Annals of biomedical engineering
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Identifying the level of overpressure required to create physiological deficits is vital to advance prevention, diagnostic, and treatment strategies for individuals exposed to blasts. In this study, a rodent model of primary blast neurotrauma was employed to determine the pressure at which acute neurological alterations occurred. Rats were exposed to a single low intensity shock wave at a pressure of 0, 97, 117, or 153 kPa. ⋯ These data indicate that neurotrauma induced from a shock wave may lead to cognitive deficits in short-term learning and memory of rats. Additional histological evidence supports significant and diffuse glial activation and cellular damage. Further investigation into the biomechanical aspects of shock wave exposure is required to elucidate this pressure range-specific phenomenon.
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Traumatic brain injury (TBI) from blast produces a number of conundrums. This review focuses on five fundamental questions including: (1) What are the physical correlates for blast TBI in humans? (2) Why is there limited evidence of traditional pulmonary injury from blast in current military field epidemiology? (3) What are the primary blast brain injury mechanisms in humans? (4) If TBI can present with clinical symptoms similar to those of Post-Traumatic Stress Disorder (PTSD), how do we clinically differentiate blast TBI from PTSD and other psychiatric conditions? (5) How do we scale experimental animal models to human response? The preponderance of the evidence from a combination of clinical practice and experimental models suggests that blast TBI from direct blast exposure occurs on the modern battlefield. Progress has been made in establishing injury risk functions in terms of blast overpressure time histories, and there is strong experimental evidence in animal models that mild brain injuries occur at blast intensities that are similar to the pulmonary injury threshold. ⋯ Principal areas of uncertainty include the need for a more comprehensive injury assessment for mild blast injuries in humans, an improved understanding of blast TBI pathophysiology of blast TBI in animal models and humans, the relationship between clinical manifestations of PTSD and mild TBI from blunt or blast trauma including possible synergistic effects, and scaling between animals models and human exposure to blasts in wartime and terrorist attacks. Experimental methodologies, including location of the animal model relative to the shock or blast source, should be carefully designed to provide a realistic blast experiment with conditions comparable to blasts on humans. If traditional blast scaling is appropriate between species, many reported rodent blast TBI experiments using air shock tubes have blast overpressure conditions that are similar to human long-duration nuclear blasts, not high explosive blasts.
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Although Head Injury Criterion (HIC) is an effective criterion for head injuries caused by linear acceleration such as skull fractures, no criteria for head injuries caused by rotational kinematics has been accepted as effective so far. This study proposed two criteria based on angular accelerations for Traumatic Brain Injury (TBI), which we call Rotational Injury Criterion (RIC) and Power Rotational Head Injury Criterion (PRHIC). Concussive and non-concussive head acceleration data obtained from football head impacts were utilized to develop new injury criteria. ⋯ Correlation analyses were performed between the proposed criteria and FE-based brain injury predictors such as Cumulative Strain Damage Measure (CSDM), which is defined as the percent volume of the brain that exceeds a specified first principal strain threshold, proposed to predict Diffuse Axonal Injury (DAI) which is one of TBI. The RIC was significantly correlated with the CSDMs with the strain thresholds of less than 15% (R > 0.89), which might predict mild TBI. In addition, PRHIC was also strongly correlated with the CSDMs with the strain thresholds equal to or greater than 20% (R > 0.90), which might predict more severe TBI.