By Genevra Pittman
Reuters
Each year in the U.S. an average of a dozen high school and college football players die during practices and games, according to a new study that finds heart conditions, heat and other non-traumatic causes of death are twice as common as injury-related ones. 

Researchers reviewed data from the National Center for Catastrophic Sports Injury Research and found 243 football deaths recorded between July 1990 and June 2010.

One hundred of the fatalities resulted from an underlying heart condition, 62 were due to a brain injury - typically a subdural hematoma - and 38 were from heat-related causes, according to findings published in The American Journal of Sports Medicine.

Kelly Dougherty, an assistant professor of pediatrics at the University of Pennsylvania Perelman School of Medicine, said she found the number of heat-related deaths in particular "quite alarming."

Many of those deaths happened in the South during preseason play, including at two-a-day practices.

"These are preventable deaths," said Dougherty, who has studied heat acclimation but wasn't involved in the new study.

"This article highlights the urgent need for future research studies that would investigate children's and especially football players' body temperature responses during practice (and) during games," she told Reuters Health.

"We have so few data to guide policy, to guide recommendations, and we really don't have a good idea of body temperature responses in the field."

Current recommendations from the American Academy of Pediatrics call for making sure kids and teens gradually adapt to exercising in the heat during the preseason and for teams to take more water breaks, and play with less intensity, on very hot and humid days. 

Some deaths on the rise
Some tests can pick up on the abnormalities that may cause sudden heart-related deaths in young athletes; however widespread screening programs are controversial, in part because of a high rate of false positives.

After heart, brain and heat-related conditions, 11 players - all African Americans with sickle cell trait - died from sickle cell crises during intense conditioning. People with sickle cell trait carry one copy of the gene for sickle cell disease, rather than two, but they can be especially vulnerable to dehydration and low oxygen, for example. 

Seven players died from asthma, seven from a sudden blow to the chest, five from a blood clot and the rest from broken necks, abdominal injuries, infections and lightning, Frederick Mueller from the University of North Carolina at Chapel Hill and his colleagues found.

The 243 deaths in total over 20 years work out to one for every 100,000 high school and college football players during that period.

High school athletes accounted for 203 of those deaths; but because there are so many more high school players, a college player was statistically almost three times more likely to die playing football than a high school player during the study period.

A representative from the National Collegiate Athletic Association (NCAA) said its health and safety committee planned to review the new study. The NCAA funds the National Center for Catastrophic Sports Injury Research.

"Through this data the NCAA has made recent policy changes in several important areas, including football preseason practice, medical examinations, safety training for coaches, concussion management plans and sickle cell trait," the representative wrote in an email to Reuters Health.

The rate of deaths related to sickle cell trait, heart conditions and heat all increased during the second decade of the study, the researchers found.

"These conditions require a greater emphasis on diagnosis, treatment, and prevention," Mueller's team wrote.

"The problem of football fatalities is real and needs to be addressed by continued surveillance and rule changes when applicable to further reduce the incidence."

Like anyone else who is getting a little older, former NFL player Wayne Clark sometimes forgets someone’s name. But unlike most people, Clark has an extra reason to worry -- as a retired  football player, he’s had more than his fair share of knocks and is now nervously watching report after report linking concussions with a brain condition known as chronic traumatic encephalopathy (CTE).

“Recalling names, which I recall used to be pretty easy for me, and now I go through stages where I think ‘Why can’t I remember that’?  I always wondered are these age-related or are they concussion-related?” Clark, 65, says.

A new study using brain scans might be able to answer that question. The technique may allow scientists to peer into the brains of the living and spot signs of the abnormally tangled clumps of a protein called "tau" that can cause such symptoms as memory loss, impulse control, mood volatility and, eventually, dementia in people with CTE.

Researchers from the University of California, Los Angeles, used the new technique to scan the brains of five former NFL players 45 and older, along with five healthy men of the same age, according to a preliminary report published Tuesday in the American Journal of Geriatric Psychiatry.

