnoidal surface from margin of clot. Macrophages ingest blood. Gradually a fibrous neomembrane forms over both surfaces of the clot. Two to three weeks are required for a grossly visible, completely encapsulating membrane. Granulation tissue gradually replaces the clot, although a dark brown liquid center may remain in large hematomas.
      
      
• Subdural Hygroma
  
  
  • Results from arachnoidal tear, with leakage of CSF into subdural space, without significant hemorrhage.
  • Becomes encapsulated, like a hematoma.
  • May behave like a chronic subdural hematoma, though usually less serious.
    
    
• Contusion and Laceration from Closed Head Injuries
  
  
  • Contusion means bruising of the brain, commonly directly beneath site of blow (coup). May cause focal neurologic signs. If severe enough, laceration of pia and cortex also occurs.
  • Small subpial, cortical and superficial white matter vessels rupture, characteristically over crests of gyri. Often hemorrhage is wedge-shaped, apex directed into white matter. CSF contains blood, and edema around the lesion may be marked.
  • All layers of cortex are destroyed within contusion. Same sequence of events follows as if this were an infarct. A fibro-glial scar forms, as necrotic debris is removed, that becomes brownish-yellow in color due to hemosiderin. Called cerebral cicatrix, or "plaque jaune".
  • With severe injuries, contusions may be large and extend more deeply. Laceration usually is prominent, with significant extravasation of blood, both subarachnoid and intracerebral.
  • Contrecoup contusion- Any blow may be associated with contrecoup injury, i.e., contusion at opposite pole of brain. Actually, however, these are usually located at tips of frontal and temporal lobes, even though the blow may be on the side or top of the head. Contrecoup contusions are common and have the same appearance as coup contusions. Mechanism: most likely a result of rotational stress causing sheering of tips of frontal and temporal lobes on irregular underlying bony surface of anterior and middle fossae.

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IV. DIFFUSE AXONAL INJURY (DAI) FROM CLOSED HEAD INJURIES

• Most important single factor governing outcome in non-missile head injury.
  
  
• Commonest cause of vegetative state in patients surviving more than four weeks.
  
  
• Commonest underlying pathology when there is no skull fracture and the brain appears normal externally.
  
  
• Characteristic Structural Features
  
  
  • Focal lesions in corpus callosum and dorsolateral quadrant of brain stem
  • Widespread damage to axons

V. SECONDARY EFFECTS OF HEAD INJURIES

• Hypoxia
  
  
• Edema
  
  
• Brain Shift (Transtentorial or Cerebellar Herniation)

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VI. DELAYED EFFECTS OF CLOSED HEAD INJURY

Two most important are:

• Post-Traumatic Epilepsy
  
  
• Post-Traumatic Personality Disorder

VII. CERVICAL SPINE TRAUMA

Brain injury is always associated with cord injury until proven otherwise.

• Hangman's Fracture: Fracture of neural arch of the axis with subluxation of C2-C3.
  
  
• Cervical Spondylosis: Degenerative changes at disc space lead to compromise of the intraspinal canal.
  
  
• Laceration of Vertebral or Carotid Artery

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