Concussions and Chronic Traumatic Encephalopathy
What can players of varying ages, sports, number of years played and causes of death all have in common? Chronic Traumatic Encephalopathy. For instance, 26 year old Bengals wide-receiver, Chris Henry died after falling off a truck during a domestic dispute. Frank Gifford died of natural causes at the age of 84. Mike Webster died at the age of 50 from a heart attack. John Grimsley died at the age of 45 after he accidentally shot himself. Ray Easterling killed himself at the age of 62. Bob Probert of the NHL died of heart failure at 45 years old. Also of the National Hockey League, Reg Fleming passed away at 73 years old after years of declining health following a heart attack and stroke. WWE Wrestler Andrew Martin died from an oxycodone overdose. 21 year old Penn State Football Player Owen Thomas killed himself. Ryan Freel of the MLB committed suicide. Ken Stabler, former Oakland quarterback died of colon cancer at the age of 69. 1 This is just a very short sampling of the lives lost that have since been diagnosed with Chronic Traumatic Encephalopathy.
Dr. Omalu 2 was a neuropathologist who happened to be doing an autopsy on Mike Webster, a retired former professional football player who was suffering greatly with memory loss, mood and behavioral disturbances though he passed away due to a heart attack. Through in-depth study of Webster’s brain, Dr. Omalu discovered evidence of what had been previously known as being punch drunk syndrome, or dementia pugilistica, and he went on to make popular the term, Chronic Traumatic Encephalopathy. Dr. Omalu was able to give Mike Webster justification to the last several very difficult and sad years of his life and provide an explanation to the family for Mike's actions. Dr. Omalu then went on to do autopsies of other players and Dr. Omalu found similar neurological pathway lesions in their brains.
There was not much literature on concussions before the year 2000, but because of Dr. Omalu’s work, we have a different understanding. Since then the research has really exploded. He has reframed what we know and how we treat concussions and repetitive concussive impacts. Because of his work, we give concussions and brain trauma much more validity.
Dr. Omalu deserves so much credit after heroically standing up for what he observed, even amongst persecution. He is also the cornerstone of the story behind the movie “Concussion.” Regardless of your opinions on professional sports, Dr. Omalu’s work has brought validity to the suffering that many players went through years of playing contact sports. His work also helps us today at Gates Brain Health as we seek to find, address and heal brain injuries.
Dr. Omalu’s first study, “Chronic Traumatic Encephalopathy in a National Football League Player” 3 is a great piece and likely something we will read about in textbooks fifty years from now.
More recently, Dr. Ann McKee’s group at Boston University have taken the ball and run with it as they continue to study CTE. Dr. McKee should be considered a heroine for her stand on the truth though it is often unpopular.
Dr. Omalu and Dr. McKee have profoundly affected so many lives and brought understanding to what has been a mystery and has been brushed off for so many years. We encourage you to read about these doctors and look into videos about them and their research on YouTube. They have some pretty interesting viewpoints.
4 Image: Normal brain, early stages of CTE, later stages of CTE.
So what is Chronic Traumatic Encephalopathy (or CTE)?
Dr. Ann McKee defines it as, “Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease associated with exposure to contact and concussions sports (CCS), including American football, boxing, association football (soccer), rugby, and ice hockey.” 5 CTE is only able to be diagnosed post-mortem when Doctors can see neuropathological lesions due to hyperphosphorylated tau protein in the brain.
What is tau?
You could think of tau as the 2x4’s of your neurons. Imagine then that you can shrink yourself down to fit in a room that is one of your neurons. This neuron room, like the rooms in your house, have 2x4’s that are imperative to the integral structure of the room. Tau helps to hold the structure of your neurons. Tau is also a kind of cytoskeletal protein which traffics molecules to and fro. Imagine that the while the tau works as the 2x4's it also works as cables stretched across the room to traffic things from side to side.
