By Emma Tinney, PhD candidate at Northeastern University

Recovering from a traumatic brain injury (TBI) is about more than just medical treatment—it’s about getting back to daily life, including physical activity. Regaining strength, endurance, and confidence can feel daunting, but regular exercise is one of the keys to improving your brain health, cognitive function, and overall well-being. With the right approach, individuals can safely ease back into movement and enjoy the benefits of an active lifestyle after a TBI. 

The Importance of Exercise after TBI

Physical activity is a powerful way to support your long-term health. Research suggests that regular exercise could prevent up to 5.3 million deaths worldwide each year from non-communicable diseases. Beyond the physical benefits, staying active is crucial for brain health, helping with memory, processing speed, and executive function—areas often impacted by TBI^1,2,3,4.

However, many people with TBI face challenges making it harder to stay active, such as cognitive difficulties, physical limitations, and environmental barriers. Finding practical solutions to these obstacles can make exercise more accessible and sustainable.

Common Challenges to Exercise after TBI

1. Cognitive Barriers:
   • Difficulty planning and sticking to exercise routines due to executive functioning⁵
   • Memory issues that make it hard to remember workout schedules or goals
   • Attention deficits can make structured or group activities feel overwhelming⁶
2. Physical Barriers:
   • Challenges with movement due to motor impairments, balance issues, or chronic pain⁷
   • Fatigue, a common consequence of TBI, can make exercise feel exhausting rather than energizing
3. Environmental Barriers:
   • Limited access to adaptive fitness programs and
   • Lack of social support, which may reduce motivation to engage in exercise^8,9

Without regular exercise, individuals with TBI are at higher risk for cardiovascular disease, metabolic syndrome, and neurodegeneration—conditions which are especially common in this population¹⁰. Inactivity can also impact cognitive and emotional resilience, potentially worsening disability over time.

The Cognitive Benefits of Exercise in TBI Recovery 

While more research is needed, studies suggest that exercise can support cognitive function^11,12,13,14, particularly in:

• Thinking and decision-making skills (how quickly you process information, adapt to changes, and control impulses)
• Memory (short-term memory for daily tasks and long-term memory for past events)
• Reaction time and coordination (how fast you respond to things and how well your brain and body work together)

For individuals with TBI, these benefits may be even more significant due to the brain’s ability to adapt after injury. However, not all cognitive challenges improve equally with exercise. For example, if memory is a primary concern, combining physical activity with cognitive rehabilitation may be especially helpful.

Practical Tips for Safely Resuming Exercise after TBI

1. Start Slow & Listen to Your Body
   • Begin with low-impact activities like walking, gentle yoga, or seated exercises
   • Pay attention to signs of fatigue, dizziness, or headache, and adjust accordingly
2. Create a Structured Routine
   • Use reminders, apps, or written schedules to keep track of workouts
   • Set small, achievable goals to build consistency and confidence
3. Incorporate Balance & Coordination Training
   • Exercises like tai chi or stability ball movements can help improve balance and reduce fall risk
4. Modify Workouts to Accommodate Physical Challenges
   • Adaptive equipment and seated exercises can provide accessible options
   • Resistance bands and body-weight movements can help rebuild strength safely
5. Engage in Social or Supervised Exercise
   • Working out with a friend, caregiver, or physical therapist can provide motivation and support
   • Group classes tailored to individuals with neurological conditions may offer a sense of community
6. Monitor Progress & Adjust as Needed
   • Track improvements in endurance, strength, or daily energy levels.
   • Celebrate small milestones to stay motivated

Moving Forward with Confidence 

Reclaiming your fitness after a TBI is a journey that requires patience, adaptation, and resilience. While challenges exist, they can be navigated with the right strategies and support. By gradually incorporating movement into daily life, individuals with TBI can experience the profound benefits of exercise—not just for physical health, but for cognitive function, emotional well-being, and overall quality of life.

If you’re on this journey, know that progress is possible! With every step forward, you’re that much closer to reclaiming strength, confidence, and independence.

You can download this helpful infographic here.

References:

1. Cabral DF, Rice J, Morris TP, Rundek T, Pascual-Leone A, Gomes-Osman J. Exercise for Brain Health: An Investigation into the Underlying Mechanisms Guided by Dose. Neurotherapeutics. 2019;16(3):580-599. doi:10.1007/s13311-019-00749-w
2. Erickson KI, Hillman C, Stillman CM, et al. Physical Activity, Cognition, and Brain Outcomes: A Review of the 2018 Physical Activity Guidelines. Med Sci Sports Exerc. 2019;51(6):1242-1251. doi:10.1249/MSS.0000000000001936
3. Bherer L, Erickson KI, Liu-Ambrose T. A Review of the Effects of Physical Activity and Exercise on Cognitive and Brain Functions in Older Adults. J Aging Res. 2013;2013. doi:10.1155/2013/657508
4. Gomez-Pinilla F, Hillman C. The Influence of Exercise on Cognitive Abilities. Compr Physiol. 2013;3(1):403-428. doi:10.1002/cphy.c110063
5. Stuss DT. Traumatic brain injury: relation to executive dysfunction and the frontal lobes. Curr Opin Neurol. 2011;24(6):584. doi:10.1097/WCO.0b013e32834c7eb9
6. Allan JL, McMinn D, Daly M. A Bidirectional Relationship between Executive Function and Health Behavior: Evidence, Implications, and Future Directions. Front Neurosci. 2016;10. doi:10.3389/fnins.2016.00386
7. Basford JR, Chou LS, Kaufman KR, et al. An assessment of gait and balance deficits after traumatic brain injury. Arch Phys Med Rehabil. 2003;84(3):343-349. doi:10.1053/apmr.2003.50034
8. Burgess C, Tian EJ, Tyack E, Kumar S. Barriers and enablers to physical activity for individuals living with traumatic brain injury: a mixed methods systematic review. Brain Inj. 2024;38(14):1157-1170. doi:10.1080/02699052.2024.2381053
9. Hamilton M, Khan M, Clark R, Williams G, Bryant A. Predictors of physical activity levels of individuals following traumatic brain injury remain unclear: A systematic review. Brain Inj. 2016;30(7):819-828. doi:10.3109/02699052.2016.1146962
10. Kursancew ACS, Faller CJ, Piva-Uchida EM, et al. Metabolic disorders after traumatic brain injury: a narrative review of systemic consequences. Metab Brain Dis. 2025;40(1):93. doi:10.1007/s11011-024-01524-3
11. Lal A, Kolakowsky-Hayner SA, Ghajar J, Balamane M. The Effect of Physical Exercise After a Concussion: A Systematic Review and Meta-analysis. Am J Sports Med. 2018;46(3):743-752. doi:10.1177/0363546517706137
12. Morris TP, Tormos Muñoz JM, Cattaneo G, Solana-Sánchez J, Bartrés-Faz D, Pascual-Leone A. Traumatic Brain Injury Modifies the Relationship Between Physical Activity and Global and Cognitive Health: Results From the Barcelona Brain Health Initiative. Front Behav Neurosci. 2019;13. doi:10.3389/FNBEH.2019.00135
13. Morris T, Gomes Osman J, Tormos Muñoz JM, Costa Miserachs D, Pascual Leone A. The role of physical exercise in cognitive recovery after traumatic brain injury: A systematic review. Restor Neurol Neurosci. 2016;34(6):977-988. doi:10.3233/RNN-160687
14. Sharma B, Allison D, Tucker P, Mabbott D, Timmons BW. Cognitive and neural effects of exercise following traumatic brain injury: A systematic review of randomized and controlled clinical trials. Brain Inj. 2020;34(2):149-159. doi:10.1080/02699052.2019.1683892

