Cincinnati Bengals receiver Chris Henry (age 26) had suffered from chronic traumatic encephalopathy (CTE) before he died tragically in December 2009, media attention is once again focused on the possible long term effects of multiple concussions on the brain. Co-directors of the Brain Injury Research Institute at West Virginia, Julian Bailes, neurosurgeon, and Bennet Omalu, California medical examiner, made the stunning announcement earlier this year (Los Angeles Times, 2010).

Stunning because Henry was only 26 years old at the time of his death, yet his brain already showed the pathophysiological effects of CTE. This case provides more evidence to the growing data showing that repetitive blows to the brain may permanently alter the brain.

Chronic traumatic encephalopathy is a degenerative brain disease that results in behaviors similar to Alzheimer’s disease (AD). However, according to researchers, CTE has a clear environmental cause (repeated brain trauma) rather than a genetic cause. In other words, CTE is the only preventable form of dementia.

Originally termed “dementia pugilistica” otherwise known as “punch drunk”, this disorder was first described in 1928 in boxers because boxers suffered from slowed movement, confusion, speech problems, and tremors (Sports Legacy Institute, 2010).

Although only recently termed chronic traumatic encephalopathy (first documented in the medical literature in 1996), CTE is now the preferred medical term for this disease.

The disease is characterized by a number of neurological and physiological changes in the brain including the buildup of an abnormal protein called tau. This protein builds up in places in the brain where it is not supposed to be and congregates in clumps in and around the brain disrupting its function.

The clinical symptoms associated with CTE vary in severity depending on which clinical stage the individual is in (McKee, A.C., et. al., 2009). Initial symptoms include the following:

The individual may progress through three stages of the disease beginning in the first stage with affective disturbances and psychotic symptoms. As the disease progresses to stage two, the individual may suffer from social instability, erratic behavior, memory loss, and the initial symptoms of Parkinson’s disease (McKee, A.C., et.al., 2009) .

The final stage consists of a progressive deterioration to dementia and may have other symptoms including the signs associated with Parkinson’s disease, speech difficulties, gait abnormalities, dysarthria (speech disorder characterized by neuromuscular weakness or lack of control of facial muscles), dysphagia (difficulty swallowing), and ptosis (drooping eyelid) (McKee, A.C., et.al., 2009).

Unfortunately, at this time, there are no specific markers or tests to detect CTE in a living athlete. Currently, CTE is diagnosed through studying brain tissue under a microscope after death.

Hopefully with the current research underway at the Center for the Study of Traumatic Encephalopathy, there will be ways to diagnose CTE in living athletes early in the future.

Although initially seen primarily in professional boxers, cases have now been identified in a number of athletes competing in different sports. According to Mckee et al. (2009), of the 51 confirmed cases of CTE, 90% of the cases occurred in athletes. The athletes included the following:

Furthermore, statistics from the Center for the Study of Traumatic Encephalopathy (CSTE) identified that 17 of the 18 deceased contact sport athletes studied showed evidence of CTE (Sports Legacy Institute, 2010).

Because repetitive closed head injuries seems to be the cause of CTE, athletes involved in contact sports may be at risk including athletes in the sports of football, boxing, wrestling, rugby, hockey, lacrosse, soccer, and skiing. CTE has also been identified in “epileptics, head bangers, and domestic abuse victims” (Mckee, A.C., et. al, 2009).

While athletes in collision sports (football and boxing) may sustain higher numbers of concussive and subconcussive brain injuries, any athlete in any sport who may have sustained more than one concussive injury may be at risk for CTE.

Unfortunately, at this time, there are no specific markers or tests to detect CTE in a living athlete. Currently, CTE is diagnosed through studying brain tissue under a microscope. This means that there is no way to tell if an athlete with a history of concussions is at risk for CTE.

Unfortunately, the research is not at the point to determine the exact number of concussive injuries it takes to initiate permanent brain deterioration. What is known is that repetitive brain injury causes CTE. The questions that need to be answered include:

A lot of questions need to be answered. Fortunately, the Center for the Study of Traumatic Encephalopathy was created in 2008 for the sole purpose of conducting research to determine the neuropathology and pathogenesis of CTE. Once the pathology of the disease is better understood, then the risk factors can be identified along with how to prevent and treat this disease.

According to a press release by one of the co-directors of CSTE, Dr. Robert Stern, a large study is underway involving a number of former NFL players to study their lives and then examine their brains following their death. To this end, more than 250 current and former athletes, including 60 retired NFL players, have agreed to donate their brain and spinal cord to the CSTE upon death (CSTE Press Release, 2010).

