Junior Seau's Suicide, And What We Know About Traumatic Brain Injury

SAN DIEGO, CA - FILE: Junior Seau #55 linebacker for the San Diego Chargers watches the offense work versus the Seattle Seahawks in their preseason game on August 16, 2002 at Qualcomm Stadium in San Diego, California. According to reports May 2, 2012, Seau, 43, was found dead in his home in Oceanside, California. (Photo by Stephen Dunn/Getty Images)

After Junior Seau took his own life on Wednesday, many speculated that CTE -- a degenerative brain condition cause by head trauma -- could have been the cause. SB Nation's Medical Expert explains more about the issue and how it affects athletes.

The tragic death of Junior Seau, the future NFL Hall of Fame linebacker who committed suicide at the age of 43 on Wednesday, may have been hastened by the violent nature of the sport he loved and, sadly, the breathtaking speed and ferocity with which he played his entire career. While the circumstances that led to his suicide may not be known for some time (or ever), his death has once again sparked conversation about the deleterious effects of repetitive head trauma on the long-term health of athletes who play contact sports, regardless of age or level of competition.

It is notable that Seau’s was the third suicide among former professional football players in the past 15 months, and the previous two – former safeties Dave Duerson and Ray Easterling – were thought to have suffered from chronic traumatic encephalopathy (CTE) acquired over their years in the NFL. And as researchers continue to make progress in their understanding of CTE -- a degenerative brain condition linked to head trauma that can lead to memory impairment, loss of impulse control, depression, and dementia -- questions continue to mount over what can be done to curb its rising incidence.

CTE results in behaviors similar to Alzheimer’s disease but differs in that it has a clear environmental cause (repeated brain trauma) rather than a genetic cause. The condition is characterized by a number of neurological and physiological changes in the brain, most importantly the buildup of an abnormal protein called tau. With continued traumatic brain injury, as occurs in concussions or even with injuries that do not lead to concussive symptoms, tau protein congregates in clumps in and around the brain, disrupting its function. Its effects on behavior can take place over a span of months to decades, making CTE nearly impossible to diagnose until the patient has died and the brain itself can be inspected for changes suggestive of the condition.

The clinical symptoms associated with CTE vary in severity depending on which of three clinical stages the individual is experiencing. In the first stage, which may take place over months to years, a patient may suffer from a number of symptoms including headaches, dizziness, confusion, depression, and psychosis. As the disease progresses to the second stage, the individual may suffer from social instability, erratic behavior, memory loss, and the initial symptoms of Parkinson’s disease. The final stage consists of a progressive deterioration to dementia and may have other symptoms including those associated with Parkinson’s disease.

Because repetitive closed head injuries seem to be the cause of CTE, athletes involved in contact sports may be at highest risk. However, while athletes in collision sports such as football and boxing may sustain higher numbers of concussive and pre-concussive brain injuries, an 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 tests to detect CTE in a living athlete, and currently it is diagnosed through studying brain tissue under a microscope. Until more research is completed among athletes who have died from the condition, there will be no way to tell if an athlete with a history of concussions is at risk for CTE, or how many concussive injuries it takes to initiate permanent brain deterioration.

Because the cause of CTE is known, to date the prevention of CTE has focused on the proper diagnosis and management of athletes who have sustained concussions, along with adhering to guidelines before returning to play. Current guidelines recommend a graduated increase in the level of activity following a concussion, progressing from the initial stage of "light exercise" toward "full contact" activity once the athlete is completely symptom-free at rest. This progression may be completed in as little as 5 days or may take as long as a team trainer or physician deems necessary.

Up until 2009, the grand majority of CTE described in all medical literature were among boxers. However, in recent years, athletes from a host of other sports, including, but not limited to, former NFL stars Chris Henry, Mike Webster, and Andre Waters; NHL enforcer Bob Probert; and professional wrestlers Chris Benoit and Andrew "Test" Martin were found to have signs of CTE on post-mortem examinations. It is notable that these athletes spanned a wide range of ages at their times of death, and that each struggled with a history of conditions and behaviors known to be associated with CTE. It is also notable that some were never formally diagnosed with or missed playing time because of concussions; such was the case for Seau.

Although it is unclear as of yet whether Seau too suffered from CTE, his untimely death has called attention to the need for professional athletes and their coaches, trainers, and physicians to exercise vigilance about guarding against head injury and allowing for sufficient healing to take place before re-entering the athletic arena. Until scientists can devise equipment that better protects against significant head injury, or unless the rules of these sports are changed entirely, the best that can be done is to stress prevention and increase education among those engaged in athletics at all levels of competition.

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