Traumatic brain injury induced by exposure to blast overpressure via ear canal

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.

Download Full-text

Ameliorative Effects of Antioxidants on the Hippocampal Accumulation of Pathologic Tau in a Rat Model of Blast-Induced Traumatic Brain Injury

Oxidative Medicine and Cellular Longevity ◽

10.1155/2016/4159357 ◽

2016 ◽

Vol 2016 ◽

pp. 1-15 ◽

Cited By ~ 14

Author(s):

Xiaoping Du ◽

Matthew B. West ◽

Weihua Cheng ◽

Donald L. Ewert ◽

Wei Li ◽

...

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Auditory Pathway ◽

Antioxidant Treatment ◽

Tertiary Butyl ◽

Early Onset Dementia ◽

Mossy Cells ◽

Blast Overpressure ◽

Promising Therapeutic Approach ◽

Central Auditory Pathway

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.

Download Full-text

Significant Head Accelerations Can Influence Immediate Neurological Impairments in a Murine Model of Blast-Induced Traumatic Brain Injury

Journal of Biomechanical Engineering ◽

10.1115/1.4027873 ◽

2014 ◽

Vol 136 (9) ◽

Cited By ~ 33

Author(s):

David M. Gullotti ◽

Matthew Beamer ◽

Matthew B. Panzer ◽

Yung Chia Chen ◽

Tapan P. Patel ◽

...

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Shock Tube ◽

High Speed ◽

Biochemical Characterization ◽

Chronic Traumatic Encephalopathy ◽

Military Population ◽

Pressure Transducers ◽

Blast Overpressure ◽

Blast Neurotrauma

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.

Download Full-text

Blast overpressure induces shear-related injuries in the brain of rats exposed to a mild traumatic brain injury

Acta Neuropathologica Communications ◽

10.1186/2051-5960-1-51 ◽

2013 ◽

Vol 1 (1) ◽

Cited By ~ 57

Author(s):

Miguel A Gama Sosa ◽

Rita De Gasperi ◽

Alejandro J Paulino ◽

Paul E Pricop ◽

Michael C Shaughness ◽

...

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Mild Traumatic Brain Injury ◽

Blast Overpressure ◽

The Brain

Download Full-text

Low-Level Primary Blast Induces Neuroinflammation and Neurodegeneration in Rats

Military Medicine ◽

10.1093/milmed/usy330 ◽

2019 ◽

Vol 184 (Supplement_1) ◽

pp. 265-272 ◽

Cited By ~ 4

Author(s):

Yansong Li ◽

Zhangsheng Yang ◽

Bin Liu ◽

Celina Valdez ◽

Mikulas Chavko ◽

...

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Neuronal Degeneration ◽

Chronic Traumatic Encephalopathy ◽

Inflammatory Cells ◽

Post Traumatic Stress ◽

Post Injury ◽

Blast Overpressure ◽

Blast Traumatic Brain Injury ◽

Combat Casualty

AbstractObjectiveMild blast traumatic brain injury is commonly prevalent in modern combat casualty care and has been associated with the development of neurodegenerative conditions. However, whether primary lower level blast overpressure (LBOP) causes neurodegeneration and neuroinflammation remains largely unknown. The aim of our present study was to determine whether LBOP can cause neuroinflammation and neurodegeneration.MethodsAnesthetized rats were randomly assigned to LBOP group (70 kPa, n = 5) or sham group (without blast, n = 5). Histopathological and cytokine changes in brain tissue at 5 days post-injury were evaluated by hematoxylin-eosin staining and Bioplex assay, respectively.ResultsHistopathological assessment revealed neuronal degeneration and increased density of inflammatory cells in frontal and parietal cortex, hippocampus and thalamus in rats exposed to LBOP. LBOP exposure significantly elevated levels of pro-inflammatory cytokines (EPO, IL-1β, IL-6, IL-12, IL-18, and TNF-α) and chemokines (GRO and RANTES) as well as of an anti-inflammatory cytokine (IL-13) in the frontal cortex.ConclusionsThis study reveals a role of neuroinflammation in neurodegeneration after mild blast traumatic brain injury. Therapies that target this process might in warfighters might function either by attenuating the development of post-traumatic stress disorder, chronic traumatic encephalopathy and Alzheimer’s disease, or by slowing their progression.

