The neurological significance of subclinical blast exposure
By: Andrew Baker, MD, FRCPC and Eugene Park, PhD
Blast injury results from trauma caused by explosions. During recent conflicts in Iraq and Afghanistan, improvised explosive devices have caused a large number of injuries. At the same time during these conflicts, there has been an increased frequency of identified traumatic brain injury, including concussions, and post-traumatic stress disorder (PTSD).
Explosions or blasts cause trauma through exposure to thermal and chemical stress, through the blunt impact of the wind (sufficient to cause amputations), and through the impact and penetration of high velocity debris and shrapnel. However, preceding all of these sources of trauma is the primary blast wave of over pressure. This primary blast wave is characterized by an instantaneous increase in ambient pressure, heat and density, followed by a prolonged negative pressure.
The primary blast wave trauma is now the focus of much research internationally aimed at understanding the mechanisms, prevention and treatment strategies of injury. Primary blast waves will transfer energy and cause injury primarily at the interfaces between tissues of differing density and especially differing phase (gas, liquid, solid). Thus, the tympanic membrane, the lung and bowel are commonly injured and characterize this trauma exposure.
While armour and other barriers have reduced penetrating injuries to the body, the emergence and persistence of brain injuries has raised the question of the relationship of blast exposure to this problem. Our laboratory is particularly interested in determining the potential relevance of blast exposure to mild traumatic brain injury, or even as an organic contributor to PTSD.
A common practical issue following an explosion is the triage of people exposed to blast wave. Symptoms and signs of injury to the tympanic membrane, lung or bowel—or even obvious neurologic changes—would indicate that the patient has been injured and needs careful attention. However, if there are no obvious or immediate physical injuries present, it is not clear whether there have been any neurologic implications following exposure to a blast at a distance. In short, sub-clinical or mild blast trauma could cause easily missed injuries in the brain that would ultimately manifest as symptoms and signs of either mild traumatic brain injury or organic contributors to PTSD. This raises an important question. In soldiers not otherwise affected by intense primary blast wave energy, was it possible that there were organic effects of primary blast exposure?
To examine this question further, we developed a model of primary blast injury in the laboratory. In association with the U of T Institute for Aerospace Studies, we characterized the physics of blast wave dynamics. Rats were randomly exposed to sham or blast wave conditions. We varied the intensity until we found the minimum that would affect the lung parenchyma, and lowered this intensity by 30%. The rats were then examined with various neuropsychological tests, and their brains were examined with both imaging and electrophysiological functional studies.
This study showed that rats exposed to blast had worse coordination or concentration on the Rotarod (a rotating rod that normal rats like to run on, much like a wheel for a pet rodent). They exhibited more anxiety in open field and light/dark box studies (measuring confidence to exit their safe dark box and explore in the light exposed pen). The brains of blast-exposed rats demonstrated evidence of cytoskeletal proteolysis by twelve hours, and cell death in the corpus callosum and periventricular white matter areas. There was reduced amplitude of the stimulated compound action potential in the corpus callosum.
Taken together, these results demonstrated that subclinical primary blast exposure resulted in measureable changes to the brain. We saw evidence of axonal injury, impaired white matter function and cell death. There was evidence of impaired neuropsychological measures including anxiety and coordination or concentration. Prior to these studies, it was not clear that subclinical exposure to primary blast wave could result in measurable organic brain injury. These studies demonstrated that primary blast waves, of intensity too low to injure the lung or bowel, may indeed harm neurons.
These studies have raised many questions in our minds. For example, could apparently harmless exposure to a primary blast wave actually cause organic brain injury that would result in measurable symptoms and signs? Further, if so, could this be related to the relatively high prevalence of symptoms and signs that are attributed to either mild traumatic brain injury and to PTSD?
Our group is pursuing these questions in both civilian and military populations. We hope to identify the underlying mechanisms and look for prophylactic and early treatments. Finally, we hope this information will lead to more questions that will ultimately be helpful for our military personnel.