Hyperphosphorylation of tau is analogous to this neuron room crumpling around you and the cables are not able to traffic things from side to side. This is what happens to your brain when you have hyperphosphorylated tau. In a nutshell, there is some serious dysfunction happening in your brain.
What does this mean? Well most of us know that when somebody has Alzheimer’s, there is a neurodegenerative process at work. There are also other neurodegenerative diseases such as Parkinson’s frontotemporal dementia, etc. These diseases all cause areas of the brain to atrophy in different ways and then experience resulting symptoms. For instance, Alzheimer's affects the memory and other closely surrounding areas. Alzheimer’s is due to Beta amyloid plaques but also there is hyperphosphorylated tau like in CTE.
Note in the image above that different diseases affect different areas of the brain. What Dr. Omalu discovered with CTE was that this hyperphosphorylation of tau was found particularly in the frontal lobes.
Note and compare in the image below, the varying stages of CTE and Alzheimer's.
Generally we all understand that we can lose a few brain cells, but when you lose many brain cells in a specific area it is only natural that you will start developing correlating symptoms. “Clinically, impulsivity, explosivity, depression, memory impairment, and executive dysfunction most commonly occur in CTE...” 13 With CTE, though, there also seems to be different manifestations of these symptoms based on the age range of the patient.
A younger age group manifest primarily emotional and behavioral symptoms while older age groups primarily experience dementia symptoms.
Younger individuals overall are now manifesting neuropsychological symptoms, or memory related symptoms that they shouldn’t have, just due to heavy hitting sports.
Annals of Neurology published one of Dr. McKee’s latest studies “Duration of American Football Play and Chronic Traumatic Encephalopathy”.11 In this recent study they stated “In total, 223 of 266 participants met neuropathological diagnostic criteria for CTE. More years of football played were associated with having CTE (odds ratios [OR] = 1.30 per year played.”
Basically the odds of having CTE doubled every two years of football played. This is highly significant! Also, in essence, the more subconcussive head impacts, the more association of CTE after death.
In the diagram below, note images B and C. Image B is what normal tissue should look like. The maroon spots in C are the accumulation of hyperphosphorylated tau protein. In image E, note the mild deposition versus severe in image F.
This over accumulation of hyperphosphorylated tau is what Dr. Mckee consistently sees in the majority of the brains of retired football players among others.
In her study, “Among 202 deceased former football players (median age at death, 66 years [interquartile range, 47-76 years]), CTE was neuropathologically diagnosed in 177 players (87%; median age at death, 67 years [interquartile range, 52-77 years]; mean years of football participation, 15.1 [SD, 5.2]), including 0 of 2 pre–high school, 3 of 14 high school (21%), 48 of 53 college (91%), 9 of 14 semiprofessional (64%), 7 of 8 Canadian Football League (88%), and 110 of 111 National Football League (99%) players. Neuropathological severity of CTE was distributed across the highest level of play, with all 3 former high school players having mild pathology and the majority of former college (27 [56%]), semiprofessional (5 [56%]), and professional (101 [86%]) players having severe pathology.” 13
Let’s reiterate: 3 out of the 14 high schoolers were diagnosed with CTE and 110 of 111 NFL players were diagnosed with CTE. Of the 111 players, 101 were diagnosed with severe pathology. This is notable.
