Why White Matter Matters in TBI
Date: March 1, 2010
When 21-year-old Tommy Martinson eased out of a coma in Hopkins’ neurocritical care unit, two months had passed since a stranger leaving a bar hammered him with a left temporal punch. Fortunately for Martinson, he was “out” while successive teams administered what neurointensivist Robert Stevens calls “the full weight of neurological critical care.”
The young man had a subdural hematoma, a subarachnoid hemorrhage and an internal brain hemorrhage—not unheard of with the concussive and acceleration-deceleration injuries that mark severe traumatic brain injury (TBI). He developed resistant status epilepticus that only a pharmacologically induced coma and antiseizure meds relieved. Then came the severe pneumonia and hypoxic respiratory failure that demanded high levels of ventilator support. The wages of survival, though, was acute kidney injury, and Martinson went on dialysis. “That’s not to mention the pulmonary embolism and multiple infections,” Stevens adds.
The fact that a grateful Martinson is now back in college and has picked up his old life, “shows, by any measure, a spectacular recovery,” Stevens adds. Amazingly, his new classmates wouldn’t begin to suspect what he’s been through. It’s only by Martinson’s own reports that lingering symptoms first came to light.
“My reaction time has changed some,” Martinson explains, “in that I take a little longer to ‘get’ something.” He also has trouble interpreting where sounds come from. Those quieter, cognitive problems, Stevens believes, may come when axons are sheared as the brain decelerates suddenly.
Immediate life-threatening injuries, of course, take priority in neurointensive care, but Stevens’ team also has a new focus on this subtler damage—diffuse axonal injury(DAI)—in the brain’s white matter. Relieving it he says, would bring a huge change in brain trauma therapy.
“White matter damage is definitely prevalent,” Stevens explains. “Virtually all brain trauma patients have it in some form.” They don’t need to suffer severe trauma—people can experience it after a concussion, a fleeting loss of consciousness, he says.
Symptoms of DAI include difficulties in consciousness, executive function, memory or attention that can last months to years after injury. And though there are therapies such as cognitive rehab, stimulants and psychotherapy, for example, none cure it.
But change is coming, Stevens believes, in part from a wealth of imaging techniques his team plans to apply to brain injury. Among them is diffusion tensor imaging (DTI), a way to view the white matter tracts that connect brain to brain. Stevens collaborates with Hopkins’ “father of DTI,” neurophysicist Susumu Mori, both to advance research on white matter damage and explore DTI as a diagnostic tool.
“We are exploring a link between white matter injury, the functional disruption of the tracts and specific cognitive changes,” says Stevens. If there is such a tie, he adds, “we could, perhaps, find ways to reconnect the tracts.” Though that may seem so much pie-in-the-sky just now, Hopkins is committed to finding care that goes beyond the supportive.
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