America is becoming a punch-drunk place. With the NHL season raging along and the NFL gearing up for its bone-crunching round of playoffs starting this month, most fans try not to give too much thought to how the players themselves are bearing up. But there was another tragic reminder recently, with the announcement that hockey superstar Derek Boogaard, who died of a drug and alcohol overdose last May at age 28, was the latest in a growing line of athletes whose premature deaths have been attributed to chronic traumatic encephalopathy (CTE), a brain condition similar to Alzheimer’s disease but caused by nothing more mysterious than getting hit too much.
Signs of CTE appear as memory loss, impulsive behavior, psychosis and other symptoms often associated with dementia. CTE has been linked to the death of Chris Henry, who played for the Cincinnati Bengals until 2009, when he was killed after jumping onto the back of his fiancée’s pickup truck following an argument, leading to a fatal tumble into the road. It was diagnosed in wrestler Chris Benoit, who in 2007 murdered his wife and son and then hanged himself. In 2004, former Pittsburgh Steeler Justin Strzelczyk, another CTE victim who suffered from hallucinations, died when he drove his car into a tractor-trailer while fleeing police. CTE was also found in University of Pennsylvania football star Owen Thomas, who committed suicide in his off-campus apartment in April 2010, having never before exhibited any sign of concussion or mental illness.
At risk of head trauma are legions of athletes (and nonathletes), even outside the professional ranks. As I reported in a TIME magazine story last January:
Up to 3.8 million Americans are getting concussed per year, according to the Centers for Disease Control and Prevention, and even that big a figure is a moving target. In 2005, the number of children who visited emergency rooms for treatment of concussions was more than twice what it had been in 1997, according to a new study in the journal Pediatrics. High school football players alone sustain 100,000 full-blown, diagnosed concussions per year. Flying under the radar are injuries mild enough to get passed off by coaches as a mere ding or ignored by players anxious to get back on the field.
What does the damage in all of these cases can be explained by simple physics. The brain sits snugly inside the skull, but it’s not a completely flush fit — there is still a layer of fluid between bone and soft tissue that serves as a natural shock absorber. Some shocks, however, can’t be absorbed, and when the head gets clobbered too hard, the brain can twist or torque or rattle around inside its skeletal casing. This can lead to swelling — which leads to concussions — and sometimes brain bleeds, which can be quickly fatal without surgery.
What worries doctors is that recovery from even a routine concussion may never be perfectly complete. As neurosurgeon Julian Bailes of Chicago’s NorthShore University Neurological Institute, who conducted the postmortem examination of Chris Henry’s brain, explained to me, a blow to the head can cause connecting fibers between nerves to wrench and tear. The brain tries to repair itself, but if the blows continue, it can’t keep up, leading to deposits of tau proteins, a major structural component of nerve fibers.
“The taus begin to accumulate,” Bailes says. “I compare them to sludge. Any concussion could lead to taus, but what we’ve learned is that it’s the repetitive nature of what used to be called mild brain injury that causes problems.” Scarily, football helmets, which do a fine job of protecting against scalp laceration and skull fracture, do little to prevent concussions and may even exacerbate them, since even as the brain is rattling around inside the skull, the head is rattling around inside the helmet.
What makes CTE crueler is that, like Alzheimer’s disease, it can’t be conclusively diagnosed until after death, when the brain can be sliced and stained and microscopic tau deposits can be spotted. The families of many athletes — incensed at the sports leagues and hoping to make games safer overall — are increasingly making the brains of players who die prematurely and suspiciously available for study.
Some athletes are even making the bequest themselves. When Dave Duerson, a former player with the Chicago Bears and New York Giants, committed suicide last February, he shot himself in the chest, not the head, and left a simple, poignant note: “Please, see that my brain is given to the NFL’s brain bank.”
Boston University’s Bedford V.A. Medical Center, where Boogaard’s brain was studied, currently has a registry of more 300 people at risk for CTE, whose blood is being regularly tested for tau proteins and whose brains will be dissected after they die. The blood tests alone do little good since even if they reveal tau proteins, they are not proof of anything. “Tau is detectable in the blood and cerebrospinal fluid,” says Robert Cantu, a Bedford neurosurgeon, “but it’s just not highly correlated with CTE.”
For now, as with so many things, the best cure is smart prevention. High school and collegiate sports are imposing tougher rules, limiting when players can return to the field after getting their bells rung and mandating baseline testing before the season so that cognitive function can be tracked. Similar rules are in place in the pros, but it’s up there — at the big-money, big-bling, big-fame level — that still more has to be done. Far stricter rules for the kinds of hits that are permissible and the kind that aren’t, and far stiffer penalties for both players and coaches violating those limits — including full-season suspensions and permanent expulsion for repeat offenders — is the only way to spare the health of the athletes, not to mention the kids who watch them and follow their leads. Devoting yourself to any game ought never mean dying for it too.