Soldiers exposed to roadside bomb blasts and athletes who have suffered repeated concussions show the same long-lasting changes to brain cells, a new study reports.
The research connects two growing — and for many sufferers, chronically debilitating — health problems in the United States. It adds to the evidence that injuries once officially termed “mild” may be anything but.
Specifically, head trauma that doesn’t knock a person unconscious may nevertheless kill some brain cells and damage the architecture of others, setting up a semi-permanent state of brain inflammation. That may lead to the foggy thinking and poor memory that thousands of soldiers and football players experience even after they’ve “recovered” and been sent back to the battlefield or playing field.
“Whether your head is accelerating because you’ve been hit by a linebacker or the blast from an exploding [improvised explosive device], the injury to the brain appears to follow a similar course,” said Lee E. Goldstein, a doctor and neuroscientist at Boston University who co-led the study, published Wednesday in Science Translational Medicine.
The abnormalities found in the brains of troops and athletes studied after death are similar to those found in the brains of mice exposed to the equivalent of a moderate-size bomb blast, an experiment the 35-member research team also conducted.
The study doesn’t immediately suggest ways to prevent or treat blast injuries in soldiers or concussions in athletes. The researchers hope that future mouse experiments may point in that direction. But the findings will almost certainly draw more attention to a problem that’s now part of the medical histories of thousands of Americans.
“The take-home message is that concussions need to be taken seriously at all ages,” said Ann C. McKee, a neuropathologist with the Veterans Affairs Boston Healthcare System. “We don’t want our kids exposed to these injuries in the pursuit of amateur athletics.”
Traumatic brain injury (TBI) has been called the “signature wound” of the Iraq and Afghanistan wars.
A key question is whether a blast alone can cause permanent brain damage, as opposed to a blast that smashes a soldier’s head against a solid object, such as a vehicle roof. By one estimate, more than 320,000 troops may have experienced some form of TBI over the past decade.
Until this study, however, there’d been almost no detailed descriptions of the brains of people who survived battlefield blast injuries.
“Surprisingly, what is happening under the microscope after a blast-related TBI hasn’t been made public, except for one previous [published] case,” said David L. Brody, a brain-injury researcher at Washington University’s School of Medicine in St. Louis.
Most soldiers exposed to roadside bombs survive; there’s no way to see what their brains look like on the cellular level after the blasts. In addition, it’s nearly impossible to find someone whose only head trauma is from an improvised explosive device. Virtually all soldiers report suffering concussions previously in their military careers or as civilians, making it hard to determine the effect of a single blast.
For athletes, the picture is similarly confusing. Football and hockey players whose brains end up in neuropathology labs tend to be ones who’ve had many concussions.
The Boston researchers tried to minimize these problems by looking at deceased young adults whose history of head trauma was known. In all cases, however, the subjects had more than one brain insult.
Using both conventional and electron microscopes, they studied the brains of 12 men, most in their 20s. Four were veterans exposed to one or two explosions who later died of other causes (at least one by suicide). Four were athletes (three football players and one wrestler) with multiple concussions who died of various causes (one by suicide). Four men had no head trauma; two of them were suicides.
The brains of the veterans and athletes each showed a loss of neurons and damage to axons, the wirelike filaments that allow neurons to communicate with each other. The brain cells also showed tangles of “tau protein,” a substance found in axons. That second abnormality is the central feature of “chronic traumatic encephalopathy.” McKee has seen it in postmortem studies of the brains of about 65 athletes with multiple concussions.
“Not only do we find it in young athletes, we find it in [military] veterans that have experienced blast and concussion,” she said.
The mice studied were exposed to bursts of compressed gas equivalent to the explosion of a 120-millimeter artillery 18 feet away, which the researchers described as “within the range of typical IED detonations.” Their brains showed some axon damage and abnormal tau protein, although the latter was not found in the wild tangles seen in the human samples.
Douglas H. Smith, who directs the Center for Brain Injury and Repair at the University of Pennsylvania and was not involved in the study, said the damage looked “quite minor” to him. He said “the jury is still out whether blast exposure alone” can cause the kind of damage seen in more conventional head trauma.
To make the mouse experiment more closely resemble battlefield conditions, the Boston researchers didn’t immobilize the heads of the anesthetized animals. Films showed that the 340-mph blast wind caused the heads to oscillate. The scientists speculate that a single IED blast may be the equivalent of multiple concussions happening over about 8 milliseconds.
Afterward, the mice showed marked problems in tests of learning and memory and had slower nerve impulses in certain regions of the brain.
“If you hear people complain, ‘Doc, I’m thinking slow, I can’t remember things’ — these are the impairments we see in the mice,” Goldstein said. “But none of these mice have played hockey, and none have been to war.”