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Commentary: We Can’t Blame CTE for Aaron Hernandez’s Demise

The tragic case of Aaron Hernandez is but the latest of the controversies surrounding chronic traumatic encephalopathy (CTE) and professional sports. After the former New England Patriots tight end was posthumously diagnosed with the brain condition, speculation has arisen as to whether the violent behavior that led to his imprisonment can be blamed on CTE.

In cases such as that of Hernandez or other acts of violence in the news, we would like to know what could have possibly motivated the perpetrator or what factors and circumstances led to their behavior. The neuropsychology of the human brain and behavior is exceedingly complex, however, and we cannot infer that microscopic findings in a brain at autopsy prompted someone to commit a specific act such as murder several years earlier.

This case provides an opportunity for us to put into context the facts and fiction of CTE. The condition has been recognized for decades but gained tremendous media attention in recent years. These rare cases have generated a great deal of public, political, and scientific interest. CTE has become a buzzword that stirs attention and fear, yet we must make sure that the pendulum of awareness and concern does not swing too far in either direction, particularly since so little is known about the condition.

Many factors complicate our understanding of CTE. First, CTE is defined primarily by the accumulation of the tau protein in a certain pattern within the brain. But tau is found in many other neurological conditions, and other pathologies are often found in brains with CTE.

Second, the clinical symptoms retrospectively reported in cases of CTE overlap with other conditions like depression and various types of dementia, currently making a diagnosis of CTE during life a matter of conjecture. We do not understand the relationships between the pathological findings and behavioral changes reported in CTE, and there are currently no accepted diagnostic criteria for CTE during life.

At present, we are left examining brains suspected of dysfunction that are donated for research, and thus do not have the larger population-based view of CTE needed to learn about its prevalence, causes, course, or related symptoms. It should be kept in mind that while the presence of tau in certain quantities and locations in the brain may be necessary for CTE, it is not sufficient for explaining behavior.

I understand the speculation that football concussions may be responsible for the sad mental demise of Hernandez and others with CTE. But we as a society should become better consumers of science and not fall prey to media or scientific hype, and should not draw premature conclusions in the absence of rigorous research and scientific evidence.

Most people who get concussions do not develop CTE. We need to understand how common CTE really is, who is at risk, and why. To do this we will need to carefully study over the course of their lives large samples of people who have sustained various brain injuries (including those with and without particular symptoms) and who have other neurological conditions.

It may be comforting to infer a “cause” of behavior in tragic situations, as it helps us understand the unknown. However, the complexities of human behavior and the brain from which it derives often defy our attempts to comprehend. We must realize that at this point, the science on CTE doesn’t support many of the fears that have fueled its ongoing controversy.

Munro Cullum is a neuropsychologist and professor of psychiatry, neurology, and neurosurgery with the O’Donnell Brain Institute at UT Southwestern Medical Center.