Researchers find new way to treat blast induced traumatic brain injuries suffered in combat

Head injuries due to blast trauma – such as what can happen to war fighters in combat – is different than head impact injuries. Currently, there are no preventive measures that specifically target Blast-induced traumatic brain injury.

However, researchers have now successfully tested the use of surfactants (poloxamers P188) to partially repair the damaged brain tissue due to blast trauma, according to an article about the research published in the Annals of Biomedical Engineering.
According to one of the authors, Dr. Michael Cho, researchers are still determining the differences and similarities between blast and impact trauma.
The two injuries were once thought to be different.
“The blast-induced incidents likely involve generation of transient vacuum during which cavitation (e.g., micron-size bubbles) may be formed and subsequently collapse with a significant pressure,” Cho said. “The potential location of microcavitation is usually the interstitial region where the acoustic impedance discontinuity exists and liquid provides the phase change for microbubble formation.”
“In contrast, head impact trauma is expected to produce compressive and shear forces that may cause microscopic disruption of brain tissue. However, recent studies suggest that blunt force to the head can generate both positive and negative intra-cranial pressure, thus suggesting microcavitation can be formed in response to head impacts.”
More research will be required to learn about the similarities of the two injuries, he said. However, the biophysical mechanism of microcavitation could be applicable to both blast-induced traumatic brain injury \and blunt force trauma to the head, he said.
Poloxamer 188 (P188) was approved by the FDA nearly 50 years ago as a therapeutic reagent to reduce viscosity in the blood before transfusion. The most striking characteristic of P188 is its ability to repair damaged cell membranes. Since the effect of P188 is not limited to the brain but to any damaged tissue, the real world application could include injection into the circulatory system to rapidly reach the damaged tissue.
Treatment would be required within a time window of the injury, Cho said.
“P188 has a half-life of ~ 18 hours and been demonstrated to be safe when administered for up to 72 hours,” he said. “It would be ideal if the injured warfighter is treated with P188 in this window of treatment time. Moreover, it is just as plausible to administer P188 as a measure of preventive treatment before the warfighter goes to battlefield. It can also be contemplated that the medical personnel will be able to repeatedly administer the preventive measure.”
Specific to the brain trauma, P188 has been demonstrated to cross the blood brain barrier (BBB). In case of leaky BBB due to trauma, researchers hypothesize that P188 may mitigate disruption of the tight junctions between brain endothelial cells.
“We are currently applying tissue engineering techniques to engineer BBB models and validate the efficacy of P188 to restore the BBB integrity,” Cho said. “We are also in the initial phase of designing animal studies to determine the formation and visualization of microcavitation in the brain and to validate the reparative effect of P188 to minimize the impact of bTBI or blunt force trauma.
The study's authors include Cho, Johnwesly Kanagaraj, Bo Chen and Shu Xiao. The research instituitons include:  University of Illinois at Chicago, Old Dominion University and University of Texas at Arlington.