How Chronic Traumatic Encephalopathy Works

One concussion doesn't mean you'll wind up with chronic traumatic encephalopathy; years of small, medium and large hits might put you at risk, however.
One concussion doesn't mean you'll wind up with chronic traumatic encephalopathy; years of small, medium and large hits might put you at risk, however.
David T. Foster, III/Charlotte Observer/TNS via Getty Images

Say you don't own one of those cars where the seatbelt automatically slides back over your shoulder when you close the door. Say you forget to buckle yourself in, and thanks to terrible bad luck, you accidentally step on the gas and ram into a brick wall at 25 miles per hour (40 kilometers per hour). Scientists would say your head hit the windshield with an approximate g-force of 100.

Now let's say none of that happened. Instead, you're a defensive lineman playing college football. On a typical morning you suit up for practice, trot out to the field and go through drills with the rest of your team. Soon enough you crash headfirst into another player. As you do so, six sensors inside your helmet remotely feed information to a laptop sitting on the floor of a small building near the field. The laptop records a hit of 80 gs to the front of your head. Ten minutes later in another drill you hammer into a teammate and get a 98-g blow in the same place. That's the equivalent of two car crashes so far, but thanks to good technique and a thickly padded helmet, you're fine. It's just another typical day on the field.

Then there's an evening practice. The laptop shows you sustained a 64-g hit to the front of your head again. You're fine. Up you get, and it's back to the fray. A little later during a routine play, you get a bit of an elbow from a passing offensive player. Just 63 gs, but down you go with a concussion.

Nine weeks later you're over the concussion and back in play. During warm-ups you get hit with 76 gs, but you're OK. Then it's game time. First play, and you get hammered in the ear with 102 gs. You stagger off the field. For days light hurts your eyes, and you have a hard time staying awake. You've had another very serious concussion.

When it comes to chronic traumatic encephalopathy (CTE), concussions aren't the only problem. CTE is a degenerative neurological disease that has symptoms resembling Alzheimer's and Parkinson's, but unlike those conditions, CTE is caused by repetitive injury to the brain. That day in practice, you didn't just get four big impacts; if you add up all the small, medium and large hits, they come to 31 in total. Now multiply that by a couple thousand. The real issue is all those sub-concussive hits you take day in day out, week in week out, year after year throughout your time playing football [source: Gladwell].

The Background

After he died of a heart attack at 50, former Steelers player Mike Webster was found to have CTE.
After he died of a heart attack at 50, former Steelers player Mike Webster was found to have CTE.
Sporting News/Sporting News via Getty Images

Those sensors in the football helmet and that laptop recording impacts were all part of a 2009 study conducted by researchers following the University of North Carolina football team. This is one example of the attention now being paid to the issue of CTE. It wasn't always so.

Back in 1928, Dr. Harrison S. Martland published an article in the Journal of the American Medical Association in which he identified a syndrome long noted by boxing fans, known colloquially as "punch drunk" syndrome. Symptoms included unsteadiness, mental confusion and slowing movement. Martland drew the connection between the symptoms and its cause: repetitive brain injury, an occupational hazard for boxers. Scientists consider this one of the first mentions in medical literature of the condition that would become known as CTE [source: Martland].

For the rest of the century, CTE was thought to be limited to boxers — a rare condition affecting a small minority of the population. For more than 80 years we've known that if you're a serious competitive boxer your chances of developing dementia are much higher than they are for the general population. In the 1950s, some medical professionals called for the sport to be banned, but their voices went unheeded. Boxers kept boxing, and fans kept watching [source: Gladwell].

Then, in 2002 a coroner and neuropathologist named Bennet Omalu autopsied Mike Webster. Webster, a retired center for the Pittsburgh Steelers, was a Hall of Famer who died of a heart attack at age 50. When Omalu looked at the former footballer's brain, there was an abundance of tau proteins. Found in people with Alzheimer's, tau proteins build up in brain cells and shut them down. But in Alzheimer's, tau usually shows up alongside another protein called beta-amyloid, which, the theory goes, sets the stage for tau proteins to do their work and produce the second, critical phase in which the symptoms of the disease appear.

