Concussions & Post Concussion Syndrome

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Concussions, head injury, and Secondary Injury

What Someone Who Has a Concussion or TBI Wants You To Know

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I need a lot more rest than I used to. I’m not being lazy. I get physical fatigue as well as a “brain fatigue.” It is very difficult and tiring for my brain to think, process, and organize. Fatigue makes it even harder to think.

My stamina fluctuates, even though I may look good or “all better” on the outside. Cognition is a fragile function for a brain injury survivor. Some days are better than others. Pushing too hard usually leads to setbacks, sometimes to illness.

Brain injury rehabilitation takes a very long time; it is usually measured in years. It continues long after formal rehabilitation has ended. Please resist expecting me to be who I was, even though I look better.

I am not being difficult if I resist social situations. Crowds, confusion, and loud sounds quickly overload my brain, it doesn’t filter sounds as well as it used to. Limiting my exposure is a coping strategy, not a behavioral problem.

If there is more than one person talking, I may seem uninterested in the conversation. That is because I have trouble following all the different “lines” of discussion. It is exhausting to keep trying to piece it all together. I’m not dumb or rude; my brain is getting overloaded!

If we are talking and I tell you that I need to stop, I need to stop NOW! And it is not because I’m avoiding the subject, it’s just that I need time to process our discussion and “take a break” from all the thinking. Later I will be able to rejoin the conversation and really be present for the subject and for you.

Try to notice the circumstances if a behavior problem arises. “Behavior problems” are often an indication of my inability to cope with a specific situation and not a mental health issue. I may be frustrated, in pain, overtired or there may be too much confusion or noise for my brain to filter.

Patience is the best gift you can give me. It allows me to work deliberately and at my own pace, allowing me to rebuild pathways in my brain. Rushing and multi-tasking inhibit cognition.

Please listen to me with patience. Try not to interrupt. Allow me to find my words and follow my thoughts. It will help me rebuild my language skills.

Please have patience with my memory. Know that not remembering does not mean that I don’t care.

Please don’t be condescending or talk to me like I am a child. I’m not stupid, my brain is injured and it doesn’t work as well as it used to. Try to think of me as if my brain were in a cast.

If I seem “rigid,” needing to do tasks the same way all the time; it is because I am retraining my brain. It’s like learning main roads before you can learn the shortcuts. Repeating tasks in the same sequence is a rehabilitation strategy.

If I seem “stuck,” my brain may be stuck in the processing of information. Coaching me, suggesting other options or asking what you can do to help may help me figure it out. Taking over and doing it for me will not be constructive and it will make me feel inadequate. (It may also be an indication that I need to take a break.)

You may not be able to help me do something if helping requires me to frequently interrupt what I am doing to give you directives. I work best on my own, one step at a time and at my own pace.

If I repeat actions, like checking to see if the doors are locked or the stove is turned off, it may seem like I have OCD — obsessive-compulsive disorder — but I may not. It may be that I am having trouble registering what I am doing in my brain. Repetitions enhance memory. (It can also be a cue that I need to stop and rest.)

If I seem sensitive, it could be an emotional response as a result of the injury or it may be a reflection of the extraordinary effort it takes to do things now. Tasks that used to feel “automatic” and take minimal effort, now take longer, require the implementation of numerous strategies and are huge accomplishments for me.

I need a cheerleader now, as I start over, just like children do when they are growing up. Please help me and encourage all efforts. Please don’t be negative or critical. I am doing the best I can.

Don’t confuse Hope for Denial. I am, We are learning more and more about the amazing brain and there are remarkable stories about healing in the news every day. It would be easy to give up without Hope.

 

Find more helpful hints on how to deal with and recover from a concussion or TBI, from impact to recovery.

What You Don’t know About Concussions, The Secondary Injury

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WARNING: The link below may be emotional for some audiences:

View My Son’s Post Concussive Seizures Here

 

The Secondary Injury
Though each traumatic brain injury (TBI) and concussion are unique to each individual, medical science has discovered that the occurrences that follow during the secondary injury are proven to be probable and foreseeable. While the biological events occur in a very calculable fashion, the degree of damage during the secondary injury can be altered if the appropriate measures are taken.
In order to effectively be able to treat a TBI or concussion you must be aware of what takes place during the secondary injury following the initial, also called primary injury.
A multiple of very calculated sequential events occur in the brain; contributing to symptoms, or an increase in symptoms, that can continue for up to 48 hours after the initial primary injury has taken place.
There are three major events that take place effecting brain function during the secondary injury.
1. Ionic shifts
2. Metabolic Changes
3. Impaired neurotransmission

In this blog, we will be covering excerpts from Keys2Concussion’s book, The Complete Concussion Protocol.

