The roughly three-pound mass inside the human skull has the consistency of not-quite-set Jello, and it's just as fragile.
The brain is highly vulnerable to shakes, shock waves from nearby blasts and other trauma, and while some injuries can seem mild at first, the brain's intricate chemical and biological makeup can still go haywire over time, leading to long-term or permanent impairment — or death.
“The brain is exquisitely sensitive to rapid movement,” and that's partly why this most complex of all organs is so vulnerable to damage, says David Cifu, national program director for physical medicine and rehabilitation (PMR) services for the Department of Veterans Affairs (VA) and a professor of PMR at Virginia Commonwealth University. Because of this sensitivity, traumatic brain injury (TBI) occurs not just when the head hits a hard object but in numerous other scenarios, such as when whiplash snaps the head back and forth in an auto accident, or an invisible blast wave from a nearby explosion sweeps through a soldier's body.
While much of the brain is gelatinous, some parts are more dense than others. The differences in density increase the brain's sensitivity to injury because trauma causes certain areas to move, start and stop at different rates, stressing and straining the organ.
The brain's “gray matter” — consisting of what are sometimes called brain cells, or neurons — is somewhat less dense than the “white matter,” which is composed of fat-coated cells that carry out functions vital to the brain's operation. These cells include axons, or nerve fibers, that carry signals through the brain.
“Some areas of the brain are more elastic and flexible whereas other regions are stiffer and less compliant to stretching,” wrote David Hovda, director, and Richard Sutton, an adjunct associate professor, at the Brain Injury Research Center at the University of California, Los Angeles. As a result, “the signature of anatomical damage in TBI reflects this complicated interaction” between the exact trauma a brain suffers and the organ's physical characteristics, they wrote.
But the complications go far deeper. The initial trauma-induced sloshing and tearing is only the “primary injury,” says Thomas McAllister, a professor of psychiatry and neurology at Dartmouth Medical School, in New Hampshire. The brain functions partly by sending neurotransmitters — different chemicals that act as signaling devices — among its cells, and “in the hours, days and weeks” that follow a TBI “a complicated cascade of neurochemical events is set off that amplify” the initial trauma by changing the brain's chemical environment, says McAllister.
For example, part of the chemical cascade causes more calcium than usual to enter the cells, producing an “energy crisis” in the injured brain, says Hovda. “You don't store energy in the brain,” Hovda explains. Instead, small parts of the brain cells called mitochondria manufacture the energy from glucose in the blood. In the case of calcium overload, the mitochondria “suck up the calcium, and if there's too much they die” or at least stop functioning. That “energy crisis” can be dire because, while the brain accounts for a mere 2 percent of the body's weight, it requires at least 20 percent of all the energy the body produces.
“This is why people can't think hard” and have trouble coping with “fear, stress, anything that causes an increase” in the brain's energy needs following a TBI, Hovda says. “During the time the brain is expressing this neurobiology, it is very vulnerable to a second insult or a challenge” such as a seizure, hard mental or emotional work or a second, even mild, TBI, which among young people, especially, can even be fatal.
Also occurring after the initial trauma is a continuing breakdown of the signal-carrying axons, which are crucial to a functioning brain. That's because “a disconnected neuron is a useless neuron,” says David Brody, an associate professor of neurology at Washington University School of Medicine, in St. Louis.
In experiments with mice, Brody's lab found that in severe TBIs, axons “were broken immediately,” but “in the milder concussive injury, it does not look like they break right away. They're abnormal right away but not broken,” suggesting that subsequent changes in the brain cause a continued breakdown of axons after the initial trauma.
In the past, “it was thought that the biomechanical load on the brain” during a TBI “produced shearing forces that literally pulled apart the connections between brain regions,” Hovda and Sutton wrote. But newer research suggests that “stretching of axons at the time of trauma” sets neurochemical and other reactions in motion. Over time, they wrote, that leads to “axon disconnection.”
— Marcia Clemmitt