Our brains are very soft organs that are surrounded by spinal fluid and are protected by the hard outer covering of our skulls.
Under normal circumstances, spinal fluid cushions the brain and keeps it from crashing into the skull. However, if our heads or our bodies are hit hard, our brains can slam into our skulls and result in traumatic brain injuries (TBIs). TBIs are also caused when the skull is fractured and the brain is directly damaged by outside force.
Although concussions, which we’ll discuss later, are sometimes referred to as mild TBIs, the reality is that no injury to the brain is mild and repeated injuries will lead to neurological degeneration that includes dementia.
TBIs are complex neurological injuries that result in a wide variety and severity of symptoms and disabilities.
In the category of TBIs from falling, most of the falls occur disproportionately in the very young (55% of falls among children occur in children between the ages of 0 and 14) and the very old (81% of falls among adults occur in adults who are 65 or older).
Most of the TBIs in the Other category (19%) are from personal firearms and military weapons.
A type of TBI that is more frequently in the headlines today is Chronic Traumatic Encephalopathy (CTE). CTE is brain damage that occurs as a result of repeated concussions (a concussion is defined as injury to the brain from a direct blow to the head or from the head or upper body being violently shaken).
The first identified variant of CTE was described in 1928 by forensic pathologist Dr. Harrison Stanford Martland as pugilistic (from the Latin word pugil, which is translated as “boxer” or “fighter”) dementia. The symptoms included tremors (Parkinsonism), slowed movement, mental confusion, and speech difficulties.
In 1973, the neuropathology of pugilistic dementia was discovered and described by a team of pathologists led by J. A. Corsellis who documented their findings after performing thorough autopsies on the brains of 15 deceased boxers.
Former boxing heavyweight champion Muhammad Ali began boxing in Kentucky when he was 12 years old.
By the age of 18, he had boxed his way to the heavyweight gold medal at the Olympics (1960).
A few months later Ali began his professional boxing career. He quickly gained national prominence because of his skill in the ring and his trademark quote: “Float like a butterfly, sting like a bee. The hands can’t hit what the eyes can’t see.” He boxed professionally until his retirement in 1981.
In 1984, Ali was diagnosed with Parkinsonism (the tremors of pugilistic dementia) and his neurological health has deteriorated steadily to include all the advanced symptoms of this variant of CTE.
His wife, Lonnie, is his caregiver and contributed to a moving article that AARP published last year about what she and Ali deal with on a daily basis as a result of the neurological degeneration that CTE has caused.
CTE has increasingly become a major health concern in the high-contact sports of professional wrestling, ice hockey, soccer, and football as more and more current and retired athletes are showing symptoms consistent with CTE.
In recent years, football – and especially professional football – has become the focal point for a closer examination of CTE. Not only has this sport become more violent in terms of how the game is played, but how concussions are treated – or not treated – has also come under greater scrutiny.
Although NFL team doctors assert that CTE is “rare” or “overexaggerated,” the hard scientific neurological and physiological evidence proves that these doctors are simply paid hirelings who care more about their paychecks than they do about the overall health of the players.
Let’s examine the facts. In a 2014 landmark study by the largest brain bank in the United States, 76 of the 79 brains of deceased NFL players that pathologists examined had TBI, and specifically, CTE.
A class action lawsuit has been filed – and a tentative agreement reached with the NFL – by retired NFL football players and/or their families (some of the players have already died from neurodegenerative causes) which claims that players were not (a) adequately protected from suffering concussions, (b) medically treated properly following concussions, and (c) provided adequate medical compensation to treat the burgeoning costs of CTE as it progresses.
This gist of this lawsuit is that the NFL used – and abused – these players to fabulously guild the seemingly-endless coffers of the NFL, often forcing the players by intimidation or fear to get back on the field as soon as they could after suffering a concussion (often in the same game), and then abandoned their responsibility to their former employees (as part of their contractual agreement) as soon as the employees began costing them money instead of making them money.
Even more damning to the NFL is the actuarial report accompanying the lawsuit that indicates that at least 1/3 of NFL players will suffer CTE.
If there is a silver lining in all of this, it is that the younger NFL players have a much greater awareness of the relationship – and their increased risk – between professional football and CTE.
They are aware of the very real probability that they will be one of the 1 out of every 3 players who develops CTE.
And they’re choosing their long-term health, including their brain health, over temporary fame and fortune.
An unprecedented number of younger – and in-their-prime in the professional football world – NFL players have already retired before the 2015-2016 season begins.
While Finnegan, Locker, and Worilds did not publicly cite CTE as a factor in their premature retirements from the NFL, there can be no logical reason to doubt that the mounting evidence was a factor in their decisions.
Chris Borland, on the other hand, made no secret that the high probability of CTE was the reason for his decision to retire.
Borland just finished his rookie season (2014-2015) with the San Francisco 49ers, but he revealed after the season that he suffered a concussion in training camp last fall. Instead of reporting the concussion, Borland covered it up so that he could continue to practice and win a starting position on the team.
This is the kind of competitive pressure that gets put on these young players by the NFL (yes, Borland made the decision and he bears the responsibility for it, but had he reported the concussion, he would have been replaced and lost the starting spot and may not have played all season).
Fortunately, though, Borland came to his senses and realized how much he had jeopardized – and would continue to – his neurological health.
We can only hope that more athletes in high-contact sports will know the higher risks of TBIs they face, not just in the professional leagues, but at the amateur levels, and they will choose to walk away from certain neurological damage.
In the meantime, we have a better understanding just in our daily lives of how TBIs can happen and what the results can be, so I hope that we’re a little more observant and attentive after falls with our little loved ones and our older loved ones, especially those already going through the journey through dementias and Alzheimer’s Disease, as they are even more prone to falling than the general elderly population.