Distinct scarring on the brains of soldiers exposed to IED blasts in Iraq and Afghanistan may be the physical fingerprint of a condition seen in World War I veterans known as “shell shock.”
The honeycomb pattern of broken and swollen nerve fibers differs from brain damage caused by car crashes, drug overdoses, or collision sports. The pattern is found throughout critical regions of the brain, including those that control executive function, researchers say.
“This is the first time the tools of modern pathology have been used to look at a 100-year-old problem: the lingering effect of blasts on the brain,” says Vassilis Koliatsos, professor of pathology, neurology, psychiatry, and behavioral sciences at Johns Hopkins University School of Medicine.
“We identified a pattern of tiny wounds, or lesions, that we think may be the signature of blast injury,” he says. “The location and extent of these lesions may help explain why some veterans who survive IED attacks have problems putting their lives back together.”
Doctors treating IED survivors “often see depression, anxiety, post-traumatic stress, and substance abuse or adjustment disorders,” Koliatsos says.
“Life is very difficult for some of these veterans. It’s important to understand that at least a portion of these difficulties may have a neurological foundation.”
Blast neurotrauma
Soldiers have struggled with bomb-induced brain damage since 1914, when German and Allied forces tried to blast one another out of entrenched positions with months-long bombardments. Many World War I fighters survived the barrage outwardly unscarred, but with an array of cognitive and psychological difficulties then known as “shell shock.”
After World War I, mass bombardments of troops were rare, and shell shock became far less common. Now renamed “blast neurotrauma,” or blast injury to brain, it has re-emerged due to insurgent forces’ widespread use of IEDs in Iraq and Afghanistan.
For the study, published in Acta Neuropathologica Communications, researchers examined the brains of five male US military veterans who survived IED attacks.
Three later died of methadone overdoses that could have been accidental, Koliatsos says, since the drug is commonly prescribed to treat soldiers’ chronic pain. One died of a gunshot wound to the head, and one died of multiple organ failure.
The veterans’ brains were compared to those of 24 people who died of a range of causes, including motor vehicle crashes, opiate overdoses, and heart attacks.
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The researchers used a molecular marker to track a protein called APP that normally travels from one nerve cell to another via a long nerve fiber, or axon.
When axons are broken by an injury, APP and other proteins accumulate at the breaks, causing swelling. In the brains of people killed in car accidents, the swellings are large and bulb-shaped. In cases of methadone overdose, these axonal swellings are small.
In the brains of four of the five veterans who survived wartime blast injuries, the axonal bulbs were medium-sized and usually arrayed in a honeycomb pattern near blood vessels. “We did not see that pattern in other types of brain injury,” Koliatsos says.
These distinctive lesions were found in a number of places in the veterans’ brains, including in the frontal lobes, which control decision making, memory, reasoning, and other executive functions.
The lesions may be fragments of nerve fibers that broke at the time of the blast and slowly deteriorated, or they may have been weakened by the blast and broken by some later insult like a concussion or drug overdose.
“When you look at a brain, you are looking at the life history of an individual, who may have a history of blasts, fighting, substance abuse, or all of those,” Koliatsos says.
“If researchers could study survivors’ brains at different times after a blast—a week, a month, six months, one year, three years—that would be a significant step forward in figuring out what actually happens over time after a blast.”
Other contributors to the research are from Johns Hopkins and the Veterans Administration Medical Center in Washington, DC Johns Hopkins Alzheimer’s Disease Research Center and gifts from the Kate Sidran Family Foundation and the Sam and Sheila Geller family funded the study.
Source: Johns Hopkins University
