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      Porcine Head Response to Blast

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          Abstract

          Recent studies have shown an increase in the frequency of traumatic brain injuries related to blast exposure. However, the mechanisms that cause blast neurotrauma are unknown. Blast neurotrauma research using computational models has been one method to elucidate that response of the brain in blast, and to identify possible mechanical correlates of injury. However, model validation against experimental data is required to ensure that the model output is representative of in vivo biomechanical response. This study exposes porcine subjects to primary blast overpressures generated using a compressed-gas shock tube. Shock tube blasts were directed to the unprotected head of each animal while the lungs and thorax were protected using ballistic protective vests similar to those employed in theater. The test conditions ranged from 110 to 740 kPa peak incident overpressure with scaled durations from 1.3 to 6.9 ms and correspond approximately with a 50% injury risk for brain bleeding and apnea in a ferret model scaled to porcine exposure. Instrumentation was placed on the porcine head to measure bulk acceleration, pressure at the surface of the head, and pressure inside the cranial cavity. Immediately after the blast, 5 of the 20 animals tested were apneic. Three subjects recovered without intervention within 30 s and the remaining two recovered within 8 min following respiratory assistance and administration of the respiratory stimulant doxapram. Gross examination of the brain revealed no indication of bleeding. Intracranial pressures ranged from 80 to 390 kPa as a result of the blast and were notably lower than the shock tube reflected pressures of 300–2830 kPa, indicating pressure attenuation by the skull up to a factor of 8.4. Peak head accelerations were measured from 385 to 3845 G’s and were well correlated with peak incident overpressure ( R 2 = 0.90). One SD corridors for the surface pressure, intracranial pressure (ICP), and head acceleration are presented to provide experimental data for computer model validation.

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          Traumatic brain injury in the war zone.

          Susan Okie (2005)
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            Blast overpressure in rats: recreating a battlefield injury in the laboratory.

            Blast injury to the brain is the predominant cause of neurotrauma in current military conflicts, and its etiology is largely undefined. Using a compression-driven shock tube to simulate blast effects, we assessed the physiological, neuropathological, and neurobehavioral consequences of airblast exposure, and also evaluated the effect of a Kevlar protective vest on acute mortality in rats and on the occurrence of traumatic brain injury (TBI) in those that survived. This approach provides survivable blast conditions under which TBI can be studied. Striking neuropathological changes were caused by both 126- and 147-kPa airblast exposures. The Kevlar vest, which encased the thorax and part of the abdomen, greatly reduced airblast mortality, and also ameliorated the widespread fiber degeneration that was prominent in brains of rats not protected by a vest during exposure to a 126-kPa airblast. This finding points to a significant contribution of the systemic effects of airblast to its brain injury pathophysiology. Airblast of this intensity also disrupted neurologic and neurobehavioral performance (e.g., beam walking and spatial navigation acquisition in the Morris water maze). When immediately followed by hemorrhagic hypotension, with MAP maintained at 30 mm Hg, airblast disrupted cardiocompensatory resilience, as reflected by reduced peak shed blood volume, time to peak shed blood volume, and time to death. These findings demonstrate that shock tube-generated airblast can cause TBI in rats, in part through systemic mediation, and that the resulting brain injury significantly impacts acute cardiovascular homeostatic mechanisms as well as neurobehavioral function.
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              Sepsis-associated encephalopathy and its differential diagnosis.

              Sepsis is often complicated by an acute and reversible deterioration of mental status, which is associated with increased mortality and is consistent with delirium but can also be revealed by a focal neurologic sign. Sepsis-associated encephalopathy is accompanied by abnormalities of electroencephalogram and somatosensory-evoked potentials, increased in biomarkers of brain injury (i.e., neuron-specific enolase, S-100 beta-protein) and, frequently, by neuroradiological abnormalities, notably leukoencephalopathy. Its mechanism is highly complex, resulting from both inflammatory and noninflammatory processes that affect all brain cells and induce blood-brain barrier breakdown, dysfunction of intracellular metabolism, brain cell death, and brain injuries. Its diagnosis relies essentially on neurologic examination that can lead one to perform specific neurologic tests. Electroencephalography is required in the presence of seizure; neuroimaging in the presence of seizure, focal neurologic signs or suspicion of cerebral infection; and both when encephalopathy remains unexplained. In practice, cerebrospinal fluid analysis should be performed if there is any doubt of meningitis. Hepatic, uremic, or respiratory encephalopathy, metabolic disturbances, drug overdose, withdrawal of sedatives or opioids, alcohol withdrawal delirium, and Wernicke's encephalopathy are the main differential diagnoses of sepsis-associated encephalopathy. Patient management is based mainly on controlling infection, organ system failure, and metabolic homeostasis, at the same time avoiding neurotoxic drugs.
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                Author and article information

                Journal
                Front Neurol
                Front Neurol
                Front. Neur.
                Frontiers in Neurology
                Frontiers Research Foundation
                1664-2295
                08 May 2012
                2012
                : 3
                : 70
                Affiliations
                [1] 1simpleInjury Biomechanics Laboratory, Department of Biomedical Engineering, Duke University Durham, NC, USA
                [2] 2simpleDepartment of Psychiatry and Behavioral Sciences, Durham VA Medical Center, Duke University Medical Center Durham, NC, USA
                [3] 3simpleDepartment of Aeronautics and Astronautics, Institute for Soldier Nanotechnologies, Massachusetts Institute of Technology Cambridge, MA, USA
                Author notes

                Edited by: Ibolja Cernak, University of Alberta, Canada

                Reviewed by: Reuben H. Kraft, U.S. Army Research Laboratory, USA; Andrew Merkle, Johns Hopkins University Applied Physics Laboratory, USA

                *Correspondence: Jay K. Shridharani, Department of Biomedical Engineering, Duke University, 136 Hudson Hall, Durham, NC 27705, USA. e-mail: jay.shridharani@ 123456duke.edu

                This article was submitted to Frontiers in Neurotrauma, a specialty of Frontiers in Neurology.

                Article
                10.3389/fneur.2012.00070
                3347090
                22586417
                5fbf60b7-2e5d-4bd5-9309-28f2faa867e7
                Copyright © 2012 Shridharani, Wood, Panzer, Capehart, Nyein, Radovitzky and Bass.

                This is an open-access article distributed under the terms of the Creative Commons Attribution Non Commercial License, which permits non-commercial use, distribution, and reproduction in other forums, provided the original authors and source are credited.

                History
                : 30 November 2011
                : 11 April 2012
                Page count
                Figures: 13, Tables: 4, Equations: 4, References: 43, Pages: 12, Words: 7002
                Categories
                Neuroscience
                Original Research

                Neurology
                blast,traumatic brain injury,brain,pig,corridor,head,injury,porcine
                Neurology
                blast, traumatic brain injury, brain, pig, corridor, head, injury, porcine

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