Chronic traumatic encephalopathy (CTE) is a permanent neurodegenerative brain disease brought on by repeated head trauma. Often, people interpret this to mean CTE is caused by concussions, however, a recent study shows concussions don’t necessarily have to be a part of the equation.
“The concussion is really irrelevant for triggering CTE,” Dr. Lee Goldstein, an associate professor at Boston University School of Medicine and College of Engineering, and a corresponding author of the study, told The Washington Post. “It’s really the hit that counts.
“Although that’s the headline, this is the best scientific evidence to date, in fact some of the only scientific evidence, that we have that that’s so. . . . This is the first really solid evidence that we have where we have controlled experiments where we can make that case very strongly and convincingly.”
The study published in the journal Brain by researchers from Boston University evaluated the brains of teenagers with head injuries and used mice to recreate this head trauma. The scientists say the data collected from this reveals more about the origin of CTE and its tenuous relationship with TBI or concussions.
“The same brain pathology that we observed in teenagers after head injury was also present in head-injured mice. We were surprised that the brain pathology was unrelated to signs of concussion, including altered arousal and impaired balance, among others. Our findings provide strong causal evidence linking head impact to TBI and early CTE, independent of concussion,” Goldstein said. “The results may explain why approximately 20 percent of athletes with CTE never suffered a diagnosed concussion.”
While these findings could have significant implications for both the military and athletics, Goldstein notes that there are several other groups at risk for repeated head trauma.
“There are many vulnerable populations at greatly increased risk of repetitive head injury including domestic abuse, incarcerated populations, homeless,” Goldstein said. “It’s a big problem for the NFL, a bigger problem for amateur athletics and an even larger problem still for the greater public.”
Goldstein believes that much of the confusion surrounding concussions and their relationship with CTE comes from conflating CTE, TBI, and concussions.
Concussions, according to Goldstein, are a syndrome defined “by consensus really every couple of years, based on the signs and symptoms of neurological syndrome, what happens after you get hit in the head. It’s nothing more than that, a syndrome. You take one [symptom] from column A, one from column B.”
A traumatic brain injury isn’t the same thing, though it may cause a concussion. “[TBI] is an injury, an event,” he said. “It’s not a syndrome. It’s an event and it involves damage to tissue. If you don’t have a concussion, you can absolutely have brain injury and the converse is true.”
Meanwhile, Goldstein defines CTE as “a bona fide neurodegenerative disease. It will progress independently of whether you have future hits and a lot of people think that the injury is the disease and it’s not. There is an injury and then it goes on to spread in the brain, like other neurodegenerative diseases.”
The intense focus on concussions as the perceived source of CTE is a matter of trying to treat a symptom rather than the root illness in Goldstein’s eyes.
“My analogy for this is it’s like having health officials focus on the hacking cough in smokers rather than the lung cancer,” Goldstein said. “A cough can be related to smoking — there can be many other causes of a cough. But the fact that you have or do not have a cough is irrelevant to whether you have cigarette-caused lung cancer. . . . It’s the same with chest pain and a heart attack. We would no more rely on chest pain to be the single indicator of whether you’ve had a heart attack.
“So concussion may or may not be a TBI and equally important not having a concussion may or may not be associated with a TBI. A concussion doesn’t tell you anything about a TBI. Nor does it tell you anything about CTE.”
Instead of being caused by a single concussion, Goldstein and his team say CTE is more likely attributed to the cumulative effect of smaller “subconcussive” hits.
The Concussion Legacy Foundation explains that subconcussive hits are those which are below the concussion threshold: “the brain is shaken, but not so violently that the damage to brain cells is severe.”
In isolation, these hits don’t cause any clear effect on the brain. Over time, though, they build up and lead to CTE.
For the study, Goldstein and colleagues examined the brains of four teenage athletes who had experienced a closed-head impact injury within 128 days of their death. Of those teens, two were 18 and two were 17. Two of the subjects had committed suicide and one died suddenly 10 days after a second sports-related head injury. The last had died after sustaining three sports-related concussions within the month before his death.
Analysis of the brains showed early-stage CTE in one of the teens and the early signs of tau protein build up in two other teens. Tau protein accumulation is believed to be one of the hallmark signs of CTE.
“You get hit the first time and a minute later you get hit again. We learned that from blasts because those happen in milliseconds. In football, it happens in minutes, tens of minutes or over a day or week. But the cumulative effect, when the brain is not fully healed, particularly in younger people, is really, really damaging,” Goldstein said, “and that’s the problem. You won’t see it by focusing on concussion. In fact it’s guaranteed that you won’t see it.
“There are many players who are hit, who are hurt and who aren’t getting help because it’s clear that they’re not at the level of concussion. Their brains are not in good shape and they go on to the next hit and the next one.”