Football isn’t a contact sport, it’s a collision sport. Dancing is a contact sport. — Vince Lombardi
Last October, a 17-year-old Montclair, N.J., linebacker collapsed following a routine tackle. A month earlier, he had sustained a mild concussion but had recovered and been cleared to play. This time, though, when he stood up on the field, he collapsed again. He died three days later of an acute brain hemorrhage.
Fortunately, such disasters are rare. In 2007, according to the National Center for Catastrophic Sports Injury at the University of North Carolina, only three deaths were attributed to head injuries among the 1.8 million U.S. teenagers playing high school football. On the other hand, it’s conservatively estimated that high school and college athletes annually sustain at least 300,000 concussions, or “dings.”
Add the growing number of kids playing soccer, hockey, lacrosse and extreme sports, and the concussion rate is staggering. But youth is about taking risks and proving oneself, not about trying to avoid life. Being KO’d or having your bell rung is a rite of passage, proof that you can take whatever is dished out. Parents be damned; let the games begin.
A timeout may in order, however. In the past few years, long-term studies suggest that seemingly uncomplicated concussions, like those sustained in high school sports, may put an athlete at increased risk for Alzheimer’s disease. Is this a real and well-established association, or just scare mongering?
A concussion — often referred to as a mild traumatic brain injury — is generally defined as a blow to the head followed by transient alterations in mental state ranging from confusion, disorientation and short-term memory defects to an actual loss of consciousness of less than 30 minutes in duration. Traditionally, concussion is divided into degrees of severity based on the duration of posttraumatic amnesia: the failure to accurately recall events that occur subsequent to the head injury. It’s generally accepted that a mild concussion results in less than 30 minutes of amnesia, a moderate concussion causes 30 minutes to 24 hours of amnesia, while with a severe concussion, the amnesia persists for greater than 24 hours.
Fortunately, the vast majority of minor concussions clinically resolve themselves within a short time, ranging from a few minutes to a few days to a week. Follow-up neuropsychological testing rarely demonstrates any residual cognitive problems in otherwise healthy young athletes. As a result, minor concussions have been considered self-limiting and without any significant long-term risk. Until now.
Perhaps the best place to begin is with a systematic review of the medical records of a group of 548 veterans who sustained a moderate or severe concussion during World War II. Over the subsequent 40 years, the incidence of Alzheimer’s disease in the moderate concussion group was twice the rate in those soldiers without a prior head injury. Those with a severe concussion had a risk four times that of the control group. The effect of minor concussion was not adequately assessed in this study.
In 2003, an editorial in the Journal of Neurology, Neurosurgery, and Psychiatry opined that, at least in males, the risk of Alzheimer’s in patients with mild traumatic brain injury was sufficient to advise head-injured patients of the risk of further injuries.
In 2005, scientists at the National Center for Catastrophic Sports Injury tested more than 2,500 retired professional football players. Those with three or more concussions were five times as likely to have cognitive declines classified as mild cognitive impairment, and three times as likely to have significant memory problems as retirees without a history of concussion. Although the researchers didn’t find a definite association between recurrent concussion and Alzheimer’s disease, keep in mind that the majority of patients with mild cognitive impairment eventually progress to full-blown Alzheimer’s. As tentative supporting evidence, the researchers observed an earlier onset of Alzheimer’s in the retirees than in the general American male population.
Again, these findings were seen in athletes with a minimum of three concussions; one or two concussions did not have any clearly increased risk of subsequent cognitive impairment.
How brain injuries might predispose someone to Alzheimer’s disease remains conjectural. It’s clear that significant forces are required for a concussion. An ongoing study at the University of North Carolina found that the impact magnitude of hits delivered by youth hockey players aged 13 to 15 was similar to that experienced by college football players. The average head impact among the youth hockey players was around 20 Gs, but some surpassed 100 Gs — the forces sustained by a car-crash dummy when a car traveling at 25 mph smashes into a brick wall.