The events that take place after the initial head injury or primary injury are referred to as the secondary injury. Most individuals aren’t aware that this secondary injury even takes place.
The secondary injury welcomes an entire new set of symptoms and damaging effects. It is because of this secondary injury that the current concussion assessments on the sidelines during sporting events might not be enough.

Any time the brain suffers a violent force or movement, the soft, floating brain is slammed against the skull’s uneven and rough interior. The internal lower surface of the skull is a rough, bony structure that often damages the fragile tissues within the brain as it moves across the bone surface. The brain may even rotate during this process. This friction can also stretch and strain the brain’s threadlike nerve cells called axons.

When the head has a rotational movement during trauma, the brain moves, twists, and experiences forces that cause differential movement of brain matter. This sudden movement or direct force applied to the head can set the brain tissue in motion even though the brain is well protected by the skull and very resilient.

Upon impact and severe motion brain cells called neurons can be stretched and often squeezed, completely tearing. Neural cells require a precise balance and distance between cells to efficiently signaling and sending messages between cells.  The stretching and squeezing of brain cells from these forces can change the precise balance, which can result in problems in how the brain processes information.

Different cognitive functions can be altered depending on the area of the brain that has been effected by the trauma.

Though the stretching and swelling of the axons may seem relatively minor or microscopic, the impact on the brain’s neurological circuits can be significant.  Even a “mild” injury can result in significant physiological damage, behavioral and emotional imbalances, and cognitive deficits.

If a person’s head is whipped around, a small tearing effect called shearing occurs throughout the brain, resulting in a diffuse axonal injury. Axons are the hair-like extensions of nerve cells that transmit messages. In a diffuse axonal injury, the messages either get mixed up, or they don’t come through at all.

Click here to receive the full report FREE on this secondary injury and What You Don’t Know About Concussions

Now Available The Concussion Recovery Guide

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The mysteries of concussions are as great as the debts of the brain itself; however, much scientific research and studies have been done to shed some light on these previously uncharted waters.

In 2012, the CDC estimated 329,290 children, age 19 and under, were treated in emergency medical departments for concussions, or mild traumatic brain injuries, also known as, MTBI.  In 2015, a Harris Poll finds that nearly 90% of Americans cannot correctly identify, nor define a concussion and are not aware of, or are familiar with, the post-concussion You are not alone. Hundreds of thousands of people have faced concussions and TBI’s. There is a community, a family and a network of support here for you!

According to the DVBIC, the Defense Department’s office responsible for tracking traumatic brain injury (TBI) data in the U.S. military, since 2000, 361,092 military enlisted have sustained a traumatic brain injury. 

With such astronomically high statistics, we can no longer afford to be un-educated and un-prepared in the face of concussions.

TBI’s including concussions are the number one cause of unintentional death and disability among children. They rob professional athletes of their livelihood, and their footprints torment our heroes and veterans of war.

The Concussion Recovery Guide coaching program is your guide from “Impact to Recovery”. The first 48 hours following a concussion are crucial in determining the impact and long term effects on the concussed individual. No concussion or TBI are the same. They are as unique as their victims. The Complete Concussion Protocol is supported by cutting edge research, describing, what you don’t know about concussions, and metabolic upset including the neurological cascade that follows during the first 48 hours. Through simple explanations and supported by medical research, The Complete Concussion Protocol will walk you through the concussion journey from the initial impact through the recovery stages. In section one, you will learn what to do and what not to do in the “First 48 hours” following a concussion. 

You will learn: 
  • How to identify concussions and post -concussion syndrome, what tests doctors use to diagnose a concussion and Post-Concussion Syndrome. 
  • You will be provided with a step by step symptom tracker and plan for safe recovery. 
  • You will learn how to eat to help the brain heal after a concussion, including food lists itemizing what to eat and what not to eat to best aid in brain health. 
  • In section three, “The Aftermath” you will receive a personalized reintegration plan; including emotional healing, how to work with educators and employers, and the creation of your personalized concussion protocol plan. 

This book utilizes helpful links, PDF documents with instructions to walk you through the planning and recovery stages. The brain health recommendations and reintegration program techniques were developed to include our veteran heroes and to help support their efforts in recovery from PTSD. 

