New research shows brain injuries from blasts similar to football impacts
Chronic traumatic encephalopathy (CTE), a progressive degenerative disease that occurs in individuals with a history of multiple concussions and other head injuries, is shown in this view of the brain of a 45-year-old male U.S. military veteran who was exposed to a single close-range improvised explosive device blast exposure two years before his death. The abnormal dark brown staining in the image identifies neurofibrillary tangles (NFTs), abnormal brain cells laden with phosphorylated tau protein. NFTs are characteristic CTE lesions found in the brains of athletes with repetitive concussive injury, and as reported in this study, U.S. military veterans with blast exposure. The investigators also identified CTE neuropathology in the brains of blast-exposed mice.
In an advance that may someday provide health benefits for soldiers and athletes, a team of researchers has discovered a mechanism that could be the cause of traumatic brain injuries (TBI) in blast-exposed soldiers.
The breakthrough study, published in the journal Science Translational Medicine, finds that the brain injuries suffered by soldiers from improvised explosive devices (IEDs) are due to the head rotation or motion from the blast wind.
The research team created a blast neurotrauma mouse model that controlled head motion during blast exposure. The study showed that the brain injuries observed in mice exposed to blasts -- equivalent to battlefield exposures -- are identical to the brain injuries suffered by soldiers from military blasts, such as IEDs, when the heads were allowed to move.
However, when the head motions were restrained, there were no brain injuries or other neurological effects in the mice.
The researchers also compared brain tissue samples from four soldiers with known blast exposure and/or concussive injury with brain tissue samples from three amateur American football players and a professional wrestler with histories of repetitive concussive injuries. In addition, they compared the brain tissue samples to those from a control group of four young men without a history of blast exposure, concussive injury or neurological disease.
The results showed that the brain damage in blast-exposed veterans is similar to the brain injuries observed in football players who have sustained repetitive concussive head injuries. This result is a significant finding because it demonstrates a common link between what has previously been believed to be two disparate injury mechanisms.
The three-year-long study, believed to be the first and only research effort that has clearly identified an injury mechanism from the direct effects of blasts, involved 35 researchers from 14 university research centers, medical schools, hospitals or other centers.
The research team was led by Lee Goldstein, a medical doctor and associate professor at Boston University School of Medicine (BUSM) and Boston University College of Engineering, and Ann McKee, a medical doctor, professor at BUSM and director of the Neuropathology Service for the Veterans Affairs New England Healthcare System. It included William Moss, a physicist in B Division at Lawrence Livermore National Laboratory.
In addition to Boston University, the Veterans Affairs Boston Healthcare System and LLNL, among the other institutions participating in the study were New York Medical College, Harvard Medical School, Massachusetts General Hospital, Emerson Hospital (Concord, Mass.), the Veteran Affairs Medical Center (White River Junction, Vt.), and the University of Massachusetts, Lowell.
As a co-author of the paper, Moss contributed to the sections describing the blast characteristics and the discussion leading to the conclusion that blast-induced head motion was the predominant brain injury mechanism. He also showed that the experimentally produced blast waves were similar -- in amplitude and duration -- to military exposures.
Moss and other members of the research team believe that once a person has undergone a blast exposure, it may still be possible some day to stem some of the effects of the brain damage in the days and weeks after such an explosion.
"A medical solution may be more practical than an engineering or physics-based solution," Moss said. "Because the brain injuries don't appear immediately upon exposure -- and take time to develop -- this suggests there may be a way to medically intervene with drugs or other therapies that could inhibit or prevent the damage from occurring," Moss said.
Moss has been studying the causes of -- and ways to mitigate -- TBI in soldiers for more than five years.
Last year, Moss and colleague Mike King, an LLNL mechanical engineer, concluded a one-year study that found that soldiers using military helmets one size larger and with thicker pads could reduce the severity of TBI from blunt and ballistic impacts. Their research was funded by the U.S. Army and the Joint IED Defeat Organization.
In an article published in September 2009 in Physical Review Letters, Moss and King found that non-lethal blasts may induce sufficient skull rippling to generate potentially damaging forces in the brain without a head impact.