By Katianne Olson

“Daddy fell and hit his head pretty bad and won’t be home for a little bit. He’s at the hospital, but he’s strong and fighting really hard to get better.”

Those were the first words I said to my almost 4-year-old daughter Piper the day after learning about my husband Chase’s traumatic brain injury (TBI). It was the dreaded conversation I knew needed to happen sooner rather than later. Our two children, Piper and Caden, were used to my husband’s shift schedule since he’s a firefighter, but this was going to be longer than just the 48-hour overtime shift he occasionally worked. Though first responder kids have a strength of their own when it comes to being flexible, this was going to be a whole new ballgame.

I sat in her bedroom, staring at her big blue eyes and curly blonde hair, wondering if this was just a horrible nightmare. I quickly realized this wasn’t something I was going to wake up from. It was the reality I was facing.

“Is he ok? When will he be home?” she asked.

I went numb. I tried to speak … but nothing came out. I took a deep breath as my mind went racing. How do I tell her I’m not sure?  How much do I tell her?  How do I tell Caden (who was almost one year old at the time) that the “Da-Da-DADA” he’s been gabbing about all morning is fighting for his life?”

I took a quick pause and decided regardless of how young my children were, I was going to be transparent with them. Did I nail that conversation? Far from it. Did I question myself? 1000%. My hope was simply to instill the courage and bravery we were going to need to help the person we love the most navigate a TBI. That means I had to start with the truth – regardless of how much uncertainty it brought.

(Caden, left, 11 months and Piper, right, almost 4)

After that emotional conversation, I googled every variation of “how to explain a brain injury to young kids,” browsed my local library, searched endlessly on Amazon—only to be left frustrated and angry. I kept hitting dead ends. As a special education teacher who is passionate about inclusion and disability awareness, I thought, “How is there nothing out there on brain injuries for children?”

It was during that very hard conversation the concept of The Resilient Brain: Understanding Traumatic Brain Injury for Kids was created in my heart.

We‘re all at risk of experiencing a concussion or TBI and at some point in our life, if not personally, we will most likely know someone impacted by a brain injury. It can be the wrong fall, hit during a sporting event, car accident, or just freak accident. That is our story. The freak accident you never thought would happen to you.

Over the years, there have been many positive improvements: identifying brain injuries, cutting edge rehabilitation facilities, technological advancements, implementing safe return to play guidelines, destigmatizing the mantra of “toughin’ it up,” promoting helmet wearing, among others. The next step: how do we educate and build awareness to be used as empowerment?

One of my favorite quotes is from Maya Angelou who said, “Do the best you can until you know better. Then when you know better, do better.”

We shouldn’t wait until our brain is injured to see how remarkable it is. I’ll be honest and say I was in that category. It wasn’t until navigating my husband’s brain injury that I realized I took my own brain for granted and the incredible power it has given me to experience a life well-lived.

 

In reflecting now almost five years later, I learned quickly how many people face the very same challenges as our family. Our story is just one out of 2.8 million affected by TBI every year. There is nothing mild about brain injury. The long-term impacts, side effects, and overall havoc it can wreak on one’s life and their loved ones can be debilitating. The invisible nature of it all adds another layer of complication. That alone is another reason why awareness and education about brain injuries are so vital.

“When you know better, do better.”

That’s my hope for The Resilient Brain: Understanding Traumatic Brain Injury for Kids. I want it to not only be a guide for those dealing with the effects of TBI but also an educational resource. Though it’s a children’s book, the content is geared for all of us – no matter what age.

 

It is long overdue to give this invisible injury representation and visibility in this world, and that starts with our youngest of readers. A brain injury diagnosis can be dark and scary, but I hope audiences can read The Resilient Brain and understand that not only is the brain resilient, you are resilient as a person, no matter where you are at in your TBI journey.

I’m incredibly honored to bring this message to the world, but this time, with the words to say.

______________________________________________________________________

Katianne (Katie-Anne) Olson is a special education teacher and author of The Resilient Brain: Understanding Traumatic Brain Injury for Kids. She lives in Chicago with her husband and two children.

To learn more about Katianne, visit her website and follow her on Instagram.

By Dr. Chris Nowinski, Concussion Legacy Foundation co-founder and CEO

Concussions and sport-related brain trauma have been in the sports headlines for more than a decade. Nearly 1,000 former athletes have now been diagnosed with chronic traumatic encephalopathy (CTE). Most played football, but ice hockey, boxing, rugby, soccer, and other sports have all seen CTE confirmed in former athletes.

