Dr. William Brown
Special to The Lake Report
I played football in high school and remember once “seeing stars” and feeling momentarily stunned after tackling the ball carrier head-on.
The sensations lasted only a few moments, but there were other players who were unable to remember much, if anything, for the rest of a game despite continuing to play after taking a bad hit.
To us it was all a big joke to talk about in the locker room following the game.
Half a century ago, no one knew much about concussions or even the anatomical and physiological basis of consciousness – certainly not the players, the coaches, the parents, family physicians and most specialists, except for a few neurosurgeons, and then only for serious head injuries associated with hemorrhage into the brain or between the surface of the brain and inner lining of the skull or other potentially serious and occasionally lethal injuries.
Except for the latter, no one paid any attention to the long-term consequences of repeated concussions in football or any other sport for that matter, except for boxing.
A report in the American Journal of Medicine in 1928 first identified an association in boxers, especially those boxers with a history of repeated knock-outs, and the later progressive development of parkinsonian features and dementia to which the term “Dementia Pugilistica” or “Punch-Drunk Syndrome” became attached, examples of which I saw in my neurology training days in Toronto and later as consultant neurologist in Boston. That was then.
Much changed with the discovery that some professional football players in the American and National football leagues, following their retirement, went on to develop a unique form of dementia given the name of Chronic Traumatic Encephalopathy (CTE). Its clinical symptoms occasionally began toward the end of their playing career, or more commonly sometime thereafter, but in any case, well before the usual later clinical onset of Alzheimer’s disease.
Autopsy studies of some affected players revealed deposits of an abnormal protein – phosphorylated tau – in the bases of the infolded regions of the brain’s cortex, together with a bevy of less specific degenerative and inflammatory changes.
Later studies revealed similar changes, albeit accompanied with more inflammatory changes, in the brains of much younger athletes, some in their teenage years with a history of multiple concussions. All of which understandably alarmed the parents of young athletes participating in contact sports – not just American football.
Recently a former colleague of mine in Boston, Allan Ropper, a world expert on traumatic brain injuries and concussion, summarized the chain of events that lead to CTE.
It begins usually with a history of several concussions, “which leads to inflammation or protein misfolding, aggregation of tau protein that leads to degeneration of neurons and supporting elements, and later the emergence of behavioural and cognitive disturbances years after exposure to play.”
Indeed a study, published in April this year in the New England Journal of Medicine, in which the brains of 26 former NFL players and 31 controls were examined using an imaging tool for tau, revealed elevated tau levels bilaterally in the posterior frontal and medial temporal lobes and, in one instance, the left parietal lobe in some of the former players but not in the controls.
There was, however, no correlation between the deposits of tau and the players’ scores on neuropsychological tests. In the accompanying editorial Ropper made the comment that, “As with Alzheimer’s disease, the CTE field is in a phase of fumbling with circumstantial evidence for a connection between tau deposition and a clinical syndrome.”
By Alzheimer’s disease he was probably referring to the lack of solid evidence that deposits of beta amyloid, or for that matter tau, play a significant role in the cause of the Alzheimer’s disease based on a trail of negative studies of different drugs designed to deplete beta amyloid stores (which they did for the most part), yet failed to change the course of the clinical manifestations of the disease in patients with early Alzheimer’s disease.
For now, despite the worries of players and families, as well as their coaches, there’s little consensus about what types and frequency of concussions to worry about, how best to protect players by changing the rules and enforcing those rules in contact sports to minimize the frequency and severity of concussions, changing the design of protective gear for players and guidelines for mandatory rest periods following concussions.
That’s a lot to be uncertain about. And we haven’t even talked about athletes, who following a single or several concussions, go on to develop distressing cognitive and behavioural symptoms that may last many months following the injury.
To hear more about all these issues, come to the next Infohealth session on Feb. 12 at 2 p.m., led by Hannah Synder, a medical student for whom I am acting as a mentor. Hannah did an excellent job early in 2019 with her comprehensive review of stroke.
Dr. William Brown is a professor of neurology at McMaster University and co-founder of the Infohealth series held on the second Wednesday of each month at the Niagara-on-the-Lake Public Library.