Doctor’s have a saying when it comes to concussions. It is, “if you’ve seen one concussion, you’ve seen one concussion.” Concussions are as unique as each individual.
 

This concussion recovery system is your guide through the entire concussion recovery process, from impact to recovery.

FINAL NOTE:
It’s important to not get over whelmed, stressed out or to give up. Remain patient and persistent while you learn what works best, this will help ensure your success through this program. Remember, no two concussions are ever the same,even in the same individual, and everyone’s personal experience will be different. This plan is designed to help you create a system that works best for you and your situation. 

My Son’s Story

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My Son’s Concussion Journey

“I feel so dumb; I don’t know what’s wrong with me.”  These were the words my son told me after suffering from his first concussion unbeknownst to me.

I was unaware of the fact that he had suffered a concussion.  I had no first-hand experience with concussions.  I looked at his pupils with a light and asked him to follow my finger with his eyes.  He didn’t pass out or vomit, so I thought we were in the clear.

That was the extent of my education and concussion screening.  After sitting down and icing his head for a couple of minutes and with no visible marks, this active 9-year-old boy asked to go outside to play soccer with his friends.  Naturally, I thought he must be ok, and released him to his free will.

After a persistent headache, the following day I took him in for a CAT scan and evaluation.  The CAT scan results came back normal, and it was not ruled a concussion, at this time.

It wasn’t until three days later when the memory loss was apparent, and we realized the severity of the concussion.

Things quickly got worse, headaches, memory loss, lethargy, depression, anxiety, sleeplessness, and even seizures.

It was the height of the hockey playoffs which he had followed religiously with his father.  He knew every player by name.  However, all of that knowledge had suddenly disappeared.   We realized something was wrong when he could not follow a conversation and repeatedly would begin speaking only to say never mind. He literally, was at a loss for words.  He repeatedly asked for the time and had a perplexed look fixed on his face when we would engage him in conversation.

Anxiety began to set in as he drew more and more blanks and realized he couldn’t remember people or events that we could.  “I feel dumb,” he said, as he could no longer complete his math homework.  He forgot all of the multiplication facts he had just recently mastered.

Unfortunately, in my son’s case we were unaware that he suffered a concussion, so we did not follow the proper concussion protocol and steps to protect him from more neurological strain, and post-concussive syndrome soon became his reality.

Severe migraines and vertigo lasted for the first month, while sleep disturbances became more evident and emotionally he was not himself.  He was placed on a homebound school program since he could perform only minimal tasks while symptoms persisted.  However, to my surprise, the school did not have a concussion plan ready to implement.  I was left to educate his educators on his condition even though, I was still learning.

Unfortunately, many people, including myself, did not understand the after-math of a concussion and it was a long difficult journey.  After initially being cleared from his concussion, the dizziness, ringing in the ears (tinnitus), and headaches were so bad they were debilitating.  The school believed that since outwardly he appeared to be fine, and projected the attitude of disbelief of his expressed continued symptoms.

Due to the nature of concussion and post-concussion syndrome, the majority of the battle was an inner struggle with no outside visible marks.  Because of this, he was often accused of “milking it” or “making things up.”  I believe this was partly due to the lack of information, education and complexity of this subject.

Unfortunately, my son’s relationships with concussions would not end with one, partly due to the severity of the initial concussion.  Research shows that once you receive a concussion your chances of getting another one increase up to 3X and it takes much less of a severe hit to the head each time.

He suffered another concussion in 2015 at school when a classmate playfully pulled his chair out from underneath him sending him falling back hitting his head on a desk.

The third concussion occurred in 2016 by what was considered a mild blow to the head during football practice.  Both times the familiar feeling of concussion filled his head, and he was immediately evaluated, and the proper steps in our concussion protocol began.

Never again would I make the same mistake, and be caught off guard by a concussion.  I was in control of the situation and ready to help by son.  I will never forget that feeling of helplessness.  No price can be placed on being prepared once a concussion takes place.

It was through these experiences that I met other individuals also suffering from the effects of concussions and I realized there was a lack of adequate information and direction for those needing answers, like myself after my son’s first concussion.

I also realized how many people were so unaware of the debilitating effects that concussions and TBI’s could bring.

It was this reason that I sought to create The Concussion Recovery Guide, initial for my son.  As I  began to implement the information I had learned and research in my own son’s life, I experienced bitter sweet emotions.  I was elated and grateful to have answers and a plan for my son, while at the same time, I was frustrated that I could not find this information in its totality after his initial concussion.

