Concussion, CTE and what we don’t know

Monday, May 14, 2018

What we wish we knew about concussion and CTE would make life easier for athletes, their parents, coaches and league administrators. It’s tough to remember that concussion research is in its infancy and the final answers about the way the brain reacts to injury, both in the short term and long term is still a mystery. Regardless of the headlines, there are many things we don’t understand. What should be common sense, may or may not be true.


The only way to diagnosis chronic Traumatic Encephalopathy is after death, by autopsy, and using special techniques to look for abnormal proteins in brain tissue. Tau proteins are located in the brain and help stabilize microtubules inside brain cells called neurons. Abnormalities of an enzyme may cause tau proteins to fold abnormally and clump into “neurofibrillary tangles”. Other brains cells may also be affected.

While the diagnosis of CTE may be suspected because of symptoms like depression, suicidal thoughts, confusion, and short term memory loss, there is no test available for patients to confirm the diagnosis while they are alive.

The pathology findings under the microscope suggest that there is a difference between Alzheimer disease and CTE based on where the tau tangles occur and the presence of amyloid plaque (a sticky protein) seen in Alzheimer.


The relationship between head injury and CTE seems to be well established. Using boxing research, it may be the number of hits to the head that make a difference as opposed to whether a concussion occurred. Studies suggest that “punch drunk syndrome” leading to dementia pugilistica found that it was the number of rounds boxed that was the important factor in determining long term brain issues, rather than the number of concussion.

This presumes that we know how to make the diagnosis of concussion and the answer is that we don’t. There is no test to confirm that a concussion has occurred. We know a concussion when we see it: a player who is temporarily confused or knocked unconscious, has a brief seizure or has an abnormal neurologic exam is an easy diagnosis. Many times, the symptoms of concussion may be delayed by hours and those symptoms may be subtle, involving sleep disturbance, ability to concentrate or minor changes in personality.

A concussion may be caused by a direct blow to the head, face or neck or it may be caused when a force to another part of the body is transmitted to the head. Imagine a car wreck where the seat belt holds the body in place but the head whips back and forth.

Not only can we not diagnosis a concussion with certainty, we also do not know when the brain has healed itself from injury and has returned to “normal”.

Cause and Effect

Making the link between head injury, concussion and CTE seems to have occurred, but the question there are plenty of questions left to answer. Does CTE risk increase with the number of concussions or does is it the age of the brain when that first concussion occurs?  Contact sports increase the risk of head injury and the prevalence of CTE in NFL players has led to lawsuits to care for players who develop debilitating symptoms after their careers have ended.

In soccer, recent research suggests that heading the ball affects brain function more than head injury caused by collision. This supports the concept that the number of minor hits may be as important or perhaps more important than a single concussion.

Newer recommendations from research have suggested that concussed brains that are not fully developed are at higher risk for future behavior problems and decreased executive thinking, including initiating activities, problem solving, and planning and organizing. The suggestion is that between the ages of 10 and 12, the brain is undergoing major growth and development and may be particularly vulnerable to injury. Recommendations suggest that tackle football should be avoided before age 12.


The NFL and NHL rightly are concerned about the long-term consequences of head injury to their players. Those who make it to the pro level have played more games at a higher level and presumably with more exposure to violence than those who didn’t make it to the college level and beyond. A case study published this year found that an 18-year-old high school football player with multiple concussions had, on autopsy, already developed abnormal tau protein tangles in his brain.It may be that the die has been cast for the pro…what happens in the major leagues may be inconsequential as to the development of abnormalities in the brain that are associated with CTE…or, it’s those concessions that occur because of collisions with larger and faster opponents may be the culprit.

The bottom line is that research teaches us much as to the consequences of head trauma and the potential for long term brain dysfunction. It also reminds us that we don’t know what we don’t know.

Protecting players at all levels of competition is a reasonable approach, but that risk of concussion will never be zero, and because of that the risk of CTE will never be zero. Asking the NFL, NHL, NCAA and high school leagues to alter the game maybe appropriate, but there is no way to know whether it will actually make a difference.

We can’t make the diagnosis of concussion. We can’t make the diagnosis of CTE. We don’t know how many concussions it takes to develop CTE and we don’t know if the brain has the ability to fix itself if it has been hurt.welcome to the world of science.

