The prevailing media narrative is that concussions or repetitive subconcussive blows "cause" chronic traumatic encephalopathy (CTE) and that there is a proven link between the two. It thus may come as a surprise that, despite widespread media coverage and speculation regarding the late-life or post-retirement risks of cognitive impairment in athletes who engaged in sports involving repetitive trauma, ... there has been very little in the way of peer-reviewed scientific literature involving data that establishes such risk. 
Rejecting the blanket conclusion that there is a definitive causal and effect connection between repetitive head trauma and CTE, the most recent international consensus statement on concussion in sport  cautions that a relationship has "not yet been demonstrated between CTE and concussions or exposure to contact sports."
It notes that "there are no published epidemiological, cohort or prospective studies relating to modern CTE. Owing to the nature of the case reports and pathological case series that have been published, it is not possible to determine the causality or risk factors with any certainty."
"As such, the speculation that repeated concussion or subconcussive impacts cause CTE remains unproven," the statement continues. "The extent to which age-related changes, psychiatric or mental health illnesss, alcohol/drug use or co-existing medical or dementing illnesses contributed to this process is largely unaccounted for in the published literature. At present, the interpretation of causation in the modern CTE case studies should proceed cautiously."
Remarkably, the consensus statement concludes with a direct shot at the media, in which it recognizes the importance of addressing the "fears of parents/athletes from media pressure related to the possibility of CTE."
Such a view was subsequently echoed by Christopher Randolph, PhD. of Loyola University in Chicago in a follow-up study of retired NFL players - who largely comprise the highly limited, self-selected universe from which the case studies of brains showing the presence of CTE have been drawn, and who the media have widely reported as being at high risk of CTE - in which he laments that "the media attention to this issue continues to far outweigh any meaningful results from sound experimental science."
Randolph found that when compared with healthy controls and with non-athlete patients with a clinical diagnosis of mild cognitive impairment (MCI), commonly presumed to reflect the earliest stage of Alzheimer's disease, the patterns of impairments of the retired NFL players involved in the study were virtually identical to those exhibited by the non-athletes with MCI, thus leading him and his colleagues to conclude that CTE might not be a distinct neurodegenerative disorder at all.
The study appears to lend support to Randolph's theory, first proposed in a 2009 paper, that a long history of repetitive head trauma in contact sports does not lead to CTE, but might eventually result in a diminished cerebral reserve leading in some unknown percentage of cases to an earlier than normal expression of other common, age-related neurodegenerative diseases such as AD and Parkinson's (PD). His theory was that the ways in which such diminished cerebral reserve would be expressed (e.g. MCI, AD, PD, ALS) would not differ from individuals with those diseases who lacked such a history of head trauma, which is precisely what his 2013 study suggests.
The Randolph study, co-authored by no less a concussion authority than Kevin Guskiewicz, Kenan Distinguished Professor, Director of the Matthew Gfeller Sport-Related Traumatic Brain Injury Research Center at The University of North Carolina at Chapel Hill, and Director of the Center for the Study of Retired Athletes at UNC, has been heavily criticized by those who have identified CTE is a distinct condition as being flawed. Chris Nowinski, co-director of the Center for the Study of Traumatic Encephalopathy at the Boston University School of Medicine, told PopSci.com  that it was "preposterous" for Randolph to conclude that CTE might not be its own disease because the retired football players had impairments similar to those of other patients with mild cognitive impairment.
Likewise, the pushback upon the release of the international consensus statement in March 2013 questioning the causal link between reptitive brain trauma and CTE, from the research group at Boston University's Center for the Study of Traumatic Encephalopathy most associated with the position that CTE is a distinct neurodegenerative disorder suffered only by athletes in contact and collision sports, and that repetitive trauma can be in some cases the sole cause of the disease, was immediate, sustained, and widely reported.
Typical was the reaction of one of the co-authors, Dr. Robert Cantu, Director of the Center. Dr. Cantu told NewJersey.com :  "When I saw that [it said] we need more data in terms of CTE, I wrote to the other authors, in essence, 'What the hell do you mean that we need more data?' The whole breadth of the document is large, and 99 percent of it it I strongly support. But that part of it, I don't support at all. Frankly, it stunned me."
Dr. Cantu's Boston University colleague, Dr. Ann McKee, likewise expressed befuddlement at the consensus statement's treatment of CTE, telling NewJersey.com, "This is a time that calls for immediate action to reduce the amount of head trauma experienced by athletes in all sports to prevent CTE."
Dr. McKee asserted that it would be "irresponsible to justify inaction by requesting a level of scientific proof that will take decades to acquire," expressing the fear that, to suggest that CTE "may not be part of the impact exposure, but rather due to other yet unidentified factors," could give tacit permission to those who play collision sports to proceed as if there is no urgent problem when concussions arise.
