College Football Player's Brain Disease Highlights Youth Risk, 10 Years After Report That Inspired Film

The case involves a 25-year-old former college player who had chronic traumatic encephalopathy, even though he never made it to the NFL. He dropped out of college after playing the game 16 years and suffering 10 concussions. He has since been identified as former Missouri State player Michael Keck.

Ten years after the report that inspired the film Concussion, scientists studying brain trauma in the National Football League have a new finding, one relevant for the more than 1 million high school football players who will never play professionally—and their parents.

JAMA Neurology reports today on the case of a 25-year-old man diagnosed with chronic traumatic encephalopathy, or CTE, after a fatal heart attack following a staph infection. His death came after a period of cognitive decline and depression that caused him to drop out of college after 3 seasons. He never played a minute in the NFL.1'(Since this report, the player has been identified as Michael Keck, who played for Missouri and Missouri State.)

What makes this case noteworthy, besides the man’s youth, is that Boston University researchers conducting the UNITE study (Understanding Neurologic Injury Traumatic Encephalopathy), had already interviewed and tested this young man before his death and were not certain he had CTE, as opposed to post-concussion syndrome or depression.1,2 The National Institutes of Health and the NFL have funded UNITE to examine former football players’ brains.

One factor fueling the uncertainty was the man’s age. But after his death, CTE was confirmed in the autopsy, the only way this can be done today.

“This shows you don’t have to be a professional athlete to develop this disease,” Ann C. McKee, MD, director of the Neuropathology Core at Boston University’s CTE Center, and the paper’s corresponding author, said in an interview with The American Journal of Managed Care.

The case could reignite discussion on how to protect children and teenagers who play football in youth leagues and school teams—at ages when their brains and bodies are still developing. McKee says young children’s heads are oversized relative to their bodies, and this demands extra caution.

Fortunately, work at BU and elsewhere is, quite literally, changing the rules of the game—from the NFL down to youth leagues, tackling methods have changed to protect players’ heads, and some youth leagues do not allow any tackling among younger children.

Research is bringing medicine closer to the day when positive diagnoses of CTE will be possible while players are alive. But as McKee, her co-authors and an accompanying editorial point out, there are scores of unanswered questions, including why some athletes seem more vulnerable to the disease than others.

“How can we prevent this from happening to others?” McKee asked.

The young man in the case report played football 16 years, starting at age 6, and suffered 10 documented concussions (the report notes there could have been more). He was talented enough to play 3 years in NCAA Division I, first as a red shirt and then in his freshman and sophomore years of eligibility before leaving school.

His mental decline was steep and swift; he began smoking marijuana, and as his symptoms progressed, he developed feelings of apathy and worthlessness, as well as suicidal ideations. Once a solid student with a 3.8 grade point average (GPA) in high school, he had a 1.9 GPA when he left college, 12 credits shy of his degree. “At age 23 years, he became verbally and physically abusive toward his wife, a change from his prior demeanor,” the authors wrote. He later became dependent on his wife.

Complicating factors included a family history of depression and addiction, which could have accounted for his mental state. This points to one of the “essential questions” about CTE described in the editorial: are there genetic factors that cause some athletes to respond differently to concussions, or that require some athletes to take more time to recover?2

In the editorial, James M. Noble, MD, MS, CPH, writes, “What biomarkers can establish a recent injury has occurred and perhaps, more importantly, provide assurance that recovery is complete?”

McKee discussed these questions and challenges in the interview with AJMC. For some reason, this young man was particularly susceptible to the effects of repeated head trauma; the case report says he seems to have suffered a particularly damaging blow in his freshman year of college. But, as McKee said, right now researchers don’t know how to tell which athletes face greater risks.

There are still more questions to be asked about making football safe, McKee said, especially about reducing the amount of routine hits. CTE looks different from the brain injuries sustained by boxers; the damage is not just the result of actual concussions but also the slightly less severe head blows that do not cause any immediate symptoms. Accumulation of tau protein on the brain is a distinguishing feature. While most associated with American football, CTE can occur in ice hockey, professional wrestling, and other contact sports. Compared with generations past, McKee said, “Athletes in general are bigger, stronger, and faster, so the hits are generally more violent.”

Today’s report comes at a time of increased attention to CTE, in large part because of the work of the BU team and UNITE. In September, the group announced that 96% of all former NFL players whose brains it studied had CTE and 79% of all patients who had played football at any level had the condition.

Noble points out that the case study comes on the 10th anniversary of the 2005 report by Bennett Omalu, MBBS, MPH, MBA,3 who triggered the discussion of CTE in American Football following his autopsy of Mike Foster, who played for the Pittsburgh Steelers and died in 2002. Omalu’s experience—and the NFL’s effort to discredit him before later funding work on CTE—is depicted in the film, Concussion, which opened December 25, 2015.

Despite increased awareness and rule changes, Noble’s editorial says that procedures for handling concussions at high school games vary by state. While the field of CTE research has grown markedly, he writes, there is no systematic way of documenting all the damage that has been done.

In 2015, for example, the public learned that not all damage is the same; declines that once might have once been written off to aging could, in fact, be influenced by CTE. Last August, the NFL posthumously inducted the San Diego Chargers’ Junior Seau into the Hall of Fame. Seau committed suicide in 2012 while experiencing symptoms that were later diagnosed as CTE. Within days of that ceremony, NFL legend Frank Gifford, who sustained one of the most famous hits in the history of the game, passed away quietly at home. Three months later, the Gifford family released a statement that he, too, had suffered effects of the brain disease, despite a long career in broadcasting after retiring from the New York Giants.

References

1. Mez J, Solomon TM, Daneshvar SH, Stein TD, McKee AC. Pathologically confirmed chronic traumatic encephalopathy in a 25-year-old former college player [published online January 4, 2016.] JAMA Neurol. doi:10.1001/jamaneurol.2015

2. Noble JM. The long drive ahead to better understanding chronic traumatic encephalopathy: First (case) and 10 (years later) [published online January 4, 2016]. JAMA Neurol. doi:10.1001/jamaneurol.2015.4297.

3. Omalu BI, DeKosky ST, Minster RL, Kamboh MI, Hamilton RL,Wecht CH. Chronic traumatic encephalopathy in a National Football League player. Neurosurgery. 2005;57(1):128-134.