While concussion, as with any form of traumatic brain injury (TBI), needs to be taken seriously [1], the impact on an athlete's day-to-day life is usually shortlived. Three-quarters of concussed high school athletes in one recent study [2] [1] were found to be symptom-free within a week; only 15% had symptoms lasting more than a week but less than a month, and only a very small number (1.5%) were still experiencing symptoms more than a month after injury.
Recent evidence [3], however, suggests that "mild" TBI, including repetitive concussive and subconcussive brain trauma [4], [2] can lead to long-term or progressive symptoms (postconcussion syndrome [5]), disability, and pathologic changes, especially in cases of repetitive concussion:
The reported clinical symptoms of CTE are "tremendously broad" [19], but can include:
A 2013 meta-analysis of CTE[19] ("Gardner study") cautions, however, that "It may be that the description of the modern CTE symptomatology is confounded by the retrospective nature of the data collection and the heavily biased case selection. Consequently, the reported clinical observations (ie, suicidality, emotional liability, aggression and disinhibition) are likely to be skewed by selection bias.
Moreover, the Gardner study notes that, because the "clinical features [of CTE] overlap with a number of known psychiatric conditions and neurodegenerative diseases," the recent characterization of CTE "does not adequately consider plausible differential diagnoses, mediating variables, moderating variables, or multifactorial neuropathological processes." In other words, it is, in the view of many leading concussion experts, overly inclusive and simplistic.
A controversial 2013 study [26] by Christopher Randolph, PhD, of Loyola University in Chicago, and 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, even goes so far as to suggest that CTE may not a distinct neurodegenerative disorder at all.
In a study of retired NFL players - who largely comprise the universe from which the case studies of brains showing the presence of CTE have been drawn, and who the media have widely reported are at high risk of CTE - Randolph found that they did not actually suffer from CTE; 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, and that the patterns of their impairments were virtually identical to those exhibited by the non-athletes with MCI.
The study supported, Randolph said, the hypothesis he had proffered in a 2009 paper[30] that a long history of repetitive head trauma in contact sports might eventually result in a diminished cerebral reserve, leading to an earlier expression of common, age-related neurodegenerative diseases such as AD and Parkinson's (PD), but that the ways in which such diminished cerebral reserve would be expressed (e.g. MCI, AD, PD) would not be expected to differ from individuals with those diseases who lacked such a history of head trauma.
The Randolph study was heavily criticized as flawed by those who viewed CTE as a distinct condition. Chris Nowinski, co-director of the Center for the Study of Traumatic Encephalopathy at the Boston University School of Medicine (CSTE), told PopSci.com [34] that it was "preposterous" for Randolph to conclude that CTE might not be its own disease because retired football players had impairments similar to those of other patients with mild cognitive impairment.
While the study was reported by some in the scientific and medical media[34,35,36] at the time it was published, it did not gain a foothold in the mass media and soon faded from view.
It has since been proved to be an outlier.
In February 2015, a conference of pathologists sponsored by the National Institute of Neurological Disorders and Stroke of the National Institutes of Health convened in Boston to begin the process of generating consensus guidelines for the pathological diagnosis of CET. The group reported "general agreement" that CTE was a distinct neuropathological disease, different from other tauopathies (e.g. neurodegenerative diseases associated with the pathological aggregation of tau protein in the human brain).[69] The feature considered most specific to CTE, the group reported, and the one that distinguished the disorder from other neurodegenerative diseases such as Alzheimer's, was the where the tau was distributed in different regions of the brain.
Not only is there no unanimity about whether CTE constitutes a distinct neurodegenerative disease, but experts disagree about how it should be classified. One of the two main research groups studying CTE (the CSTE group led by Drs. Ann McKee, Robert Stern and Robert Cantu) classifies CTE into four disease "stages" [21] while the other (led by Dr. Bennett Omalu) describes four "phenotypes"). [20, 22]
According to McKee and her colleagues, the four stages are:
Stage 1: preclinical. No symptoms.
Stage 2: Deterioration in attention, concentration, and memory, as well as disorientation and confusion, and occasionally accompanied by dizziness and headaches.