But the public and even scientists have struggled to understand why the number of concussions an athlete has suffered does not predict their odds of developing CTE. Many professional athletes I speak to believe they aren’t at risk for CTE because they only had “one or two concussions,” but that couldn’t be further from the truth.

My colleagues and I believe part of the confusion comes from the word we use to describe head impacts and head injuries – subconcussive – so I wrote an editorial with collaborators from Harvard University, Boston University, the Mayo Clinic, and the Concussion Legacy Foundation that was just published in the British Journal of Sports Medicine, the most influential medical journal on sports medicine.

We believe the problem stems from how we think about concussions. We think of concussions as the hardest hits to the head an athlete receives. But when you look more closely at the research, you are reminded that they are not.

We reviewed published helmet sensor studies and found that around 10% of head impacts experienced by football players are harder than the average concussion. Those hits add up quickly. For example, if a football player takes 1,000 head impacts in a season and had one diagnosed concussion, he took around 100 hits harder than that concussion.

But concussions don’t occur every season. A different study of college football players found for every diagnosed concussion, an athlete takes 340 head impacts harder than that concussion. If we want to focus on where CTE risk is coming from, we should not be looking only at the concussions, but at all other hits, and especially those 340 extreme impacts.

We believe the terminology used to describe hits to the head also causes confusion. Scientists have been referring to head impacts that don’t cause concussion symptoms as “subconcussive impacts,” which implies they are less than concussions. This has even led to CTE experts saying CTE is caused by “small, repetitive impacts.” But when it comes to size of the hit, 10% of head impacts are more than concussions. We recommend replacing “subconcussive” with “nonconcussive” to better describe these impacts. After a head impact, a concussion was either diagnosed or it wasn’t.

The term subconcussive has not only confused the discussion around head impacts, but also around traumatic brain injuries. Studies consistently show that athletes exposed to hundreds of repetitive head impacts, in the absence of a concussion, still have changes to brain function, blood biomarkers of brain injury, and structural changes on imaging that look similar to changes in athletes with diagnosed concussions. The concept of subconcussive injury has been shoehorned into the conversation to explain this “missing link.”

We suggest we stop using “subconcussive injury” because it’s also misleading. The missing link is better described as subclinical traumatic brain injury (TBI). Subclinical TBI happens when there are changes in brain function, biomarkers, or imaging without concussion signs or symptoms.

There is no question in my mind that subclinical TBI happens regularly. Beyond the existing studies showing a link, consider this question: the human brain has about 86 billion neurons – if you injured one neuron, could you feel it? Look at the amazing image below, from a new project at Harvard that scanned 1 cubic millimeter of the human brain, to begin to understand the complexity of the human brain.

Photo credit: Google

We cannot hear when one tree falls in a forest of 86 billion trees. It is well known that someone can suffer a significant brain injury without signs or symptoms, simply because the injury occurred in an area that is not responsible for common concussion symptoms like memory, thinking, vision, balance, hearing, speech, etc.

By changing the nomenclature, we hope to remove some of the mystery as to why concussions do not predict CTE risk, whereas the number and strength of repeated head impacts do. We need to name the impacts and injuries that we can’t see to advance the conversation.

This is analogous to understanding sun exposure and skin cancer. I was putting sunscreen on my kids recently to prevent them from getting sunburn, which is linked to skin cancer. Sunburn is something I can see. Sunburn is something my kids will complain about because it hurts. Sunburn is analogous to concussion, which we can see and people can feel.

But I recently learned from my travels cofounding the Australian Sports Brain Bank that if I lived in Australia, I would be taught to be worried about how much time my children spend in the sun overall, not just sunburn, because “healthy” sun exposure also causes skin cancer. In Australia, some primary schools have a “No Hat, No Play” policy for children at outdoor recess. Thanks to research, Australians realized they cannot just focus on the shiny objects of sunburns to prevent skin cancer, as overall minutes in the sun matter, too.

To me, that sun exposure is analogous to subclinical TBI. We haven’t cared about it because we can’t see it, and athletes don’t complain about it because they don’t feel it. We also haven’t understood the downstream effects – but now we do. To prevent CTE and other outcomes, we need to focus on preventing subclinical TBI, too.

Photo credit: Just A Little Further

The next time you see that big hit in an NFL game and it makes you hold your breath, you shouldn’t necessarily exhale and celebrate just because the player pops up. They may have suffered a subclinical traumatic brain injury that they cannot feel – but may contribute to developing CTE down the road.

I’m not saying you cannot enjoy watching the game. But I hope you choose to support efforts to limit the number and strength of those impacts – such as the new NFL kickoff, or the elimination of hitting in practice, spearheaded by the late Dartmouth coach Buddy Teevens.

By using the right terms to understand what causes CTE, and letting the science drive changes to how we play sports, we can prevent a lot of cases of CTE.

By Dr. Chris Nowinski, Concussion Legacy Foundation co-founder and CEO

This week, I coauthored the largest study ever of CTE in youth, high school and college athletes who died before the age of 30, published here in JAMA Neurology. Led by the brilliant Dr. Ann McKee and the scientists of the Boston University CTE Center and UNITE Brain Bank, and made possible by our amazing Legacy families who donated the brain of a loved one, this study provides important learnings:

1. Nearly half (41.4%) of 152 cases had CTE. As Dr. McKee said, this study clearly shows that the pathology of CTE starts early. The fact that more than 40% of young contact and collision sport athletes in the UNITE Brain Bank have CTE is remarkable – considering that studies of community brain banks show that fewer than 1% of the general population has CTE. To me, it is powerful that so many families correctly predicted their child or husband had CTE. It suggests three possible things, at least one of which must be true:

• CTE causes telltale symptoms in young people.
• CTE does not cause symptoms in young people, but the head hits and concussions those athletes suffered are causing chronic symptoms.
• CTE is far more widespread in young people with high exposure to contact sports than we want to believe.

We need to study more young brain donors not exposed to contact and collision sports, to better understand which symptoms are related to concussions, RHI, and CTE.

