Last week I wrote about traumatic brain injury (TBI). By coincidence, the BMJ just published a study looking at a type of TBI called chronic traumatic encephalopathy (CTE), which is caused by repeated head injuries over a long period of time, even those not severe enough to cause an acute TBI. They were looking specifically at former NFL football players, because that sport is known to cause multiple minor head traumas, especially over a long career. The findings, while not surprising, are alarming.
The researchers looked at the medical histories of 1,712 former NFL players who died during 2008-21. They were all players after 1949, when hard helmets came into standard use. Of these players, 338 had donated their brains for examination after death, and so they were available for pathological examination.
The fact that these brains were voluntarily donated is the biggest caveat in this study, because it means that this is a self-selective group. The obvious potential bias is that those players who were motivated to donate their brains were concerned that they might have CTE. Players who were asymptomatic may not have even been aware of the option, let alone be motivated to do so. The authors attempt to account for this factor, as you will see.
They found:
“Among 1712 NFL players who died, 338 (19.7%) players’ brains were studied, 315 (93.2%) of whom had a diagnosis of CTE; thus, among all 1712 NFL players who died, the possible CTE prevalence at death ranged between 18.5% and 98.7%.”
The range is so large because of the potential for biased selection. In other words, if there were a 100% selection bias, meaning every player with CTE donated their brains, then you get the maximally conservative estimate of 18.5% of all the players having CTE. If everyone who did not donate their brain had CTE, then you get the 98.7%. Likely the number is somewhere in between, but probably closer to the lower end.
Of note, CTE can only be diagnosed pathologically, meaning at autopsy. The diagnosis can be suspected clinically, but cannot be confirmed without examining the brain directly. The diagnosis is confirmed by the presence of tau protein buildup microscopically. This is not visualized by MRI scans. Clinical examination can diagnose dementia, and MRI scan can visualize some of the damage, but these cannot distinguish CTE from other causes on dementia. Only microscopic examination can. This is why this study is important to understanding CTE, because it examined so many brains to confirm CTE.
Of the brain donors in the study, about 60% had clinically diagnosable dementia. Disappointingly, they did not do an assessment for dementia in the non-donors, so we don’t really know what this means about the total dementia risk for these NFL players. The range of possible incidence is from 11.8–92.1%, which doesn’t really tell us much.
They also looked at deaths during the period from 1016-2021, when brain donation was most common. During that period the minimum CTE risk was 24.5%, which is why you might see headlines that at least a quarter of NFL players develop CTE.
What does this mean for the NFL? Defenders will argue that the NFL has already made adjustments to reduce CTE risk, which is true. The data in this study are from older players, those that dies between 2008 and 2021. We won’t have definitive data on recent players for decades. But we do have some indicators.
Modern helmet design does continue to improve, reducing the forces on the heads of players. There have also been numerous rules changes, limiting head impacts during play. What we can look at is concussion rates. In this study NFL concussion rates decreased by 38% after rules changes implemented in 2018.
However, concussions may or may not be a good indicator or CTE risk. There is evidence that CTE results from repeated forces to the brain that are below the threshold for causing concussion. In other words, you can get CTE without ever suffering a single acute concussion. Further, modern helmets, while good at reducing concussion risk, may not reduce the risk of these lesser traumas, which can result from rapid acceleration of the head without the blow necessary to cause concussion.
So essentially, we don’t know if these recent interventions have actually reduced CTE risk, and if so by how much. It is plausible that the risk is lower, but lower than 18-25% (and remember, this is at the low end) is not very encouraging. That could still mean a very high risk of this severe neurological outcome for players.
