Experts warn about repeated brain blows in football
June 28, 2010 4:00 AM
Ernest Coleman/Cincinnati Enquirer
By Chuck Finder Pittsburgh Post-Gazette
The brain of the late Cincinnati Bengals pass receiver Chris Henry contained so many signs of chronic disease -- sludge, tangles and threads associated with late-in-life dementia or Alzheimer's -- that it shows a football player can sustain life-altering head trauma without ever being diagnosed with a concussion.
The brain damage may have contributed to Mr. Henry's troubled behavior and, ultimately, his death in December at age 26.
These conclusions, among others following tissue study by scientists affiliated with West Virginia University, make Mr. Henry the first active National Football League player to be discovered suffering from the progressive generative disease known as Chronic Traumatic Encephalopathy, or CTE.
Julian Bailes and Bennet Omalu, with the Brain Injury Research Institute in Morgantown, W.Va., have examined 10 other retired players, among them ex-Steelers Mike Webster, Terry Long and Justin Strzelzcyk. The researchers found frightful similarities between those brains and that of Mr. Henry. Those men were older than Mr. Henry and had taken thousands of blows to the helmet during long football careers.
Finding CTE in a current pro football player wouldn't surprise Robert Cantu, whose Boston University research group has received funding from the NFL.
In a microscopic view of tissue from the brain of the late Cincinnati Bengals receiver Chris Henry, the brown spots are Tau protein stains that surround and damage the brain cells. "It's blue normally," said Julian Bailes, a brain injury researcher. "I look at it like sludge. [The brain] tries to clear it, and it can't." The wispy lines are neuritic threads, dead and leftover connections between cells. "You shouldn't see any of this, ordinarily," Dr. Bailes said.
"It also wouldn't surprise me that somebody as young as 26 would have it, either," Dr. Cantu said of Mr. Henry. "What would be a big surprise is if the amount of Tau protein. ... would be as excessive as it is in people who had much more lengthy careers and died at a much later age."
Mr. Henry never missed a game because of a concussion with either the Bengals or WVU, where he played in college.
"It didn't look like the brain of a 26-year-old," said Dr. Omalu, a former Allegheny County pathologist who first found CTE in an autopsy of Mr. Long in September 2005.
"This is not something to celebrate. It is not something to be joyful about. It is something that is very humbling, very introspective. It is a call to action.
"I'm not calling for the eradication of football; no, I'm asking for full disclosure to the players. Like the surgeon general considers smoking to be dangerous to your health, repeated impacts of the brain are dangerous to your health and will affect you later in life. Period. The players need to know this.
"I think it's an epidemic. It's beneath the radar. We simply didn't identify it [early and properly]. The more I encounter NFL players, the more I realize ... it is much more prevalent than we had identified."
Added Dr. Bailes, who serves on the NFL Players Association brain-trauma committee: "Is it an epidemic? I don't know. But it was pretty alarming, that study."
Among the Henry study's findings, scheduled to be announced today at a news conference in Morgantown:
• The single, highlight-video concussive blow isn't the most dangerous part of the game. Rather, it is the constant thumping of the helmet and the brain inside the skull that causes long-term harm. The scientists found in Mr. Henry's tissue "chronic changes that have been there for several years," Dr. Bailes said. "And these are not all NFL-caused," meaning they stem from youth, high school and college football, as well.
• A gene that is a precursor -- an identifying factor for susceptibility to CTE -- has been found in 70 percent of the late athletes researched by Dr. Bailes and Dr. Omalu at the institute, among them former professional wrestler Chris Benoit, who killed his wife and 7-year-old son before committing suicide in 2007. An autopsy found steroids in his system.
The gene identified in Mr. Benoit is Apolipoprotein E, known as APOE, and is found in roughly 25 percent of the general population.
"Maybe what our research will lead to is the realization that, maybe in the future, genetic testing would be important for these athletes to know," Dr. Bailes said.
• Multiple or repetitive brain impacts appear to be the leading cause in an athlete's behavioral changes, akin to the onset of dementia, though it is an area that scientists agree remains open for more study.
Mr. Henry died Dec. 17 from a fractured skull and other head injuries sustained when he fell from a moving pickup truck in the driveway of his fiancee's family home near Charlotte, N.C. Those injuries were visibly separate from Mr. Henry's chronic condition caused by football, both doctors said.
