Article

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: 1.07). 01/2009; 72(1). DOI: 10.1016/j.mehy.2008.08.015
Source: arXiv

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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    • "Therefore the free-floating head FE model has been considered to reduce the cost of the simulations. Some other researchers simply fix the base of the FE head model and study the biomechanical responses of the head under the blast loads during the first few milliseconds [1] [2] [3] [4] [5] [6] [7] [8] [9] [10]. While considering the whole body is computationally expensive, in some circumstances the effects of the trunk cannot be ignored. "
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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.
    Full-text · Conference Paper · Nov 2013
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    • "The mechanisms of blast-induced brain injury remain controversial [3,11,26]. Blast pressure waves may cause brain injury by directly transmitting blast energy into the brain and/or indirectly through dysfunction of the pulmonary and circulatory systems. Activation of the autonomic nervous system and the neuroendocrine-immune system may contribute to molecular changes and cellular injuries in the brain [19,27-35]. "
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    ABSTRACT: Blast-induced traumatic brain injury has dramatically increased in combat troops in today's military operations. We previously reported that antioxidant treatment can provide protection to the peripheral auditory end organ, the cochlea. In the present study, we examined biomarker expression in the brains of rats at different time points (3 hours to 21 days) after three successive 14 psi blast overpressure exposures to evaluate antioxidant treatment effects on blast-induced brain injury. Rats in the treatment groups received a combination of antioxidants (2,4-disulfonyl α-phenyl tertiary butyl nitrone and N-acetylcysteine) one hour after blast exposure and then twice a day for the following two days. The biomarkers examined included an oxidative stress marker (4-hydroxy-2-nonenal, 4-HNE), an immediate early gene (c-fos), a neural injury marker (glial fibrillary acidic protein, GFAP) and two axonal injury markers [amyloid beta (A4) precursor protein, APP, and 68 kDa neurofilament, NF-68]. The results demonstrate that blast exposure induced or up-regulated the following: 4-HNE production in the dorsal hippocampus commissure and the forceps major corpus callosum near the lateral ventricle; c-fos and GFAP expression in most regions of the brain, including the retrosplenial cortex, the hippocampus, the cochlear nucleus, and the inferior colliculus; and NF-68 and APP expression in the hippocampus, the auditory cortex, and the medial geniculate nucleus (MGN). Antioxidant treatment reduced the following: 4-HNE in the hippocampus and the forceps major corpus callosum, c-fos expression in the retrosplenial cortex, GFAP expression in the dorsal cochlear nucleus (DCN), and APP and NF-68 expression in the hippocampus, auditory cortex, and MGN. This preliminary study indicates that antioxidant treatment may provide therapeutic protection to the central auditory pathway (the DCN and MGN) and the non-auditory central nervous system (hippocampus and retrosplenial cortex), suggesting that these compounds have the potential to simultaneously treat blast-induced injuries in the brain and auditory system.
    Full-text · Article · Nov 2013 · PLoS ONE
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    • "This could occur if the main pressure wave was being transmitted through the Virchow-Robin compartment. Several studies have documented that intracranial pressure increases acutely following blast exposure [7,15,20-27,31,32]. Increased CSF pressure transmitted through the Virchow-Robin compartment could generate local pressure differentials at the interface between the vascular basal lamina and the surrounding tissues. "
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    ABSTRACT: Blast-related traumatic brain injury (TBI) has been a significant cause of injury in the military operations of Iraq and Afghanistan, affecting as many as 10-20% of returning veterans. However, how blast waves affect the brain is poorly understood. To understand their effects, we analyzed the brains of rats exposed to single or multiple (three) 74.5 kPa blast exposures, conditions that mimic a mild TBI. Rats were sacrificed 24 hours or between 4 and 10 months after exposure. Intraventricular hemorrhages were commonly observed after 24 hrs. A screen for neuropathology did not reveal any generalized histopathology. However, focal lesions resembling rips or tears in the tissue were found in many brains. These lesions disrupted cortical organization resulting in some cases in unusual tissue realignments. The lesions frequently appeared to follow the lines of penetrating cortical vessels and microhemorrhages were found within some but not most acute lesions. These lesions likely represent a type of shear injury that is unique to blast trauma. The observation that lesions often appeared to follow penetrating cortical vessels suggests a vascular mechanism of injury and that blood vessels may represent the fault lines along which the most damaging effect of the blast pressure is transmitted.
    Full-text · Article · Aug 2013
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Questions & Answers about this publication

  • Wei Zhao added an answer in Brain Trauma:
    Can brain trauma be caused due to thoracic pressure surges?

    I am a mechanical engineer studying mechanisms of brain trauma. Of the mechanisms that I have studied, I found the evidence of brain trauma as a result of thoracic pressure surge only due to blast waves. I would like to know if any other kind of impact in the thorax could lead to brain trauma due to thoracic pressure surge. For eg. if someone gets kicked in the thorax portion are there any chances of their experiencing brain trauma.

    Wei Zhao

    This concept is what I learned in my advisor's class. I was not able to found a reference for it. However, I found another paper which could be helpful.

    Based on this Thoracic mechanism as discussed in the following paper, one experiencing a blast wave around chest like the blast from airbag could sustain brain pressure-induced injury.

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      [Show abstract] [Hide abstract]
      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.
      Full-text · Article · Jan 2009 · Medical Hypotheses