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The Downward Spiral of Chronic Traumatic Encephalopathy

The Downward Spiral of Chronic Traumatic Encephalopathy

In the final months before retired football player Dave Duerson committed suicide in 2011, he complained of headaches, blurred vision and a deteriorating memory.1

For most of his life, he’d been met with remarkable success. In college, he was an All-American defensive back at Notre Dame. During his 11-year National Football League (NFL) career, he won Super Bowls with the Chicago Bears and the New York Giants.2 After he retired in 1993, he had a successful career in the food-services industry.1 He earned an economics degree from the University of Notre Dame and a certificate from Harvard Business School’s Executive Education program.3

Then things began to fall apart. Outwardly, his marriage ended, his business failed and he went bankrupt. Inwardly, he feared he was suffering from symptoms of a brain disease called chronic traumatic encephalopathy (CTE), a form of dementia that shares similarities with Alzheimer’s disease.4 Just before he shot himself in the chest, Duerson sent text messages and wrote a note to his family with this request: “Please, see that my brain is given to the NFL’s brain bank.”1

That brain bank is Boston University’s Center for the Study of Traumatic Encephalopathy, which has examined dozens of former football players’ brains for the telltale signs of CTE. The Center autopsied Duerson’s brain and did, indeed, diagnose him with CTE. In fact, they’ve found CTE in the majority of the players’ brains they’ve examined.5

CTE is a degenerative disease found in individuals with a history of repeated mild head injuries. For decades, it was believed that only boxers were susceptible to CTE. The disease was first described in a 1928 article titled “Punch Drunk,” written by pathologist and medical examiner Harrison Martland, MD.6 Dr. Martland wrote that he found the condition in “nearly one-half of the fighters who have stayed in the game long enough.” These boxers were nicknamed “punch drunk” for the tremors and signs of dementia that can occur in the later stages of the disease. It was later termed “dementia pugilistica,” meaning dementia of a fighter.7

But the symptoms of CTE—including painful headaches—are not exclusive to boxers. They’ve been reported in football players, hockey players, professional wrestlers, soccer players, jockeys, soldiers exposed to blasts and even a frequent parachutist.8 Further, head trauma isn’t exclusive to professional athletes. The New York Times recently reported that a Tulane University football player broke his neck in September during a tackle, and countless other high school athletes are likely enduring concussions that could result in long-term decline.9 To account for this widespread impact of head trauma, dementia pugilistica was renamed “chronic traumatic encephalopathy” (i.e., a chronic disease of the brain caused by trauma) in the 1960s. Fifty years later, CTE research remains in its infancy and there is still much to be learned about the disease. Prevention is currently the only way to avoid the downward spiral.7

Chronic Headaches and Signs of Dementia

Matthew McCoyd, MD, remembers being shocked by the news of Duerson’s suicide but says Duerson’s history was “fairly characteristic of the disease.” Dr. McCoyd is a Notre Dame alumni himself and a neurologist at Chicago’s Loyola Medical Center where he runs a concussion clinic for athletes.

The downward spiral of CTE can start years or even decades after the head trauma. In athletes, symptoms typically emerge in mid-life, after they’ve retired from sport. In the first phase of CTE, individuals notice problems with concentration and memory, disorientation, dizziness and chronic headaches. Over time, those individuals become more irritable and confused, may show aggressive or violent behavior, and may have speech disorders.8

Family and friends often speak of a change in personality. Duerson exhibited worsening cognitive and social functioning that led to problems with his relationships and poor money management. Among all CTE sufferers, there’s a high frequency of depression, drug overdose and suicide.

In the final phase of CTE, individuals can develop loss in motor functions that, as Dr. McCoyd describes, “looks something like Parkinson’s disease,” and they may also develop dementia.

In all stages of the disease, chronic headaches (in particular, chronic migraine or chronic tension-type headaches) seem to be common, Dr. McCoyd says. This is what sets CTE apart from Alzheimer’s disease. “The pathology is similar to what we see in Alzheimer’s, but the Alzheimer’s patients don’t seem to have headaches,” Dr. McCoyd says.

It isn’t clear why headaches are connected to CTE, Dr. McCoyd says. Then again, much of CTE is still a mystery.

Understanding the CTE Brain

CTE is difficult to understand in large part because, currently, it can only be diagnosed after a person dies by doing an autopsy of the brain. Pathologists look for tangled threads of tau, a protein that accumulates in the brain tissue of people with CTE and other illnesses that cause dementia. “Your body can’t get rid of the protein, so it stores it in nerve cells,” Dr. McCoyd says. “This clogs up the nerve cells, which makes them unable to work properly or pass messages along.”

Tau build-up is present in both CTE and Alzheimer’s, yet the tangles are more uniformly widespread in Alzheimer’s disease. In CTE, tau is typically found in high-density clumps close to the interface between the blood vessels on the brain’s surface and the brain itself.1 “When you’re getting hit in the head repetitively, your brain is shaking and may be bouncing up against these rigid blood vessels,” Dr. McCoyd says.