Stage 3: Social instability, erratic behavior, lack of insight, poor judgment, memory loss and initial symptoms of Parkinson disease
Stage 4: General cognitive disfunction progressing to dementia, often accompanied by full-blown Parkinsonism, as well as speech and gait abnormalities.
As other studies have noted, the stages proposed by McKee et al [21] are based on the level of neuropathological evidence of disease on autopsy rather than on clinical presentation. [19] In light of the lack of currently available biomarkers to observe the natural history of CTE in living patients, Dr. Barry Jordan, the author of a 2013 study reviewing the clinical spectrum of sport-related traumatic brain injury,[20] viewed the characterization of pre-clinical CTE (before symptoms are observed) and prodromal CTE (between the time initial symptoms appear and onset of the full blown disease) as premature. Instead, Jordan proposed classifying the clinical criteria for the diagnosis of CTE into four categories (definite, probable, possible, and improbable CTE) in line with other neurological disorders. His view appears to be shared by Randolph in his 2013 NFL retiree study,[26] in which Randolph notes a "substantial pathological overlap and a lack of clear clinical-pathological correlation."
On the basis of currently available evidence, the Gardner study[19] proposed a fourth, conservative, operational definition for the modern CTE diseased process:
Although historically, CTE was primarily associated with boxing, it has been identified among athletes playing American football, hockey, wrestling, rugby and among those suffering blast or concussive injury in military service. [13]
A 2012 study [13] by CSTE researchers found evidence of CTE in 80% of a small group of deceased individuals with a history of repetitive mild traumatic brain injury (64 athletes, including 33 former NFL players, and 21 military veterans), from which evidence the authors concluded that "repetitive mild traumatic brain injury alone is sufficient to trigger CTE in some people." (emphasis supplied)
The Gardner study [19] estimated, however, the incidence of CTE among professional American football players at less than 4%, based on the numbers of cases obtained in a given period versus the number of athletes who died during the same period. If all of those professional athletes at risk were to be used as the exposure, the study authors argue, then the incidence rate would be less than 1/100th of a percent (0.01%). Gardner estimated that of the 85 autopsies only 20% had 'pure' neuropathology consistent with CTE, 52% had CTE plus other neuropathology, 5% had neuropathology but no CTE, and 24% had no neuropathology.
For his part, Dr. Randolph, the author of the 2013 study on NFL retirees,[26] said he believed that, if there was indeed an increased risk of late-life cognitive impairment in NFL retirees compared to men in the general population, it was probably due to diminished cognitive reserve. "We still do not know if NFL players have an increased risk of late-life neurodegenerative disorders," Randolph said.[28]
The idea that concussion may speed up the brain's natural aging process and lead to a more rapid depletion of cerebral reserve is consistent with a theory advanced by researchers at the University of Michigan in a 2012 study [9][27] of collegiate athletes with a history of concussion in which they found subtle changes in concussed athletes on tests of balance and gait that, they speculated, put the athletes at greater risk of falls later in life.
Recent biomechanical studies suggest that athletes in collision sports such as football may experience over one thousand hits during the course of a single season,[26, citing studies] precisely the kind of "repeated sublethal brain trauma" a recent study suggests may ultimately lead in an unknown percentage of cases to CTE even if none, individually, leads to a formal diagnosis of concussion. [Indeed, the 2009 Randolph study [30] hypothesized that concussion per se was unlikely to be as signficant a factor in the development of age-related neurodegenerative diseases like MCI, AD and PD as such routine repetitive trauma.]
In a groundbreaking 2010 study [10] [5, 46] by researchers at Purdue University, athletes repeatedly subjected to such so-called "sub-concussive hits" (particularly offensive and defensive linemen) were shown to have measurable short-term impairment of neurocognitive function (primarily visual working memory) on neurocognitive tests [11], as well as altered activation in neurophysiologic function on sophisticated brain imaging tests (fMRI), even though they displayed no clinically-observable signs of concussion [12],
Moreover, even though the players in the Purdue study who suffered short-term cognitive impairment from repeated sub-concussive blows appeared to fully recover cognitive function before the next season, exhibiting results on fMRI and neurocognitive tests comparable to their previous baseline scores, the Purdue researchers cautioned that return to baseline did not necessarily mean that there was 100% recovery.