This entry was tagged , , , , ,

cte: what we don’t know

Sunday, July 31, 2016

The press has not been kind to Gary Bettman this week and this time, the press is wrong. The NHL Commissioner wrote a letter in response to questions asked by Connecticut Senator, Richard Blumenthal, that outlined the league’s position regarding concussion and the long term effects of head injury. The New York Times called out his “reluctance to link hits to the head in hockey with a degenerative brain disease”.  Sports Illustrated wrote of the “refusal to acknowledge a possible link between concussions and CTE has proved to be controversial.”

“I was surprised and appalled, because I thought the response would be more receptive,” Blumenthal told via telephone from Philadelphia. “I would’ve welcomed an acknowledgement for stronger action and a commitment to determining whether the game is causing these heartrending injuries with such painful consequences, rather than dismissing the link between hockey and CTE.” 

Mr. Bettman’s 24-page letter acknowledged the potential for head injury and concussion in all contact sports and also summarized the medical literature that has yet to prove that chronic traumatic encephalopathy (CTE) is caused by concussion. While it seems intuitive that CTE is caused by trauma, there are major questions that remain unanswered.

Association v. Causation

There is no doubt that there is an association between traumatic brain injury and CTE, but the research is just beginning as to what causes some people to develop CTE and others to be spared. Or have they been? With todays’ science and technology, CTE can only be diagnosed after death by autopsy, and then only if the brain is dissected and special stains are used to look at cells under the microscope. Of the athletes whose brains have been studied, there seems to be a correlation between the many concussions that they had sustained and CTE findings in the lab. Unfortunately, there is a problem with the statistics.

For a cause and effect to be found, brains from different groups of athletes need to be studied:

  • Those who had no concussion history and no signs or symptoms of depression or dementia
  • Those who had no concussion history but developed signs or symptoms of depression or dementia
  • Those who had a concussion history and had no signs or symptoms of depression or dementia.

As of now, researchers have mostly studied those who have had a history of concussion and developed signs of mental illness and/or dementia.

What do we know?

There is evidence that there is a link exists between a severe traumatic brain injury and the eventual development of dementia. There also may be a dose relationship, meaning the more severe the head injury, the more likely dementia becomes a future possibility.  However, there is not necessarily that same link that connects repetitive minor head injuries with CTE. Lots of small concussions does not necessarily equal one major head injury.

…specifically for rTBI (recurrent mild traumatic brain injury), there has been an unavoidable case-selection bias and a virtual absence of control material from uninjured cases in reports of CTE, rendering interpretations of the incidence of this pathology meaningless in the context of exposure to repetitive mild injury. –  Hay J, et al. Annual Review of Pathology. May 2016

While the public is hearing about brain chemistry and anatomy, including tau proteins and neurofibrillary tangles, other research is ongoing looking at other markers of brain injury. These include amyloid deposits, DNA binding proteins, neuroinflammtion, brain white matter degradation and neuron (brain cell) loss. Chromosome research may offer some clues to CTE development, with certain genes more likely to be associated  CTE after a brain injury and others that might injure the brain by activating certain enzymes. 

What don’t we know?

Traumatic brain injury is known to be the biggest risk factor for developing dementia. The question is how much brain trauma is needed to cause CTE.

  • Does it take one or multiple concussions?
  • Are concussions spaced closer together more dangerous? Or does the same damage occur even when they are spaced years apart.
  • Is concussion in children and teenagers more important than later in life? or are their brains better able to adapt and heal themselves?
  • Do brains heal themselves and become pristine after a period of time, or is the concussion damage permanent?
  • Why do some concussion patients develop depression and dementia, while other do not?

The bottom line is that while a relationship exists between head injury and degenerative brain disease, scientific research has yet to prove that concussion causes CTE. There are many next steps for research to take, including being able to diagnose CTE in live patients without having to wait until they die to perform an autopsy. For now, we know that we don’t know a lot.

There are known knowns. These are things we know that we know. There are known unknowns. That is to say, there are things that we know we don’t know. But there are also unknown unknowns. There are things we don’t know we don’t know. – Donald Rumsfeld.


This entry was tagged , , , , , , ,