The fresh cut grass and crisply-painted yard lines. The sound of helmets clashing in an epic stack of large men vying for a single ball. Stands packed high with thousands upon thousands of crazed, prideful, body-painted fanatics. The cheerleaders. The roar of the crowd. Chips, dip, and booze. Hilarious touchdown dances. Dementia, confusion, and depression.
That last bit may not be present on game day, but for many football players, it's brewing all along—with every clash, tackle, and fall.
Cases of chronic traumatic encephalopathy, or CTE, are only now beginning to unfold with postmortem diagnoses and early symptoms of memory loss, depression, confusion, and aggression being reported by former NFL players.
And with the recent settlement involving 4,500+ former footballers against the NFL, the topic of CTE has quickly shifted from being more than just a medical issue.
Brett Favre, former Green Bay Packers quarterback, announced last month on Sports Talk 570 in Washington that he couldn't remember his daughter playing youth soccer one summer.
|Brett Favre, retired after 17 years of|
Favre, though widely-known and well-respected, is not the first to "come out" with CTE symptoms.
Like a number of neurodegenerative diseases, such as Alzheimer's, CTE can only be conclusively ruled after examining brain tissue. As of last December, 33 former NFLers have been diagnosed post-mortem.
Encephalopathy is defined as any disease of the brain. Its prefixes, chronic traumatic, are aptly named. CTE is a result of months to years to decades of repetitive impacts on the brain and its resulting damage to axons, the portion of the neuron at which impulses are conducted to communicate with other neurons.
Symptoms of CTE range from changes in mood (apathy, anxiety, suicidality) to behavior (aggression) to cognition (memory loss) to, in some cases, difficulty with balance and gait.
It's not just footballers. Boxers, wrestlers, ice hockey, soccer, and rugby players tend to be more prone to head traumas than athletes of other sports.
And despite athletes getting the most attention, they're not the only ones affected. Combat militants, domestic abuse victims, and even those with a history of seizures are all ticking time bombs for CTE.
In February 2011, former Bears, Giants, and Cardinals safety Dave Duerson, at the age of 50, sent a text message to his family requesting that his brain be used for research at Boston University School of Medicine, location of the largest CTE brain bank in the world.
He promptly held a gun to his chest and shot himself dead.
Dr. Robert Stern, co-director of the research group, and his colleagues uncovered elevated levels of tau protein in Duerson's brain, clumped especially around its deep wrinkles, called sulci.
Duerson is just one of a number of suicides and murder-suicides recorded among athletes in recent years.
And the suicide of 21-year old University of Pennsylvania football player Owen Thomas in 2010 was a startling reminder that more than just the old veterans are affected by this kind of trauma.
The brain bank at Boston University was established in 2008 and, after just two years, had possession of over 250 current and former athletes' brains and a no-strings-attached $1 million grant from the NFL.
This group was preceded by the Brain Injury Research Institute (BIRI) in 2002, of which forensic pathologist Bennet Omalu, M.D. was a founding member. Omalu was the first to characterize CTE in the brains of five former NFLers who committed suicide.
He was surprised to find Alzheimer's- and dementia-like brain damage in these relatively young men.
The typical brain afflicted with CTE will have a reduced brain volume, particularly in the frontal and temporal lobes. This reduction is associated with enlarged ventricles, or fluid-filled brain cavities.
Reduced blood flow and, eventually, atrophy to several key brain regions, including the amygdala (emotion) and hippocampus (memory formation) likely explains the physical and personality changes associated with the disease.
A view under the microscope reveals neuron loss, beta-amyloid peptide, and neurofibrillary tangles formed from deposits of tau protein—cornerstones of our current knowledge of Alzheimer's.
In rodent models, traumatic brain injury has been followed by neurodegeneration for as long as a year after impact. The pathology, or cause, between point A (trauma) to point B (dementia) is not well-understood beyond these observations, unfortunately.
Just two weeks ago, Hall of Fame running back Tony Dorsett and two other former NFLers were diagnosed with CTE after undergoing three months of brain scans and other tests at UCLA.
Dorsett was among the 4,500+ former players involved in a $765 million lawsuit against the NFL that was settled at the end of August. Ninety percent of the settlement will compensate former players for concussion-related injuries over the next 20 years, while the remaining 10% will be used for performing baseline medical exams.
Although the NFL denies the allegations, former players insist that the organization hid the known risks of concussion from players to, they say, "protect its image."
Brett Favre, now 44, was sacked over 525 times in his career. "In some respects," he told Matt Lauer in an interview with TODAY, "I'm almost glad I don't have a son because of the pressures he would face."
"I would be real leery of him playing."
Some youth organizations have begun implementing flag football as an alternative to tackle football in kids—that critical developmental period when concussions are all but necessary. But that proposal is unlikely to catch on. Not with the obsession, reverence, and hero worship for the Great American Sport.
After all, said former player and head coach Duffy Daugherty (1915-1987): "Football is not a contact sport. It's a collision sport.
"Dancing is a good example of a contact sport."
With 3,000 brain injuries per year and an average of 0.41 concussions per game in the NFL alone, the quote could not be truer.
Shively, S, AI Scher, DP Perl, and R Diaz-Arrastia. Dementia resulting from traumatic brain injury: What is the pathology? Arch Neurol 69(10): 1245-1251 (2012).
Image credit: Michelle M. Dickson, PSUMark2006, NIH (via Wikimedia Commons), Riplee, slemmon (via Flickr).