Filed under: Athletes, Athletic Trainers, Coaches, Uncategorized | Tags: Brain Bank, Brain Injury, Chronic Traumatic Encephalopathy, concussion, CTE, Dr. Ann McKee, Head Injuries, NFL, tau protein
Chronic Traumatic Encephalopathy (CTE) is a relatively new disease that first came to light in 2008. There have not been many cases of CTE diagnosed, in fact, as of 2009 only 49 cases have been studied. With such a small sample size, the argument could be made that why should we care? Here is why; CTE is a degenerative disease that stems from repeated brain injuries that cause an abnormal build-up of tau protein. This build up is seen as tangles that closely resemble the tangles associated with Alzheimer’s disease. These tangles destroy brain cells and end up compromising entire sections of the brain.
Dr. Ann Mckee is a neuropathologist that is currently doing research at the Veterans Administration Hospital in Bedford, Massachusetts. She is developing a “brain bank” of various athletes who have decided to donate their brain due to their suspicion of the disease. This disease is typically asymptomatic until 8 or 10 years after the period of time that the concussions were sustained. The average age for onset of symptoms has been 43. The most common symptoms are mood changes, depression, memory problems, aggression, loss of impulse control, personality changes and dementia. Once these symptoms emerge they steadily get worse eventually leading to full blown dementia and sometimes death. CTE can only be diagnosed post-mortem. Perhaps the most shocking finding is that CTE can develop without any significant brain trauma or concussion. It can stem just from the day to day jostling of the brain that is associated with aggressive sports such as boxing, hockey and football.
Bob Prober and Reggie Flemming were among the first to be diagnosed and since then many former NFL and NHL athletes have fallen victim to this disease. John Grimsley, Mike Webster, Andre Waters, Justin Strzelcyk, Terry Long, Tom McHale and Dave Duerson are recent NFL players that have been diagnosed with this disease, and it is suspected that CTE was a major attribution to each of their deaths. A lot of the players who have been diagnosed with CTE have committed suicide at a young age, and they have purposefully shot themselves in the chest so they can donate their brains to Dr. Mckee’s brain bank. Junior Seau is among the most recent athlete to have suspected CTE. As of now there is no current treatment for CTE. There is also no set number of brain injuries that have to be sustained in order to develop CTE. This is even more reason to treat concussions more conservatively in order to allow proper time for the brain to heal.
Below is a timeline of the NFL’s response to this growing trend and links that support current findings on CTE.
1994 The NFL establishes its Mild Traumatic Brain Injury (MTBI) Committee.
2002-2007: NFL’s Response. In response to Omalu’s report of CTE in Mike Webster’s brain tissue, NFL MTBI Concussion Committee members Ira Casson, Elliot Pellman, and David Viano identified the report as “some bullshit theory,” essentially shrugging off the conclusions.
Spring 2007 The “88 Plan” is launched to provide financial support for retired players suffering from dementia.
June 2007 Concussion Summit. All 32 teams required to send their doctors and athletic trainers to the MTBI Committee’s first league wide Summit on Concussions where independent scientists presented conclusions and findings linking football related brain injury and concussions and long-term effects of player concussions.
August 2007 Ignoring the Concussion Summit findings, the NFL produces a pamphlet for players designed to inform them about the league’s policy on concussions, the symptoms and signs of concussions, and related subjects. The pamphlet included the following text:
“If I have had more than one concussion, am I at increased risk for another injury? Current research with professional athletes has not shown that having more than one or two concussions leads to permanent problems if each injury is managed properly. It is important to understand that there is no magic number for how many concussions is too many. Research is currently underway to determine if there are any long-term effects of concussion in NFL athletes.”
2008 NFL’s Response. In response to Dr. McKee’s studies, former NFL MTBI Concussion Committee Co-Chair, Dr. Ira Casson, characterizes each study as an isolated incident from which no conclusion could be drawn. Dr. Casson further maintains that “there is not enough valid, reliable or objective scientific evidence at present to determine whether…repeat head impacts in professional football result in long term brain damage.”
December 2, 2009 NFL changes Return-to-Play Rules: Players with concussions cannot return-to-play the same day. Once removed, player cannot return-to-play until fully asymptomatic, normal neuro exam, normal neuropsych testing, and clearance obtained by both team physician and an independent consultant. Players are to be candid with medical staff and to disclose any symptoms.
2010 Following the 2009 season, the NFL enacts the following rule changes for the 2010 season designed to protect players who could be particularly vulnerable to a blow to the head during the game: (1) When a player loses his helmet, an official will whistle the play dead; (2) A defensive payer cannot line up directly across from the “snapper.” The defensive player “must have his entire body outside the snapper’s shoulder pads.”; and (3) A player may not launch himself into a receiver who has caught the ball, but “has not had time to protect himself.”
July 2010 The NFL and NFLPA release a poster on concussions for NFL players that includes a very different message (from the 2007 pamphlet) regarding long-term effects of brain injuries. The poster includes the following language:
“Unlike other injuries, there may be significant consequences of ‘playing through’ a concussion. Repetitive brain injury, when not treated promptly and properly may cause significant damage to your brain….TBI can cause a wide range of short-or long-term changes affecting thinking, sensation, language, or emotions.”
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