American football is characterized on every play by collisions carried out with varying intensity. Wide receivers, defensive backs and punt returners are particularly vulnerable to hits that capture the attention of fans and commentators alike. Linemen sustain substantial hits on every play.
Most of the time, the colliding athletes spring to their feet. A small number will suffer concussions.
During five collegiate football seasons beginning in 2004, the National Collegiate Athletic Association documented more than 41,000 injuries among players at member institutions. The injury rate was 8.1 per 1,000 exposures for athletes in games or practices. Concussions accounted for 7.4 percent of injuries during this time period. The problem with this data is that many concussions are either unreported or undiagnosed.
Recent studies on collegiate and professional players show decreased volume in the hippocampus, a component of the brain, in individuals with histories of game-related concussions. These changes are detected by sensitive imaging studies. The hippocampus plays a vital role in the storage and retrieval of long-term memory. Shrinkage of the hippocampus is associated with decreased speed in performing cognitive tests.
Multiple impacts to the brain that do not result in concussion may still, over time, lead to structural changes in the hippocampus. A study published in 2014 compared hippocampal volume in 25 collegiate players with documented concussions versus 25 players without concussion. Players with a history of concussions had smaller hippocampi. The more years that any player, with or without concussive histories, participated in practice and games, the more likely he was to have a diminished hippocampus and slowed cognitive function.
A study from 2013 evaluated 67 volunteers representing three collegiate teams. In games at the end of the season, blows to the head were monitored by video and post-game interviews. Blood samples were collected before and after the games and also six months later to measure a protein derived from brain cells.
The presence of the protein in the blood indicates a disruption of the normal chemical barrier between brain and bloodstream. With enough protein in the blood, the body develops antibodies against it as an immune response. Such antibodies may attack and damage brain cells over a sustained period of time. The alterations in brain structure correlate with changes in cognition and might be the basis of chronic traumatic encephalopathy — the condition seen in autopsied brains of professional football players who suffered from early-onset dementia.
In the study of college teams, the brain protein was only detected in blood samples from players who sustained the greatest number of hits to the head; the more hits, the higher the concentration of protein. A player with a high level of the antibody was more likely to have a altered brain structure and slowed cognitive function, showing that brain injury leads to leakage of a protein into the bloodstream.
These studies involve small samples of players. The research is costly and must be carried out over long periods of time by teams of researchers. Much larger numbers of players must be followed over a number of years — ideally from high school to college and beyond — to assess the full significance of brain injuries associated with football.
The NCAA and the National Football League are the logical funders of this research. The outcome of the research would likely lead to changes in rules, procedures, equipment and medical evaluation to enhance the safety of football for all participants.
Contact Clif Cleaveland at firstname.lastname@example.org.