The shock wave of an explosive device such as bomb can propel objects into the cranium but there is also a direct form of organ damage from the dissipation of energy that occurs at the interfaces of tissues of different densities. This form of barotrauma invariably ruptures the tympanic membranes, a sign that is a marker of blast injury (Xydakis et al). Deafness, tinnitus, and vertigo are common accompaniments from cochlear concussion. The lung is next most often affected.
Loss of consciousness may occur but there is little understanding of the mechanism aside from the conventional configuration of flinging of the skull from the pressure wave. As summarized in an editorial by one of the authors, the initial shock wave is followed by a supersonic blast wind and a reverse and prolonged front of underpressure. Tissues are damaged when energy is dissipated at the interface between air and liquid that presents a change in acoustic impedance. The subsequent blast wind is the source of separate injury, throwing people against fixed objects and dispersing projectiles that penetrate the body. Potential modes of conduction of the force of the blast to the cranial contents include the acceleration and deceleration of the head as a wave passes by, which essentially results in concussion; skull deformation which squeezes the brain; the indirect passage of the shock wave through the lungs; and the entry of the wave through the openings in the cranial vault, specifically the acoustic and optic canals and the foramen magnum.
Acute gas embolism of the brain vessels has also been reported in the military medical literature. DePalma and colleagues and also Ropper have reviewed blast injuries but the neurologic literature is quite deficient and does not settle whether the percussion wave can produce unconsciousness by direct “concussion” in the original sense of the term, causing “commotion” of brain tissue or perhaps momentary cessation of cerebral blood flow.
Posttraumatic Epilepsy (See Also Chap. 15)
Seizures are the most common delayed sequela of craniocerebral trauma, with an overall incidence of approximately 5 percent in patients with closed head injuries and 50 percent in those who had sustained a compound skull fracture and direct wounds of the brain. The basis is nearly always a contusion or laceration of the cortex. As one might expect, the risk of developing posttraumatic epilepsy is also related to the overall severity of the closed head injury. In a civilian cohort of 2,747 head-injured patients described by Annegers and colleagues (1980), the risk of seizures after severe head injury (defined by loss of consciousness or amnesia for more than 24 h, including subdural hematoma and brain contusion) was 7 percent within 1 year and 11.5 percent in 5 years. If the injury was only moderate (unconsciousness or amnesia for 30 min to 24 h or causing only a skull fracture), the risk fell to 0.7 and 1.6 percent, respectively. After mild injury (loss of consciousness or amnesia of less than 30 min), the incidence of seizures was not significantly greater than in the general population. In a subsequent study, Annegers and colleagues (1998) expanded the original cohort to include 4,541 children and adults with cerebral trauma. The results were much the same as those of the first study except that in patients with mild closed head injuries, there was only a slight excess risk of developing seizures—a risk that remained elevated only until the fifth year after injury. The likelihood of epilepsy is said to be greater in parietal and posterior frontal lesions, but it may arise from lesions in any area of the cerebral cortex. Also, the frequency of seizures is considerably higher after penetrating cranial injury, as cited earlier.