The findings led Randall Benson, a neurologist at Wayne State University in Detroit, to speculate in Sports Illustrated [31] that the Purdue researchers may have taken what amounted to a "real-time snapshot" of the early stages of CTE, and that it was possible that the damage would only be known over the long term, years later.
Since publication of the first Purdue study, similar findings about the effects of RHI, both in the short- and medium-term, have been reported by many other researchers [45, 47-62], with several of the studies finding changes which persisted for weeks and even months after a football season ended.
Summarizing the state of the research in 2015, a study by researchers at the University of Virginia[[53] found that, in the short term, RHI has been "linked to increased susceptibility to concussion, decreased cogntitive function, altered gray matter functional connectivity, and changes in white matter microstructure," and that, in the long term, "retired football players who have sustained high levels of subconcussive impact over their careers have been hypothesized to have an increased risk of developing neurodegenerative disorders, like amytrophic lateral sclerosis [e.g. Lou Gehrig's disease], Alzheimer's disease, Parkinson's disease, and chronic traumatic encephalopathy (CTE)."
While the severity of CTE seems to correlate with the length of time engaged in the sport and the number of traumatic injuries, whether a single TBI can trigger the onset of CTE, and the number of concussions and/or amount of cumulative subconcussive trauma necessary to produce such pathology, remains unknown, leading some experts to conclude that, as of yet, "no reasonable basis exists to predict which athletes might be at risk other than perhaps to identify very broadly those involved in sports with exposure to repeated high-impact forces to the head (e.g boxing, American football)."[13]
It is important to note, however, that, while few studies have evaluated repeated concussive head trauma as a risk factor for later neurodegenerative disease, two studies that did failed to identify [13] an increased risk of neurodegeneration among participants in contact/collision sports.[33,38]
A 2012 Mayo Clinic study [13] of high school students who played football from 1946 to 1956 [33] found that, 50 years later, the did not appear to be at increased risk of later developing dementia, PD or ALS compared with their non-football playing high school male classmates.
The authors, however, were careful to note the many differences between today's high school football players and those of the distant past: while today's players have better equipment, trainers and physicians who are more knowledgeable about concussions, play under rules which prohibit - at least in theory - leading with the head when blocking and tackling, and may be marginally more likely to report concussive symptoms than players from a prior era, they also tend to be larger and quicker, increasing the force of impact, and wear helmets which, while "dramatically different from the marginally protective headgear of the earlier era, do not eliminate concussions and may give them a false sense of protection."
As a consequence of these differences, they cautioned that the results of their study, while they could be viewed as "somewhat reassuring to high school players from 50 years ago, they should give no reassurance to today's players."
A 1990 study [38] of individuals with Alzheimer's disease also found no association between risk of disease and participation in contact sports, although, as Jordan noted in his 2013 paper,[20] the robustness of the study's finding was limited by its small sample size.
Just as some athletes sustain concussion and others do not, despite experiencing blows to the head of similar magnitude and number, it is important to note that, while there is increasing evidence in the research to support the view that an accumulation of undiagnosed subconcussive head trauma and/or history concussive injury may lead to (or be the leading risk factor) for CTE, with a 2015 study[68] finding that a history of concussive injury was the only risk factor consistently associated with CTE, "the apparent low incidence of CTE makes it challenging to draw definite conclusions on the condition's risk factors."[67] In other words, all neuropathologically confirmed cases of CTE involved individuals with a history of brain trauma exposure, but clearly not all individuals exposed to brain trauma develop CTE. [3,67]
Among the other factors which may increase the risk of CTE besides repetitive head impacts include :
Because the study of CTE is in its infancy, [3,14,16.68,70] many critical questions remain, among them: "how much brain trauma is causative, what type, and how frequent, the age when players are most susceptible and whether some individuals are genetically more prone than others."
As Dr. Robert Stern of the CTE Center at Boston University [15] told the CBS News magazine's Steve Kroft in November 2015 [16],[70] "We know from all the neuropathologically confirmed cases of CTE that every case has had one thing in common, a history of repetitive head impacts. That means that... [i]t's not good for you. It's a necessary variable to get this disease. But just because you hit your head a bunch, doesn't mean you'll get the disease. So we have to figure out why one person gets it and another person doesn't."
