FAQs: Concussions, CTE, risks & research
Doctors advising the NHL and NHL Players’ Association have challenged some of the claims that have been made about the research by the Boston University Center for the Study of Traumatic Encephalopathy.
Ruben Echemendia is a clinical neuropsychologist and the NHL’s neuropsychological consultant. He chairs the NHL/NHLPA concussion working group.
Jeffrey Kutcher is an associate professor at the University of Michigan and a consultant to the NHLPA. He chairs the Sports Neurology Section of the American Academy of Neurology.
Chris Nowinski co-founded the Sports Legacy Institute to advance the study, treatment and prevention of the effects of brain trauma in athletes and other at-risk groups. He is a co-director of the BU CSTE and is pursing his doctorate in behavioral neuroscience.
QUESTION: How does Boston University define chronic traumatic encephalopathy?
From BU’s website: “Chronic Traumatic Encephalopathy (CTE) is a progressive degenerative disease of the brain found in athletes (and others) with a history of repetitive brain trauma, including symptomatic concussions as well as asymptomatic subconcussive hits to the head.
“CTE has been known to affect boxers since the 1920s. However, recent reports have been published of neuropathologically confirmed CTE in retired professional football players and other athletes who have a history of repetitive brain trauma.
“This trauma triggers progressive degeneration of the brain tissue, including the build-up of an abnormal protein called tau. These changes in the brain can begin months, years, or even decades after the last brain trauma or end of active athletic involvement. The brain degeneration is associated with memory loss, confusion, impaired judgment, impulse control problems, aggression, depression, and, eventually, progressive dementia.”
Q: Does everyone agree that repetitive brain trauma causes CTE?
Echemendia: “We don’t know what’s causing that. There is at this point speculation and hypotheses about what’s causing that, but the data do not support any causal statements. For example, the data do not the support a statement at this point in time that repetitive blows to the head cause CTE. What we know is that some players have CTE that have been examined that we don’t know what the cause is. Now it’s possible it’s repetitive blows to the head, but we don’t know that in any scientific sense at this point in time.”
Kutcher: “If we take the first assumption, that multiple head traumas cause long-term brain injury or brain dysfunction, does that happen? Yes. That’s something that has been described for a long time, especially in boxers. That’s not a new concept. … I think we suspect that, and there’s a reasonable sort of anecdotal evidence that trauma causes tau. So far that has not been shown experimentally to be true. But I know there’s some research ongoing.”
Q: Do we know what tau does?
Echemendia: “The presence of CTE and the extent to which that automatically implies behavioral changes, the types of behavioral changes, that link has not been made scientifically at this point in time.”
Kutcher: “Tau, to be clear, is a very common protein … It’s a common problem for many neurological diseases, degenerative brain diseases, such as Alzheimer’s, where it’s assumed tau deposition in the neurons messes with their ability to work at some point. … Tau is a protein that’s around. It’s in you normally. But we’re talking about sort of conglomerates of tau, kind of stuck together that become a problem. … The short answer is, no. We don’t know what tau does to the brain.”
Nowinski: “There are a lot of diseases with tau deposition. This is a specific disease which to our knowledge after studying 60 brains of it in the last few years – different age groups, different backgrounds – is that it progresses in a specific way [in the brain]. We can define the way it progresses – where it starts, where it goes next. That’s defined. … You cannot control the rate of progression. We do not know the rate of progression.”
Q: What is the risk of an athlete developing CTE?
Echemendia: “We don’t know who is susceptible to this. We don’t know who is not susceptible to this, and we don’t know the combination of factors that then lead to CTE at this point in time. My hope is that we will in the near future, but at this point in time, we don’t have that information.”
Kutcher: “How often does that happen is the question. What’s the risk of that in the average population? What’s the rate of it? There’s a sense that that is an individual number depending on the genetics of the brain and how that brain responds to trauma.”
Nowinski: “It’s an unknown risk. We’re finding it in more athletes who played a long time than we’d like. We’re finding it in young athletes who didn’t play a long time, which is concerning, but we have no idea again what the percentage is. But it’s a real risk, and we should change our behaviors.”
Q: How is CTE different from other brain diseases?
Kutcher: “Degenerative neurological processes are for the most part predictable. Alzheimer’s is pretty predictable. Parkinson’s, predictable. These are predictable diseases that tend to start in an age group and they go a certain way. Yeah, they’re different patterns, but I can tell you what they are. What is the CTE pattern? There isn’t one. According to people who look at these brains, it’s happening to 17-year-olds, it’s happening to 80-year-olds, it’s causing depression, it’s causing dementia, it’s not [causing dementia]…”
Nowinski: “Well, it’s certainly not defined like other diseases that have been studied by dozens of institutions over decades. [Alzheimer’s is] moderately predictable. I’ve give him that. Not everyone’s Alzheimer’s disease course is the same, by any stretch of the imagination, and again, remember that the drug industry is focused on presymptomatic Alzheimer’s disease, because that’s the best place to intervene. Once tissue is gone, it’s much harder to bring it back than it is to stop a disease progression.”
Q: What can we do while waiting for more research?
Echemendia: “The NHL has been working on this as you know since 1997. We’ve been moving on this for a very long time. Over the past few years, we’ve made some specific changes, but I don’t think those changes are related to what’s been happening in CTE but rather our concern overall that we want to provide the best care that we can with respect to evaluating and managing this injury.”
Kutcher: “I think there are two main things we can do. One is along the lines of the acute injury itself. If somebody gets hit enough so that their brain produces symptoms – i.e. they have a concussion – we recognize all those injuries, we remove them from play and we let them recover. … [We can also] look at overall dose. Something I tell my patients a lot: If you’re going to play a contact sport, get good at that contact sport and play one. I’ve got kids that go from football to wrestling to track or whatever. But I’ve got some kids that play football, hockey at the same time, hockey for their club team, football for the high school, then they go and they wrestle and they play rugby. … You can give your brain some time to rest. Those are thing we can do reasonably that I don’t need the science to really get behind making those types of changes.”
Nowinski: “The biggest low-hanging fruit comes in football and soccer. You can reduce somebody’s exposure by 50 percent and theoretically reduce their risk of CTE possibly more by limiting contact in practice. That’s hitting in football. That’s headers in soccer. You start monitoring and limiting that, and you have a dramatically safer sport – an overwhelmingly safer sport, and no one is talking about that. Do I think we’ve gone far enough in convincing people this is real? No. The game does not suffer with those changes at all. The things we’re asking for do not hurt the games.”
Other popular stories on Yahoo! Sports:
• Lou Gehrig’s last home run bat has ties to famous actor’s dad
• Alex Ovechkin gets into cussing rift with Capitals coach
• Mets pitcher risks $4M salary on mountain climb