Kelvar Vest Protection Against Blast Overpressure Brain Injury: Systemic Contributions to Injury Etiology

2013 ◽  
Author(s):  
Joseph B. Long
2019 ◽  
Vol 1723 ◽  
pp. 146400 ◽  
Author(s):  
Shalini Jaiswal ◽  
Andrew K. Knutsen ◽  
Colin M. Wilson ◽  
Amanda H. Fu ◽  
Laura B. Tucker ◽  
...  

2010 ◽  
Vol 69 (4) ◽  
pp. 795-804 ◽  
Author(s):  
Stanislav I. Svetlov ◽  
Victor Prima ◽  
Daniel R. Kirk ◽  
Hector Gutierrez ◽  
Kenneth C. Curley ◽  
...  

2019 ◽  
Vol 13 ◽  
pp. 117906951987221 ◽  
Author(s):  
Daniel W Bryden ◽  
Jessica I Tilghman ◽  
Sidney R Hinds

Traumatic brain injury (TBI) is a well-known consequence of participation in activities such as military combat or collision sports. But the wide variability in eliciting circumstances and injury severities makes the study of TBI as a uniform disease state impossible. Military Service members are under additional, unique threats such as exposure to explosive blast and its unique effects on the body. This review is aimed toward TBI researchers, as it covers important concepts and considerations for studying blast-induced head trauma. These include the comparability of blast-induced head trauma to other mechanisms of TBI, whether blast overpressure induces measureable biomarkers, and whether a biodosimeter can link blast exposure to health outcomes, using acute radiation exposure as a corollary. This examination is contextualized by the understanding of concussive events and their psychological effects throughout the past century’s wars, as well as the variables that predict sustaining a TBI and those that precipitate or exacerbate psychological conditions. Disclaimer: The views expressed in this article are solely the views of the authors and not those of the Department of Defense Blast Injury Research Coordinating Office, US Army Medical Research and Development Command, US Army Futures Command, US Army, or the Department of Defense.


2016 ◽  
Vol 2016 ◽  
pp. 1-15 ◽  
Author(s):  
Xiaoping Du ◽  
Matthew B. West ◽  
Weihua Cheng ◽  
Donald L. Ewert ◽  
Wei Li ◽  
...  

Traumatic brain injury (TBI) can lead to early onset dementia and other related neurodegenerative diseases. We previously demonstrated that damage to the central auditory pathway resulting from blast-induced TBI (bTBI) could be significantly attenuated by a combinatorial antioxidant treatment regimen. In the current study, we examined the localization patterns of normal Tau and the potential blast-induced accumulation of neurotoxic variants of this microtubule-associated protein that are believed to potentiate the neurodegenerative effects associated with synaptic dysfunction in the hippocampus following three successive blast overpressure exposures in nontransgenic rats. We observed a marked increase in the number of both hyperphosphorylated and oligomeric Tau-positive hilar mossy cells and somatic accumulation of endogenous Tau in oligodendrocytes in the hippocampus. Remarkably, a combinatorial regimen of 2,4-disulfonylα-phenyl tertiary butyl nitrone (HPN-07) andN-acetylcysteine (NAC) resulted in striking reductions in the numbers of both mossy cells and oligodendrocytes positively labeled for these pathological Tau immunoreactivity patterns in response to bTBI. This treatment strategy represents a promising therapeutic approach for simultaneously reducing or eliminating both primary auditory injury and nonauditory changes associated with bTBI-induced hippocampal neurodegeneration.


2022 ◽  
Vol 17 (1) ◽  
pp. 115
Author(s):  
Yi Pang ◽  
Hong Zhu ◽  
Yang Ou ◽  
BradA Clifton ◽  
Jinghui Li ◽  
...  

2014 ◽  
Vol 136 (9) ◽  
Author(s):  
David M. Gullotti ◽  
Matthew Beamer ◽  
Matthew B. Panzer ◽  
Yung Chia Chen ◽  
Tapan P. Patel ◽  
...  