It was during that epiphany that I realized, the information I used to help my son needed to be documented and put to print for others out there struggling and searching for solutions and answers.

The information in this program is a composition of scientific and medical research, case studies, and real life applications brought together over a span of 5 years.

I have such gratitude in knowing my son didn’t suffer in vain. I believe as challenging as it can get, life happens for us and our family struggles brought answers that can help others.

I have compiled my research and findings in a free article  What You Don’t Know About Concussions.

This article will fill in the gaps regarding what goes on in the brain during and after impact and astound you as you discover hard truths like why sideline concussion screenings simply aren’t enough just to name a couple. 

Click here more information regarding the complete Concussion Recovery Guide Program including Audios, Videos, pdf’s and tools and techniques to help guide and support your intentions during the recovery  process. 

(CTE) Chronic Traumatic Encephalopathy

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What is CTE?

According to the Boston University Research Center and the Concussion Legacy Foundation; Chronic Traumatic Encephalopathy (CTE) is a progressive degenerative disease of the brain found in people with a history of repetitive brain trauma (often athletes), including symptomatic concussions as well as asymptomatic sub-concussive hits to the head that do not cause symptoms. Chronic Traumatic Encephalopathy (CTE) is found in athletes, military veterans, and others with a history of repetitive brain trauma.

 In CTE, a protein called Tau forms clumps that slowly spread throughout the brain, killing brain cells. CTE has been seen in people as young as 17, but symptoms do not generally begin appearing until years after the onset of head impacts.

CTE has been known to affect boxers since the 1920’s (when it was initially termed punch drunk syndrome or dementia pugilistica). Just take a look at the degenerative  Mohamed Ali and the aggression of Mike Tyson.

In recent years, reports have been published of neuropathologically confirmed CTE found in other athletes, including football and hockey players (playing and retired), as well as in military veterans who have a history of repetitive brain trauma. CTE is not limited to current professional athletes; it has also been found in athletes who did not play sports after high school or college.

Early symptoms of CTE usually appear in a patient’s late 20s or 30s, and affect a patient’s mood and behavior. Some common changes seen include impulse control problems, aggression, depression, and paranoia.

As the disease progresses, some patients may experience problems with thinking and memory, including memory loss, confusion, impaired judgment, and eventually progressive dementia. Cognitive symptoms tend to appear later than mood and behavioral symptoms, and generally first appear in a patient’s 40s or 50s. Patients may exhibit one or both symptom clusters. In some cases, symptoms worsen with time (even if the patient suffers no additional head impacts). In other cases, symptoms may be stable for years before worsening.

The repeated brain trauma triggers progressive degeneration of the brain tissue, including the build-up of an abnormal protein called tau. These changes in the brain can begin months, years, or even decades after the last brain trauma or end of active athletic involvement. The brain degeneration is associated with common symptoms of CTE including memory loss, confusion, impaired judgment, impulse control problems, aggression, depression, suicidal thoughts or tendencies, Parkinsonism, and eventually progressive dementia.

In the photographs below, the brain tissue has been immunostained for tau protein, which appears as a dark brown color.

Tau immunostained sections of medial temporal lobe from 3 individuals:

Whole brain section from a 65 year old control subject showing no tau protein deposition.Whole brain section from a 73 year old world champion boxer with severe dementia showing very severe tau protein deposition in the amygdala and thalamus.Whole brain section from John Grimsley showing abundant tau protein deposition in the amygdala and adjacent temporal cortex.

Microscopic section from 65 year old control subject showing no tau protein deposition.Microscopic section from John Grimsley showing numerous tau positive neurofibrillary tangles and neurites in the amygdala.Microscopic section from a 73 year old world champion boxer with severe dementia showing very severe tau protein deposition in the amygdala and thalamus.

A BRIEF HISTORY OF CTE
CTE was first described in 1928, when Dr. Harrison Martland described a group of boxers as having “punch drunk syndrome.” Over the next 75 years, several researchers reported similar findings in boxers and victims of brain trauma, but fewer than 50 cases were confirmed. In 2005, a pathologist named Bennet Omalu published the first evidence of CTE in an American football player: former Pittsburgh Steeler Mike Webster. Shortly thereafter, the Concussion Legacy Foundation partnered with Boston University and the U.S. Department of Veterans Affairs to form the VA-BU-CLF Brain Bank, led by Dr. Ann McKee. The Brain Bank has revolutionized how we understand the disease, with more than 500 brains donated, over 300 of which have been found to have CTE.