Chris Nowinski, 34, a former professional wrestler with World Wrestling Entertainment, is on a mission to help the research community better understand the CTE brain. Repeated concussions left Nowinski with severe headaches and depression and ended his sports career. Headaches were a rare event before his sixth—and last—concussion, which he sustained during a wrestling match. After that day he began experiencing short-term memory loss and a constant, dull-aching headache that lasted for five years. Nowinski says medications didn’t make a dent in the pain. Time was the only healer, he says, noting that he only experiences one or two headache days a month now.

Currently there is no cure for CTE; physicians can only treat the symptoms. Nowinski also hopes that will change through the work of his Sports Legacy Institute in Boston (which seeks to advance the study, treatment and prevention of brain trauma in athletes) and through its collaboration with Boston University through the Center for the Study of Traumatic Encephalopathy. Nowinski has persuaded a number of families to donate the brains of deceased athletes for research, including the family of former NFL player Andre Waters, who committed suicide in 2006 at the age of 44.10 The neuropathologist who examined Waters’ brain, Bennet Omalu, MD, determined that Waters had developed CTE.11

When, in 1994, Waters was asked by the Philadelphia Inquirer how many concussions he’d sustained, he said, “I think I lost count at 15.” He also admitted to ignoring the concussions, sniffing smelling salts and returning to the game.11

Waters’ story illuminates one thing that researchers do know about CTE: it takes repeated head injuries to trigger the disease. “But only a small number of people have been diagnosed with CTE and there are still many questions: How many hits do you need? Why do some people seem to have long careers with histories of head injuries and not get it? Is it a combination of the number of hits and being predisposed?” Dr. McCoyd says.

Genetics may be a factor that makes some people susceptible. A gene variation seen in Alzeimer’s has been found in approximately 57 percent of individuals with CTE.12 Dr. McCoyd hypothesizes that other health problems (e.g., hypertension, diabetes) or age might influence the process.

“Younger athletes might be more at risk because they aren’t as strong and their skulls aren’t as thick as older athletes,” Dr. McCoyd says.

Indeed, CTE has been discovered in the brains of two football players who died young, one at age 21 and the other at age 18.13,14 In one study using a system called HITSTM, Stefan M. Duma of the Center for Injury Biomechanics installed sensors in the helmets of seven or eight-year-old football players.15 His research showed that the players averaged more than 100 head impacts during the course of about nine practices and five games. Some hits exceeded a force equivalent to a big hit in college football.16

Reducing the Risk

In June 2012, Pop Warner, the nation’s largest youth football organization, announced new rules of play, including prohibiting contact for two-thirds of each practice. The new policy may help the largest group of vulnerable players (more than 285,000 children ages 5 to 15) in the country. Adult leagues are also making moves to reduce the risk. Both the NFL and Ivy League college teams have reduced the number of full-contact practices. The NFL imposed stiffened penalties for hits to the head and neck, requiring athletes be barred from returning to play on the same day of a concussion if they exhibit any symptoms.17,18 Helmet technology has also improved, with the addition of more padding and helmets that are designed to better distribute the force of impact.19

Such prevention is critical. An estimated 1.6 to 3.8 million sports-related concussions occur annually in the United States.7 Once a person suffers one concussion, they’re more likely to sustain another. It is this accumulation of concussions that is of utmost concern. By the time an NFL player has played through high school, college and 10 years of pro football, he could have been hit 18,000 times, according to HITS data.

Still, as Dr. McCoyd says, “football is a contact and collision sport designed to run into people. You’re never going to take the hits out of the game completely.”

Thus, while prevention is key, it is also important for people who experience head trauma to report it and seek help right away. Unfortunately, in sports and the military where strength and a fighting spirit are celebrated, Dr. McCoyd says many people won’t report their symptoms.

“[In athletics], most players know that if they develop symptoms that are suspicious for concussions, they’re going to get pulled from the game and they’re not going to be able to play,” says Dr. McCoyd.

Therefore it is also important for people to police one another. Coaches should be alert for concussion symptoms among their players, parents should ask their children if they’ve been hit in the head during practice, etc. If mild or severe head trauma is found, it should be reported and treated promptly to avoid worsening of symptoms and new blows to the head. An environment where people feel safe to report their symptoms and where coaches, trainers, parents and fellow soldiers work to prevent trauma could go a long way in reducing the risk for CTE and the number of people lost to the degenerative disease.


Government, Athletics Supporting CTE Research

CTE research has grown exponentially in recent years.7 On September 5, 2012, the NFL donated $30 million in funding to the Foundation for the National Institutes of Health for research into brain injuries and degen- erative diseases.20

In addition to studies among athletes, the Veterans Administration (VA) is researching CTE among veterans.

