Our brain, the seat of our consciousness, the essence of us, floats around in fluid inside our skull. When your head bumps into something at high speed, your brain can keep moving in that fluid and crash into your skull, sometimes with serious consequences.
When the four-time Pro Bowl football safety Dave Duerson deliberately checked into a hotel in 2011, left a suicide note asking that his brain be donated to science and shot himself carefully in the chest, he clearly believed that the terrible cognitive impairments and depression he was experiencing were more than he could bear and wondered if his career had something to do with it.
The suicides of other athletes like standout defensive back Andre Waters and much-beloved linebacker Junior Seau add to this suspicion. As difficulties with memory, cognition, mood and suicidal thoughts grow among our military and our veterans, speculation grows about the connections between traumatic brain injury (TBI) and these long-term effects.
Recent work in my laboratory at New York Medical College in Valhalla, N.Y., in collaboration with colleagues at the Boston University School of Medicine, the Boston Veterans Administration and other institutions, has discovered that events with similar outcomes can be set in motion in soldiers exposed to the nearby detonation of an improvised explosive device. Whether in athletes who have suffered multiple concussions or in blast-exposed soldiers, the consequences of TBI can be serious and persistent -- and can worsen with time.
We found that people exposed to either concussive injury or blast developed a syndrome called chronic traumatic encephalopathy (CTE). CTE is a progressive degenerative disease of the brain first observed in boxers and other high-contact-sport athletes with histories of repetitive brain trauma.
The disease is associated with increased incidents of impaired judgment, impulse control problems, aggression, depression, memory loss, confusion and eventually dementia. The key word here is "progressive," because this indicates that CTE is a process that can continue with worsening brain damage long after an initial trauma, but also offers the hope that we have enough of a time window to try to treat and arrest this process to minimize the damage.
While these associations suggest the possibility of a causal relationship between TBI and CTE, proving such a connection is made difficult by the many confounding events that occur in the course of people's lives.
To circumvent this problem, we designed a method for exposing experimental mice (who have never been in combat or played football) to a blast wave that mimics the power of an improvised explosive device.
These mice showed changes in their brains that were indistinguishable from CTE in people: They had persistently impaired learning and memory, and communication between cells in their brain was slowed. The mice also experienced impairment of the normal long-lasting strengthening of connections between cells that is thought to be a key part of the way that memories are stored. But if the animal's head was kept from moving during the blast, this damage was largely prevented.
Our work offers the first evidence in a controlled study of a connection between blast TBI and CTE and will help us begin to identify the types of functional damage to the brain that underlie the cognitive, memory and mood dysfunctions experienced by both soldiers and athletes following brain trauma.
A burning question on the minds of both scientists and parents is what kinds of trauma to the head (and brain) we should worry could cause long-term detrimental effects.
The short answer is that we just don't know. My colleagues and I are starting to suspect that repeated bouts of much milder traumas than those leading to concussions may be enough to trigger the beginning of the march toward CTE in susceptible individuals. If so, we will need to be far more cautious about assessing the brain function of our young athletes and soldiers, and we will need to start finding new ways to protect and monitor them.
An equally critical question is what we can do to reduce or prevent the consequences of TBI and CTE, once initial traumas have occurred.
To answer this question, it will be essential to test experimental treatments in careful animal experiments before doing so in people. By mimicking in animals what happens in brain injuries in people, we aim to identify protective strategies that can be applied before -- and drug and behavioral treatments that can be effective after -- either blast-related or impact-related brain trauma.
Discoveries will have to be validated by careful observations and studies in people, but I believe our research gives new hope of rescuing the lives of many of our athletes and veterans. We owe it to them to do our very best.
For more on CTE, go here.