WHAT CAUSES CTE?
The best available evidence tells us that CTE is caused by repetitive hits to the head sustained over a period of years. This doesn’t mean a handful of concussions: most people diagnosed with CTE suffered hundreds or thousands of head impacts over the course of many years playing contact sports or serving in the military. And it’s not just concussions: the best available evidence points towards sub-concussive impacts, or hits to the head that don’t cause full-blown concussions, as the biggest factor.

 

WHO IS MOST AT RISK FOR CTE?
Every person diagnosed with CTE has one thing in common: a history of repetitive hits to the head.1 CTE is most often found in contact sport athletes and military veterans, likely because these are some of the only roles in modern life that involve purposeful, repetitive hits to the head. CTE has been found in individuals whose primary exposure to head impacts was through tackle football (200+ cases confirmed at the VA-BU-CLF Brain Bank), the military (25+ cases), hockey (20+ cases), boxing (15+ cases, 50+ globally), rugby (5+ cases), soccer (5+ cases, 10+ globally), pro wrestling (5+ cases), and, in fewer than three cases each, baseball, basketball, intimate partner violence, and individuals with developmental disorders who engaged in head banging behaviors.

Importantly, not everyone who has suffered repetitive hits to the head will develop CTE. There are several risk factors at play that make some people more prone to develop CTE than others, including:

Age of first exposure to head impacts
Athletes who begin playing contact sports at younger ages are at greater risk for CTE. Several published studies show that exposure to head impacts before age 12 is associated with worse outcomes than starting after age 12.

Length of exposure to head impacts
Athletes with longer careers playing contact sports are at greater risk than athletes with shorter careers. Among those diagnosed with CTE, athletes with longer careers are more likely to have more severe pathology than those with shorter careers.

There are very likely other risk factors that have yet to be discovered, including possible genetic differences that make some people more prone to develop CTE than others. More research will help scientists determine what those factors might be, and could help us understand how to prevent and treat the disease.

HOW IS CTE DIAGNOSED?
Currently, CTE can only be diagnosed after death through brain tissue analysis. Doctors with a specialty in brain diseases slice brain tissue and use special chemicals to make the Tau clumps visible. They then systematically search areas of the brain for Tau clumps with a unique pattern specific to CTE. The process can take several months to complete, and the analysis is not typically performed as a part of a normal autopsy. In fact, until recently there were relatively few doctors who knew how to diagnose CTE.

In 2015, researchers from the VA-BU-CLF Brain Bank, led by Dr. Ann McKee, collaborated with the National Institutes of Health to develop diagnostic criteria for CTE, so that any neuropathologist familiar with brain diseases can accurately diagnose CTE. This important work has made it possible for more and more scientists to be on the lookout for CTE, helping accelerate progress.

I SUFFERED A CONCUSSION. IS THAT GOING TO GIVE ME CTE?
One concussion in the absence of other brain trauma has never been seen to cause CTE.

The best evidence available today suggests that CTE is not caused by any single injury, but rather it is caused by years of regular, repetitive brain trauma. There are also many individuals who suffer years of head impacts, but do not develop CTE. More research will help us understand these factors in the future.

WHAT TREATMENTS EXIST FOR CTE?
Treating a disease that can’t be officially diagnosed until after death is difficult. Luckily there are lots of things that patients worried they have CTE can do to address their symptoms and find relief. Most treatments for CTE involve identifying the symptoms that are causing patients the most difficulty, and treating those symptoms with targeted therapies.

Mood changes
Mood changes, including depression, irritability, and anxiety, may be treated with cognitive behavioral therapy. Working with a cognitive behavioral therapist can help patients develop strategies that help them manage the particular mood symptoms that are causing the greatest problems.

Headaches
A variety of treatment options exist for headache, including craniosacral therapy, massage, acupuncture, or medications. Working with a doctor to determine the type of headache is helpful for determining the best treatment options.

Memory problems
Memory training exercises, including consistent note-taking strategies, can be helpful for continuing a patient’s activities of daily living, despite increasing difficulty with memory.

The Science of CTE

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[The following information is courtesy of the Concussion Legacy Foundation and based on the cutting edge research of  DR. Ann McKee]

CTE is a disease of the brain. To really understand the science of what’s going on, we’ll need some background on what the brain is like when it is healthy. A good place to start is by looking at our brain cells, or neurons.

