By Jessica Rizzo and Dylan Henry, of Montgomery McCracken
When Antonio Brown disrobed in the middle of a Tampa Bay Buccaneers game this January, threw his clothes into the stands, and ran off the field, many rushed to play “armchair doctor,” publicly speculating that the wide receiver was suffering from chronic traumatic encephalopathy (“CTE”), the progressive brain disease associated with repeated concussive and sub-concussive blows. The problem? CTE can only be diagnosed through postmortem brain autopsy. That means anyone who may be suffering from CTE is currently unable to be diagnosed with the disease (which is indicated by abnormal deposits of a protein in specific parts of the brain).
Speculation about Brown’s erratic behavior follows the postmortem CTE diagnoses of his fellow NFL players Vincent Jackson, Phillip Adams, and Aaron Hernandez, who join the list of many other professional athletes who have been diagnosed with CTE postmortem.
Jackson was a wide receiver for the Buccaneers and the San Diego Chargers for 11 years. Last February, he was found dead in a hotel room at the age of 38. Doctors examined his brain and determined that he had stage 2 CTE.
Jackson had been reported missing by his family at the time of his death. In his mid-thirties, Jackson began exhibiting behavioral changes, becoming increasingly depressed and paranoid. He struggled with memory loss and difficulty solving problems and he grew extremely isolated towards the premature end of his life.
Phillip Adams was a defensive back for five years. After his NFL career ended, he often complained to his family of frequent memory lapses. Adams had a hard time with impulse control and, like Jackson, seemed to be growing increasingly paranoid. Last April, he went on a violent rampage, shooting and killing six people in Rock Hill, South Carolina before barricading himself in his family home and fatally shooting himself at the age of 32. Doctors who examined his brain after the massacre found that he had stage 2 CTE.
Hernandez was just 27 when he hanged himself with a bedsheet in his prison cell in 2017. The former New England Patriots tight end had previously been convicted of shooting and killing a friend, ending his NFL career. A posthumous examination of his brain revealed that he had stage 3 CTE, with damage akin to what researchers see in the brains of players in their 60s.
While CTE research is still in its infancy, the disease has gotten a lot of buzz over the last decade because of high profile cases like these. Because it has become a household name, some players suffering from cognitive decline after repeated head trauma may be tempted to diagnose themselves as having CTE, which many see as a death sentence. This is unfortunate, as focusing on one possible affliction to the exclusion of others may mean prematurely ruling out causes of symptoms that can be diagnosed and treated while the patient is still alive. For example, modern medicine is better equipped to help patients with Alzheimer’s, dementia, and bi-polar disorder.
While our current inability to diagnose CTE in the living prevents us from developing methods to treat, manage, minimize, and ultimately, prevent the disease, this may not always be true—recent studies have indicated that we may soon be able to diagnose CTE in living patients.
A panel of expert clinician-scientists in neurology, neuropsychology, psychiatry, neurosurgery, physical medicine, and rehabilitation has developed new consensus diagnostic criteria for traumatic encephalopathy syndrome (“TES”), the clinical disorder associated with CTE. The panel was convened as a part of the First National Institute of Neurological Disorders and Stroke Consensus Workshop to Define the Diagnostic Criteria for TES. The experts determined that diagnosis of TES requires (1) substantial exposure to repetitive head impacts from contact sports, military service, or other causes; (2) core clinical features of cognitive impairment (in episodic memory and/or executive functioning) and/or neurobiological dysregulation; (3) a progressive course; and (4) that the clinical features are not fully accounted for by any other neurologic, psychiatric, or medical conditions. Patients meeting these criteria will then receive a grade on a scale from one to five, one indicating that the patient is independent and five indicating that the patient has severe dementia.
Developed primarily for the purpose of facilitating future CTE research, the criteria is not yet ready for physicians to use in diagnosing living patients. It will, however, help scientists move closer to achieving that goal. The authors of the paper publishing the criteria note that they represent a critical step towards identifying a biomarker for CTE in the living.
Separately, Boston University researchers have published the results of a study indicating that it may be possible to use magnetic resonance imaging (“MRI”) technology to locate evidence of CTE in living patients. The researchers compared the brain scans of 55 deceased male brain donors with CTE to 31 healthy living men and found that the men with CTE had experienced shrinkage in certain regions of their brains. The frontal lobe, temporal lobe, and hippocampus, which plays a major role in learning and memory, were all affected.
The medical community has only just begun to understand the prevalence of CTE. A recent study of the brains of deceased Australian athletes, for example, found that more than half showed signs of CTE. All of the athletes whose brains were examined had, while alive, participated in sports with risks of repetitive injury such as rugby and football. Half of the donors with CTE had died by suicide.
Diagnosis In The Living
When we are able to diagnose CTE in living patients, healthcare providers and families will be better equipped to provide the support those suffering from the disease need. For example, a formal diagnosis could have helped Evan Hansen, the 21-year-old Wabash College football player who killed himself shortly after researching CTE on his laptop, possibly as part of an effort to self-diagnose. Had Hansen, whose self-diagnosis turned out to be accurate, received the terrible news that he had the disease from a doctor, he could have simultaneously received guidance for managing symptoms like depression.
The ability to diagnose CTE in living patients will also likely lead to increased damages in lawsuits, as patients and families use this knowledge as a basis for incorporating costs of treatment and life care plans into relief requests.
There is currently no treatment for CTE, in part because it cannot be diagnosed in the living. Those close to someone who may be suffering from the disease can only look on helplessly, hoping tragedy does not strike, as it has for so many former NFL players and other athletes. Identifying a way to reliably diagnose CTE in living patients will bring us closer to making timely intervention, treatment, management, and, ultimately, prevention, possible.