In Webster's case, there was tau but no beta-amyloid, which meant Webster had dementia, but not Alzheimer's. The presence of tau had been caused by repeated head trauma, and Omalu diagnosed CTE. It was the first time a former NFL player was found to have the disease. It was not the last [source: Gladwell].

Since then, Omalu and a leading neuropathologist named Ann McKee have discovered that Webster's case was not isolated. CTE is endemic to the sport of football.

Football is, of course, wildly popular, and unlike boxing, it's a sport played by millions of people from grade school through college. That's why CTE is making front-page headlines. It's not just a question of whether it's ethically OK to watch NFL gladiators hammer one another in the head; it's also a question of whether we're putting our children at risk by letting them trot out to play for their high school team.

And it's not just football that puts people at risk of CTE. The condition has been found in people who've participated in wrestling, soccer, baseball, hockey, rugby, karate, horseback riding, parachuting, lacrosse and skiing. Some epileptics and domestic abuse victims have also been diagnosed with CTE [source: McKee et al.].

The Symptoms

Neurology researcher Ann Mckee stores brains at the Bedford Veterans Administration Medical Center, repository for the Brain Bank, where she's studying the pathology of concussive head trauma in ex-athletes.
Neurology researcher Ann Mckee stores brains at the Bedford Veterans Administration Medical Center, repository for the Brain Bank, where she's studying the pathology of concussive head trauma in ex-athletes.
Brian Cahn/ZUMA Press/Corbis

When neuropathologists look at a brain with CTE they might see any of a number of features, such as scar tissue, a shrunken, atrophied cerebral cortex and medial temporal lobe, neurofibrillary and astrocytic tangles in the temporal and frontal cortices and limbic regions, and degeneration of axons and white matter fiber bundles [source: McKee et al., "Spectrum"].

Of course, unless you're a medical professional, preferably a neurologist, none of this means much. Suffice it to say that the brain looks unhealthy — and unhealthy in a specific way that indicates it's been bounced around inside the skull far more than it should have been.

For the layperson, the symptoms of CTE are much more familiar. Although the condition is caused by injury rather than disease, people who suffer from it have symptoms that resemble those of people with other neurodegenerative illnesses such as Parkinson's and Alzheimer's, although CTE usually shows up much earlier than those diseases (often when people are in their 40s).

The condition can be progressive, and there are three stages of deterioration. Sometimes accompanied by dizziness and headaches, the first stage includes:

  • Shorter attention spans
  • Difficulty concentrating and remembering
  • Increasing disorientation and confusion leading to poor reasoning, judgment and problem-solving
  • Aggression and poor impulse control

In the second stage, people with CTE can begin to behave oddly and experience memory loss. Finally, people suffering from severe CTE can enter a third stage characterized by symptoms such as slowing movements, staggering, difficulty speaking, trembling and deafness [source: McKee et al., "Athletes"].

However, just because a person exhibits these symptoms doesn't necessarily mean he or she has CTE. One of the largest problems facing CTE researchers is that they can diagnose the disease only through special screening methods during an autopsy. In other words, as of January 2016, CTE diagnosis is post-mortem only.

As if that weren't enough, the other big problem is that there's no known cure for the condition. The best thing we can hope for is to prevent the brain trauma from happening in the first place. But exactly how to do that is an open question. How much head-banging can a brain put up with? Does it matter at what angle you get hit, how many times you get hit, how thick your neck muscles are? For the moment, it seems that kids under 14 are more at risk, and girls are more vulnerable than boys. In both groups, the risk is tied to having thinner or weaker necks, among other factors. But the research on how to prevent, never mind cure, CTE is still in its early days [source: Sneed].

Concussion Repercussion

Ann McKee, professor of neurology and pathology at Boston University School of Medicine and co-director of the Veterans Affairs Center for the Study of Traumatic Encephalopathy, inspects a brain in the Bedford Veteran Medical Center.
Ann McKee, professor of neurology and pathology at Boston University School of Medicine and co-director of the Veterans Affairs Center for the Study of Traumatic Encephalopathy, inspects a brain in the Bedford Veteran Medical Center.
Stan Grossfeld/The Boston Globe via Getty Images

Since McKee and Omalu began their research into the connection between CTE and contact sports, professional sports organizations have been under pressure. In April 2015, the NFL settled a lawsuit with 5,000 retired players for $1 billion. The lawsuit claimed that the league had covered up evidence of the harm caused by concussions [source: Beck].