It wasn't intended to have such an implication, Dr. Rosemarie Scolaro Moser, Director of the Sports Concussion Center of New Jersey and MomsTEAM.com's sports concussion neuropsychologist, told NewJersey.com. Instead, she cautioned that it would be jumping to conclusions to say, 'If you play football, you're probably going to get CTE.' Which is not the case. So what differentiates those with CTE from those who don't have it? That's what we need to know."
The numbers of those in the medical, scientific, and concussion research communities voicing serious doubts about whether the link between repetitive brain trauma and CTE is nearly as strong as Drs. McKee and Cantu claim, or that proving scientifically that it can be caused solely by such trauma is inevitable, has been growing, even in the face of continued media reports elevating the purported link to scientific fact.
"Her study of brains with CTE appear to be all former NFL players, 1 from high school and 1 from college, but what about soccer players?" wondered Scott L. Bruce, MS, ATC, co-author of the 2004 NATA Position Statement on Sports-related Concussions and Founder of the Chattanooga Concussion Prevention Initiative, after viewing the PBS Frontline documentary "League of Denial" featuring Dr. McKee.
"Or what about athletes from other sports? What about females vs. males? What about those players who play college football, but never go on to play in the NFL? Of the number of high school players  who never play college football? Are any of their brains examined for CTE? If so, what were the findings?"
Indeed, while the Boston group is quick to point to the fact that almost all the brains it has autopsied showed signs of CTE, other researchers have not found it be the case. In a 2013 study,researchers in Canada autopsied the brains of six former CFL players with a history of multiple concussions and significant neurological decline. They found that only 3 of the six had post-mortem neuropathological findings consistent with CTE. The other 3 had pathological diagnoses of AD, ALS and PD. Even in the athletes whose brains post-mortem showed signs of CTE showed evidence of cancer, vascular disease, and AD.
The case studies, said lead author, Lili-Naz Hazrati of the Tanz Center for Research in Neurodegenerative Diseases in Toronto, "highlight that not all athletes with history of repeated concussions and neurological symptomology present neuropathological changes of CTE." In other words, "a history of participation in professional football and a history of multiple concussions, combined with positive clinical signs and symptoms of progressive neurodegenerative disease, were not inevitably associated in each of the 6 cases with a post-mortem diagnosis of CTE."
The absence of cross-sectional, epidemiological, prospective or longitudinal studies on CTE has thus led many of the most respected experts and researchers in the concussion community to part company with Drs. McKee and Cantu, at least on the conclusions that can - and can't - be drawn from the science.
Like Randolph and others, Hazrati said that the preliminary findings of the Canadian study of CFL players "support the need for further research into the link between concussion and CTE as well as the need to expand the research to other possible causes of taupathy in athletes," and "point to a critical need for prospective studies with good sampling methods to allow us to understand the relationship between multiple concussions and the development of CTE."
Until recently, the fact that the mainstream of the concussion research community does not share the views of the Boston group, has not been widely reported. It appears, however, that some in the media are beginning to pay attention to the science. In a recent interview , for instance, a leading concussion researcher, Dr. Michael McCrea, singled out for criticism a statement by Dr. McKee in "League of Denial" in which she "really wonder[ed], on some level, if every single football player doesn't have [CTE]."
"This is one of those situations where the story has really raced out in front of the science," McCrea told a reporter for the Milwaukee Business Journal. He agreed that concussion is a serious injury and the sports industry should take it seriously. But McCrea had a problem with "League of Denial" using what he considered speculation that has yet to be proven in clinical research
In an article in Deadspin , Matthew McCarthy, a physician at New York-Presbyterian Hospital, writes about the "puddles of ink" that will be "spilled linking head trauma to chronic traumatic encephalopathy ... written by sportswriters who, frankly, don't understand the science and have long overstated what is actually known about the condition."
About the consensus statement's conclusion that no cause and effect relationship had been demonstrated, Dr. McCarthy points out that the statement "runs counter to almost everything you have read about CTE, but it received virtually no media attention in the United States when it was released. In part, that's because it speaks to the far higher burden of proof in the scientic community than the one in the public consciousness. But that's the point. The popular consensus has far outstripped the science."
As for Dr. McKee's statement to NewJersey.com, McCarthy observes that she admits that, while there was not scientic proof, there was enough evidence to start thinking about making changes. But he wondered whether it is the right thing for scientists to choose "to bang the drum, loudly, even if they can't be sure of the exact message once we're listening."
McCrea and McCarthy are not alone in urging caution.
In a June 2013 meta-analysis of the scientific literature on CTE in the prestigious British Journal of Sports Medicine, Andrew Gardner, MD, of the Centre for Translational Neuroscience and Mental Health in Callaghan, New South Wales, Australia, and two highly respected colleagues, Grant Iverson and Paul McCrory (the lead author of the last three international consensus statements on sport-related concussion, including the 2013 statement that prompted the expressions of outrage by McKee and Cantu), characterized the "strongly presented causal assumptions in the literature relating to concussive and subconcussive brain impact exposure" as "scientifically premature."