2. The study includes the first women’s soccer player diagnosed with CTE, a 28-year-old collegiate soccer player from the United States whose identity remains private. Last month, the first female athlete was diagnosed with CTE by the Australian Sports Brain Bank, which we cofounded in 2018. Heather Anderson was a 28-year-old Australian Football League player. With two young female athletes diagnosed with CTE in two months, we look forward to engaging with women’s sports organizations and leaders to discuss CTE Prevention Protocols.

3. The majority of subjects did not have CTE. “The study suggests that some of the symptoms these young athletes are experiencing are not caused by the early tau pathology of CTE,” said Dr. McKee. “It is imperative that young athletes who are experiencing neuropsychiatric symptoms seek out care, as it is likely that the symptoms can be reduced with effective management and follow-up.” If you or someone you love is experiencing symptoms, please reach out to the CLF HelpLine for doctor recommendations and support.

Clinical symptoms were common among the athletes, whether or not they had CTE, including: depression (70.0%), apathy (71.3%), difficulty controlling behaviors (56.8%), and problems with decision making (54.5%). Substance abuse also was frequent, with alcohol abuse present in 42.9% and drug abuse in 38.3%.

4. Nearly all the young athletes had mild CTE, stages 1 and 2; although 3 donors had CTE stage 3. (There are 4 possible stages of CTE with stage 4 being the most severe). To put that in perspective, three college football players who died before 30 had more severe CTE pathology than Junior Seau. In those with CTE, there was often other evidence of brain injury, including the presence of a cavum septum pellucidum, enlargement of the ventricles, and more perivascular macrophages in the white matter.

5. CTE is not just a problem for professionals. Amateur athletes comprised 71.4% of those diagnosed with CTE, and included American football, ice hockey, soccer, and rugby players, and wrestlers. Those diagnosed with CTE were older (average age at death 25.3 years vs. 21.4) and had significantly more years of exposure to contact sports (11.6 vs 8.8 years). Like all brain bank studies, the brain donors are different from the general population of young athletes, in part because they are more likely to have symptoms. CTE cannot yet be diagnosed in the living, and the true prevalence of CTE in any population remains unknown.

6. We cannot thank our donor families enough. I still call families after learning they have lost a loved one, and it’s hardest calling parents who have lost a child and young wives who have lost a husband, often with young children. Almost all these deaths are unexpected, so families are less likely to initiate brain donation by calling BU – instead, they hear from me within 72 hours of losing their loved one. The fact that we had 152 people in this study reminds me of the best of humanity – these families, in their saddest moments, were still focused on helping others.

7. Finally, I have tremendous respect for Mike and Kia Locksley sharing that their son Meiko was part of the study and diagnosed with CTE. Meiko was murdered in 2017 at the age of 25. Mike is the head football coach at the University of Maryland. Watch Mike and Kia share with the New York Times why they went public, and what they hope will come from this research.

If this study makes you as uncomfortable as it makes me and you want to make a difference today, sign up for our research registry, or consider making a donation.

For more information about the BU CTE Center, the UNITE Brain Bank, and CTE, please visit www.bu.edu/cte. The study was primarily funded by The Department of Veterans Affairs, NINDS and NIA, part of NIH, the Buoniconti Foundation, and the Mac Parkman Foundation.

The Boston University CTE Center has diagnosed CTE in 345 of 376 (91.7%) NFL players studied at the UNITE Brain Bank since it was co-founded in 2008 by Boston University, the VA Boston Healthcare System, and the Concussion Legacy Foundation. Below are 10 NFL draft picks from the last 20 years who went on to suffer, and later be diagnosed, with the neurodegenerative brain disease.

1. Max Tuerk – 2016 NFL Draft, Round 6, Pick 3

The San Diego Chargers selected USC center Max Tuerk with the third pick of the third round in 2016. Shortly after the draft, Tuerk began isolating himself and stopped communicating with his family. He grew increasingly paranoid and struggled with hallucinations, psychosis, and extreme depression. By the middle of the 2017 season, Tuerk was out of football, and his symptoms made it difficult to maintain a job. In 2020, he collapsed on a hiking trail in his hometown, where he died at 26 from an enlarged heart. Diagnosis: Stage 1 CTE

Photo credit: Gregory Bull/Associated Press

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By Dr. Chris Nowinski, Concussion Legacy Foundation co-founder and CEO

Today the Boston University CTE Center released they have now diagnosed CTE in 345 of 376 (91.7%) NFL players studied at the UNITE Brain Bank since it was co-founded in 2008 by Boston University, the VA Boston Healthcare System, and the Concussion Legacy Foundation. These numbers are updated from the 2017 publication in the Journal of the American Medical Association that reported 110 of 111 NFL players (99%) had CTE.

A lot has happened since that 2017 study that helps us interpret what these new NFL numbers mean. Before we get to that, the goal of releasing the numbers is to drive those at risk for CTE to resources and research.

“While the most tragic outcomes in individuals with CTE grab headlines, we want to remind people at risk for CTE to know that those experiences are in the minority,” said Ann McKee, MD, director of the BU CTE Center and chief of neuropathology at VA Boston Healthcare System. “Your symptoms, whether or not they are related to CTE, likely can be treated, and you should seek medical care. Our clinical team has had success treating former football players with mid-life mental health and other symptoms.” Here are links to resources and research opportunities:

1. Symptoms that could be related to CTE or concussion can be effectively treated. Reach out to the CLF HelpLine for treatment recommendations and support.
2. CLF is collaborating with the BU CTE Center to learn how to prevent, diagnose and treat CTE and other symptoms related to head impacts, including Project S.A.V.E., which is recruiting men and women over the age of 50 who played contact sports. To learn about studies with active recruiting, click here.
3. To sign up for our research registry to be informed of future studies, click here.