The evidence, as Dr. McKee states in a 2012 CTE study, [13] "clearly shows that, for some athletes and war fighters, there may be severe and devestating long-term consequences of repetitive brain trauma that has traditionally been considered only mild."
"The last thing we want is for people to panic. Just because you've had a concussion does not mean your brain will age more quickly or you'll get Alzheimer's," says Steven Broglio, PhD, ATC, Assistant Professor of Kinesiology and Director of the Neurotrauma Research Laboratory at the University of Michigan School of Kinesiology and the author of the 2012 study [9] suggesting that concussions may speed up the brain's natural aging process.[27]
Broglio stressed that the influence of various lifestyle and environmental factors, such as smoking, alcohol consumption, physical exercise, family history (genetics), whether or not a concussed athlete "exercises" their brain, and even how dense the gray matter in a person's brain is, which gives them greater "cognitive reserve" to draw upon may also impact the brain's aging process, and that "concussion may only be one small factor."
In addition, he said, this line of research is still in its infancy. "'It's not entirely clear," Broglio told the Kalamazoo News [17], "if and how the brains of young athletes are affected by the sports they play. 'We are realizing it's probably not how many concussions you have that makes a difference, but the total exposure' to concussive and sub-concussive blows."
"What we don't know is if you had a single concussion in high school, does that mean you will get dementia at age 50?" Broglio said. "Clinically, we don't see that. What we think is it will be a dose response."
"So, if you played soccer and sustained some head impacts and maybe one concussion, then you may have a little risk. If you went on and played in college and took more head balls and sustained two more concussions, you're probably at a little bigger risk. Then if you play professionally for a few years, and take more hits to the head, you increase the risk even more. We believe it's a cumulative effect."
Does the average high school athlete face risks similar to those of former professional football players - such as those whose brains, upon examination after death, show signs of CTE or who, even if still alive, exhibit signs of serious depression or early-onset dementia which researchers have linked to their years on the playing field?
Broglio says that there is little to no evidence that they do. "We're not seeing an epidemic of men in their early 50s with early Alzheimer's because they played high school football," Broglio told a Michigan newspaper [17] in commenting on his 2012 study. His observation is supported by the 2012 study [13][33] by Mayo Clinic researchers which found no increased risk of neurodegenerative disease in men in their 60's and 70's who played high school football in the 1940's and 1950's.
Boston University's Cantu has also been, at times, a voice counseling restraint. "For my patients who've had multiple concussions and fear that they are at risk for developing CTE later in life, I offer simple advice: Relax. The connection has been greatly overstated."[44]
The authors of a 2015 editorial in the British Journal of Medicine[67] agreed: "While cases continue to surface and receive tremendous media attention, the fact remains that current evidence suggests that the risk is very low when we consider the total number of athletes who have played American football."
Dr. Cantu's colleague, Dr. Robert Stern, told [16] the CBS newsmagazine, Sixty Minutes, the same thing: [J]ust because you hit your head a bunch, doesn't mean you'll get the disease," says Stern, who made it clear to the program's Steve Kroft "that most NFL players don't," and that the number of confirmed cases is still small, with thousands of former NFL players seemingly unaffected.[70]
The simplest way to decrease the risk of CTE, whatever it is, say a growing number of experts, is to:
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 ("Zurich statement") [13] 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 [including the McKee studies], 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 Zurich 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. [As a result], the interpretation of causation in the modern CTE case studies should proceed cautiously."
Remarkably, the Zurich statement discussion of CTE 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 is echoed by Randolph in the 2013 NFL retiree study[26] which laments that "the media attention to this issue continues to far outweigh any meaningful results from sound experimental science," and in four other recent literature reviews.[39-42]
There was, not surprisingly, immediate pushback upon the Zurich statement's release in March 2013 from the research group at CSTE, the group most associated with the argument - repeated by many in the media - that such a causal connection has already been proven.
Said one of the Zurich statement co-authors, Dr. Robert Cantu, MomsTEAM concussion expert emeritus and CSTE director, in an interview with NewJersey.com [29]. [15] "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 colleague, Dr. Ann McKee, likewise expressed befuddlement at the Zurich 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." She 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, 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."
