Military personnel are exposed to occupational levels of blast overpressure during training. This study characterizes the pressure-time histories of air, underwater, and localized blast, and correlates blast parameters with neuropathology. Blast overpressure was produced by a howitzer, a bazooka, an automatic rifle, underwater explosives, or a shock tube. Anesthetized pigs were exposed in positions that simulated real training scenarios. Underwater exposures were performed using explosives at distances recommended by safety requirements. In other experiments, rats were exposed via a shock tube. The pressure changes were recorded with a hydrophone sensor in the brain of the pig and in rats with an optical fiber sensor. Histological examination of porcine brains revealed small parenchymal and subarachnoid hemorrhages, predominately in the occipital lobe, cerebellum, and medulla oblongata. Relative to the peak pressure in air, that in porcine brain (Pmax brain/air) was 0.7 for the bazooka and 0.5 and 0.7, respectively, for the 9- and 30-kPa howitzer. The attenuation was stronger in water: the detonation pulse had a brain/water ratio of 0.1, and the secondary pulses had ratios of 0.3-0.4. The results indicate that low-frequency spectra penetrate easily from air or water into the brain, but high-frequency spectra appear to be filtered by body structures. In addition, blast waves were recorded in the brain and abdomen of pigs after local exposure via shock tube to either the abdomen or the top of the skull. When the abdomen was exposed, the maximal peak value in the brain was only 3% of that in the abdomen. Moreover, part of this pressure could have been derived from the air outside the head. The results gave little support to significant transmission of pressure within the body.

There is little information on threshold levels and critical time factors for blast exposures, although brain damage after a blast has been established both clinically and experimentally. Moreover, the cellular pathophysiology of the brain response is poorly characterized. This study employs a rat model for blast exposure to investigate effects on the neuronal cytoskeleton. Exposure in the range of 154 kPa/198 dB or 240 kPa/202 dB has previously been shown neither to cause visual damage to the brain, nor to affect the neuronal populations, as revealed with routine histology. Here, the brains were investigated immunohistochemically from 2 h to 21 days after blast exposure. A monoclonal antibody was used which detects only the phosphorylated epitope of the heavy subunit of the neurofilament proteins (p-NFH). This epitope is normally restricted to axons, that is, not demonstrable in the perikarya. Eighteen hours after exposure in the 240-kPa/202-dB range, p-NFH immunoreactivity accumulated in neuronal perikarya in layers II-IV of the temporal cortex and of the cingulate and the piriform cortices, the dentate gyrus and the CA1 region of the hippocampus. At the same time, the p-NFH immunoreactivity disappeared from the axons and dendrites of cerebral cortex neurons. The most pronounced immunostaining of neuronal perikarya was found in the hemisphere, which faced the blast source. The perikaryal accumulation of p-NFH was present also at 7 days but the neuronal perikarya had become negative at 21 days, at which time the axons again displayed p-NFH immunoreactivity. Exposure in the range of 154 kPa/198 dB caused similar, although less marked accumulation of p-NFH immunoreactivity in the neuronal perikarya. The findings are interpreted to show a dephosphorylation of NFHs in axons and dendrites and a piling up of p-NFHs in the perikarya due to disturbed axonal transport.

No abstract

A concussion model was developed to simulate the high velocity of impact and rapid head DeltaV of concussions in National Football League players. The new procedure can be used to evaluate immediate and latent effects of concussion and more severe injury with greater impact mass.