It is difficult even for experts to interpret what 345 of 376 NFL players having CTE means. Here are some ways to understand the data:

1. The study does not necessarily mean that 92% of all current and former NFL players have CTE. Brain bank samples are subject to selection biases. The prevalence of CTE among NFL players is unknown since CTE can only be definitively diagnosed after death.
2. College, high school, and youth players face lesser odds of being diagnosed with CTE. A 2020 study from the UNITE Brain Bank found the odds of being diagnosed with CTE increase by 30% per year of football played.
3. The odds of an NFL player getting CTE appear extraordinarily higher than people who haven’t played contact sports. For comparison, a 2018 Boston University study of 164 brains of men and women donated to the Framingham Heart Study found that only 1 of 164 (0.6 percent) had CTE. The lone CTE case was a former college football player. The extremely low population rate of CTE is in line with similar studies from brain banks in Austria, Australia and Brazil.
4. The data provides more evidence that repeated traumatic brain injuries and repetitive head impacts cause CTE. In 2022 we published a review of the CTE literature and concluded the evidence is overwhelming that sports like football cause CTE. The National Institutes of Health agreed and three months later updated their definition of CTE.
5. As the study sample size grew, we expected the 99% odds from 2017 to decrease to something closer to the actual prevalence. The small drop in odds from 99% to 92% with a much larger sample is concerning. In 2017, CTE critics said we were getting “the worst of the worst” in those first eight years of the brain bank, so the 99% number was meaningless. In the intervening six years, we’ve more than tripled the sample size, and yet still more than 90% of players have CTE.

This leaves us with two important questions:

1. Does the high CTE odds suggest that if we were able to diagnose CTE in the living, we’d learn that a very high share of NFL players (>50%) have CTE?
2. Or, if we are still getting the worst of the worst, most symptomatic cases, does that mean that among NFL players, CTE can be easily diagnosed by families? If so, how can we turn that into a diagnostic protocol for doctors?

CLF is here for current and former NFL players and their families who may be worried about CTE. Submit a form to the CLF HelpLine and our staff will be in touch to provide personalized support and resources. We also offer Zoom support groups for suspected CTE patients and caregivers to discuss shared experiences. Learn more here, and know above all: you are not alone, and help is available.

We are very grateful to our Legacy Donors and their families for making this research possible, and the for the scientists for their commitment to understanding and treating CTE. Without their contributions, we wouldn’t know anything about CTE, or have any new data to release. Read their stories here.

By Dr. Chris Nowinski, Concussion Legacy Foundation co-founder and CEO

Monday, Miami Dolphins head coach Mike McDaniel announced quarterback Tua Tagovailoa was placed in the concussion protocol after he “displayed and admitted to having concussion symptoms” after their loss to the Green Bay Packers on Sunday night.

This is likely Tua’s third concussion of the season, after what appeared, from my perspective, to be an obvious concussion on September 25 that the team refused to call a concussion, followed by a clear concussion on September 29 where Tua was knocked unconscious and showed decorticate posturing. Decorticate posturing is a rare brain injury sign more often seen in stroke victims, suggesting a more serious injury.

What happens next is important for Tua’s career and his life, and it’s an important teaching moment, so I’ve shared some insights below. It’s also a stark reminder of how much work we have ahead of us to continue to change the conversation on concussions.

1. Tua is in the concussion protocol, but does he have a concussion?

• Almost certainly, yes, Tua has a concussion. The team reported Tua “displayed and admitted to having concussion symptoms” on Monday. Self-report of concussion symptoms after a head impact is the gold standard for diagnosis, specifically when the patient has experience with concussions. Unfortunately, Tua knows all too well what a concussion feels like.
• We also have a clear possible mechanism for concussion. Tua’s concussion was not diagnosed during the game, but looking back at the film there is a clear head to ground impact that preceded a decline in his performance. Finally, he is also displaying signs of concussion. Therefore, it would be nearly impossible for a physician to conclude he did not suffer a concussion.

2. Will the Miami Dolphins diagnose him with a concussion?

• It would seem reasonable if Tua has a concussion, he will be diagnosed with a concussion. However, because there is no objective test for concussion, a diagnosis is not certain. Remember, on September 25, Tua showed 5 unique concussion signs after a head impact:
  • He grabbed his head in pain
  • He stumbled when he stood
  • He “shook off the cobwebs” and moved his head side-to-side (which you only do in the instance of a concussion)
  • He fell
  • He then had to be held up by his teammates
• But after initially calling it a concussion, the team claimed those five signs were somehow caused by a “back injury” earlier in the game and returned him to play. They stuck with this story all week, refusing to put Tua in the formal protocol, yet they also said they tested him for a concussion for three days before the Thursday night game.
• The Dolphins have a poor track record on this, and there are other possible diagnoses teams have made in these situations. Those of us following this field over the last 20 years remember the NFL used to call concussion symptoms a “traumatically-induced migraine” (here is Terry Glenn in 2002) and let players continue to play. Earlier this month, the captain of the England rugby team said his long-term symptoms after a concussion are actually due to nerve injuries in his neck. In both situations, there is no test that can differentiate those injuries with certainty – it’s the doctor’s call. 10 years ago, it wouldn’t surprise me to see one of those two diagnoses reported for Tua. But because the Dolphins are now under a microscope, I cannot imagine they’ll try to give an alternative diagnosis again.

3. How did the NFL spotter miss this?

• In retrospect, it’s easy to suggest the video of Tua’s head hitting the ground is the concussion, but to my knowledge, Tua didn’t show concussion signs after the impact (like stumbling again), so it wouldn’t have triggered a call down and automatic removal. Changing the protocol wouldn’t fix this unless we want everyone to come out of the game when their head hits the ground.

4. Why did Tua wait until Monday to report his symptoms?

• Most likely, he didn’t “wait” until Monday. We should give him the benefit of the doubt and assume he didn’t notice his symptoms until he woke up the next day. If you are hit hard enough to have a concussion, you have been through some serious trauma, which the body can compensate for with a burst of adrenaline or other responses that can mask the subtle symptoms of a concussion. Concussion symptoms are often delayed by a day or two. In addition, we cannot expect players with malfunctioning brains to recognize their brains are malfunctioning. Instead, we should respect Tua for reporting his symptoms. Most concussions show no outward signs, and NFL players often choose to not report their symptoms because they fear that when they are put in the protocol, they might lose their job.

