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.

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passing out

Monday, April 3, 2017

Fans watch where the action is but video cameras record all, including what happens well away from the play. Low motion instant replay is usually saved for highlights or controversial plays, but for Philadelphia Flyer Michal Neuvirth, those cameras captured him collapsing in his goal, 100 feet away from the puck Without warning, Neuvirth fell to the ice and remained motionless for a few minutes until he gradually wakened and was rushed to the hospital. He was observed overnight, and with initial testing being normal, he was discharged home, no doubt to be poked and prodded to find out just what happened.

Passing out is never normal. At its very basic, the purpose of the body is to protect the brain at all costs. Brain cells need very little to function, oxygen, sugar and that’s about it, but it takes a complicated factory to deliver those two basic goods. A person needs to be able to breathe to get air into the lungs, where oxygen needs to be extracted and tacked onto red blood cells. The heart pumps those cell through arteries to the brain. Glucose is added to that oxygen supply when digestive system extracts glucose from food and dumps it into the bloodstream.

With those two building blocks, a person will be awake if two structures in the brain are working. The reticular activating system, the on/off switch in the brainstem, needs to be in the on position and at least one hemisphere of the brain needs to work. Blood supply needs to be cut to one or both of these parts of the brain for a person to become unconscious.

It may be a true emergency when a patient has a syncopal event, meaning that they passed out. If the patient remains unconscious, treatment and diagnosis happen together. Blood is tested for low blood sugar (hypoglycemia), a dose of Narcan might be given in case the person overdosed on a narcotic and an EKG with a heart rhythm strip is done, looking for a heart rhythm disturbance. Most often, though, the patient is awake by the time they are seen by the doctor and the detective work begins to look for clues as to the reason why the patient passed out, make certain that no disaster has occurred and hopefully prevent another passing out episode.

Passing out often is a fluid delivery problem. Cardiac output measures how much blood the heart pumps per minute. Enough output and the blood pressure is maintained to push blood uphill to the brain. The cardiac output formula is relatively simple:

      Cardiac output = Stroke volume x Heart Rate

Output equals how much blood is pumped per heartbeat multiplied by how often the heart beats per minute, and is a measure of how effective the heart is in meeting the body’s and the brain’s demands for energy. Problems may exist with the heart rate and rhythm or with the red blood cells and fluid. Anemia (low red blood cell count) or dehydration (decrease fluid in the body) may decrease how much blood is pumped per heartbeat. A heart that beats too slow, too fast or not at all, will also decrease cardiac output.

Some problems are not very serious, like a vasovagal episode, where the heart slows and blood vessels dilate because a noxious stimulus that stimulates the vagus nerve. Imagine a medical student fainting when he sees his first operation or a patient who passes out because of pain. Other causes can be life threatening, like a massive pulmonary embolus or blood clot to their lung (25% of patients with PE present with sudden death), a structural problem with the heart or a major electrolyte crisis in the body.

ESPN reported that Mr. Neuvirth had been recently ill recently with a virus infection and perhaps his syncope was due to dehydration. Standing in full equipment can make a goalie sweat up a storm…but while dehydration is a possibility, the big worry is whether Mr. Neuvirth had a heart rhythm abnormality, an electrical disaster like ventricular fibrillation nor ventricular tachycardia. When the bottom half of the heart does not get an organized electrical signal, it can’t squeeze in a coordinated fashion, it can’t squeeze, blood doesn’t flow through the body, including the brain, and the patient can pass out. V fib and V tach may be the cause of sudden death.

Since the patient is usually not on a monitor when the event happens, and if no other easy diagnosis can be found to explain the syncope, admission to the hospital to watch the heart rate and rhythm is usually the safest plan. Sometimes a clue can be found on the EKG or during observation, but often not. The patient is usully discharged home with no solid answer but with the expectation that further tests might need to be done. Since people live in the real world and not a hospital bed, people can have their hearts monitored in the real world for durations of 1-2 days or even months at a time. Every heartbeat can be recorded and analyzed fro potential problmes.

The treatment of syncope depends on the cause but from a practical standpoint, sometimes the cause is never found. The question then becomes, what advice should be given to the patient regarding activity. There is no right answer when the diagnosis is not known. In the ER, the unknown syncope decision is easy; the patient needs to stay in the hospital to be monitored. But once the dust has settled, it’s a risk-reward discussion between doctor and patient to decide when it’s safe to return to full activity, whether that’s work, driving a car or playing goalie in the NHL.

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