The study goes on, “Among 27 participants with mild CTE pathology, 26 (96%) had behavioral or mood symptoms or both, 23 (85%) had cognitive symptoms, and 9 (33%) had signs of dementia. Among 84 participants with severe CTE pathology, 75 (89%) had behavioral or mood symptoms or both, 80 (95%) had cognitive symptoms, and 71 (85%) had signs of dementia.” 13
“Among the 111 CTE cases with standardized informant reports on clinical symptoms, a reported progressive clinical course was common in participants with both mild and severe CTE pathology, occurring in 85% of mild cases and 100% of severe cases. Behavioral or mood symptoms were common in participants with both mild and severe CTE pathology, with symptoms occurring in 96% of mild cases and 89% of severe cases. Impulsivity, depressive symptoms, apathy, and anxiety occurred in 89%, 67%, 50%, and 52% of mild cases and 80%, 56%, 52%, and 50% of severe cases, respectively. Additionally, hopelessness, explosivity, being verbally violent, being physically violent, and suicidality (including ideation, attempts, or completions) occurred in 69%, 67%, 63%, 52%, and 56% of mild cases, respectively." 13
“Cognitive symptoms were common in participants with both mild and severe CTE pathology, with symptoms occurring in 85% of mild cases and 80 (95%) severe cases. Memory, executive function, and attention symptoms occurred in 19 (73%), 19 (73%), and 18 (69%) mild cases and 76 (92%), 67 (81%), and 67 (81%) severe cases, respectively. Additionally, language and visuospatial symptoms occurred in 54 (66%) and 44 (54%) severe cases, respectively. A premortem diagnosis of AD and a postmortem (but blinded to pathology) consensus diagnosis of dementia were common in severe cases, occurring in 21 (25%) and 71 (85%), respectively. There were no asymptomatic (ie, no mood/behavior or cognitive symptoms) CTE cases. Motor symptoms were common in severe cases, occurring in 63 (75%). Gait instability and slowness of movement occurred in 55 (66%) and 42 (50%) severe cases, respectively. Symptom frequencies remained similar when only pure CTE cases (ie, those with no neuropathological evidence of comorbid neurodegenerative disease) were considered.” 13
“Most CTE cases have been diagnosed in former amateur and professional CCS athletes, but also in military veterans with blast exposure and others who have suffered from traumatic brain injury. Among 66 men from the Mayo Clinic Brain Bank with documented CCS exposure and 198 age‐matched participants (132 men, 66 women) without CCS exposure, 21 of the 66 (32%) CCS athletes, but none of the unexposed participants, had CTE. Among 202 American football players from the Veterans Affairs (VA)–Boston University (BU)–Concussion Legacy Foundation (CLF) Brain bank, 177 (88%) players had CTE, including 3 of 14 (21%) high school players, 48 of 53 (91%) college players, and 110 of 111 (99%) National Football League (NFL) players. The NFL players commonly (95 of 110 [86%]) had severe CTE (ie, stage III or IV).” 13
Researchers can not yet explain why not everyone who experiences repetitive head trauma has CTE. Is there a genetic component? A predisposition? They are looking for these answers. But regardless, the number of cases are staggering and scary.
In essence, the more subconcussive head impacts, the more association of CTE after death.
These statistics raise some serious questions:
1. Should our children be playing competitive contact sports?
Like quoted earlier, Dr. McKee found that “Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease associated with exposure to contact and concussions sports (CCS), including American football, boxing, association football (soccer), rugby, and ice hockey.” 5 Keep in mind that this research isn’t picking solely on American football, but is bringing light to a global issue and raises questions as to whether kids under 18 should head the ball in soccer, or get into fights and hard collisions in hockey or football. Dr. Omalu’s research changed the understanding of what it is like to play sports at a younger age and likely, this is a good thing for our children’s long term health. His argument is that after the age of 18, one is old enough to determine for him or herself whether one wants to risk their health by playing sports.
2. What then, can we do to help the brain health of those who’ve sustained repetitive head impacts?
Unfortunately, there is not a definitive answer yet with studies to back it up but Dr. Gates has some theories. Remember how we discussed the gut break down that happens after a concussion (video and newsletter) and how bacteria affects our brain? Can we do something then, with diet, with supplements, with anti-inflammation measures that will maybe help to slow down this process of CTE? This is the hypothesis that we are working with currently.
Another one of Dr. Gates' favorite studies on this topic is “Limbic System Structure Volumes and Associated Neurocognitive Functioning in Former NFL Players.” 15 This study discusses the benefits of Diffusion Tensor Imaging MRI's to evaluate the severity of concussions, brain trauma, and the potential for a future CTE diagnosis. We have discussed this before (video and article.)
