Pathology and Mechanisms of TBI, Jeffrey T. Barth & Frank G. Hillary
© 1998-2000 National Academy of Neuropsychology

CLOSED AND PENETRATING HEAD INJURIES

Contra Coup Effect
Edema
Hemorrhage
Diffuse Axonal Injury
Rotational Injury (shear-strain)

In order to appreciate the potential complexity of mild TBI, one must first understand the medical and pathophysiological mechanisms and implications of the spectrum (mild, moderate, and severe) of TBI. There are two categories of brain trauma which are referred to as closed head injuries, and penetrating head injuries. The most common cause or mechanism of closed head injury is motor vehicle accident, and penetrating head injuries most often occur with gunshot wounds.

 

 

 

 

 

 

 

 

 

 

Penetrating Head Injury:
Penetrating head injuries are much less common than closed head injuries (outside of wartime experiences) and they result in death in approximately 50 percent of cases. Penetrating head injuries primarily result in direct damage to cerebral tissue and hemorrhaging from the penetrating object. Penetrating head injury can result in very focal impairment (such as in the case of an ice pick or knife blade penetrating the cerebral hemispheres), or relatively diffuse injury from gunshot wound and the secondary shaking, hemorrhaging, and edema. Other secondary factors may also complicate this injury (see below).

 

 

 

 

 

 



X-Ray: Large Bolt Penetrating The Frontal Lobes


"CT Scan: Gunshot Wound Across The Frontal Lobes In A Child

Closed Head Injury:
Figure: Necrosis of Brain Tissue in the Inferior Frontal Lobes and Anterior Right Temporal Lobe Secondary to Moderate Closed Head Injury with Hemorrhage

As stated earlier, the most common cause of closed head injury is automobile accident which involves acceleration - deceleration injury to the brain. As one can imagine, in automobile accidents (with and without seatbelt restraint -- see next chapter in this module - Whiplash and Beyond: Motor Vehicle Seatbelt Restraint Effects on TBI) focal, multifocal, and diffuse injury to brain tissue may occur. The type and extent of damage will be directly related to the speed and direction of head movements (linear or rotational acceleration) and the time and distance of deceleration. The typical head on automobile accident results in the individual's head moving forward and stopping (due to hitting the steering wheel, dashboard, or windshield, or being restrained by the seatbelt and airbag), and then, after stopping, moving backwards to land against the headrest. In this scenario, the brain, in fact, moves forward within the cranium and may rapidly impact against the irregular frontal and temporal bones which can directly damage associated tissue through contusion (bruising) or hemorrhage. After the skull and brain have terminated their forward movement, the brain can bounce backward in the opposite directly and impact (in this case) the occipital bone. This movement of the brain inside the skull in the opposite direction of the first impact is referred to as the contra coup effect. This opposite area of impact is referred to as the contra coup site, which can in fact, result in as much or more damage to brain tissue as the original site of impact. In automobile accidents where the occupant may be thrown in several directions within the vehicle, there may be multiple impact and contra coup sites. The secondary effects of such closed head injuries may include hemorrhaging (bleeding) which can occur intracerebrally from stress to the vascular system, or hematomas (collections of blood typically noted between the skull and brain associated with meningial tearing: subdural and epidural hematomas or subarachnoid hemorrhage), and edema (swelling) of the brain.


"Subdural Hematoma"

"Subdural Hematoma"

"Epidural Hematoma"

"CT Scan of Subdural Hematoma"

"CT Scans of Subdural Hematomas"

"CT Scan of Edema and Frontal Craniotomy for Pressure Release"

Hemorrhage may cause brain tissue necrosis based upon lack of oxygen saturation (ischemia), increased intracranial pressure (ICP), and the direct toxic effect of blood on brain tissue when it is not confined to arteries, vessels, and capillaries (it is treated as a foreign body in the brain by the immune system). Edema also creates ICP which can also directly effect brain tissue.


"CT Scans Of Intracerebral Hemorrhages"

Figure: Depressed Skull Fracture
Closed head injury may be accompanied by skull fracture which requires direct impact of the head on an object. Skull fractures are referred to as linear (a crack) or depressed (the skull is displaced inward).

At a histological or cellular level, acceleration - deceleration trauma, particularly when the brain twists or rotates within the skull (rotational acceleration) may cause axonal strain, tensile stress or compression which may be focal, multi-focal, or diffuse. This process was referred to in the 1940's by Holburn as "shear-strain", or more recently as diffuse axonal injury (DAI). Gennarelli's work with primate acceleration - deceleration models found just such axonal shear-strain in mild head injury when applying the Fink-Heimer silver stain to brain stem neurons.

 

Diffuse Axonal Injury:



"Normal Intact Axon With No Attached Silver (maroon) Stain"


Cellular Debris With Silver Stain In Brain Stem Of Mild TBI Primate."

At a physiological level, traumatic brain injury, of any type, may create neurochemical and neurometabolic cascade effects. As Dixon (1993) points out and is evident is Hovda's (1994) fluid percussion model, traumatic brain injury (including mild trauma) can create neuronal depolarization which in turn results neuronal discharge and the release of neurotransmitters and increased extra cellular potassium (K+). This is followed by an increased glucose demand and metabolism (hyperglycolysis) and a resultant relative ischemia from reduced cerebral blood flow. Delayed axonal injury may also occur through the influx of extra cellular calcium (which reduces cerebral blood flow through vasoconstriction) and the release of oxygen free radicals which can increase damage to neurons several hours post injury.


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