Explosive blast exposures are a leading cause of combat and training Traumatic Brain Injuries (TBI) among Service members. Blast-induced TBI result from exposure to blast overpressure, which generates shock wave energy that impacts the head through the brain tissue. However, the exact mechanisms through which this energy causes a brain injury are poorly understood because damage occurs at the subcellular level. Additionally, the damage is typically measurable only through advanced neuroimaging techniques, such as transmission electron microscopy as well as gross histopathological, biochemical, and neurobehavioral assessment. Previous research on blast-induced TBI stops short of directly associating brain tissue damage with the different components of a blast overpressure shock wave. As such, a complete understanding of shock wave-related blast-induced TBI ideally requires detailed characterization of a shock wave itself.
To address this gap, researchers studied physical blast shock wave properties, including peak pressure, rise time, positive phase duration, impulse, shock velocity, and particle velocity, together with established biological effects of blast on the mouse brain (Rutter et al., 20211; Konan et al., 20192; and Song et al., 20183). In the study, mice were exposed to open-air blast and then evaluated using neurobehavioral, histological, biochemical, and advanced neuroimaging assessments. Additionally, the different waveforms were compared for open-air and shock tube experiments, as major differences exist between these types of blast overpressure exposure.
As expected, exposure to open-field blast was associated with ultrastructural brain injury and neurobehavioral changes. Specifically, abnormalities of axons, mitochondria, and synapses, increased mitochondrial dysfunction, and oxidative stress resulting in a decline in neurobehavioral function. These results, combined with waveform comparisons between open-field and shock tube blast overpressures, give insight on the physical properties of blast shock waves. Additionally, the results provide a database of physical blast properties that allow for direct comparison to the biological findings after blast exposure, independent of open-air or shock tube modeling.
Understanding the association between shock wave physics and tissue damage that causes a brain injury will help with the treatment of TBI. Future work continuing to detail the association between shock wave physics and brain tissue damage will help with the understanding, prevention, assessment, and treatment of blast-induced TBI among Service members.
1. Barbara Rutter, PhD, Hailong Song, MBBS, PhD, Ralph G DePalma, MD, FACS, Graham Hubler, PhD, Jiankun Cui, MD, Zezong Gu, MD, PhD, Catherine E Johnson, PhD, Shock Wave Physics as Related to Primary Non-Impact Blast-Induced Traumatic Brain Injury, Military Medicine, Volume 186, Issue Supplement_1, January-February 2021, Pages 601-609, https://doi.org/10.1093/milmed/usaa290.
2. Landry M Konan, Hailong Song, Genevieve Pentecost, Delvise Fogwe, Tina Ndam, Jiankun Cui, Catherine E Johnson, DeAna Grant, Tommi White, Mei Chen, Weiming Xia, Ibolja Cernak, Ralph G DePalma, Zezong Gu, Multi-Focal Neuronal Ultrastructural Abnormalities and Synaptic Alterations in Mice after Low-Intensity Blast Exposure, J Neurotrauma. 2019 Jul 1;36(13):2117-2128. doi: 10.1089/neu.2018.6260.
3. Hailong Song, Landry M Konan, Jiankun Cui, Catherine E Johnson, Martin Langenderfer, DeAna Grant, Tina Ndam, Agnes Simonyi, Tommi White, Utkan Demirci, David R Mott, Doug Schwer, Graham K Hubler, Ibolja Cernak, Ralph G DePalma, Zezong Gu, Ultrastructural Brain Abnormalities and Associated Behavioral Changes In Mice After Low-Intensity Blast Exposure, Behavioral Brain Research, 2018 Jul 16;347:148-157. doi: 10.1016/j.bbr.2018.03.007.
This publication was made possible in part by funding from the DoD Congressionally Directed Medical Research Programs (CDMRP) for the Peer Reviewed Alzheimer's Research Program Convergence Science Research Award (PRARP-CSRA; AZ140109 and AZ180043), research funds from Department of Pathology and Anatomical Sciences from the University of Missouri School of Medicine (ZG), and Veterans Affairs Office of Research and Development BLR&D (I01 BX004313-01A1).
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