Before such a conclusion could be reached, wrote Gardner and his colleagues, systematic research was needed to address five specific unanswered questions:
First, whether similar, or even identical, neuropathological findings are observed in other samples that share clinical characteristics with CTE, such as patients with drug or steroid abuse, alcohol abuse histories, chronic psychiatric problems, cardiovascular/cerebrovascular disease or other health conditions.
Second, the extent to which the reported underlying neuropathology contributes to the reported clinical features (eg, cognitive deficits, psychiatric features).
Third, whether and to what extent genetics may contribute to the observed neuropathology.
Fourth, whether there are other possible mediator or moderator variables for the association between the neuropathology and the clinical features of the disease.
Finally, whether a methodology can be developed for identifying individuals who are at future risk or might currently have CTE.
"Psychiatric problems and cognitive impairment," wrote Gardner and his colleagues, "usually have multifactorial, not unitary causation - this will require further attention in future studies." He said that the important next step in the process of potentially answering some of the unresolved issues associated with CTE is to conduct large-scale, prospective, longitudinal, clinicopathological studies.
To be fair, both Drs. Cantu and McKee have also called for such studies. But, in the meantime, it appears that the prevailing narrative is that those that play contact and collision sports in general, and football in particular, are at serious risk of developing a frightening, degenerative, irreversible disease, even though, as noted above and by Dr. McCarthy, "the study of head injuries is a lot more confusing and murky than once suspected - that some very good researchers are now suggesting CTE might not even be a unique disease."
The media narrative, argues Dr. McCarthy, has real world consequences in which former NFL players, and all those who ever donned a football helmet, may be, to a greater or lesser degree, "collateral damage."
As he points out in his gripping first person account of an encounter with an unidentified former NFL player in the psychiatric ward of a New York hospital, the former player was paralyzed by the fear that he was "walking around with a death sentence over [his] head."
"An aging athlete," he argued, should not have to "assume that a neurologic symptom is from CTE or that his life is about to unravel. There may be an alternate treatable explanation. And, either way, a physician should be making the diagnosis," not a journalist or even a research scientist.
"The interpretation of causation in the modern CTE case studies should proceed cautiously," urges another 2013 literature review,  whose authors not only include McCrory and Gardner, but such pre-eminent concussion researchers as Willem H. Meeuwisse of the University of Alberta, and neurologist Jeffrey S. Kutcher, MD of the University of Michigan, a co-author of the 2013 American Academy of Neurology's concussion guidelines.
The authors of the Canadian study of CFL players, agreed: "Our findings," they said, "advocate caution in the clinical diagnosis of CTE in patients with histories of contact sports and neurocognitive decline, as other diagnoses of neurodegenerative diseases are also possible."
It is important to note that these researchers are not saying that such a causal link won't ever be established, and it is clear from the evidence so far that there is a link between concussions and repetitive head trauma and an increased risk of long-term neurocognitive problems. Kucher, for one, admits that, "Ultimately, scientific research might establish that participation in contact sports leads to a distinct neuropathological syndrome, and this neuropathology causes psychiatric, cognitive and physical problems." Until then, such "cause and effect relationship remains to be shown scientifically."
"Until the risk factors for developing CTE are better defined," says Steven Broglio, PhD, AT, of Michigan NeuroSport and Director of the NeuroSport Research Laboratory at the University of Michigan, strategies designed to reduce those risks will necessarily remain "an educated guess, at best."
"Ultimately, a comprehensive approach that includes, but is not necessarily limited to, modifications of head impact exposure, equipment modifications, rule changes and enforcement, and changes in game culture may all be needed to reduce injury risk," Broglio concludes.
November 15, 2013 update: The latest evidence that journalists in the popular press appear to be willing to get ahead of the science on CTE came today with the publication of an article  by Dan Flynn in the Brietbart Report  about news reports by numerous media outlets, including CBS News and The Atlantic stating as fact that eight former NFL players, including Hall of Fame running back Tony Dorsett and fellow Hall of Famer Joe DeLaumielleure, had been diagnosed with CTE, when it appears that the tests they underwent, while finding signs consistent with the presence of the disease, made no definitive diagnosis of CTE, because, as TauMark, the company that made the test, itself noted on its website, "A definite diagnosis is only possible with autopsy when tau proteins are found in distinctive brain areas," and all of the 8 were still very much alive. "Just as the press touts an unpublished, nonexistent study by researchers standing to profit from the claims [that their test has been proven to diagnose CTE in living patients], actual peer-reviewed science [such as the Canadian study ] clashing with the mere claims .. goes overlooked." Perhaps Flynn puts it best in concluding that "[satisfying the scientific method requires more than making an unverified claim. Headlines aren't so demanding."
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Posted October 18, 2013, most recently revised November 15, 2013