The War's Invisible Wounded
Credit: Zuma

The science of blast injury, less than a decade old, is so preliminary that even basic tenets can only be guessed at now. How far can you be from a pressure wave without being at risk? Can TBI occur when there's no loss of consciousness? How many blast exposures is too many, and does that vary from person to person? One such question is most germane to men like Workman: Why do some soldiers heal on their own, while others go on suffering without end?

Estimates vary according to who's doing the counts, but between 50 and 80 percent of the milder cases do resolve themselves. But for a "miserable minority," as clinicians call them, the symptoms are intractable and so disabling that they can't go back to their life's work. If there's hope for them, it rests with people like Colonel Ling, the neurologist who treated TBI patients in Baghdad and came back in 2006 ablaze to find a cure. As a program manager at DARPA, the military's gold-star research lab, he secured $9 million to fund a pathbreaking study that defined both the syndrome and the science. Putting out a call to the top universities, he built a team of multiple disciplines, pairing astrophysicists with biochemists and mechanical engineers. He tasked his scientists to come back to him in a year with, first, a detailed understanding of the cause of brain-blast harm, and, second, an analysis of what that harm looked like, down to the cellular level.

Conventional ways of examining the damage were all but useless here, as most of it was far too subtle to see on CT scans and MRIs. Nor, for obvious reasons, could you excise tissue from a soldier who was still alive. So one group of scientists turned to pigs as subjects, putting them in harnesses and setting off charges nearby. Another group at Harvard took neurons from rats and subjected them to simulated bombs, using tiny magnets and blast bioreactors to overstress the cells the way a wave of pressurized air would. A third crew, working out of MIT, developed software models to measure blast waves and see how they acted inside the skull.

The investigators of project PREVENT (Preventing Violent Explosive Neurotrauma) discovered that of all a blast's components – the heat, light, and noise; the cloud of chemical toxins; and a surge of electromagnetic force – the most lethal, by far, was the supersonic wave of overpressurized air. "Here," says Ling, clicking a tab on his laptop: "A picture's worth a thousand words." On his screen loops a video taken at an ATF blast facility. A 20-kilogram bomb, squarely encased in metal, blows up, and in superslow motion, a monstrous fist of visible air pounds a painted rail of 2x4s. The planks twist in one direction, then another from the underpressure, an inverse surge of suction force. "Your brain is 80 percent aqueous," says Ling, "so it's rippling under the wave. With even the mild cases" – those farthest from the blasts – "we're seeing inflammation and widespread damage to the fibers of the axons," the trunks through which cells communicate and carry out complex functions.

In animals, that caused impaired gait, sleep, and memory, which told Ling's team that the affected areas were at the front and back of the brain. This dovetailed with what Ling saw in his practice as a neurologist at Walter Reed, where TBI soldiers complained of a linked set of symptoms. They had, besides migraines, the vertigo and nausea caused by lesions to the cerebellum, the walnut-shaped region at the rear of the brain that manages motor balance. More ominous was the damage to the frontal lobe, where higher functions are controlled – planning, judgment, problem solving. It is also where sleep and mood are regulated, and is, in essence, the home of the personality. Small wonder that the spouses and parents of some of these soldiers said they barely knew them anymore. Erratic and listless, easily confused: They acted like old men in young men's bodies, drifting in and out of their own lives.

But so dizzyingly overwired is the human brain that, to understand the failure of a cortex bundle, it is necessary to start with a single cell. At Harvard, one of DARPA's partner teams is studying discrete neurons battered by microstressors. Associate professor Kit Parker, who heads the project, has a distinctive investment in the work, having served a tour in northern Afghanistan as an army reserve captain in '02. His lab manager, Josh Goss, a twice-deployed marine, leads me around the benchtop stations, where miniature marvels of the team's invention are put to abstruse tasks. In one room, a pair of tiny tweezers pushes and pulls a neuron, the effects of which are filmed, then scanned, on a 3-D microscope. In another room, the plunger of a bioreactor pounds a tray of nerve cells with a whomp. "We developed these tools to ask a fundamental question: What does a cell feel after a blast?" says Goss.

Parker speculates that neurons left intact by the blast are "swimming in a soup of dying cells," starving for oxygen as the blood vessels spasm, and caught in a tide of errant proteins as the axons shoot off wildly. It may be several years before he and fellow researchers know which proteases and enzymes are at fault. But once they've pinned those down, existing drugs might ease symptoms until new smart-bomb medicines come along. "We lack biomarkers, as we lacked them in AIDS, before we came up with viral load and CD4 counts," says Zafonte, of Harvard Medical School. "But when we found those signs and fixed them, we also fixed the outcome."

Parker isn't quite as sanguine. "There are so many complex questions," he says, that "it's going to take a big tent" to resolve them. "We need scientific nation building, a TBI czar, and enough money to pay for the kind of innovation that has repeatedly put this country on top." He takes pains not to add what so many in the field have muttered off the record: that the National Institutes of Health, the government colossus with a $30 billion annual budget, has largely hugged the sideline on brain-blast trauma. "My fear is we're going to see a wave of 40-year-old soldiers showing up at the VA with dementia," says Parker. "They played hurt and went on fighting after multiple blasts, and I hope we return their loyalty when they need it."

Parker might have told me this much in person when I dropped by his lab in May. But at the time, he was engaged in other matters, leading a company of the 10th Mountain Division from Kabul to the Pakistani border. It's his second tour of duty, and the bombs he swept for were vastly more potent than in '02. "My convoy got blown up," he told me via e-mail from his base very late one night. "Flipped an MRAP in front of me, triggering a brutal firefight when me and another dude pulled out casualties. Watching an MRAP go up in the air, [attached to] a two-ton mine roller, gives you some idea of the force." A third of his staffers at Harvard have done combat tours in Iraq or Afghanistan, and are "after it like a ball of fire," Parker writes. "I've got friends with TBI."