Animal studies show that at a cellular level, brain injuries cause metabolic changes that range from the quickly reversible to the release of chemicals that are toxic to neurons. Some animal studies have shown that such toxic effects can include the production and deposition of beta amyloid plaques, a central feature of the pathology of Alzheimer’s disease.
One Alzheimer’s disease researcher, Daniel Laskowitz, an associate professor of medicine and the director of the Neurovascular Laboratories at Duke University Medical Center, suspects that this amyloid deposition can trigger an inflammatory response, which in turn leads to further neuronal injury and cell death. Such a process might explain the long lag time between the initial injury and the later-life development of dementia.
Another possibility is that mild traumatic brain injury causes some degree of neuronal loss that is tolerated in young people. This relative depletion of neurons, though, might leave one with less brain “reserve” in older age.
On the other hand, several excellent studies have failed to demonstrate an association between minor concussions and Alzheimer’s. After more than 20 years of research, there isn’t a true consensus of opinion. The problem, in large part, stems from the methodology of assessing head injuries.
To begin with, imagine the inherent difficulties of doing a good neurological examination during the middle of a close, hard-fought football game. By necessity, evaluations tend to be brief and rudimentary. Over the roar of the crowd, team trainers or physicians without adequate neurological training make complex mental health assessments. Even in the NFL, where all 32 teams use sophisticated neurocognitive testing to evaluate the severity of a concussion, the evaluations are considered imperfect. A further limitation is the hard reality that, by definition, an uncomplicated concussion manifests no specific objective neurological findings on brain scans.
A second problem is that self-reporting from athletes is notoriously unreliable: They lack awareness of the significant symptoms of a concussion and fear that reporting a head injury may sideline them. In a postseason survey, more than 50 percent of high school football players failed to report documented concussions; 70 percent of those who did report experiencing symptoms of a concussion denied any specific history of concussion on pre-participation exams.
Ultimately, good medical advice boils down to opinions based on the best available medical data. Evidence-based medicine is far superior to individual experience and gut feelings. But there is often a long lag time between suspicion and definitive proof.
Take the issue of cholesterol and coronary artery disease. Although it was known in the 1960s that elevated cholesterol was associated with coronary artery disease, it took another couple of decades to acquire hard data that elevated cholesterol contributes to coronary artery disease and that it is a modifiable risk factor. During this extended period between suspicion and proof, many physicians, out of a combination of doubt and inherent conservatism, downplayed or completely ignored the possibility that lowering an elevated cholesterol might also reduce the incidence of coronary artery disease. Retrospectively, it is hard to calculate how many lives were adversely affected.
To put this argument into a practical perspective, consider what happens to your brain in ordinary childhood. In a population-based study of 1.3 million children and adolescents attending school in Ontario, the cumulative incidence of concussion over their entire 12 years of primary and secondary schooling was less than 2 percent in males and less than 1 percent in females. By contrast, in a given football season, 10 percent of all college and 20 percent of high school players sustain a mild traumatic brain injury. The same incidence has been shown in high school soccer.
Of even greater significance is the fact that players who sustained one concussion in a season were three times as likely to sustain a second concussion in the same season as uninjured players. It’s a downward spiral: Concussions beget concussions. (Remember Roger Staubach?) If you play long enough, odds are high that you will sustain at least one concussion. In a study of soccer players, the 10-year incidence of sustaining at least one concussion was greater than 50 percent.
The American Academy of Neurology has issued fairly stringent guidelines for the management of sports-related head injuries. For the most severe concussion, it recommends that the player be withheld from sports for at least two weeks. If the athlete sustains a second concussion, he is withheld from sports until he is asymptomatic for at least a month or longer. But the guidelines are primarily concerned with immediate cognitive deficits that arise from the actual head injury; they are not designed to specifically address the possibility of long-term risks like Alzheimer’s disease.
Whether or not to play contact sports, especially after having sustained one or more concussions, isn’t an easy decision. There are no right answers. In the end, it boils down to athletes using their heads off the field to determine what using their heads on the field might cost them.