There is an outdated dogma that neurologic impairments caused by primary blasts are rare because the skull provides excellent protection for the brain; that is, brain injury is solely a consequence of air emboli in cerebral blood vessels (Clemedson, 1956; Owen-Smith, 1981). Despite recent clinical findings (Cernak et al., 1999a, 1999b, 1999c, 2000), experimental findings (Saljo et al., 2000; Cernak et al., 2001a, 2001b), and experience in contemporary military operations that suggests substantial short-term and long-term neurologic deficits caused by blast exposure without a direct blow to the head, old belief prevails in the professional literature and in clinical practice. Indeed, information on blast injuries (Table 2.3) lists mainly the consequences of secondary and tertiary blast mechanisms. Although BINT is one cause of in-theater injuries, it is often underdiagnosed. Its complex clinical syndrome is caused by the combination of all blast effects (Figure 2.6).
It is noteworthy that blast injuries are usually manifested in a form of polytrauma, that is, injury involving multiple organs or organ systems. Primary blast injury of the chest produces bradycardia, hypotension, and apnea via vagal reflexes, which may induce cerebral hypoxia and ischemia (Cernak et al., 1996a, 1997; Ohnishi et al., 2001). Bleeding from injured organs, such as the lungs and intestine, causes a lack of oxygen in all vital organs, including the brain. Damage of the lungs reduces the surface for oxygen uptake from the air and reduces the amount of the oxygen delivered to the brain (Cernak et al., 1997). Tissue destruction initiates the synthesis and release of hormones and mediators into the blood that, when delivered to the brain, change the brain’s function (Cernak et al., 1996b). Irritation of the nerve endings in injured peripheral tissue and organs also contributes to BINT (Irwin et al., 1999).