The mechanisms by which blast pressure waves cause mild-to-moderate traumatic brain injury (mTBI) are an open question. Possibilities include acceleration of the head, direct passage of the blast wave via the cranium, and propagation of the blast wave to the brain via a thoracic mechanism. The hypothesis that the blast pressure wave reaches the brain via a thoracic mechanism is considered in light of ballistic and blast pressure wave research. Ballistic pressure waves, caused by penetrating ballistic projectiles or ballistic impacts to body armor, can only reach the brain via an internal mechanism and have been shown to cause cerebral effects. Similar effects have been documented when a blast pressure wave has been applied to the whole body or focused on the thorax in animal models. While vagotomy reduces apnea and bradycardia due to ballistic or blast pressure waves, it does not eliminate neural damage in the brain, suggesting that the pressure wave directly affects the brain cells via a thoracic mechanism. An experiment is proposed which isolates the thoracic mechanism from cranial mechanisms of mTBI due to blast wave exposure. Results have implications for evaluating risk of mTBI due to blast exposure and for developing effective protection.

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Blast-associated shock wave-induced traumatic brain injury (bTBI) remains a persistent risk for armed forces worldwide, yet its detailed pathophysiology remains to be fully investigated. In this study, we have designed and characterized a laboratory-scale shock tube to develop a rodent model of bTBI. Our blast tube, driven by a mixture of oxygen and acetylene, effectively generates blast overpressures of 20–130 psi, with pressure-time profiles similar to those of free-field blast waves. We tested our shock tube for brain injury response to various blast wave conditions in rats. The results show that blast waves cause diffuse vascular brain damage, as determined using a sensitive optical imaging method based on the fluorescence signal of Evans Blue dye extravasation developed in our laboratory. Vascular leakage increased with increasing blast overpressures and mapping of the brain slices for optical signal intensity indicated nonhomogeneous damage to the cerebral vasculature. We confirmed vascular leakage due to disruption in the blood-brain barrier (BBB) integrity following blast exposure. Reactive oxygen species (ROS) levels in the brain also increased with increasing blast pressures and with time post-blast wave exposure. Immunohistochemical analysis of the brain sections analyzed at different time points post blast exposure demonstrated astrocytosis and cell apoptosis, confirming sustained neuronal injury response. The main advantages of our shock-tube design are minimal jet effect and no requirement for specialized equipment or facilities, and effectively generate blast-associated shock waves that are relevant to battle-field conditions. Overall data suggest that increased oxidative stress and BBB disruption could be the crucial factors in the propagation and spread of neuronal degeneration following blast injury. Further studies are required to determine the interplay between increased ROS activity and BBB disruption to develop effective therapeutic strategies that can prevent the resulting cascade of neurodegeneration.

We report observation of the signature of very-long-period orbits in the Stark spectrum of lithium in a regime of classical chaos. We identify recurrences associated with the orbits parallel to the electric field, including those beyond the 100th return of the primitive orbit. We also identify recurrences due to scattering of an incoming wave from one orbit into another by the alkali-metal core.PACS numbers: 32.60.+i, 03.65.Sq, 05.45. +b Periodic-orbit theory provides an important link between quantum theory and classical dynamics in regimes of disorderly (chaotic) motion [1]. The closely related closed-orbit theory [2,3] predicts the photoabsorption spectrum of a system from knowledge of its closed classical orbits. Long-period orbits are of particular inter-

This paper reviews the history and evidence related to remote wounding effects of ballistic pressure waves imparted to tissue by the impact of a bullet. Such remote effects are often referred to as hydraulic or hydrostatic shock. In spite of considerable published evidence and a long history, some medical professionals continue to regard the ability of a bullet to injure tissue that is not directly crushed or stretched as mythical (Jandial R, Reichwage B, Levy M, Duenas V, Sturdivan L. Ballistics for the neurosurgeon. Neurosurgery. 2008:62:472-480.) Early references to these effects date to the 19 th century; however, compelling experimental support and medical findings in human case studies did not become available until the late 20 th and early 21 st century. Keywords: ballistics, traumatic brain injury, TBI, blast wave, ballistic pressure wave Without citing data in support for the claim, the otherwise excellent review paper, Ballistics for the neurosurgeon, 1 asserts that "hydrostatic shock" is a "relatively recent myth." However, remote effects of ballistic pressure waves known as "hydrostatic shock" or "hydraulic shock" have considerable support and a long history. Reference to "hydraulic shock" can be found as early as 1898 in an article describing experiments in which fish were killed by a remote pressure mechanism similar to underwater dynamite explosions by firing a rifle into the water within 24 inches or so of the fish. 2