In the wake of that settlement, the NFL has implemented changes designed to reduce serious head trauma. These changes include banning tackles that injure the crown of the head. They're even thinking of changing the nature of tackling altogether, making it closer to the rugby style of grabbing legs. But as we now know, concussions are just the tip of the iceberg. Researchers are discovering CTE in the brains of deceased rugby players, hockey players and even soccer players [source: Branch]. It seems any activity that involves players getting repeatedly hit in the head, whether it's by other players or by soccer balls when heading, could have long-term consequences for brain health.

One recent study looked at the brains of 165 people who had played football at some point in their lives, whether it was in high school, college or the NFL. Of those, 131 had CTE — that's 79 percent — and 91 of them played in the NFL. Eighty-seven of those 91 pros had CTE — that's fully 96 percent [source: Beck]. Even if you account for the fact that people who donate their brains to research are probably more likely to have suffered from some disorder, those statistics are extraordinary.

A 2008 survey discovered that 4.6 percent of former NFL players had been diagnosed with Alzheimer's, dementia or some other memory-related condition. That rate is six times higher than the prevalence in the general population [source: Engber]. Whether these diagnoses are actually the result of CTE remains unknown, of course, and will remain so until after those surveyed die and are autopsied (if they are).

One problem with trying to find a way to prevent CTE from occurring is that, in the case of contact sports like football, it would seemingly require altering the game to the point of it becoming unrecognizable. Would football still be football if it didn't involve gladiatorial, head-crunching impacts? Would fans still be excited to watch it?

The Future of CTE

Forensic pathologist and neuropathologist Dr. Bennet Omalu is credited with discovering chronic traumatic encephalopathy in former football players.
Forensic pathologist and neuropathologist Dr. Bennet Omalu is credited with discovering chronic traumatic encephalopathy in former football players.
Pete Marovich/Getty Images

Will Smith stars as the coroner Bennet Omalu in the recent film "Concussion." The movie follows the story of Omalu's groundbreaking autopsy of Mike Webster, his subsequent research into the prevalence of CTE in pro-football players and his efforts to publicize the results. Critics have noted that "Concussion" drastically oversimplifies the problem of CTE, altering Omalu's story to do so and drawing a direct line between Webster's early death and CTE. The film also claims that there's a causal link between CTE, depression and suicide. Statistically, this seems implausible. Studies have shown that ex-NFL players are less prone to depression than people in the population at large. They're also less likely to commit suicide — 59 percent less likely, to be precise. Not only that, the pros tend to have fewer illnesses and be longer-lived than the rest of us [sources: Engber, "Lies"; Engber, "Panic"].

So if they have more CTE but live longer, happier, healthier lives, what does that tell us about the disease? It may be that the consequences of having CTE are not quite as dire as some people fear. Perhaps most people can live with a little chronic traumatic encephalopathy and exhibit few symptoms.

The problem is, we just don't know. The science of CTE is only getting started. Critics aside, maybe "Concussion" will help mobilize public awareness and focus attention on the issue long enough to encourage more scientists to add to the growing body of research on the topic. In 2013 there was great excitement when it was announced that an "in vivo" test for CTE had been developed. Though the test has since proven unreliable, researchers remain hard at work trying to refine testing methods [source: Mez et al.].

But this raises another possible problem. What if neuropathologists come up with a perfect test that can say without a shadow of a doubt that you have CTE? What then? If people believe the disease will lead to inevitable mental decline, dementia, depression and death, they might take drastic measures. Perhaps, before a test is developed, it would be wise to determine just how debilitating CTE really is.

Author's Note: How Chronic Traumatic Encephalopathy Works

I played soccer in high school and as a left fullback headed my share of long kicks back up the field. As I researched this article I became increasingly paranoid that I might have CTE. Could I attribute my inability to remember the names of recent acquaintances to chronic traumatic encephalopathy? What about all the times I've forgotten items on the grocery list even though they're ON THE GROCERY LIST? After all I'm well into my 40s, the common age when CTE is said to develop. The problem with this self-diagnosis, beyond its hypochondriacal absurdity, is that I've always been this way. It's just getting incrementally worse as I age.

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Sources

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