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.
Highlights
While an uncommon cause of traumatic brain injury (TBI) in civilian life [1], blast-related TBI has been of long-standing interest in military head trauma
We considered as low-level blast those studies that utilized blast exposures of ≈ 75 kPa or less based on the considerations discussed above and where sufficient pathological information was available to conclude there was no gross pathology hemorrhages that would be incompatible with mild traumatic brain injury (mTBI)
Blast-related mTBI associated with diffuse, global pattern of reduced fractional anisotropy (FA); pattern not affected by history of previous civilian mTBI; with history of more than one blast mTBI trend toward larger number of low FA voxels than with a single blast injury
Summary
While an uncommon cause of traumatic brain injury (TBI) in civilian life [1], blast-related TBI has been of long-standing interest in military head trauma. The 2014 Institute of Medicine report [36] on the long-term consequences of blast injury concluded that based on human studies, there is “limited/suggestive evidence that most of the shared symptoms are accounted for by PTSD and not a direct result of TBI alone” and that for post-concussion symptoms and persistent headaches following blast-related mTBI, there was only sufficient evidence to suggest an association.
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