A Thoracic Mechanism of Mild Traumatic Brain Injury Due to Blast Pressure Waves

Department of Physics, United States Military Academy, West Point, NY 10996, United States.
Medical Hypotheses (Impact Factor: 1.15). 01/2009; 72(1). DOI: 10.1016/j.mehy.2008.08.015
Source: PubMed

ABSTRACT The mechanisms by which blast pressure waves cause mild to moderate traumatic brain injury (mTBI) are an open question. Possibilities include acceleration of the head, direct passage of the blast wave via the cranium, and propagation of the blast wave to the brain via a thoracic mechanism. The hypothesis that the blast pressure wave reaches the brain via a thoracic mechanism is considered in light of ballistic and blast pressure wave research. Ballistic pressure waves, caused by penetrating ballistic projectiles or ballistic impacts to body armor, can only reach the brain via an internal mechanism and have been shown to cause cerebral effects. Similar effects have been documented when a blast pressure wave has been applied to the whole body or focused on the thorax in animal models. While vagotomy reduces apnea and bradycardia due to ballistic or blast pressure waves, it does not eliminate neural damage in the brain, suggesting that the pressure wave directly affects the brain cells via a thoracic mechanism. An experiment is proposed which isolates the thoracic mechanism from cranial mechanisms of mTBI due to blast wave exposure. Results have implications for evaluating risk of mTBI due to blast exposure and for developing effective protection.

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    ABSTRACT: The results of a computational study on the effect of the body on biomechanical responses of a helmeted human head under various blast load orientations are presented in this work. The focus of the work is to study the effects of the human head model boundary conditions on mechanical responses of the head such as variations of intracranial pressure (ICP). In this work, finite element models of the helmet, padding system, and head components are used for a dynamic nonlinear analysis. Appropriate contacts and conditions are applied between different components of the head, pads and helmet. Blast is modeled in a free space. Two different blast wave orientations with respect to head position are set, so that, blast waves tackle the front and back of the head. Standard trinitrotoluene is selected as the high explosive (HE) material. The standoff distance in all cases is one meter from the explosion site and the mass of HE is 200 grams. To study the effect of the body, three different boundary conditions are considered; the head-neck model is free; the base of the neck is completely fixed; and the head-neck model is attached to the body. Comparing the results shows that the level of ICP and shear stress on the brain are similar during the first five milliseconds after the head is hit by the blast waves. It explains the fact that the rest of the body does not have any contribution to the response of the head during the first 5 milliseconds. However, the conclusion is just reasonable for the presented blast situations and different blast wave incidents as well as more directions must be considered.
    ASME 2013 International Mechanical Engineering Congress and Exposition; 11/2013
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    ABSTRACT: Traumatic Brain Injury is a major health issue that is hard to diagnose since it often occurs without signs of external injuries. While it is well known that exposure of biological cells to shock waves causes damage to the cell membrane, it is currently unknown by which mechanisms damage is caused, and how it depends on physical parameters such as shock wave velocity, shock pulse duration, or shock pulse shape. In this computational study, we use a coarse-grained model of the lipid vesicle as a generic model of a cell membrane to elucidate the general principles of the cellular damage induced by the shock wave direct passage through the cranium. Results indicate that the extent of the liposome compression does not strongly depend on the pressure pulse and that liposome extension is very sensitive to the change in the negative pressure phase. The structural integrity of the vesicle is altered as pores form in the lipid membrane at overall pressure impulses generated by supersonic shock waves, which are greater than 5 Pa·s at single or repetitive exposure. Consequently, these permeability changes may lead to changes in the influx of sodium, potassium, and calcium ions.
    The Journal of Chemical Physics 11/2014; 141(18):184904. DOI:10.1063/1.4901130 · 3.12 Impact Factor
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    ABSTRACT: High-pressure blast waves can cause extensive CNS injury in human beings. However, in combat settings, such as Iraq and Afghanistan, lower level exposures associated with mild traumatic brain injury (mTBI) or subclinical exposure have been much more common. Yet controversy exists concerning what traits can be attributed to low-level blast, in large part due to the difficulty of distinguishing blast-related mTBI from post-traumatic stress disorder (PTSD). We describe how TBI is defined in human beings and the problems posed in using current definitions to recognize blast-related mTBI. We next consider the problem of applying definitions of human mTBI to animal models, in particular that TBI severity in human beings is defined in relation to alteration of consciousness at the time of injury, which typically cannot be assessed in animals. However, based on outcome assessments, a condition of "low-level" blast exposure can be defined in animals that likely approximates human mTBI or subclinical exposure. We review blast injury modeling in animals noting that inconsistencies in experimental approach have contributed to uncertainty over the effects of low-level blast. Yet, animal studies show that low-level blast pressure waves are transmitted to the brain. In brain, low-level blast exposures cause behavioral, biochemical, pathological, and physiological effects on the nervous system including the induction of PTSD-related behavioral traits in the absence of a psychological stressor. We review the relationship of blast exposure to chronic neurodegenerative diseases noting the paradoxical lowering of Abeta by blast, which along with other observations suggest that blast-related TBI is pathophysiologically distinct from non-blast TBI. Human neuroimaging studies show that blast-related mTBI is associated with a variety of chronic effects that are unlikely to be explained by co-morbid PTSD. We conclude that abundant evidence supports low-level blast as having long-term effects on the nervous system.
    Frontiers in Neurology 12/2014; 5:269. DOI:10.3389/fneur.2014.00269

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