Say you are a military vet who has been exposed to several blasts and now your spouse is noticing that you are acting differently and deal with impulsivity in ways you didn’t prior, Or that you are easier to anger and feel more depressed than you used to. Or maybe you are a boxer, or a former NFL Player and have noticed these symptoms. To evaluate the possibility of CTE, you could get a volumetric MRI which looks at the density of certain areas of the brain compared to age normals.
Image description: “Diffusion tensor imaging section. Diffusion tensor images captured on a 3 T magnet analyzed with streamline tractography using Slicer 3. Control brain on the left and the brain of a former professional boxer in his 40’s on the right. The top two images are sagittal views with the callosal fiber tracts delineated; it is notable that the boxer’s fiber tracts are markedly shorter than the control. The bottom two images are a coronal view of the same two individuals and it can be seen that the athlete’s corpus callosum (red structure in the middle of the brain) is noticeably thinner than the control” 16
Diffusion Tensor Imaging measures a different percentage of what is happening in your brain and also gives you a baseline of what is normal for that gender and age group. If you are losing density in the emotional processing area of your brain, then we need to do something about this. This is the hypothesis that we are working with at Gates Brain Health: to treat with diet, anti-inflammatory, supplementation and targeted neuroplasticity exercises to build density in certain areas of the brain based on the MRI with DTI.
Typical care after a concussion:
There is much confusion surrounding concussions but there IS an explanation, it IS a visible injury if the right imaging is ordered.
There is still much to be discovered about Chronic Traumatic Encephalopathy and there have been great strides made recently in being able to diagnose while the patient is still alive. We need to be more aware and cautious of the implications of subconcussive brain injuries and raise awareness that would result in healthy changes made and support for players and military dealing with symptoms of CTE.
If you are ready to begin your path to healing or have any questions, contact us at (775) 507-2000 or email email@example.com
This Article by Gemma Ward based on information shared by Dr. Gates here.
1. News Articles: Top 20 Notorious Cases of CTE Head Injuries and NFL Players with CTE
2. Articles: Meet Bennet Omalu and When Bennet Omalu, MD, Identified a Degenerative Brain Disease.
3. Omalu, Bennet I et al. “Chronic traumatic encephalopathy in a National Football League player.” Neurosurgery vol. 57,1 (2005): 128-34; discussion 128-34. doi:10.1227/01.neu.0000163407.92769.ed
5. Mez, Jesse et al. “Duration of American Football Play and Chronic Traumatic Encephalopathy.” Annals of neurology vol. 87,1 (2020): 116-131. doi:10.1002/ana.25611
8. Image Hussain, Rashad et al. “Neurodegenerative Diseases: Regenerative Mechanisms and Novel Therapeutic Approaches.” Brain Sciences 8.9 (2018): 177. Crossref. Web
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11. Mez, Jesse et al. “Duration of American Football Play and Chronic Traumatic Encephalopathy.” Annals of neurology vol. 87,1 (2020): 116-131. doi:10.1002/ana.25611
12. Image. Copyright © 2019 The Authors. Annals of Neurology published by Wiley Periodicals, Inc. on behalf of American Neurological Association. This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.
13. Mez J, Daneshvar DH, Kiernan PT, et al. Clinicopathological Evaluation of Chronic Traumatic Encephalopathy in Players of American Football. JAMA. 2017;318(4):360–370. doi:10.1001/jama.2017.8334
15. Lepage, Christian et al. “Limbic system structure volumes and associated neurocognitive functioning in former NFL players.” Brain imaging and behavior vol. 13,3 (2019): 725-734. doi:10.1007/s11682-018-9895-z
16. Image Baugh, C. et al. “Chronic traumatic encephalopathy: neurodegeneration following repetitive concussive and subconcussive brain trauma.” Brain Imaging and Behavior 6 (2012): 244-254.