CASSON, IRA R. MD
Dr. Casson, an attending neurologist at Long Island Jewish Medical Center in New Hyde Park, NY, is an assistant professor of clinical neurology at Albert Einstein College of Medicine in the Bronx, NY. He formerly served as the co-chairman of the NFL Committee on Mild Traumatic Brain Injury.
The perspective expressed here in the Viewpoint column is the independent opinion of the author and does not necessarilly reflect the view or endorsement of the American Academy of Neurology.
Recent newspaper reports and House Judiciary Committee discussions on concussion have offered evidence that permanent brain damage caused by repeated head impacts, known as chronic traumatic encephalopathy (CTE), is an epidemic in retired professional football players that constitutes a national health crisis. The reports also question the seriousness with which the National Football League (NFL) has addressed concussion in professional football. I believe the evidence from available studies and NFL efforts to promote safety suggests otherwise. As Charles Darwin said: “False facts are highly injurious to the progress of science for they often endure long.” Let's look at the available “facts.”
Three mail-in/telephone survey studies have been cited as proof that a career in the NFL increases the risk of dementia and depression later in life, and all have inherent methodological limitations. The data collected depends on the subjects' motivation and memory. The researchers can never be sure that the percentage of subjects who respond are truly representative of the entire study population. These self-report questionnaires are also limited by the possibility of bias: the subjects may respond to all the questions in a patterned manner (response bias) and their responses may be based on what they think they should answer rather than what they may actually think (social desirability response set bias).
The two papers from the University of North Carolina regarding the risks of depression and late-life cognitive impairments in retired NFL players use data from the same subjects and their spouses; thus, they are based on one survey population, not two separate independent studies. Moreover, these studies suffer from the absence of any objective clinical verification of the respondents' condition by physician or diagnostic reports.
The response rates to the surveys were poor: 30.7 percent of the subjects did not respond to the first mailing, and the follow-up elicited a non-response rate of 66.8 percent. If many of the non-respondents did not answer because they were healthy and had no medical, neurologic, or psychiatric complaints, this would bias the study results toward reporting a higher incidence of cognitive or depression symptoms than were truly present in the entire study population.
These reports also relied solely on their subjects' ability to recollect data on concussion history 20 to 50 years prior; yet, the authors reported that many of these same subjects had cognitive and memory problems. This raises serious doubts about the reliability of the data. The absence of a valid control group makes any comparisons to the general population difficult to interpret.
The authors reported that 11.1 percent of the respondents had been diagnosed with clinical depression, which they state is “generally consistent with” the incidence in the general U.S. population. This suggests that retired NFL players do not have an increased risk of depression. The authors also reported that subjects with a history of no concussions had a 6.5 percent incidence of depression, those who had one or two concussions had a 9.74 percent incidence of depression, and those with three or more concussions had a 20.17 percent incidence of depression. Does this mean that professional football players who sustained two or fewer concussions during their careers have lower rates of clinical depression than the general public and are somehow protected from developing depression later in life compared to other American men who never played professional football? I strongly doubt that is the case.
The third self-report “study” that has been cited as indicating that retired NFL players have an increased incidence of cognitive and memory impairments was done at the University of Michigan by Dr. David Weir and was funded by the NFL. In Dr. Weir's testimony to the House Judiciary Committee in October 2009, however, he said: “The study was not designed to diagnose or assess dementia. The study did not conclude that football causes dementia.”
There have also been recent reports of abnormal tau deposition in the brains after autopsy of a few retired NFL players. Tau pathology in the CNS is not exclusive to head trauma. Some tau pathology can be seen in normal aging, and it is one of the neuropathological components of Alzheimer disease. Predominant tau pathology occurs in a number of other neurologic diseases that have never been linked to athletics or head trauma. Some of these diseases have genetic causes, some have environmental/toxic causes, and others, despite intensive scientific investigations, are still of unknown cause. The clinical features of these other tau diseases, including CTE in boxers, is very different than that reported in the football cases.
Tau pathology has also been reported in men who played college football but never played professionally, not to mention an 18-year-old high school athlete. In view of these findings, it is possible that head trauma or some other event occurring in childhood or adolescence is a factor.
Some of the reported neuropathological details in the football cases are not fully consistent with the accepted features of CTE in boxers. The reports of tau deposition in the lower reaches of the spinal cord in some of these football cases raises the question of how trauma to the head could result in pathology at such a distance.
The dearth of objective contemporaneously obtained clinical history information on any of these players while they were alive along with the heavy reliance on posthumously obtained reports from family members certainly limits our ability to determine what, if any, clinical picture might be related to the tau pathology.
Figure. DR. IRA R. CASSON
NFL team physicians and athletic trainers have been treating concussed players in a cautious conservative manner for many years. Since the early 1990s, NFL players were not cleared to return to play after concussion until they had no symptoms and had a completely normal neurological examination by a team physician. This standard is much more rigorous than that recommended by the AAN in 1997, which allows some concussed athletes to return to play on the day of the injury without even being seen by a physician!
Over the past eight years, NFL team medical staffs have adopted an even more conservative approach, which has resulted in fewer players returning to play on the day of concussion, an increase in the average number of days they are held out from play, and more players being held out of play seven days or more. These more cautious actions have occurred despite the fact that the severity and number of signs and symptoms of concussions has not changed.
That said, players must be forthright in reporting their injuries. Toward that end, the NFL has made a concerted effort to educate players and their families, as well as coaches and other team personnel, about the importance of reporting any symptoms that might be related to concussion to team medical personnel.
In other efforts to reinforce safety, the NFL has supported the development of new tests to evaluate the force attenuation properties of helmets in conditions associated with concussion in NFL players. The helmets used today perform better than those designed in the 1990s. Continued helmet testing is resulting in design improvements that better manage impact forces.
In addition, the NFL has established and enforced rules that reduce the risk of concussion during game play by preventing unnecessary helmet-to-helmet impacts of defenseless players, as well as other blows to the head.
The public has been led to believe that dementia and depression are frequent and an inevitable consequence of a career in professional football. This “false fact” is belied by the presence of a large number of retired players who, despite experiencing multiple concussions, have gone on to have brilliant careers in broadcasting and other endeavors as well as the numerous retired players who testified so eloquently and articulately before Congress. Many also believe that all retired players who have dementia and depression are suffering as a result of multiple head injuries sustained during their NFL careers. This “false fact” implies that retired NFL players are somehow immune to the multiple risk factors and diseases that are associated with dementia and depression in the general population.
I believe the issue of concussion and its possible long-term effects must be taken seriously and that player health and safety is of paramount importance. The rule changes, improved equipment safety, and conservative management of concussion are prudent and should continue. I also believe the reason for tau buildup in the brains of some retired players needs to be found and that an>in vivo means of diagnosing abnormal brain tau levels in active and retired football players and other athletes needs to be developed.
• Guskiewicz KM, Marshall SW, Cantu RC, et al. 2007;39:903–909.