During this tragic time the inbox has been besieged by many stories, questions and information. One such email came in on Wednesday night;
In light of Junior’s death, which dovetails with the Saints bounty fallout, I thought I’d pass along this paper I wrote in grad school last year about the long-term risks associated with concussions in professional football. Its something of a review article, that covers the development of CTE and physiology of concussions. I played football in high school and “sucking it up,” as you know, is part of the gridiron culture, but we need to education players, parents, and trainers about the difference between having your bell rung and developing a neurological disorder. This paper hasn’t been peer-reviewed by anyone except my professor, who was a medical writer, not a neurologist but I stand by the science. I started this article by asking for advice from Dr. Robert Stern, the chairman of the Center For The Study of Traumatic Encephalopathy at Boston University. I drew on their research and many of their articles and they do excellent work.
I also wanted to thank you all for following this issue, which is becoming a major concern for athletes, fans, and families.
The author of the email and of the paper is Doug Taylor and I feel it is a very good piece for all to read. Although, as Doug notes, the paper is not “peer-reviewed” it does not mean there isn’t valuable information for everyone to read and think about. I would like to thank Doug for sharing this.
Long Term Effects of Concussions – Doug Taylor
Sports-related concussions are one of the most common injuries sustained by professional football players. The acute symptoms that follow a mild traumatic brain injury are well established, with many instances of headaches, confusion, dizziness, and short spells of amnesia. The long-term effects of these injuries are less comprehensively understood. It is clear that repeated blows to the head can cause physiologic distress that develops into a degenerative neurological syndrome known as Chronic Traumatic Encephalopathy (CTE). This disease is characterized by pathologic protein aggregations that eventually lead to behavioral disturbances culminating in dementia. Several individuals diagnosed with CTE have committed suicide, though evidence conclusively linking the disease with such actions remains elusive. Original claims that the disease develops only after many years of playing football are being reevaluated as younger players are being diagnosed with CTE.
Unlike a concussion, which is a temporary physiologic disruption, chronic traumatic encephalopathy (CTE) is a degenerative neurological disease with established pathological abnormalities.2,19 CTE is not an accumulation of these concussive or subconcussive hits but rather a disease set in motion by these events. It is currently not known how many brain injuries are necessary to initiate CTE, but data suggest a single concussion is insufficient.10,19 It is clear that CTE is a result of the repeated mild brain injuries suffered thousands of times each year by professional football players. The initial clinical symptoms of CTE are akin to those documented in postconcussive patients. These include attention deficiencies, memory loss, profound confusion, dizziness, and chronic headaches. As the disease progresses more serious symptoms such as difficulty problem solving, impaired judgment, and emotional instability become apparent.29 In the case of one former professional football player posthumously diagnosed with CTE, cognitive disturbances such as asking the same question repeatedly and the inability to recall movies he had previously seen were
documented by friends and family before his death.29-31
The second stage of the CTE progression is characterized by impaired speech and the onset of Parkinson’s symptoms such as tremors and inconsistent muscle control. Advanced cognitive dysfunction and infrequent violent or erratic behavior constitute phase III of CTE, with intermittent bouts of depression, lethargy, or anxiety throughout.30,31 The progression of CTE is largely dependent on the individual patient, with various factors including length of career, family medical history, and co-morbidity affecting the outcomes.29
Initial study of CTE in football players showed the onset of symptoms after retirement 29,30 Two frequently cited examples are of two 45-year-old former professional football players who developed CTE after they left the game and died violent deaths (though one was an accidental self-inflicted gunshot wound) (Figure 2).29,30 Both men played professional football for at least 8 years and were diagnosed with at least 8 concussions during their careers. Neither man was diagnosed with post-concussive syndrome or required hospitalization after the head injury. Each man lost consciousness only once in his professional career.29,30
The link between repeated concussive or subconcussive hits and long-term brain damage has been established in recent years. The physiological aftermath of a concussion coincides with the pathological findings in the brains of patients with CTE. There is overwhelming evidence showing the condition to be the direct result of these repeated sublethal hits to the head. Further data suggest the condition can be prevented by longer rehabilitation time after an initial head injury, though precisely what amounts to adequate recovery time is not yet clear and varies on an individual basis. The thousands of hits to which professional football players are subjected over the course of the season are not necessarily damaging on their own, but the cumulative effect of these impacts over time is catastrophic. Of special concern to researchers is the development of CTE in younger players, most of whom have not yet experienced the ultra-violent hits encountered on the professional level. The appearance of tau neurofibrillary tangles in these young men suggests CTE may be extremely widespread in professional football players. The National Football League has instituted guidelines for its players, coaches, owners and medical staff designed to identify concussive traumas and keep players off the field until they are deemed fit to return to action by an independent neurologist. The effectiveness of this new protocol and the consequences on NFL players remains to be seen.
From a clinical perspective, researchers need more athletes to participate in CTE studies. The Center for the Study of Traumatic Encephalopathy and the Sports Legacy have been petitioning players to donate their brains with some success; 40 current or retired NFL players have agreed to donate their brains. This is an important step in curbing the development of CTE in professional football, but the key to stopping the disease appears to be broader education of athletes, trainers, physicians, and parents on the risks associated with repeated brain injuries. Organizational intercession to prevent injuries players from returning to the field is essential and could drastically decrease the prevalence of all brain injuries at every level.