Although blast-induced traumatic brain injury (bTBI) is well recognized for its significance in the military population, the unique mechanisms of primary bTBI remain undefined. Animate models of primary bTBI are critical for determining these potentially unique mechanisms, but the biomechanical characteristics of many bTBI models are poorly understood. In this study, we examine some common shock tube configurations used to study blast-induced brain injury in the laboratory and define the optimal configuration to minimize the effect of torso overpressure and blast-induced head accelerations. Pressure transducers indicated that a customized animal holder successfully reduced peak torso overpressures to safe levels across all tested configurations. However, high speed video imaging acquired during the blast showed significant head accelerations occurred when animals were oriented perpendicular to the shock tube axis. These findings of complex head motions during blast are similar to previous reports [Goldstein et al., 2012, “Chronic Traumatic Encephalopathy in Blast-Exposed Military Veterans and a Blast Neurotrauma Mouse Model,” Sci. Transl. Med., 4(134), 134ra160; Sundaramurthy et al., 2012, “Blast-Induced Biomechanical Loading of the Rat: An Experimental and Anatomically Accurate Computational Blast Injury Model,” J. Neurotrauma, 29(13), pp. 2352–2364; Svetlov et al., 2010, “Morphologic and Biochemical Characterization of Brain Injury in a Model of Controlled Blast Overpressure Exposure,” J. Trauma, 69(4), pp. 795–804]. Under the same blast input conditions, minimizing head acceleration led to a corresponding elimination of righting time deficits. However, we could still achieve righting time deficits under minimal acceleration conditions by significantly increasing the peak blast overpressure. Together, these data show the importance of characterizing the effect of blast overpressure on head kinematics, with the goal of producing models focused on understanding the effects of blast overpressure on the brain without the complicating factor of superimposed head accelerations.


Author(s):  
Miguel A Gama Sosa ◽  
Rita De Gasperi ◽  
Alejandro J Paulino ◽  
Paul E Pricop ◽  
Michael C Shaughness ◽  
...  

Author(s):  
Shailesh Ganpule ◽  
Robert Salzar ◽  
Namas Chandra

Blast induced neurotrauma (BINT), and posttraumatic stress disorder (PTSD) are identified as the “signature injuries” of recent conflicts in Iraq and Afghanistan. The occurrence of mild to moderate traumatic brain injury (TBI) in blasts is controversial in the medical and scientific communities because the manifesting symptoms occur without visible injuries. Whether the primary blast waves alone can cause TBI is still an open question, and this work is aimed to address this issue. We hypothesize that if a significant level of intracranial pressure (ICP) pulse occurs within the brain parenchyma when the head is subjected to pure primary blast, then blast induced TBI is likely to occur. In order to test this hypothesis, three post mortem human heads are subjected to simulated primary blast loading conditions of varying intensities (70 kPa, 140 kPa and 200 kPa) at the Trauma Mechanics Research Facility (TMRF), University of Nebraska-Lincoln. The specimens are placed inside the 711 mm × 711 mm square shock tube at a section where known profiles of incident primary blast (Friedlander waveform in this case) are obtained. These profiles correspond to specific field conditions (explosive strength and stand-off distance). The specimen is filled with a brain simulant prior to experiments. ICPs, surface pressures, and surface strains are measured at 11 different locations on each post mortem human head. A total of 27 experiments are included in the analysis. Experimental results show that significant levels of ICP occur throughout the brain simulant. The maximum peak ICP is measured at the coup site (nearest to the blast) and gradually decreases towards the countercoup site. When the incident blast intensity is increased, there is a statistically significant increase in the peak ICP and total impulse (p<0.05). Even after five decades of research, the brain injury threshold values for blunt impact cases are based on limited experiments and extensive numerical simulations; these are still evolving for sports-related concussion injuries. Ward in 1980 suggested that no brain injury will occur when the ICP<173 kPa, moderate to severe injury will occur when 173 kPa<ICP<235 kPa and severe injury will occur when ICP>235 kPa for blunt impacts. Based on these criteria, no injury will occur at incident blast overpressure level of 70 kPa, moderate to severe injuries will occur at 140 kPa and severe head injury will occur at the incident blast overpressure intensity of 200 kPa. However, more work is needed to confirm this finding since peak ICP alone may not be sufficient to predict the injury outcome.


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