The Concussion Crisis by Linda Carroll

Author:Linda Carroll
Language: eng
Format: epub
Publisher: Simon & Schuster

Figure 8.2: Sequence of photos following an axon from right after it’s stretched until two hours later. (Courtesy of Douglas H. Smith, M.D.)

Figure 8.3: Evolution of an axon bulb and disconnection of the axon following a brain injury. (Courtesy of Douglas H. Smith, M.D.)

All of Smith’s findings so far were in axons stretched by forces similar to those in a severe TBI. He began to wonder whether the same kinds of damage would be seen in milder brain injuries, like the concussions so prevalent in sports. There was evidence from an autopsy study that this might be the case. Australian researchers had looked at the brains of five people who had suffered a concussion and then died from other causes, such as pneumonia, days to months after their head injures. The study, which was published in 1994 in The Lancet, found the same kinds of axon damage—including bulbs of protein—that Adams had found in the brains of people with severe TBIs.

Over the years, Smith had seen plenty of cases in which people with concussions—so-called mild traumatic brain injuries—had taken a long time to recover or had never completely recovered. “I like to say that the expression ‘mild traumatic brain injury’ is an oxymoron,” he says. “It’s only mild compared to the train wreck of severe TBI that can leave you in the hospital for years. But for people with concussions that just want to get back to being themselves, it’s not at all mild.”

Smith figured he had all the tools to answer an intriguing question: Do mild traumatic brain injuries cause permanent changes to the axons? He was very familiar with post-concussion syndrome, so he knew that something serious could occur even in mild head injuries. He started to wonder whether a first concussion might lead to axonal damage so small that it was difficult to detect. Subtle changes in the axons might predispose them to significant damage if they were stretched again soon after the first stretch. Maybe, Smith thought, post-concussion syndrome was due to an accumulation of axonal injuries. The damage from the first jolt might simply make an axon more vulnerable to a second hit.

He came up with a new experiment. He designed a stretch study that scaled back the intensity of the tug to approximate what an axon would experience in a concussion. When he and his colleagues examined the lightly stretched axons, they found no damage to the microtubules, and the axons outwardly appeared completely normal. The axons were then stretched a second time, twenty-four hours later, in exactly the same way as the first. Smith’s suspicions turned out to be right. When axons were stretched lightly two times in a row, they began to deteriorate. Some took on a wavy appearance. Some developed bulbs of protein. Some eventually died. Smith had proven that the damage from two light stretches could be equivalent to a single strong stretch.

Now he wanted to know what it was about the first stretch that seemed to make the axons more vulnerable.

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