5. Will Tua play again this season?

• Tua should not play again this season. Full stop. But the Dolphins should make the playoffs, which could give Tua enough time to become asymptomatic and clear the concussion protocol. What Tua may not know is that the concussion protocol is imperfect and is not the only variable to consider when deciding whether to return this season. Clinical experience (and my personal experience) suggests that the more concussions one has, and the closer together they are, the longer they take to recover from, and the more likely symptoms are to become permanent. Tua would be further risking his career to return this season, but a doctor may not be willing to tell him that.
• The Dolphins will likely send Tua to multiple doctors around the country for PR reasons as they consider what to do. The doctors that pro teams refer professional athletes to in these situations are often the doctors that are most likely to tell the team what they want to hear – that there is no permanent damage, and it is safe to return. Consider it from the team’s perspective – would you keep sending players to a doctor who often advises them to sit out when have no symptoms if you could send them to many other doctors who will tell them to play? Conservative doctors may stop getting referrals.

6. Is Tua “concussion-prone” and should he retire?

• It’s not fair to Tua to label him as concussion-prone, and he does not have to retire. A cluster of concussions, or even long-term symptoms, does not prevent a successful return or long career. Remember a decade ago when people were predicting Sidney Crosby would need to retire after fighting concussions? He’s still playing. Tua has had multiple concussions this season, but I’d argue his medical management of his September 25 apparent concussion is to blame – Tua’s been playing football a long time and never had issues before. Let’s hope, given proper rest, he doesn’t again.
• However, Tua should receive all the support he needs in his recovery, including mental health support. There is no good data on what happens to athletes after three concussions in three months because it is so rare. The anecdotes, however, are concerning. I recently counselled a professional athlete and connected him to better medical resources after he suffered three concussions in the last year and attempted suicide.

7. What does Tua’s experience mean for other athletes?

• No one is being watched more closely for concussions right now than Tua. Yet everyone missed it – the NFL spotters, the team medical staff, the coaches, the announcers, and the players on the field. If we can’t spot Tua’s concussion, what are the chances we do a good job spotting the concussions of youth athletes, who don’t have the benefit of 30 medical professionals at each game, multiple camera angles and replays, coaches and teammates who know what concussions look like, and the experience of having had prior concussions? That’s why we launched our Stop Hitting Kids in the Head Campaign, which encourages parents to choose non-contact sports for their kids before high school. For children, our primary focus should be concussion prevention.

By Adam Finkel, ScD & Chris Nowinski, PhD

The five questions below about repetitive head impacts (RHI) and CTE are based on natural observations that are frequently made by sports organizations, former athletes, and even some physicians.

Unfortunately, they have been inappropriately used by doctors associated with sports leagues, including NFL advisors and NFL- and NHL-sponsored neuropsychologists, to trivialize CTE or to attempt to refute that RHI causes CTE, and that CTE causes dementia.

We wrote this blog to clear up any confusion and to accompany our recent publication on CTE causation, Applying the Bradford Hill Criteria for Causation to Repetitive Head Impacts and CTE.

It’s important to note these five questions do not provide actual counterevidence, only anecdote. However, none of the observations below, even if they were supported by data rather than anecdote, cast any doubt on the conclusions that RHI causes CTE and that CTE is a grave disease.

Sometimes analogy can be helpful. Everyone has known for decades that smoking causes lung cancer. Imagine if someone told you

“Smoking doesn’t cause lung cancer, because…”

I heard of someone who smoked heavily and didn’t get lung cancer…
I heard of someone who got lung cancer but never smoked…

or

“Lung cancer doesn’t cause serious symptoms, because…”

I heard of someone whose lung cancer was mild…
I heard of someone who was short of breath but didn’t have lung cancer…

Or

“It’s OK for that child to smoke two packs-a-day because…”

I heard they plan to stop by age 18.

Would any of these statements change your mind about whether cigarette smoking causes lung cancer? Of course not. It’s not surprising to hear these statements from some physicians, neuropsychologists, or researchers if they don’t have training in public health. But public health professionals, trained in interpreting evidence, never offer these statements to doubt causation.

Adapted by Nowinski CN & Finkel AM from Brand KP, Finkel AM. A Decision-Analytic Approach to Addressing the Evidence About Football and Chronic Traumatic Encephalopathy. Semin Neurol. 2020 Aug;40(4):450-460.

By Dr. Chris Nowinski, Concussion Legacy Foundation co-founder and CEO

As the lead author of the 2nd through 5th Consensus Statement on Concussion in Sport, Dr. Paul McCrory may be the most influential neurologist in sports over the past 20 years. The Statement is famous for both its extraordinary conflicts of interest and for downplaying the link between head impacts and CTE.

The conference that produces updated statements is funded or organized by international sports governing bodies like FIFA and the IOC and 32 of the 36 authors have financial ties to organized sports. Some have suggested that their statement on CTE, “a cause-and-effect relationship has not yet been demonstrated between chronic traumatic encephalopathy and sport related concussion and exposure to contact sports” is critical to successfully defend class-action lawsuits from former athletes. (In contrast, the CDC CTE Fact Sheet says evidence demonstrates a cause-and-effect relationship).

Over the last month, McCrory has had two editorials retracted for plagiarism, faces additional allegations of plagiarism, and is being asked to explain how he treated athletes with concussion symptoms during a time the Medical Board of Australia said he was not allowed perform neurodiagnostic procedures. I also wrote a blog about how he has also misrepresented BU’s research in public talks.

While we’re looking into McCrory’s influence on the global CTE conversation, would you be surprised to learn he is a was also one of the key promoters of the theory that CTE can be caused by the use of opioids? Professional sports organizations embraced it and repeated it because they know their athletes suffer injuries that often require surgery and the use of painkillers. In 2015, McCrory was senior author on an opinion piece that questioned the link between CTE and sports, claiming:

“The correlation between opioid abuse and hyperphosphorylated tau deposition is well described, and should be factored as a key variable in any assessment of causation [in CTE].”

We reached out to the world’s expert on how opioids and alcohol impact the brain neuropathologically, and in the following video he debunks McCrory’s nonsensical claim that CTE could be caused by substance abuse. Dr. Gabor Kovacs is an internationally renowned neuropathologist and researcher in the field of neurodegenerative diseases. In 2021, he received the Alfred Meyer Memorial Lecture and Prize from the British Neuropathological Society for his expertise on tau-related conditions. He is currently affiliated with the University of Toronto and the University Health Network (UHN), where he holds numerous roles including consultant Neuropathologist at the Laboratory Medicine Program at the UHN, Principal Investigator at the Tanz Centre for Research in Neurodegenerative Disease, and Senior Scientist at the Krembil Brain Institute.