[Update: it is important to note that the Zurich statement was issued after a conference held more than three years ago, so that, in light of the body of research in the last three years, its statements on CTE may now be outdated. What the 5th International Conference - rumored for Berlin in October 2016 [30] - will decide is anybody's guess. Stay tuned!]
There nevertheless remains continued skepticism by many in the medical, scientific, and concussion research communities as to whether CTE is caused solely by repetitive head impacts.
As an August 2015 editorial in the British Journal of Medicine editorial [67]: "It still remains unclear if brain damage is an inevitable consequence or an avoidable risk of [contact or collison sports]."
Dr. McKee's "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, in a comment to a concussion blog entry[17] after viewing the PBS Frontline documentary League of Denial in which she was featured.
"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?"
Similarly, the absence of cross-sectional, epidemiological, prospective or longitudinal studies on CTE has led many of the most respected experts and researchers in the concussion community to express caution in quantifying the risk of CTE posed by repetitive head impacts, although that fact, with some notable exceptions, has not been widely reported.
An exception was a recent article [31] in which a leading concussion researcher, Dr. Michael McCrea, singled out for criticism a statement by Dr. McKee in the PBS Frontline documentary, League of Denial, in which she said she was "really wondering 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 [32],[32] 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 Zurich 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 scientific 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 argued that, while there was not scientific proof, there was enough to start thinking about making changes, so she "and others have chosen to bang the drum, loudly, even if they can't be sure of the exact message once we're listening." (the fact, of course, is that changes are being made, most notably in the form of limits on full-contact practices)
In their 2013 meta-analysis of the scientific literature on CTE,[19] Gardner, 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 Zurich statement that prompted such expressions of outrage by McKee and Cantu), [13] characterized the "strongly presented causal assumptions in the literature relating to concussive and subconcussive brain impact exposure" as "scientifically premature."
In order to reach that conclusion, writes Gardner, systematic research is needed to address five specific unanswered questions:
First, it is not known 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. [Author's note: A 2015 meta-analysis of all reported cases of CTE[68] appears to suggest otherwise, however, finding no evidence to link substance abuse, genetic factors such as APOE, or pre-existing medical conditions to an increased risk of CTE]
Second, the extent to which the reported underlying neuropathology contributes to the reported clinical features (eg, cognitive deficits, psychiatric features) is uncertain.
Third, the potential existence of a genetic contribution to the observed neuropathology has not been determined. [Author's note: Again, the 2015 meta-analysis of CTE cases[68] found no evidence to support the view that genetic factors increased risk of CTE]
Fourth, possible mediator or moderator variables for the association between the neuropathology and the clinical features have not been identified.
Finally, we do not have a methodology for identifying individuals who are at future risk or might currently have CTE. Psychiatric problems and cognitive impairment usually have multifactorial, not unitary causation - this will require further attention in future studies. 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. [Note: the NCAA has recently begun such long-term studies]
To be fair, both Drs. Cantu and McKee have also called for such studies, as have many others.[67] Indeed, Dr. Cantu, in a moment of honest and candid reflection on the impact he has as a leading authority on concussions, even went so far as to acknowledge in a postscript included in the paperback edition of his book, Concussions and Our Kids,[44] that if there was "one thing that isn't explained as fully in the book as [he] wish[ed] ... it is the precise relationship between total head trauma (concussions and also subconcussive blows) that a child absorbs playing football and hockey and, to a lesser degree, soccer and basketball and the possibility of developing a degenerative brain disease such as CTE as an adult. We don't know yet," he admits. "The research continues, and it is possible that we will have an answer to that critical question soon, perhaps with a decade."
But, in the meantime, it appears that the prevailing narrative - at least in the mainstream media and among pundits and commentators - is that those that play contact and collision sports in general, and football in particular, and youth football even more specifically, are at serious risk of developing a frightening, degenerative, irreversible disease, when, as noted by Dr. McCarthy, "the study of head injuries is a lot more confusing and murky than once suspected."
