Neuropathology and Pathophysiology

TBI results in neuropathology via overt alterations in brain tissue as well as disruptions in brain function at a cellular level. Observable injuries resulting from head trauma can be classified into two broad categories: primary and secondary. Primary injuries

Table 27-1. Ratings of traumatic brain injury severity




GCS = 13-15

GCS = 9-12


PTA< 1 hour

PTA= 1-24 hours

PTA > 1 day

LOC< 30 minutes

LOC= 1-24 hours

LOC > 24 hours

Note. GCS = Glasgow

Coma Scale; LOC = length of loss of consciousness;

PTA=length of posttraumatic amnesia.

result directly from the trauma itself. They include skull fractures, contusions and lacerations, and mechanical injuries to nerve fibers and blood vessels. Secondary injuries arise indirectly from the trauma and in children include brain swelling and edema, hypoxia and hypotension, increased intracranial pressure, mass lesions such as epidural hematomas, and seizures (Pang 1985).

The primary injuries that arise from head trauma reflect biomechanical forces, which can result in the tearing or bruising of blood vessels that gives rise to focal contusions or hemorrhage, as well as in the shearing or straining of white matter nerve fibers. Shear and strain forces have been thought to be responsible for diffuse axonal injury, which triggers a process of Wallerian degeneration in distal axonal projections and results in the diffuse loss of synaptic terminals (Povlishock et al. 1992).

Focal contusions are especially likely to occur in the frontal and temporal cortex because of their proximity to the bony prominences in the anterior and middle fossa of the skull. In contrast, shear/strain injuries appear to be most common at the boundaries between gray and white matter. Although diffusely distributed, they occur most often around the basal ganglia, periventricular regions near the hypothalamus, superior cerebellar peduncles, fornices, corpus callosum, and fiber tracts of the brain stem.

Brain swelling and cerebral edema are two major secondary complications of TBI and may be more common in children than among adults (Aldrich et al. 1992; Bruce et al. 1979, 1981; but see Lang et al. 1994). Brain swelling and cerebral edema are thought to result from a disruption of the normal relationships between blood, brain tissue, and cerebrospinal fluid. In contrast to brain swelling and cerebral edema, mass lesions are less common in children than adults (Bruce 1995). Mass lesions involve the accumulation of fluid, usually blood associated with contusion and hemorrhage. Epidural hematomas result from bleeding into the space between the dura and the skull, often in association with a skull fracture that disrupts the middle men-

ingeal artery. Subdural hematomas result from bleeding into the space between the dura and the arachnoid membranes, frequently because of a tear in the bridging veins of the sagittal sinus, and are more often acute in nature. Intracerebral hematomas occur within the brain parenchyma and often follow the same spatial distribution as contusions. Subarachnoid or intraventricular hemorrhages are also common in TBI (Bruce 1995).

Head trauma can result in a variety of neuro-chemical events (Novack et al. 1996). Excessive production of free radicals can affect cell membrane integrity and cause lipid peroxidation or attack cell organelles, such as the mitochondria. Excitatory amino acids can be harmful in excessive amounts, disrupting cell function and eventually resulting in cell death. Glutamate and aspartate, two common excitatory amino acids, have an affinity for receptors prevalent in the hippocampus and thalamus. The release of these amino acids is especially sensitive to hypoxic-ischemic events and increases dramatically after TBI, which may help explain the vulnerability of the hippocampus to the effects of TBI. The disruption of cellular calcium homeostasis by hypoxia-ischemia is another indirect source of brain injury. Hypoxic-ischemic insults interrupt normal ion pumping mechanisms and induce the release of in-tracellular calcium. In addition, the calcium influx triggers other chemical events, including the release of free radicals and excitatory neurotransmitters. The disruption of calcium homeostasis also can result in vasoconstriction, leading to further hypoxic-ischemic insult.

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