Primary Blast Traumatic Brain Injury in the Military:
The Case for Acknowledging Primary Blast Concussions (Part One in Series)
Veterans returning from Operations Enduring Freedom and Iraqi Freedom (OEF/OIF) have presented with a wide range of cognitive symptoms without clear head injury events. Many of these veterans, however, have been exposed to low-pressure blast waves from Improvised Explosive Devices (IEDs). Existing mechanical models have not demonstrated that concussions may be contracted through low-pressure blast waves; nevertheless, OEF/OIF veterans with blast exposure present with concussion symptoms. Should exposure to low-pressure blast waves be a proximal cause of concussion, then many blast-exposed veterans may be unaware that they have contracted mild Traumatic Brain Injuries (mTBIs). This provides a complicated diagnostic picture because 1) mTBIs are not visible or immediately apparent, and 2) veterans may not complain of concussion or classic post-concussional symptoms (Dikmen, Machamer, Fann, & Temkin, 2010). To further complicate the situation, many of the symptoms of concussion/mTBI mirror the symptoms of PTSD. Because exposure to blasts is almost necessarily psychologically traumatic, it is often difficult to parse what symptoms are related to posttraumatic stress (or other psychiatric issues) versus mTBI. Furthermore, given the chronologically simultaneous actions of experiencing brain injury and psychological trauma, the two conditions are highly co-morbid (Bogdanova & Verfaellie, 2012). Not only is it difficult to distinguish PTSD from the mTBI, but if both conditions are present, symptoms may be attributable to one condition, both, or their interactions. Finally, the fact that many of the symptoms associated with mTBI and/or post-concussional syndromes are subjective means that it often not possible to obtain objective measures of the symptoms of either condition (Davenport, Lim, & Sponheim, 2015; Dikmen, Machamer, Fann, & Temkin, 2010). Part 1 of this two-part series reviews the types of damage associated with IED explosions and identifies why existing models may be insufficient for understanding blast-related mTBI. Part 2 describes the diagnostic/detection process for blast-related mTBI and offers treatment suggestions.
Types of IED Damage
Blasts are defined as large dispersions of energy, pressure, and heat. Because such propulsions emanate from explosive devices, they propel projective fragments at high velocity, greater or equal to the speed of sound (Jak, 2013). The IEDs of OEF/OIF were often surrounded by additional barbs or garbage to produce increased shrapnel damage and injury. The explosive energy that does not propel resulting fragments is over-pressurized. It reacts with the normal air around the explosive site and pushes forth with high velocity to achieve barometric equilibrium. The result is an explosive wave that is powerful enough to move large objects, including many vehicles and people, which may be flung through the air (Jak, 2013; Plurad, 2011). This explosive wave expands with a variation of overpressure-underpressure that is translated to bodily tissue. When impacting the body, it compresses and expands alveoli, which can result in significant damage to the lungs, gastrointestinal tract, and middle ears (Jak, 2013; Plurad, 2011).
Secondary blast injuries are caused by impact from energized debris. Secondary blast injuries are significantly more common than primary injuries, and they are the injuries that the bombs were initially designed to create (Plurad, 2011). Tertiary damage results from displacement of the person by the blast or impact. That is, injury may be suffered from being thrown into buildings, walls, vehicles, or other environmental hazards. Structural collapse or nearby buildings may also cause tertiary damage. Fracture, traumatic amputation, open brain injury, and focal closed brain injury are possible (Center for Disease Control, n.d.; Jak, 2013). Additional environmental factors, including chemical burns, heat burns, inhalation injuries, and psychiatric injury (e.g., PTSD) are considered quarternary injury (Center for Disease Control, n.d.; Jak, 2013; Plurad, 2011). If bombs propel infectious substances or radiation, injuries contracted from these agents may be considered quinary (Champion, Holcomb, & Young, 2009).
Models and Mechanisms of Primary Blast Damage
The classic human/civilian model for mTBI is sports concussion, which is typically an acceleration-deceleration injury. In this non-blast injury, lesions may emerge at the site of the coup and contracoup. Rotational forces may cause some diffuse axonal injury in addition to the effects of the blunt injury. Physical mechanisms of damage include tissue damage, focal and diffuse bleeding, and shear stress and strain in the white tracts, especially in the temporal lobes. White matter shearing can in turn contribute to further tissue damage (Lew et al., 2007). If the acceleration-deceleration model can be applied in blast injuries, then the brain would accelerate into the far neural wall (often the occipital region connecting with the posterior skull), decelerate, and accelerate into the near neural wall (often the orbitofrontal region connecting with the anterior skull (Cernak et al., 2011). It is difficult to immediately apply the acceleration-deceleration model to primary blast injuries, however. This is because the blast is translated through air, so stress can be transferred into the body without an acceleration-deceleration force. Although exact mechanisms are presently unknown, blast injuries are believed to be caused by the overpressurized wave’s interacting with the brain. The concussive wave’s striking the body may vibrate the body, such that oscillations are sent through the brain via wave conductance, and the brain in thusly injured (Courtney & Courtney, 2009). In the currently adopted VA model, the changes in atmospheric pressure move in waves, which result in the displacement, shearing, and stretching or multiple bodily organs, with slight variance in velocities. Organs are thereby mechanically moved at different speeds, resulting in shearing and diffuse injury (Taber, Warden, & Hurley, 2006).
Animal studies have demonstrated that high pressure primary blasts can do significant neurological damage as well as impair coordination, strength and balance (Moochhala, 2004; Taber, Warden, & Hurley, 2006). The IED blasts experienced in OEF/OIF, however, are low pressure blasts. Because low pressure blasts were typically associated with secondary damage (and fatality) prior to OEF/OIF, some have questioned whether the low pressure primary blast waves of modern IEDs can produce brain injury. As a result, there has been some debate as to the authenticity of veterans’ symptom reporting (Elder et al., 2014; Taber, Warden, & Hurley, 2006). The primary problem with using any physical or scientific models for reproducing mTBI is that the ecology of Iraq and Afghanistan is rather unusual. This is because primary blasts have historically been studied in open fields; whereas, much of the combat in Iraq and Afghanistan occurred in confined spaces. In such spaces, there is minimal area for the pressure wave to travel, so its greater forces travel through the body. Moreover, there is some indication that pressurized waves in contained situations cause a reverberation effect, such that waves bounce off walls. This means that in a very confined space, servicemembers may experience the effects of multiple blast waves from single explosions (Defense Veterans Brain Injury Center, 2014; Plurad, 2011).
For ethical reasons, it may not be possible to recreate such conditions in a laboratory at this time. Instead, the mTBI epidemic of the OEF/OIF conflicts may represent a grand new clinical case study (e.g., H.M., Phineas Gage). That is, these servicemembers may be their own best subject pool. From this perspective, 88% of OEF/OIF-related mTBIs were closed head injuries and thereby may have been impacted by primary blasts. Perhaps more convincingly, among a veteran sample who experienced blast injuries with known damage to the lower extremities only (i.e., no known head injuries), 36% had EEG alterations (Warden et al., 2005. This suggests that some of these individuals had unknowingly suffered primary blast-related mTBIs. At this point, it is clear that experiencing IED blasts while serving in the military in Iraq/Afghanistan may lead to the cognitive, somatic, and psychiatric symptoms typically associated with concussion/mTBI. The parsimonious conclusion is that veterans with such exposure have suffered primary blast-related mTBIs. This still does not solve the problem, however, of how to differentiate unknown primary blast-related mTBI from PTSD. (See Part 2 of this article for an explanation of how mTBI is diagnosed/detected and treated.)
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