"This is not a picture of acute brain swelling and edema. This is not an X-ray. This is a piece of tissue taken out of his brain," Dr. Bailes said. "This is chronic and long-standing."
Mr. Henry played in 55 games, including 12 starts, in his five-year Bengals career, one that included five arrests in a 28-month span and three suspensions totaling 14 games. He was once suspended at West Virginia by then-coach Rich Rodriguez, who called Mr. Henry an embarrassment to himself and the program. CTE and his chronic brain trauma could well have played a role, the scientists contend.
"The circumstances of somebody jumping onto a moving truck ... ," Dr. Omalu began.
He noted how a witness to the accident reported that Mr. Henry's last words were to his fiancee, Loleini Tonga, who was behind the wheel: "If you take off, I'm going to jump off the truck and kill myself."
"From what I know about his manifestations, I think there was ... neural-behavioral syndrome," Dr. Bailes added.
Bengals officials declined comment, as did NFL officials without knowing the specifics of the findings. But NFL spokesman Greg Aiello added in an e-mail: "We have invested $1 million in CTE research with the Boston University group. CTE was an important part of the agenda at our recent medical conference on brain injuries in Washington. We will continue to proactively address the issue through the medical experts."
Kevin Guskiewicz, a Latrobe native and former Steelers graduate-assistant trainer, is the research director at the University of North Carolina's Center for the Study of Retired Athletes. He added in an e-mail: "There is still much to learn about CTE. We do not yet know the cause, but there is increasing speculation that a contributor might be the hundreds of subconcussive -- non-injurious -- head impacts sustained over the course of a player's career."
As for those who wonder whether steroid use is linked to head trauma, Dr. Bailes said his previous research found that anabolic steroids do not appear to increase a player's chances of brain injuries from concussive blows.
Dr. Bailes, once a Steelers team doctor and currently the neurosurgeon for WVU athletic teams, maintains that this study is not advocating radical changes to the NFL or other levels of football.
But he reiterated a stance that he and other experts heralded most recently at a brain injury seminar at Duquesne University in March: Take the head out of the game to make it safer.
This research got its start in September 2005, when then-Allegheny County coroner Cyril Wecht announced that Mr. Long had died the June before as a result of traumatic brain injuries sustained during his Steelers career. The cause of death was later amended to suicide, but the discovery of CTE by Dr. Omalu, in the coroner's office, became part of football's mainstream discussion for the next half-decade and more.
The disease was previously restricted to the "punch-drunk" syndrome known to afflict boxers since the 1920s. Dr. Omalu opened the door to football; he and later Dr. Bailes studied tissue samples from a handful of NFL veterans. Since then, deceased football players as young as age 18 studied by a Boston University group and the Morgantown researchers were found to have Tau-protein stains and other signs of the disease.
The Brain Injury Research Institute was started three years ago by Dr. Bailes, the West Virginia School of Medicine's chairman of neurosurgery; Dr. Omalu and Wheeling-based attorney Bob Fitzsimmons. (Mr. Fitzsimmons represents two Post-Gazette reporters in a pair of lawsuits not related to sports.)
Dr. Omalu, now medical examiner for San Joaquin County, Calif., studied the donated Henry samples first.
"I think it was the fourth slide. I stopped. I was like, 'Whoa.' I was saddened by it, really," he said.
"This is not a mild case," added Dr. Bailes. Under a microscope, Mr. Henry's slides showed the same number of Tau-stained brown spots normal for "an 80- or 90-year-old."
The doctors said they hope the Henry case will prompt players and officials at all levels of football to take notice, if not action. Practices without helmets? Standing up linemen from a three-point stance? There are, to them, questions deeper than how many games to sideline a concussion sufferer.
"The NFL wants us to believe that documented concussions are the issue. I've always believed that it's not about documented concussions. It's about repeated impacts to the head ... sub-concussions," Dr. Omalu said. "Concussions are the extreme [end] of the spectrum. The issue is repeated impact, repeated blows to the head.
"We need to be more proactive. This is an issue of health risk. It is a public-health issue. Chris Benoit exhibited violent behavior. Many of them have died broke, without jobs. There's a societal implication. And also an issue of public safety. We need to take it more seriously."