“Imagine someone who just had an improvised explosive device set off near them: first, there’s the actual blast and then there’s a wind that can be upwards of a few hundred miles per hour,” Dr. McCoyd says. “You can imagine the type of force that’s going to put on the brain.”

The VA recently performed a neuropathological analysis to compare the brains of four military veterans exposed to blasts or concussive injury with the brains of football players and a wrestler who had experienced repetitive concussive injuries. Published in the May 2012 issue of Science Translational Medicine, the study found that all four veterans had tau tangles indicative of CTE, similar to the CTE indications found in the brains of the four athletes.21

In the same study, the researchers immobilized the head of a mouse and found that such immobilization protected the mouse from brain injury during a blast. NASCAR has tried a similar approach to prevent head injuries by mandating better seatbelts and harnesses for racecar drivers.22 “If you could do the same thing for football, you’d probably reduce the risk of concussion,” says Dr. McCoyd, “but then you can’t play the game.”

Measuring Impact

To help coaches and trainers determine whether an athlete can return to play after head trauma, many teams now use the ImPACT® (Immediate Post-concussion Assessment and Cognitive Testing) evaluation system. ImPACT is a 20-minute, computerized tool that walks the user through several concussion-related tests including attention span, reaction time and working memory. Athletes must take the test prior to a concussion to set a baseline score. Once head trauma occurs, the athlete then takes the test again to see how their score aligns with the baseline and normative data. A licensed health care professional interprets the data and makes a decision about return-to-play.

A majority of U.S. professional football and soccer teams—and all national hockey league teams—use the ImPACT test. When it comes to high schools and universities, it depends on whether the state and/or school has made ImPACT use mandatory. For a list of states, schools and teams using ImPACT, go to



  1. Schwarz. “Duerson’s Brain Trauma Diagnosed.” The New York Times. May 2, 2011.
  2. Munson. “Duerson Case Could Set Precedent.” July 16, 2012.
  3. Garriott. “NFLPA Mourns Loss of Legend Dave Duerson.” February 18, 2011.
  4. Mayo Clinic. “Dementia.” Apr. 16, 2011.
  5. BU Center for the Study of Traumatic Encephalopathy. Press release. Dec. 6, 2011.
  6. Martland. “Punch drunk.” JAMA. 1928;91(15):1103-1107.
  7. Saulle et al. “Chronic Traumatic Encephalopathy: A Review.” Rehabilitation Research and Practice. 2012:816069.
  8. McKee et al. “Chronic Traumatic Encephalopathy in Athletes: Progressive Taupathy Following Repetitive Head Injury.” Journal of Neuropathology and Experimental Neurology. 2009;68(7):709-735.
  9. Cook. “Dying to Play.” The New York Times. Sept. 11, 2012.
  10. Bialik and Fry. “Eagles Fans Mourn Death of Andre Waters.” The Wall Street Journal. Nov. 21, 2006.
  11. Schwarz. “Expert Ties Ex-Player’s Suicide to Brain Damage.” The New York Times. Jan. 18, 2007.
  12. Gavett et al. “Chronic Traumatic Encephalopathy: A Potential Late Effect of Sport-related Concussive and Subconcussive Head Trauma.” Clinical Journal of Sports Medicine. 2011;30(1):179-xi.
  13. Faris and Hinman. “Football’s Risk Factor: Brain Injuries Raise New Concerns for Young Athletes.” May 24, 2012.
  14. BU Center for the Study of Traumatic Encephalopathy. “18 Year Old High School Football Player.”
  15. Farrey. “Study: Impact of Youth Head Hits Severe.” Feb. 22, 2012.
  16. Daniel et al. “Head Impact Exposure in Youth Football.” Annals of Biomedical Engineering. 2012;40(4):976-981.
  17. O’Connor. “Trying to Reduce Head Injuries, Youth Football Limits Practices.” The New York Times. June 13, 2012.
  18. Schwarz. “NFL Issues New Guidelines on Concussions.” The New York Times. Dec. 2, 2009.
  19. Malone. “Football Turns to Helmet Technology to Tackle Head Injuries.” Reuters. Apr. 2, 2012.
  20. “National Football League Grants $30 Million to National Institutes of Health.” Sept. 5, 2012.
  21. Goldstein et al. “Chronic Traumatic Encephalopathy in Blast-exposed Military Veterans and a Blast Neurotrauma Mouse Model.” Science Translational Medicine. 2012;4(134):134ra60.
  22. Aumann. “Safety Improvements, Changes Define Racing Eras.” Feb. 16, 2011.
  23. Fenno and Rosiak. “NFL Concussion Lawsuits.” The Washington Times. June 21, 2012. 24. Grogg. “Shaun Gayle Joins NFL Concussion Lawsuit.” July 11, 2012.

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