Neuron

Neuron

BRAIN CELLS 101
If you’ve ever heard someone talking about how brains are wired, or if you’ve heard someone talking about getting their brains firing, they were talking about their neurons.

Neurons are the basic building blocks of the brain. Over 90 billion neurons connect in a complex network that allows us to interpret and react to our environment.

Every neuron has three main parts: the cell body, the axon, and the axon terminal. We’ll focus mainly on the axon, which is a long and skinny structure that behaves a lot like a wire in an electrical circuit. Neurons communicate with one another by sending electrical signals down their axons and off to adjacent cells.

CTE Axon and Hair

PROBLEMS WITH THE NEURON
The axon’s long and spindly shape helps the neuron reach far away cells in different parts of the brain, but there are two problems that come with that shape:

It makes the axons fragile, and prone to injury during concussion.
Things tend to break at their weakest point, and the axon is very often the weak point for the neuron. After a concussion, damage to axons is much more common than damage to other parts of the cell. A damaged axon has more trouble sending its signals, interfering with the brain’s ability to do its job.

It makes it difficult for the cells to distribute chemicals and materials to all areas of the cell.
Almost everything the cell needs to function is made in the cell body, but a lot of that stuff needs to be used along the axon or at the axon terminal. To get everything where it needs to go, the cell needs a transportation system.

MICROTUBULES: A FRAGILE TRANSPORTATION SYSTEM

Microtubules

To help distribute chemicals and materials throughout the cell, neurons have a special transportation system, made up of tiny tubes called microtubules. These tubes run the length of the cell, helping materials from one end make it down to the other end.

To continue with our example, if the axon were as big as a regular wire, each microtubule would only be as wide as a single strand of hair.

Remember: axons are the weakest point of the neuron, making them the first thing to break during a concussion. Microtubules are much smaller and weaker than the axons, making them vulnerable not only to concussion, but also smaller impacts that may leave the axons intact.

Since these tubes are so small, they need help supporting their structure. A special protein called Tau helps keep everything together by sticking to the tubes outside. In healthy brains, this is where the story ends: Tau supports the microtubules, microtubules help the cells function, and the brain operates normally.

In diseased brains, however, the same protein that helped keep everything together can actually cause things to fall apart.

TAU PROTEINS GOING HAYWIRE
If the microtubules break down, Tau proteins can float freely inside the cell. Under certain conditions, the free Tau proteins can change their shape (in a process called phosphorylation), causing them to clump together.

Once the clumps begin to form, they can spread to surrounding brain areas. At a certain point, the clumps take on a life of their own, and continue to grow and spread even without additional head impacts through a process known as prion spread. Scientists don’t yet know when this process begins, or if it happens to everyone who begins developing clumps or just in some people who are genetically pre-disposed.

What scientists do know is that the Tau in CTE spreads in a distinctive pattern that is unique to CTE. Scientists also believe that the slow spread of Tau clusters is likely one reason it takes so long for symptoms to show up – it takes a long time for the slow moving clumps to infect enough brain tissue to change brain function.

FUTURE DIRECTIONS OF CTE RESEARCH
The biggest question in CTE research today is: How can we diagnose CTE in a living person? Once we can diagnose CTE in a living person, we can begin evaluating potential treatments and therapies to help people who are suffering from the symptoms of CTE.

Scientists are working hard to develop such a test, and there have been promising findings using a variety of special techniques. Some of the most exciting lines of research are trying to diagnose CTE using:

Positron Emission Tomography (PET scans): Researchers inject a tracing chemical that binds to the Tau proteins in CTE, and use a special brain scanner to trace where the chemical settles in the brain. With a tracer chemical that binds to Tau (and only Tau), this technique could show us the tell-tale distribution of tau tangles while someone is still alive. Several research groups have developed such a chemical, and early studies in athletes are already underway.

Fluid based biomarkers: New techniques in biochemistry have allowed researchers to develop extremely sensitive tests, able to detect proteins and substances in the blood at extremely low levels. Researchers using these tests are looking for evidence of abnormal tau and other indicators in the blood of athletes at risk for CTE. Normally these indicators would be caught by a robust barrier between the bloodstream and the brain (called the blood brain barrier), but repeated concussions and subconcussive blows that cause CTE can also damage this barrier, allowing clues to slip out of the brain.