New Evidence Links Head Trauma, Brain Disease in Football Players

BU docs discover damage at pro and high school levels

BU neurologists have discovered two new cases of degenerative brain disease among former football players, one of whom, a high school athlete who had suffered multiple concussions, was only 18 years old.

“To me, this was earth-shattering,” says Robert Cantu, an associate professor of neurology at the School of Medicine and codirector of BU’s Center for the Study of Traumatic Encephalopathy (CSTE). “This 18-year-old played a number of collision sports, including football. To see initial-stage chronic traumatic encephalopathy at that age is hugely worrisome. It’s something no 18-year-old should have.”

Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative disease caused by repeated trauma to the head and characterized by the buildup of a toxic protein called tau throughout the brain. The abnormal protein impairs normal functioning and eventually kills brain cells. CTE sufferers display such symptoms as memory impairment, emotional instability, erratic behavior, depression, and problems with impulse control. Eventually, the disease progresses to full-blown dementia. The presence of CTE in the brain can be confirmed only after death.

The identity of the 18-year-old was not made public at the family’s request, but the case has been verified by the New York Times, according to CSTE researchers. “The net has to be cast wider now,” says Cantu, who is also chief of neurosurgery and director of sports medicine at Emerson Hospital in Concord, Mass.

high magnification shows dense tau immunoreactive NFTs around a small blood vessel (hole) and tau immunoreactive neurites in the neuropil.
Brain sample from an 18-year-old high school football player. Top left: Whole mount section of frontal cortex showing very focal deposition of tau protein around small blood vessels (red box). Bottom left: high magnification shows dense tau immunoreactive NFTs around small blood vessels (holes) and extensive tau immunoreactive neurites in the neuropil immediately surrounding the area. Top right: Another whole mount section of frontal and insular cortex showing very focal deposition of tau protein around a small blood vessel in insulara cortex (red box). Bottom right: high magnification shows dense tau immunoreactive NFTs around a small blood vessel (hole) and tau immunoreactive neurites in the neuropil.

In the second recent case, neurologists found significant CTE in the brain of former Tampa Bay Buccaneer Tom McHale, a nine-year veteran of the NFL. McHale died from a drug overdose in 2008 at the age of 45; he was the sixth former professional player to be diagnosed postmortem since 2002. Others include Andre Waters, John Grimsley, and former Pittsburgh Steelers Mike Webster, Terry Long, and Justin Strzelczyk. Waters and Long committed suicide; Grimsley, an experienced user of firearms, died in 2008 from a self-inflicted gunshot wound, which was ruled accidental. All died by the age of 50. So far, only one deceased NFL player tested, 24-year-old Damien Nash, who died in 2007, did not have CTE.

“This means that six of six deceased former NFL players between the ages of 25 and 50 have had severe brain damage that, if they had lived, would have developed into debilitating dementia,” says Chris Nowinski, a former Harvard football player and WWE wrestler, who cofounded the nonprofit Sports Legacy Institute (SLI) with Cantu.

CSTE is a collaboration between SLI and BU’s School of Medicine. The work at MED is headed by Robert Stern, an associate professor of neurology and codirector of the Alzheimer’s Disease Clinical and Research Program, and Ann McKee, an associate professor of neurology and pathology, director of the neuropathology core of BU’s Alzheimer’s Disease Center, and the director of the brain banks of the Framingham Heart Study and the Bedford VA Medical Center.

McKee conducted the neuropathological analysis on the brains of Grimsley and McHale. Her findings of significant CTE were independently confirmed by E. Tessa Hedley-Whyte, a professor of pathology at Harvard Medical School and a neuropathologist at Massachusetts General Hospital. “Although the neuropathological findings of CTE are, in some ways, similar to those we see in Alzheimer’s disease,” McKee says, “they represent a distinct disease with a distinct cause – namely, repetitive head trauma.”

A number of living former NFL players, led by three-time Super Bowl champion Ted Johnson, have agreed to donate their brains to BU after they die. Johnson, 36, a former New England Patriots linebacker who sustained multiple concussions during his 10-year career, is exhibiting signs of early-stage Alzheimer’s. The newest donors to CSTE’s brain bank include Hall of Famers Joe DeLamielleure and Willie Wood. They join Ken Gray, Brent Boyd, Dan Pastorini, Mel Owens, Chad Levitt, Wayne Hawkins, and Willie Daniel.

“We appreciate the growing support among former NFL players and their choice to give back to past, current, and future generations of athletes,” Nowinski says. “I hope this research serves as a wake-up call that radical change is needed in football to protect the millions of children playing the game.”

Three of the latest donors are members of the 88 Plan, created by the NFL in 2007 to financially support the families of former players showing signs of Alzheimer’s and dementia. The league does not, however, acknowledge a direct link between concussions and CTE. The program was named after former NFL star John Mackey, a Hall of Fame tight end who wore number 88 for the Colts in the 1960s and 1970s and suffers from severe dementia. “It’s probably a significant number of 88 Plan members who have CTE,” Cantu says, “but that won’t be known until their brains can be studied.”

In 1986, Cantu wrote guidelines for returning to play after sustaining a concussion, but they have largely been ignored. The creation of CSTE last year and Johnson’s high-profile participation have pushed the issue forward over the past two years. The case of the 18-year-old ought to turn up the volume even more, Cantu says. He and Stern stress that education is the key to injury prevention.

“First and foremost, everyone involved in football needs to take blows to the head very seriously,” Stern says. “This includes coaches, trainers, team doctors, parents of youth athletes, and the players themselves. The most important thing for all those involved to remember is that if one suffers a concussion, to stop playing football until all symptoms have completely resolved. This can take days, or more often, weeks to months.”

Last week, CSTE netted a $250,000 grant from the National Operating Committee on Standards for Athletic Equipment. Stern says that improvements in protective headgear are critical.

“However,” he adds, “it’s unlikely that even the very best high-tech helmet will prevent all concussions or sub-concussive injuries. Therefore, return-to-play guidelines need to be strengthened and strictly followed at all levels of play. With continued research from our group and others, we should be able to determine with better certainty and detail the specific risk factors for the development of CTE.”

Lisa McHale, the widow of Tom McHale, says she finds the recent results profoundly disturbing. “I just can’t conceive of anyone thinking otherwise. I have 9- and 11-year-old boys who are just beginning to play Pop Warner football. In light of Tom’s situation and the findings on the high school football player with the initial evidence of CTE, I now question their involvement in a sport that had been so important in our lives.”

BU Today story by Caleb Daniloff,