behavioral changes in blast victims might be underestimated, and valuable time for preventive therapy or timely rehabilitation might be lost (Warden, 2006; Martin et al., 2008).
Penetrating TBI is generally inflicted by munitions fragments, high-energy bullets, or other fragments generated by an explosion. In the recent warfare, penetrating TBI caused by secondary blast effects is only one of the elements of BINT. Penetration by a fragment or object depends on the energy of the projectile and the retardation caused by the fragment–tissue interaction. The retardation—which is a function of the shape of the object (the presented area), the angle of approach, and the properties of the tissue—determines the amount of energy transferred into the tissue, whereas the extent of damage depends on delivered energy (Sapsford, 2003). Projectiles with high available energy, such as fragments generated by an improvised explosive device, usually transfer large quantities of energy and cause strong stress waves and large temporary cavities (Yoganandan et al., 1997). The temporary cavities, lasting only a few milliseconds, expand fast, decreasing pressure to below atmospheric and sucking debris into the wound (Sapsford, 2003; Zhang et al., 2005b). A cavity’s collapse is preceded by several smaller expansions and contractions of decreasing amplitude. The extent of damage to tissue in a nonelastic environment like the brain is estimated to be 10–20 times the size of the projectile.
Experimental Studies. Experimental studies on wound ballistics demonstrate pathophysiologic wounding properties of a penetrating brain injury distinct from those of the other types of head injury (Carey et al., 1990b; Soblosky et al., 1992; Torbati et al., 1992; Carey, 1995; Williams et al., 2006a, 2006b). If a missile penetrates a cerebral hemisphere without severe disruption of vital brain structures, the indirect effect of ordinary pressure waves, set up by the interaction of missile and tissue, may damage the brain stem respiratory nuclei and cause death (Carey, 1995). Thus, the possibility of fatal apnea is directly related to the missile energy of deposit in the brain. Moreover, it has been shown that although transmitted ordinary pressure waves might interfere with the reticular activating system in the brainstem and induce persistent coma, specific long-lasting neurologic defects from a missile wound generally result from direct missile damage to the cerebral cortex or cortical projections (Carey, 1995). The pathobiology of penetrating TBI also includes vasogenic edema around the missile wound track in the injured hemisphere (Carey et al., 1990a, 1990b); increase in ICP; decrease in cerebral perfusion pressure (Carey et al., 1989; Carey, 1995); widespread stretch injuries of blood vessels, nerve fibers, and neurons; and distortion and displacement of the brain (Finnie, 1993). Recent experimental studies (Williams et al., 2006a, 2006b, 2007) used a unilateral right frontal trajectory to induce survivable penetrating TBI of the frontal cortex and striatum and identified three distinct phases of injury progression. Phase I (0–6 hours), the primary injury, began with immediate (<5 minutes) intracerebral hemorrhage; maximal volumetric size developed at 6 hours after the trauma. In phase II (6–72 hours), the secondary injury, cells undergoing necrotic cell death and infiltrated neutrophils (24 hours) and macrophages (72 hours) formed a core lesion of degenerate neurons surrounding the injury track. The core lesion expanded into perilesional areas and reached maximal volume at 24 hours after the trauma. Phase III, delayed degeneration, developed 3–7 days after the trauma and involved neurogenic inflammation and degeneration of neurons and fiber tracts in structures remote from the core lesion, such as the thalamus, the internal capsule, the external capsule, and the cerebral peduncle (Williams et al., 2006a, 2007).