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, [22] 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 of the University of Michigan, a co-author of the 2013 American Academy of Neurology's concussion guidelines. [23]
In October and November 2013, four more reviews of the peer-reviewed literature [33][39-42] joined the growing body of scientists pouring cold water on the now common assumption in the media and general population that contact sports inevitably causes CTE, and that CTE causes those with the disease to commit suicide.
In the first, published in the British Journal of Sports Medicine,[39] a leading concussion researcher, Grant Iverson, MD, of the Department of Physical Medicine and Rehabilitation at Harvard Medical School, finds the scientific evidence insufficient to support a finding of the existence of a strong causal relationship between CTE and suicide in former athletes.
In the second, published in the journal Behavioral Sciences and the Law, [40] scientists at the University of Colorado School Medicine conducted a state-of-the-science review of CTE, explored the evidence for links between traumatic brain injury (TBI), CTE and catastrophic clinical events such as suicide, and highlighted the complexity of specifically attributing suicide to CTE. Like Iverson, they urged caution in jumping to conclusions on the basis of preliminary case study autopsies.
In the third commentary, published in the journal Neuropsychological Review,[41] Christopher Randolph, PhD, of Loyola University in Chicago, as noted earlier, the leading skeptic about the link between CTE and contact sports, reviews the history of so-called "classic" CTE in boxers, the literature on "modern" CTE (case studies from 2005 forward), mainly in American football players, explores the sampling and methodological issues that, he says, prevent any firm conclusions about the association between athletic head trauma and neurodegenerative diseases such as CTE being drawn, and calls, like Iverson and Wortzel, for more carefully-controlled epidemiological and prospective studies to overcome current limitations in this research and stimulate further research.
Finally, commenting in the British Journal of Sports Medicine on a systematic review of the literature on CTE in sport[19] published in the same issue of the journal, Charles Tator, MD, of the Division of Neurosurgery at the University of Toronto, notes the "significant advances" over the past 10 years in understanding CTE that have allowed the sports community to understand that the issue of brain degeneration as a consequence of repetitive concussion is not confined to boxers but applies at least to hockey, football, wrestling, and rugby.
Tator emphasizes, however, says that there are many questions to be answered, among them:Like Iverson, Wortzel, and Randolph, Tator says longitudinal studies of large number of at-risk athletes are "essential." The recent editorial in the British Journal of Sports Medicine[67] takes the same view.
It is important to emphasize that such researchers are not saying that such a causal link won't ever be established. As Gardner admits, "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."[19]
Indeed, the authors of one recent paper[40] acknowledge that "it simply makes good clinical sense to continue practices to minimize the number of concussions sustained and that allow for adequate recovery after any concussion" while awaiting the results of such studies. The authors of the 2015 BJSM editorial on CTE[67] take the same view: "Despite uncertainties, strategies to reduce the number of concussive and subconcussive head impacts in American football [and in other sports, presumably, such as soccer, lacrosse, and hockey] should be a top priority."
At the same time, however, they say it is "essential to avoid embracing preliminary results derived from relatively small case numbers and methodologically problematic studies as undisputed medical fact, and to allow such results to redirect clinical practice away from established standards."
A concerted effort is thus needed, they say, to educate medical professionals and the public at large regarding the state of the science of mTBI and CTE in order to avoid "catastrophizing" mTBI, to mitigate the "collective anxiety" that has resulted, and to reduce the likelihood that outcomes after mTBI will be actually be made worse as a result of the media frenzy around CTE.
Sources:
McKee A, Cantu R, et. al. Chronic Traumatic Encephalopathy in Athletes: Progressive Tauopathy After Repetitive Head Injury. J Neuro Exp. Neurol 2009; 68(7): 709-735
Gavett B, Stern R, Cantu R, Nowinski C, McKee A. Mild traumatic brain injury: a risk factor for neurodegeneration. Alzheimer's Research & Therapy 2010; 2:18
Galetta KM, Barret J, Allen M, et. al. "The King-Devick test as a determinant of head trauma and concussion in boxers and MMA fighters." Neurology 2011; Prepublished online February 2, 2011.
Daneshvar DH, Baugh CM, et. al. Helmets and Mouth Guards: The Role of Personal Equipment in Preventing Sports-Related Concussion. Clin Sports Med 2011;30:145-163.
Footnotes:
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