Pathogenesis of craniocerebral trauma

Pathogenesis of craniocerebral traumaOne of the easiest classification schemes for TBI is based on the mechanism. Injuries can be classified as acceleration/deceleration, impact, or penetrating.

Acceleration/Deceleration Injury

Typically seen following high-speed accidents, these injuries involve sudden acceleration or deceleration. The skull and brain accelerate differentially, causing the brain to slosh back and forth within the skull. As it does, the brain impacts against intracranial bony irregularities such as the floor of the frontal fossa, the sphenoid wing or the petrous ridge, leading to the development of superficial cortical contusions. A further consequence of this differential movement between skull and brain is the stretching of cortical draining veins as they cross the subdural space before penetrating the dural sinuses. If stretched enough, these veins tear and bleed into the subdural space, thus forming subdural hematomas. The final consequence of acceleration/deceleration is the transmission of kinetic forces to the brain that cause shear injury to neurons (axons particularly) and blood vessels. This leads to diffuse axonal injury and the development of subcortical, pericentral, and posterolataral mesencephalic hematomas.

Subdural hematoma resulting from tearing of bridging cortical veins. The hematoma roughly follows the contour of the brain and causes significant left-to-right brain shift. Subdural hematoma is often associated with acceleration/deceleration-type injuries and the underlying brain injury is often quite severe.

Impact Injuries

Impact injury is often seen following assaults with blunt objects such as bats or pipes. As such, the skull absorbs much of the object’s kinetic force, though the brain often absorbs enough to cause a concussion. Skull fractures are common in this type of injury and dural injury often follows. This also results in the development of epidural hematomas as the meningeal vessels under the fracture tear. Since the skull absorbs much of the impact, the severity of injury per se is less severe than that following acceleration/deceleration injuries. Thus, the classic clinical picture is that of initial loss of consciousness at the time of impact followed by a lucid period as the patient recovers from the concussion. In some cases, a second period of decreased mentation develops after the lucid period, as the epidural hematoma expands to compress the brain stem or other vital brain areas. The thin temporal squamosa is the skull bone most likely to fracture.

Penetrating Injuries

Penetrating brain injuries can be divided into high-velocity and low-velocity injuries. The cutoff is somewhat arbitrary but is defined as missile velocity of 300 feet per second at impact. Since the energy (E) transmitted to the brain equals 1/2 the missile mass (M) times its velocity (V) squared (E = 1/2 x M x V2), the higher the velocity or the greater the missile mass, the greater the energy transmitted to the brain. Since energy varies with the square of the velocity, V has greater impact than M in determining the energy absorbed by the brain.

Since low-velocity missiles often cannot penetrate the thick cranial vault, most low-velocity injuries occur though the relatively thin skull base—particularly the orbitocranial window—causing damage to structures along the path of entry, with the cerebral vasculature being particularly vulnerable. A multitude of low-velocity missiles have been described including pens, pencils, chopsticks, branches, arrows, darts, and needlefish.

High-velocity injuries are of a different nature. Though structures along the path of entry are certainly injured, much of the damage occurs away from the missile tract. This is because the missile’s kinetic energy is absorbed by the skull and brain as it slows. The resulting transfer of energy to the brain precipitates a diffuse injury similar to that imparted to the brain following acceleration/deceleration injuries. As such, the morbidity of high-velocity injuries is significantly higher than that of low-velocity injuries. The increased use of military-style assault weapons in United States urban centers has increased the lethality of gunshot wounds, as these weapons are designed to fire with much higher muzzle velocities than conventional firearms.


Regardless of mechanism, all injuries to the brain share some common physiologic characteristics. The initial impact leads to a number of alterations, many of which are thought to involve the unregulated release of neurotransmitters from traumatic depolarization of cerebral neurons. Though many neurotransmitters are released simultaneously, the excitatory neurotransmitter glutamate is released in the greatest quantity. It is thought to initiate a biochemical cytotoxic cascade mediated through N-methyl-D-aspartate glutamate receptors. This cascade leads to alterations in cellular energy metabolism, cerebral blood flow, transmembrane ion concentration gradients, free radical production, and cytokine release.

In concert with these cellular changes are gross changes such as the development of intracranial hematomas, cerebral edema, and hydrocephalus—all of which can contribute to intracranial hypertension. Additionally, systemic problems such as hypotension, seizures, infections, and hypoxia can develop, increasing the risk of further neurologic injury.

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