Download Full-text

On the Development of Interspecies Traumatic Brain Injury Correspondence Rules

Military Medicine ◽

10.1093/milmed/usy360 ◽

2019 ◽

Vol 184 (Supplement_1) ◽

pp. 181-194 ◽

Cited By ~ 1

Author(s):

Robert Saunders ◽

X Gary Tan ◽

Amit Bagchi

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Computational Models ◽

Human Head ◽

Injury Prediction ◽

Blast Overpressure ◽

Component Material ◽

Mri Scans ◽

Correspondence Rules ◽

Ct And Mri

Abstract Traumatic brain injury analysis in human is exceedingly difficult due to the methods in which data can be collected, thus many researchers commonly implement animal surrogates. However, use of these surrogates is costly and restricted by ethical concerns and test logistics. Computational models and simulations do not have these constraints and can produce significant amounts of data in relatively short periods. This paper shows the development of a human head and neck model and a full body porcine model. Both models are developed from high-resolution CT and MRI scans and the latest low-to-high strain rate mechanical data available in the literature to represent tissue component material behaviors. Both models are validated against experiments from the literature and used to complete an initial interspecies correspondence rule development study for blast overpressure effects. The results indicate the similarities in the way injury develops in the pig brain and human brain but these similarities occur at very different insult levels. These results are extended by a study, which shows that blast peak pressure is the driving factor in injury prediction and, depending on the injury metric used, significantly different injuries could be predicted.

Download Full-text

Blast-induced mild traumatic brain injury through ear canal: A finite element study

Biomedical Engineering Letters ◽

10.1007/s13534-015-0204-0 ◽

2015 ◽

Vol 5 (4) ◽

pp. 281-288 ◽

Cited By ~ 3

Author(s):

Praveen Akula ◽

Yi Hua ◽

Linxia Gu

Keyword(s):

Traumatic Brain Injury ◽

Finite Element ◽

Brain Injury ◽

Mild Traumatic Brain Injury ◽

Ear Canal ◽

Finite Element Study ◽

Element Study

Download Full-text

Protection against Blast-Induced Traumatic Brain Injury by Increase in Brain Volume

BioMed Research International ◽

10.1155/2017/2075463 ◽

2017 ◽

Vol 2017 ◽

pp. 1-10 ◽

Cited By ~ 3

Author(s):

Ming Gu ◽

Usmah Kawoos ◽

Richard McCarron ◽

Mikulas Chavko

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Brain Volume ◽

Jugular Vein ◽

Neuronal Degeneration ◽

Vascular Dysfunction ◽

Terrorist Attacks ◽

Neuronal Nuclei ◽

Blast Overpressure ◽

Military Conflicts

Blast-induced traumatic brain injury (bTBI) is a leading cause of injuries in recent military conflicts and it is responsible for an increased number of civilian casualties by terrorist attacks. bTBI includes a variety of neuropathological changes depending on the intensity of blast overpressure (BOP) such as brain edema, neuronal degeneration, diffuse axonal damage, and vascular dysfunction with neurological manifestations of psychological and cognitive abnormalities. Internal jugular vein (IJV) compression is known to reduce intracranial compliance by causing an increase in brain volume and was shown to reduce brain damage during closed impact-induced TBI. We investigated whether IJV compression can attenuate signs of TBI in rats after exposure to BOP. Animals were exposed to three 110 ± 5 kPa BOPs separated by 30 min intervals. Exposure to BOP resulted in a significant decrease of neuronal nuclei (NeuN) together with upregulation of aquaporin-4 (AQP-4), 3-nitrotyrosine (3-NT), and endothelin 1 receptor A (ETRA) expression in frontal cortex and hippocampus one day following exposures. IJV compression attenuated this BOP-induced increase in 3-NT in cortex and ameliorated the upregulation of AQP-4 in hippocampus. These results suggest that elevated intracranial pressure and intracerebral volume have neuroprotective potential in blast-induced TBI.

Download Full-text