Because the cause of CTE is known, the prevention of CTE needs to focus on the proper diagnosis and management of athletes who have sustained concussions along with adhering to guidelines before returning to play. Unfortunately even with the advances lately in the management of concussion, they may not be enough.

According to a recent statement by Dr. Robert Stern, co-director of CSTE, new evidence shows” that 85% of concussions require about three weeks of recovery” (Abel, D., 2010). This is a longer time period than anything currently in the literature for return to play guidelines.

Current guidelines recommend a graduated increase in the level of activity of the athlete progressing from the initial stage of “light exercise” towards “full contact” activity once the athlete is completely symptom-free at rest. The athlete progresses through each stage as long as the athlete remains symptom-free during each stage. If symptoms return, then the athlete needs to stop for the day. This progression may be completed in as little as 5 days or may take as long as the athlete requires.

More research needs to be conducted to ensure that the current neurological tests that are being used in the field are accurate and correspond correctly to the state of the brain. If concussed athletes’ brains still suffer the effects of being concussed without corresponding outward signs or symptoms, then better neurocognitive tests need to be created to accurately reflect the status of the brain.

While the researchers continue to study the effects of concussion on athletes’ brains, lawmakers have moved to take the issue into their own hands by creating laws that would better protect young athletes. Bills have been introduced across this country in a number of states (i.e., California, New York, Massachusetts) to protect athletes who have been concussed by not allowing these athletes to return to play on the same day of the injury, requiring medical approval before concussed athletes are allowed to return to their sport, and by introducing training and education for coaches, athletic administrators, parents, and athletes as to the dangers of concussions (Abel, D., 2010).

Dr. Robert Stern offers his own recommendations specifically for the sport of football including reducing full-contact practices, changing the way players line up on the field, and using new helmets to reduce the force of the impact on the football players’ brains (Abel, D., 2010).

The best recommendations for the prevention of CTE is to ensure that athletes who sustain concussions be seen by sports medicine professionals who have experience in treating concussions. Because the research on concussions has changed significantly over the past several years, primary care physicians who do not specialize in sports medicine might not be aware of how to correctly diagnose a concussion using the latest guidelines, utilize the new diagnostic tools, and how to apply current treatment protocols.

Parents need to also be educated as to the signs and symptoms of concussion and be diligent to learning the current treatment protocols also. Parents may be in the best situation to detect subtle changes in their child’s behavior that others may not notice.

Last, it is the parents and the coaches’ responsibility to ensure that no athletes return to sport until they are completely symptom free of all signs and symptoms of concussion at rest and with full activity. Returning an athlete too early to sport after a concussion may also place the athlete at risk for second impact syndrome (life threatening brain injury).

Because this disease has not been able to be detected until after the death of the athlete, it is not an area that has received attention until recently. As researchers better understand the progression of CTE and its effect on the brain, researchers can then begin to focus on treatment protocols.

If you suspect that you have Chronic Traumatic Encephalopathy, it is critical to seek the urgent consultation of a local sports injuries doctor for appropriate care. To locate a top doctor or physical therapist in your area, please visit our Find a Sports Medicine Doctor or Physical Therapist Near You section.

Abel, D. (April 28, 2010). Bill addressing student concussions advances. The Boston Globe. (accessed on June 29, 2010).

Center for the Study of Traumatic Encephalopathy, Boston University, “20 More NFL Stars to Donate Brains to Research”, (accessed on June 29, 2010).

McKee, A.C., Cantu, R.C., Nowinski, C.J., Hedley-Whyte, E.T., Gavett, B.E., Budson, A.E. Santini, V.E., Lee, H., Kubilus, C.A., & Stern;, R.A. (2009). Chronic traumatic encephalopathy in athletes: progressive tauopathy after repetitive head injury. Journal of Neuropathology and Experimental Neurology 68:7, 709-735.

Los Angeles Times Staff and Wire Reports (June 28, 2010). Bengals’ Henry had chronic brain injury. Los Angeles Times.

Sportslegacy.com, “Chronic Traumatic Encephalopathy”, (accessed on June 29, 2010).

Telander, R. (June 25, 2010). What football did for us and … what football did to us: the story of the 1968-1970 Northwestern Wildcats. Sun Times. (accessed on June 29, 2010).

Zeigler, T. (June 22, 2009). Chronic traumatic encephalopathy: possible consequences of recurrent concussion. Suite101.com.