Research about CTE is still relatively limited and there are significant questions to be answered, such as the precise relationship between ApoE polymorphism and CTE or how many concussions are necessary for the disease to occur. There remains a need to establish an accurate diagnostic test for CTE in living individuals and treatments must be developed for these patients. Other environmental risk factors must be evaluated, such as the effects of childhood or adolescent brain traumas on athletes. It is clear that more expansive research on professional football players is required before a complete picture of the long-term effects on head trauma on these athletes can emerge.
The article is very well written and worth your time, I find the genetic link section very interesting and new for me.
Thanks again Doug!
Informative paper (can’t help but wonder if what new information has be discovered since it was written). I saw an article that briefly addressed the genetic factors that may influence risk.
“The “apolipoprotein E” gene or APOE is located on chromosome 19 and encodes production of the protein apolipoprotein E. Apolipoprotein E is involved in repairing the neurons following moderate to severe traumatic brain injury. As APOE is a polymorphic gene, there are three slightly different versions, e2, e3, and e4, with e3 being the most commonly found in the general population. It is thought that the presence of e3 may generate protection from severe trauma and speed up the recovery process. However, the presence of e4 may increase negative outcomes following trauma including longer periods of unconsciousness and slower cognitive recovery.”
Terrell’s study is very interesting and as more data is presented it should cause many to pause and think more critically.
While CTE has been documented in some football players the emphasis on this pathology may be overemphasized. It is dramatic and if one is seeking research funding it is timely. Nonetheless, CTE’s prevalence does not approach the levels similar to that in boxing pouplation. That being said, I would suggest will see an increase in rates of NFL-related CTE in the near future.
“Investigators have shown in an experimental animal TBI study that a synthetic apolipoprotein-like peptide improved functional recovery.”
“APOE E4 remains the main genetic risk factor for late onset AD. It appears that APOE E4 acts additively or synergistically with TBI to increase the risk of AD. Multiple studies show that APOE E4 is associated with poorer outcome after TBI21, and functional impairment 6 months after brain trauma but not with initial injury severity. APOE E4 is also a risk factor for chronic traumatic encephalopathy (CTE) in boxers. Furthermore, recent literature reviews show that pathologically verified long term enuropathological changes of CTE have been reported in athletes playing pro football, pro wrestling, and other sports.”
“Our group studied one of the largest cross-sectional sample of 196 athletes (See Appendix A) and showed a statistically significant, nearly 3-fold increase in risk of a history of self reported Concussion for those with the APOE promoter G-219T TT genotype relative to the GG genotype (OR, 2.8; 95% C1, 1:1 to 6.9) adjusted for age, sport, school, and years in primary sport.”
Click to access APOE,%20APOE%20Promoter,%20and%20Tau%20Genotypes%20and%20Risk.pdf
“The increase in aspartate and glutamate levels, multiple
ionic fluxes, and the hypoperfusion/hyperglycolysis mismatch
characteristic of the pathobiology of concussion may be
regulated by a complex set of gene-gene interactions among
the APOE gene, tau gene, APOE promoter, and perhaps the
NMDA receptor gene. APOE expression is affected by APOE
genotype and G-219T genotype, as well as the inciting head
trauma itself. Future research can focus on other genetic and
environmental factors that affect APOE expression and the
potential genetic regulation of this cascade of events.”
“Boxers and football players (especially lineman) appear to be the most likely to get the disease because of the repetitive brain trauma exposure. But, it is important to note that not everyone with a history of repetitive brain trauma will develop CTE.
Our center is currently conducting research into the other potential additive risk factors, such as genetics, age of initial brain trauma exposure, frequency and overall duration of exposure, etc. This research will hopefully lead us to understand why one person gets the disease and another person does not.”
Some harsh commentary –
“… when I accidentally channel-surfed past the eleventy-gazillion hours of live NFL draft coverage this weekend, it looked like nothing more than the debut of a new television game show: Who Wants To Be a Vegetable at 50?”
“Ray Easterling’s eventual dementia was as inevitable a result of the work he did for a living as black lung is for coal miners, or mesothelioma is for the people who work with asbestos. That this simple fact is obscured by an affection the country has for its football is a symptom of a country that has let that affection compromise its moral bearings.”
Dr. Randall Benson’s written congressional testimony, Jan. 4, 2010. (This is a couple years old, but I found the imagining information really interesting.)
Click to access Benson100104.pdf
“… head injury including mild TBI causes varying amounts of axonal injury which a) recovers slower than clinical symptoms; b) underlies the more important and longstanding functional impairments; c) gives rise to phosphorylated Tau in damaged axons and d) likely leads to CTE with repetitive concussions (possibly in genetically predisposed individuals (Teasdale, Lancet, 1997).”
Thanks for writting this. I am 37 my symptoms are out of control. I only played contact football for 12 years Thank God. Injury ended my career when iI was a senior in high school. I probably rung my bell everyday i played and knocked myself out once a week. This does not include skateboard and motircycle concussions. There is no hope for people suffering from this!!! Is it the impulsive behavior that makes them commit suicide or is it the pain and lack of hope?
Unknown Jason, but do me a favor if you are having any of those thoughts seek help, I did and it was the best thing I ever did…