The suicide of former New England Patriots tight-end Aaron Hernandez in April brought the controversy surrounding brain injury in the National Football League back to the front pages. After his death, an examination of the 27-year-old brain showed that he had severe CTE — chronic traumatic encephalopathy — a serious disease, resulting from repeated blows to the head, that’s known to have repercussions as severe as suicide.

The league has largely avoided the issue, but a study released on Tuesday — paid for by both NFLPA (the player’s union) and the NFL Foundation (which is essentially run by the league) — links specific types of positions to increased brain damage. The findings were published in the journal Radiology.

The research, conducted by Kevin Guskiewicz, Ph.D., the research director of the Center for the Study of Retired Athletes at the University of North Carolina at Chapel Hill, didn’t focus directly on the development of CTE through repeated head injuries, but it represents one of the NFL’s first serious endeavors into research into CTE prevention.

Areas highlighted in red and orange represent damage chalked up to the crossover of concussion history and career duration; blue shows damage caused by the crossover of concussion history and playing position. Radiological Society of North America

The study used two MRI techniques — diffusion tensor imaging (DTI) and functional MRI (fMRI) — to examine the brains of ex-football players to determine whether there was a link between an individual’s playing history and the amount of injury to white matter in their brains.

“Our study, by including both former collegiate and professional players, gives us the ability to examine career duration and playing position along with concussion history,” Guskiewicz said of the findings. “By doing so, we found that these factors are all important when considering the long-term effects of playing football.”

Aaron Hernandez scores a touchdown in the fourth quarter against the New York Jets in December 2010. Getty Images / Jim Rogash

Certain Positions Linked to CTE

By analyzing the brain scans of 61 former players — half played only college ball, and the other half went on to play professionally — the researchers concluded that their hypothesis was correct: Certain positions were linked to greater white matter damage due to recurring head impacts. In particular, they looked at the effects of playing speed positions, like running backs and wide receivers, versus non-speed positions, such as offensive and defensive linemen. In general, linemen tend to bear the brunt of brain impacts, especially those to the front of the helmet.

Hernandez, a tight-end, played in a position that’s a mix of position types. It requires speed but also is subject to frequent tackles.

Aaron Hernandez gets tackled with his helmet by Ray Lewis of the Baltimore Ravens during the 2013 AFC Championship game. Getty Images / Jared Wickerham

Individuals that played non-speed positions that had a history of recurrent concussions (three or more), they found, had more damage to their frontal white matter, the part of the brain where CTE takes hold. That wasn’t the case for those that played speed positions and had a history of concussions, suggesting that the way that non-speed players become concussed is different and more dangerous.

Non-speed players, like defensive tackle Jarvis Jenkins #94 of the Kansas City Chiefs, were shown to have greater brain damage due to concussions than speed players. Getty Images / Peter Aiken

They also found, perhaps unsurprisingly, that the duration of a player’s career was linked to the number of concussions they had, which in turn affected how much damage their brains suffered. There was, however, one odd caveat: While ex-college players who had three or more concussions during their careers clearly showed more widespread damage to white matter, the same couldn’t be said for the ex-professionals with the same concussion history, who had higher white matter integrity. It’s possible this was simply an effect of the ex-pros that the researchers sampled — perhaps they were just atypically healthy — though co-author Michael Clark notes in a statement that it’s also possible that the duration of a player’s career is simply not that important when considering the factors leading to serious brain injury.

This study builds on recent research that underlines the long-term effects of playing football. In July, a groundbreaking study showed that 99 percent of the deceased ex-NFL players’ brains that scientists examined had evidence of CTE and that the prevalence of CTE rose with higher levels of play.

This graphic shows the classic features of CTE in the brain of Hernandez. There is severe deposition of tau protein in the frontal lobes of the brain. Boston University

Larger studies involving more players need to be conducted to reach more solid conclusions, but the discovery of the link between player position and brain damage, at least, points to a way to alleviate at least some of the problems in the NFL, says Guskiewicz: “The mechanisms of concussions in non-speed players are fundamentally different from those of speed position players, suggesting that perhaps position-specific helmets are warranted.”

It’s far from a perfect solution to solving the complicated problem of brain damage in American football, but it’s a start.

The brain scan of Hernandez’s brain after after he hung himself in prison (he was convicted of murder) showed his CTE was on par with someone in their 60s, the test showed. Boston University, which received Hernandez’s brain via his family after he died, expressed its gratitude after its research was finished in September.

Hernandez’s family filed a lawsuit against the NFL, but later dropped it, leaving open the possibility for it to be refiled if future research shows that brain injuries suffered by NFL players directly correlate to off-field problems. According to Boston University, symptoms of CTE include “memory loss, confusion, impaired judgment, impulse control problems, aggression, depression, suicidality, parkinsonism, and eventually progressive dementia.”

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