By the end of former Pittsburgh Steelers center Mike Webster’s violent football career, the blows he had taken to his head equated to hundreds of thousands of car crashes, by his own estimation. The damage precipitated a severe case of a brain disease upending the health of football players and boxers that is invisible to the eye and so elusive to current imaging technology it’s not possible to even diagnose definitively in a living person.
But as a CLE session Tuesday outlined, growing knowledge about chronic traumatic encephalopathy (CTE) is providing crucial guidance for understanding other kinds of traumatic brain damage and, in turn, informing how cases about them are litigated.
“The nature of litigation leads us to think about injuries as an isolated event,” said Larry Cohen, an injury and wrongful death attorney based in Vermont who presented the session on brain injury litigation. “As lawyers, we want to find the event that has caused something so that we can then use that event and the behavior that led to it, typically negligence or intentional acts, and say this is the causative factor that took place here.”
But, he explained further, lawyers have to consider brain injuries as dynamic processes that go beyond a simple causal relationship. And CTE is a valuable microcosm of developing knowledge about that complex web of causes and effects. Although repeated head injuries are necessary for the condition to develop, they aren’t enough on their own to cause CTE. That relationship, Cohen said, shows the importance of the question for litigation about why different people can suffer the same injury and yet see very different outcomes.
“The naysayers who say you can never have any injury (from a mild brain trauma) account for that by saying whoever claims to have an injury is making it up,” he said. “But in fact what CTE is showing is that you can have the injury that sets a process in motion, and yet, for some individuals, that process advances and becomes disabling cognitively and psychiatrically, whereas for others who have the same injury experience, it doesn’t proceed.”
He said he has come across the opinion that mild traumatic brain injuries never result in permanent brain damage and that it is still a widely held yet problematic view that the field of knowledge needs to overcome.
Cohen emphasized that although injury contributes to CTE, the condition itself is a disease. Another important characteristic of CTE as an encapsulation of understanding brain injury as a whole field is that it can’t be seen, which means its presence has to be diagnosed by looking at indicators. A key marker of CTE is when tau, a protein abundant in the central nervous system, accumulates in the “valleys” of the brain’s soft tissue. It can accumulate when trauma to the head causes the brain to move inside the skull’s protective shell, leading to tau leaking out of damaged neurons and blood vessels. The buildup of tau in the brain’s valleys, called sulci, mark a key difference between CTE and Alzheimer’s, Cohen explained.
A coroner first described the condition in boxers in the late 1920s in the journal of the American Medical Association, and his observations continue to influence the current school of thought about CTE. Another pathologist first gave the disease its name in the 1950s. But CTE gained infamy in the early 2000s when neuropathologist Bennet Omalu discovered former NFL center Mike Webster had advanced CTE by the time he died at age 50.
Although Cohen said it’s difficult to predict how much litigation will spring up surrounding CTE, he explained there are a number of imaginable types of actions and defense arguments. The disease is now so well known that organizations sponsoring contact sports might argue assumption of risk as a defense.
But Cohen added possible causes of action might include ones such as failure to warn, misrepresentation of risk or medical negligence. Product failure is probably not a viable action, he said, because of the research showing helmets do not provide protection against CTE.
Although Cohen said medical negligence for failure to identify the condition might be a lucrative legal argument to explore, the difficulty of diagnosing CTE while a person is alive presents a challenge for making it.
Cohen continued to say increasing knowledge of CTE has furthered understanding of the part trauma plays in brain damage because repeated trauma can also overwhelm the body’s usual healing process.
“Plasticity allows the brain, where the injury is very modest, to overcome the fact of injury organically and to avoid the symptoms that are characteristic of a traumatic brain injury,” he said. “But if the injury is more pervasive … you see a presentation and a continuation of symptoms.” Cohen said while genetics are thought of as a strong factor for susceptibility to CTE, there is not yet a clear answer, and science is likely a long way from providing one.
“We absolutely need to remain humble, because the field of brain function is truly in the infancy stage,” he said, adding that he has heard the sentiment that the area of knowledge has progressed from infancy to toddlerhood.
Cohen reiterated the need for lawyers to come up with a framework of thinking to account for different outcomes in people who suffer the same trauma besides simply dismissing those who do suffer brain damage as malingerers.
“That’s the window that I believe CTE is going to provide to understand why we see the differences we do in mild traumatic brain injury,” Cohen said. “It’s going to do a whole lot more, but if it did only that, it would be a tremendous advancement over where we are.”
—Julia Cardi