The hope is that studies like this will enable scientists to better understand CTE, says Dr. Gary Small, director of the UCLA Longevity Center, who led the study.

“Then maybe we will be able to detect it sooner and possibly come up with a preventive treatment rather than trying to repair what is damaged,” Small says.

A study of five people doesn’t say much about what might be found in a larger population. But Small and his colleagues are encouraged by what they've seen.

Each of the football players in the study had a history of one or more diagnosed concussions and several had cognitive and/or mood symptoms. The players represented a wide range of positions: linebacker, quarterback, guard, center, and defensive lineman.

At the outset, the players were asked to fill out questionnaires designed to detect signs of cognitive decline and mood symptoms.

To look for signs of CTE, Small and his colleagues injected each study volunteer with a newly developed radio tracer that locks on to the tau protein and shows up in bright colors ranging from red to yellow on PET scans.

The scans from the healthy non-players showed no signs of tau build-up, but the images from the players showed a range that correlated with the number of hits they’d sustained during their football careers.

UCLA

Brain scans of living former NFL players show evidence of the damage linked to a brain-destroying condition called CTE, researchers said on Tuesday.

Though the researchers had asked 19 players initially to participate in the study, only five were willing, Small says. And only one was willing to have his name released to the public. That was Clark, a former quarterback for the San Diego Chargers.

Clark, who had sustained only one concussion while playing football, didn’t have much evidence of tau build-up. But he did have some.

“And when I first saw the scan I thought, whoa, that looks pretty extensive,” Clark says in an video interview on UCLA's website.

“Wayne’s scans show the abnormal protein deposits, just like the other football players in the study,” Small says. “Now he's in his mid-60s and he has very minor memory complaints, which could be part of normal aging, but they also could be related to his concussion. When we do further studies, we’ll be able to find out if there’s a solid connection between the two.”

Clark hopes the research will help doctors eventually identify which players might be at risk of developing permanent brain damage. “My hope is that this study will help diagnose the condition before a player dies and is autopsied,” Clark says. "If we can diagnose it when a player is alive, then we can learn how best to intervene and how to improve equipment and rules and practice habits to we can make the game safer.”

It’s not just NFL players. Brain injuries are common among war veterans, victims of accidents and younger athletes.

The researchers don’t completely understand the relationship between tau deposits and jolts to the head. Clark’s scan suggests that one hit might possibly lead to some accumulation of the abnormal protein -- just not enough to lead to symptoms.

“We don’t know how many hits it takes,” says Dr. Joseph Maroon, a professor of neurosurgery at the University of Pittsburgh Medical Center, and team neurosurgeon for the Pittsburgh Steelers. He was not involved in this study. “We don’t know if one severe hit can lead to this progression. Some players can get thousands of hits and never develop CTE. There are millions of football players in high school, college, and pro level who have taken multiple blows to the head and not developed CTE.”

Another unresolved question is whether multiple “sub-concussive” hits, such as those sustained by linemen on every play, can lead to CTE.

Perhaps the biggest question scientists hope to solve with this type of research is what percentage of concussed players end up with CTE.

Many believe that there is a genetic component that can make a person more susceptible and that those with resilient genetics can take a number of jolts to the brain without developing the disease.

Though most of the former NFL players’ brains autopsied up to this point have shown signs of CTE, those brains have come from players who tended to have pronounced symptoms of the disease before their deaths.

Two years ago when former football star Dave Duerson committed suicide, he left a note explaining that he’d decided to shoot himself in the chest, rather than the head, so scientists might examine his brain to see if the concussions he’d suffered in his 11-year NFL career as a hard-hitting safety for the Chicago Bears, the New York Giants and the Phoenix Cardinals could explain the symptoms that were making his life a misery.

Thus far, Boston University’s Center for the Study of Traumatic Encephalopathy has found evidence of CTE in the autopsied brains of 33 former NFL players, including that of Duerson, according to a report published in December in an early online version of the journal Brain.

