There are theories of the vital mechanisms of blast-wave–brain interaction underlying primary BINT. There are numerous assumptions that explain BINT as a type of postconcussion syndrome, that emphasize the psychologic dimension of blast experience (Jones et al., 2007), or, on the basis of clinical and experimental data, that posit that BINT can develop without a direct blow to the head and results from the kinetic-energy transfer of the blast wave through large blood vessels in the abdomen and chest to the central nervous system (Cernak et al., 1999a, 2001b; Bhattacharjee, 2008). As the front of the blast overpressure interacts with the body surface and compresses the abdomen and chest, it transfers its kinetic energy to the body’s fluid phase. The resulting hydraulic interaction initiates oscillating waves that traverse the body at about the speed of sound in water and deliver the kinetic energy of the blast wave to the brain. Once delivered, that kinetic energy causes both morphologic and functional damage in distinct brain structures. Although the damage might resemble the injury patterns that develop after mechanical TBI caused by direct interaction of a mechanical force and the skull, the injury manifestation, timeline, and complexity of pathologic changes make BINT a distinct health problem. Furthermore, frequency resonance between blast wave and electromagnetic pulse might also contribute to primary blast-induced neurologic disturbances (G. Ling, personal communication).
Experimental Studies. Experimental studies on primary blast-induced biologic effects routinely use shock tubes or blast tubes, cylindrical metal tubes usually closed at one end. The blast overpressure and underpressure waves are generated either by compressed air (shock tubes) or by detonation of an explosive (blast tubes) in the closed end of the tube (Nishida, 2001; Robey, 2001). Anesthetized animals are fixed individually in special holders designed to prevent