Patric Stanton, Ph.D., explains how one groundbreaking study proves that it’s hits to the head—not concussion—that trigger CTE.
As an expert in his field, with decades of experience studying synaptic plasticity in the quest to better understand neurological diseases, including traumatic brain injury, Patric K. Stanton, Ph.D., professor of cell biology and anatomy and of neurology, and a team at New York Medical College were called upon to join an elite contingent of researchers studying the origins of Chronic Traumatic Encephalopathy (CTE). The stunning results of that study provides the first solid evidence regarding the origins of CTE. According to Stanton, “It is becoming clear that simply experiencing repeated impact in contact sports, without ever having a concussion, can still increase the risk of developing CTE. We need to know how much it increases this risk, and develop new methods of monitoring impact to determine when, and for how long, a person should no longer be playing contact sports.”
In recent years, CTE has come into the spotlight because of its link to athletes and combat veterans for whom head trauma has long been considered a professional hazard. Previously, the exact origin behind CTE had remained hard to pinpoint, since studying CTE required postmortem brains of high-level athletes and veterans thought to have CTE prior to death.
Results of this study, led by the Boston University School of Medicine, were published last month in the journal Brain. “Our study is ground-breaking for a few reasons,” Stanton explains, “along with our companion blast TBI CTE paper in 2012, these are the first studies that examined both the brains of young athletes and soldiers, and showed pathological hallmarks of CTE in the brains of athletes and soldiers as young as 18.”
Specifically, Stanton and his colleagues studied human brains from teenage athletes who had sustained closed-head impact injuries prior to death, then compared those to the brains of age-matched teen athletes without recent traumatic head injury. The analysis showed post-traumatic pathology, including one case of early-stage CTE, in the head injury group and none in the teenagers without head injury. To hone in on the exact mechanism behind the pathology, researchers then studied mouse models that recreate sports-related head impact and military-related blast exposure, under controlled laboratory conditions.
“We now have strong evidence to believe that the risk of CTE to soldiers, professional and amateur athletes, is much greater than previously known,” Stanton explains. The take-away, particularly as it applies to parents and coaches of young athletes is this: It is repetitive hits to the head, with or without concussion, that cause CTE. To prevent CTE, you must prevent young athletes from incurring repetitive head impact. “Sports in particular are elective forms of entertainment, and it is the responsibility of professional and amateur sports to work to make these forms of entertainment safer. This is likely to require both changes in the way the games are played, and better monitoring and rules for when athletes need to be removed from the game. For our military personnel, we have a profound responsibility to minimize their risks of TBI, and to search for treatments that reduce the risk of CTE.”