Some hope that the new research is just the beginning.

“This is a step forward and it emphasizes the importance of what PET scanning might hold as we go forward in trying to diagnose the condition [in living players],” says Maroon.

Maroon and others say they believe that CTE is the result of a normal inflammatory response to brain injury that runs amok. The theory is that the inflammation switch gets turned on and stays on in people with a certain genetic predisposition, Maroon says.

“One might conjecture that it’s like starting a small brush fire in a dry forest,” Maroon said. “If the predisposition is there and the fire is lit, then it may continue inexorably.”

Maroon hopes that new radio tracers will be found that highlight the early signs of inflammation before tau has even begun to accumulate. Then there might be a chance to find therapies that stop CTE from developing, he says. 

See more NBC Health news: 

• Contact sports leave pattern of brain injuries, study finds
• US launches study into youth sports concussions

BOSTON -- Years of hits to the head in football or other contact sports lead to a distinct pattern of brain damage that begins with an athlete having trouble focusing and can eventually progress to aggression and dementia, a study released on Monday says. 

Researchers examining the brains of 85 former athletes and soldiers who sustained multiple mild head injuries over their lives found the condition they developed, chronic traumatic encephalopathy, came in an "ordered and predictable" four-stage pattern. 

The condition, which causes depression and erratic behavior, has attracted public concern in recent years following the high-profile suicides of former professional athletes. 

Worries about chronic traumatic encephalopathy, or CTE, have prompted youth and college football programs around the United States to take steps intended to limit the number of hits to the head athletes experience in practice and games. The National Football League has banned the most dangerous helmet-on-helmet hits. 

The latest study, published in the journal Brain by researchers affiliated with Boston University School of Medicine, spells out how the condition progresses through four stages that can begin with mild memory loss, progress to cognitive failure and eventually bring on aggression. 

Symptoms of stage one CTE include headache and loss of attention. Stage two sufferers may face depression, outbursts of anger and short-term memory loss. Those in stage three encounter executive dysfunction and cognitive impairment. Symptoms of the most severe fourth stage include dementia, aggression and difficulty finding words. 

'Dementia pugilistica'
Researchers are now able to chart CTE's progression in the brains of dead people who had suffered from the condition originally known as "dementia pugilistica" for its occurrence in boxers. But they remain unable to diagnose it in the living. 

"Until we do that, we can't fully understand the risk factors, we can't understand how common it is," said Robert Stern, a Boston University professor and co-author of the study. "The goal would be to have a variety of measures of this predictive pattern in the brain while someone is alive." 

Stern said he was working on tests that would diagnose the condition early, by using magnetic resonance imaging or testing for specific proteins linked to the problem. 

The research found CTE was closely linked to the number of years an athlete played football, but not directly tied to the number of concussions sustained. 

That suggests a steady diet of mild hits to the head, rather than a handful of more traumatic injuries, brings on CTE, Stern said. 

He cautioned the condition would not develop in all athletes and suggested that concerns about CTE should not prompt parents of young players to pull their children from the sport, though he said parents should closely monitor how the game is played. 

"We don't want people to feel that they're going to get this early dementia just because they had a concussion or two," Stern said. "This is a disease of total, overall repetitive brain trauma." 

On Saturday, Kansas City Chiefs linebacker Jovan Belcher shot and killed his girlfriend and then shot himself in front of the team's coach and general manager in an act that shocked fans of the National Football League. While CTE can bring on confusion, depression and violent behavior, there was no evidence Belcher's actions were related to brain injury. 

Belcher was only 25 and had played in the league four seasons. Other prominent suicides involved players with longer careers including Junior Seau in May, Ray Easterling in April and Dave Duerson last year. 

"An individual's suicide and aggressive behavior at such a young age is so multi-factoral, it is such a complex issue, that you can't jump to the conclusion that CTE is the cause of any individual's behavior," Stern said. 

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