By Dr. Chris Nowinski, Concussion Legacy Foundation co-founder and CEO

Over the past nine days the sports concussion and chronic traumatic encephalopathy (CTE) community has been rocked by multiple allegations of plagiarism against Professor Paul McCrory, lead author of the 2nd to 5th Consensus Statements on Concussion in Sport, which has led to multiple retractions and a dark cloud hanging over his career and any scholarship he has touched. This blog by Dr. Nick Brown outlines multiple other instances of possible plagiarism by McCrory.

McCrory has been perhaps the most influential voice representing professional sports organizations in their organized efforts to minimize and dismiss the evidence that repeated hits to the head – like those in American and Australian football, soccer, and rugby – can cause CTE. He famously belittled CTE as ”all the carry on and hoo-ha you get from the United States” in a 2016 lecture at the University of Melbourne Florey Neuroscience Institute.

A close view of that 2016 lecture reveals something potentially even more concerning than plagiarism. In his presentation, attended by a VIP audience including former AFL chief executive Ross Oakley and members of the media, McCrory dramatically misrepresented research by Boston University in ways that minimized CTE.

Before I delve into those examples, I’ll provide some background on why McCrory’s statements on CTE matter so much.

Background

The 5th Consensus Statement on Concussion in Sport, published in 2017, is the most influential document of the last decade because of one sentence deep in the document, “A cause-and-effect relationship has not yet been demonstrated between CTE and SRCs (sports-related concussions) or exposure to contact sports.”

Even by 2017, that statement did not align with the views of two of the top U.S. government officials leading CTE research, Dr. Walter Koroshetz, the director of the National Institute of Neurological Disorders and Stroke (NINDS), and Dr. Dan Perl, the head of the CTE brain bank for the U.S. Department of Defense, who both went on record in 2014 saying cause and effect was demonstrated to their satisfaction. From ESPN:

Asked about Goodell’s statement that medical people will decide if there is a link between football and brain damage, Perl said, “I think they have decided. At least some of us have.” Perl acknowledged there may be contributing factors but added: “CTE is only seen in the setting of repeated head trauma. At the end of the day, this is produced by head trauma. I’m sorry, that’s what all the research says.”

Koroshetz, of the NIH, agreed that advanced CTE cases are clearly related to head trauma. “I don’t think there’s any wiggle room,” said Koroshetz, adding that some of the earlier cases may be less certain. “It’s pretty clear this is due to head injury. Whether there are other things involved, and when it starts, that’s hard to know, but I don’t think there’s any question that it’s related to head injury.”

The National Football League went on record in 2016 at a Congressional hearing acknowledging the link.

Organizations like the NHL relied on the consensus statement to claim that causation had not been demonstrated. The NHL was fighting a lawsuit from retired players and regularly cited the consensus statements while defending its inactions.

The Consensus Statement is organized and written by members of the Concussion in Sport Group, and the meeting is sponsored by IOC, Fédération Internationale de Football Association (FIFA), International Federation for Equestrian Sports (FEI), World Rugby (WR) and the International Ice Hockey Federation (IIHF). It has been the subject of exposes from the Canadian Broadcasting Corporation, the Guardian, and the Dutch newspaper NRC because 32 of 36 members had ties to professional sports leagues. 5th annual conference co-chair McCrory, who played a leading role in selecting the members, has advised the Australian Football League, FIFA,and the IOC, has received funding from the NFL, and has served as an expert witness for the NHL.

The Lecture: “The Concussion “Crisis” – Media, Myths and Medicine”

With that background, we’ll now explore how McCrory misrepresented the research of Boston University on CTE at a 2016 lecture at the University of Melbourne Florey Neuroscience Institute, according to their 2015 annual report, he served as a professor and senior researcher,

Example 1: The first time McCrory misrepresents the research from Boston University is at 6:40, where he says,

“And the feared CTE that you’ve heard about… the best guess from the group that is pushing this most strongly says the risk is about 4% of retired athletes get it. The other way of looking at it is that 96% of athletes do not get it. Yet if you read the media, particularly from the United States, you get a very different perspective.

That is not what Boston University said. Here is the passage from which he gets the 4% number:

If one considers the prevalence in deceased professional American football players who died between February 2008 and June 2010, there were 321 known player deaths and the brains of 12 of the 321 underwent postmortem neuropathologic examination at Boston University Center for the Study of Traumatic Encephalopathy (BU CSTE). All 12 examined neuropathologically showed evidence of CTE, suggesting an estimated lifetime prevalence of at least 3.7%. If one assumes that all deceased players who did not come to autopsy did not have CTE and that the amount of head trauma in professional football has remained fairly constant over the past five decades, a prevalence of 3.7% would result. Although this represents a conservative estimate, it suggests a significant public-health risk for persons who suffer repetitive mild traumatic brain injury (TBI).

The passage is meant to infer that even if we found the only 12 cases of CTE among those 321 NFL players, it’s a major public health problem. But the paper also makes it clear that 3.7% is an absolute minimum prevalence, it is unlikely those were the only 12, and it was still statistically possible at that time that 100% of NFL players had CTE. Therefore, when McCrory said that BU said “the risk is 4%,” he is misrepresenting the research.

McCrory made the same claim in a 2013 publication, where he went further, claiming that if our 12 NFL CTE cases (out of 12 brains studied) represented all NFL CTE cases ever, “the incidence rate would be less than 0.01%.”

Journalist Wendy Carlisle was so befuddled by McCrory’s claims that in 2014 she wrote him this letter where she pointed out his misrepresentation and asked, “Why did you think it was methodologically valid to look at all the professional players who were ‘at risk’ i.e.- all those who have ever played professional football and then analyze them against the cohort of autopsied brains of players who died between Feb 2008 and June 2010?”

It’s a great question.

Example 2: The more egregious misrepresentation of the research of Boston University takes place at 31:30, where McCrory says,

“The biggest group in the world pushing this area is the Boston University Group, led by Ann McKee and Bob Cantu, and they’ve presented 64 athletes with “so-called” CTE. But interestingly, a fifth of them had no actual pathology. Yet they’re labeled as CTE. Doesn’t really make sense.”

This is an incredible misrepresentation of a 2013 study I co-authored and that is not what the publication actually says. It is not true that “a fifth of the 64 athletes diagnosed with CTE had no pathology.” Dr. McCrory appears to be referring to this passage on page 60.

We analyzed the brains of 85 individuals with a history of repetitive mild traumatic brain injury and found evidence of CTE in 80%; all males, ranging in age from 17 to 98 years (mean = 59.5 years), including 64 athletes, 21 military veterans (most of whom were also athletes) and one individual who engaged in self-injurious head-banging behavior.

100% of the 64 athletes diagnosed with CTE had CTE. What McCrory does not appear to understand is that throughout the paper we note that most of our Veterans were also athletes, so when we mention athlete and Veteran numbers, some are double counted. It is important for interpreting the data, so the point is raised in the second sentence of the abstract:

We analyzed post-mortem brains obtained from a cohort of 85 subjects with histories of repetitive mild traumatic brain injury and found evidence of chronic traumatic encephalopathy in 68 subjects: all males, ranging in age from 17 to 98 years (mean 59.5 years), including 64 athletes, 21 military veterans (86% of whom were also athletes) and one individual who engaged in self-injurious head banging behavior.

I have never seen anyone make the mistakes that McCrory has made in referencing our studies, including members of the media without medical training, bloggers, or even laypersons on their social media accounts.

These are not the only examples of McCrory misrepresenting the research of others in a way that minimizes CTE. History Professor Stephen Casper has pointed out that McCrory consistently made mistakes in citing the work of others, even making the false claim that Harrison Martland’s seminal 1928 article Punch Drunk was based on the examination of only one patient when it was five.

McCrory also makes an unfathomable error at 19:15 interpreting the number of concussions caused by sports and recreation in America, saying:

Most people think football is the big one but it’s not. In America, where we have the best statistics, the numbers of concussions – sport-related concussion I’m talking about – are probably in the order of 40 million cases a year, if you allow for the unreported cases. If you go on the U.S. Census data it’s probably10 times greater than that again.

McCrory is confused here. He is citing data from a 2006 study from the CDC. But what he doesn’t appear to understand is that the 1.6 to 3.8 million figure on his slide is an extrapolation of a prior CDC estimate of 300,000 sports-related concussions that already accounts for unreported concussions. The CDC provides such a wide estimate (2.2 million!) because they recognize the actual number may be anywhere from five to 12 times higher than their earlier estimate of 300,000.

But McCrory appears to believe the 3.8 million figure is the real number of diagnosed concussions, and then, accounting for undiagnosed concussions, the true figure is 10 times more than that – 40 million concussions. To put it another way, Paul McCrory, the supposed world’s expert, believes that one in eight Americans suffer a concussion each year through sports or recreation.

Then he doubles down yet again and says that U.S. Census data reflects it may be 10 times that number, so Paul McCrory believed, in 2016, after authoring the 2nd, 3rd, and 4th consensus statements on concussion in sport, that there are 400 million sports concussions in America – more than one concussion for every man, woman, and child – each year.

That mistake also provides context for another bizarre statement he makes about our 2013 study, when he says at 32:10: “But as you can see here, 5 (CTE) cases had no symptoms, so that’s a weird disease that doesn’t give you any problems.”

In this statement, Paul McCrory appears completely unaware of a concept widely known in the Alzheimer’s disease field as preclinical Alzheimer’s. Pathology always precedes symptoms in neurodegenerative disease. In Alzheimer’s, it has been shown that most people have pathology 15 years before they show any symptoms. People also develop CTE pathology years before they display symptoms.

Conclusion

Paul McCrory is a complicated man. This 2018 expose by journalist Wendy Carlisle provides even more background, including the discovery that up until that point, McCrory had published no original research on CTE.

These new revelations of McCrory’s plagiarism, along with the knowledge that he has been misrepresenting the research of others for years, is troubling. People are dying every day of CTE. Families are suffering. It was just announced that CTE was diagnosed in 12 of the first 21 Australian athletes whose brains were studied at the Australian Sports Brain Bank.

Yet many sports minimize the risk of CTE because they’ve been listening to Paul McCrory tell them that CTE is hoo-ha. In my opinion, this is more than just a question of ethics and academic integrity, it has harmed athletes.

Every sports organization that has relied on McCrory’s denial of the link between head trauma and CTE must start fresh. Perhaps they should start with the U.S. Centers for Disease Control and Prevention (CDC) 2019 fact sheet, which states:

The research to-date suggests that CTE is caused in part by repeated traumatic brain injuries, including concussions, and repeated hits to the head, called subconcussive head impacts.

Whatever comes next, the future of the Concussion in Sport Group is in question.

On Friday, McCrory tendered his resignation from the group and will no longer serve as chair. Who will take his place? Consider this – if the next chair says they agree with the CDC and the NFL that head impacts cause CTE, they may cost their sponsors FIFA and World Rugby billions in future payments to injured players.

Therefore, it is only logical to conclude that the sponsors of the Concussion in Sport Group may be forced to select someone not based on their merits as a scientist, but based on their willingness to continue say that “a cause-and-effect relationship has not yet been demonstrated between CTE and SRCs (sports-related concussions) or exposure to contact sports.”

Perhaps this is the time to take a new approach to advancing global concussion and CTE consensus. It is clear the conversation should not be solely driven by the sports industry due to their clear conflicts of interest. Instead, an approach that emphasizes transparency, includes public health expertise, and focuses on the long-term interests of the athletes themselves may prove more valuable. That is precisely the plan laid out by my colleagues in Toward Complete, Candid, and Unbiased International Consensus Statements on Concussion in Sport, published in October of 2021. I encourage you to read it. It is time for change.

*Disclosure: CLF co-founder and chief medical officer Dr. Robert Cantu is a member of the Concussion in Sport Group. He has been publicly critical of their CTE statements.