High-impact activities like football are known to cause creeping brain damage that can't easily be detected until after death. But promising research may give rise to new methods of diagnosing chronic traumatic encephalopathy.
In 1996, the brain of an alcoholic dwarf circus clown perplexed scientists with a disease normally limited to boxers. Over 15 years of being shot from a cannon at a circus, the clown developed dementia pugilistica, or as its 1928 discoverer Harrison Martland called it, "punch drunk." Less than ten years after the publication of a study on that cannon-rattled brain, an autopsy diagnosed deceased NFL Hall of Famer Mike Webster with the same condition, but now called chronic traumatic encephalopathy (CTE). An upswell in public interest and research following this death brought to light the danger that brain injuries present for athletes in all contact sports. A string of suicides and bizarre deaths by professional athletes, primarily football and hockey players, catalyzed a movement of more than 100 athletes to donate their brains for scientific study.
Junior Seau is the most recent athlete to donate his brain. The day after Junior Seau's suicide last week, the co-directors of the Boston University Center for the Study of Traumatic Encephalopathy published a paper, titled "Chronic traumatic encephalopathy: neurodegeneration following repetitive concussive and subconcussive brain trauma," in the medical journal Brain Imaging and Behavior. Even though Corsellis first identified the signs of CTE in the brains of boxers in 1973, significant gaps remain in our knowledge of this disease.
MORE ON SPORTS INJURY
Repeated blows to the head -- from football tackles, blasts from a circus cannon or some other trauma -- put the brain at risk for CTE. Although typically associated with concussions or serious head injuries, brains of football players with CTE but without any concussive history demonstrate that repeated, less severe "subconcussive" injuries provide sufficient trigger for this disease. While individual trauma may produce short-term symptoms, the effects of CTE manifest years after the injuries as the disease progresses and the brain breaks down. Yet many athletes with recurrent head injuries evade CTE; it appears repeated head trauma are necessary, but not sufficient, to trigger CTE. Researchers believe that the nature of the head trauma -- and the severity, frequency, and age of the recipient -- may play a role in whether or not CTE develops. But, for now, why the disease overtakes some and spares others remains a mystery.
The answer hides somewhere amidst tangled neurons and wasted brain tissue. During autopsy, scientists diagnose CTE through the pattern of brain decay and the buildup of tau protein. Normally, the tau protein stabilizes the brain cell skeleton. In both CTE and Alzheimer's, two distinct diseases, enzymes cause the protein to release from the skeleton and cluster in cells to form neurofibrillary tangles (NFTs). Researchers remain uncertain about the tangles' exact effect on the brain, says Dr. Brandon Gavett, a neuropsychologist at the University of Colorado-Colorado Springs. Unlike Alzheimer's, which is characterized by the even spread of NFTs, in CTE, NFTs cluster around blood vessels and dead tissue. According to Gavett, some researchers hypothesize that damage to blood vessels during head trauma may cause the brain to wither and form NFTs but thus far no mechanism of disease has been proven.
Brain damage associated with CTE triggers crippling psychological effects. Because the disease can only be diagnosed by autopsy, the changes in behavior and mood must be pieced together by interviews with family members after the afflicted person's death. Family members report that their loved ones exhibited problems with learning, remembering new information, and organization. Judgement and impulse control also frequently gave way to aggressive behavior and problems with addiction. Additionally, those affected by CTE frequently became depressed, agitated, and -- in what ultimately takes the lives of many with CTE -- suicidal. On top of these emotional changes, difficulty with balance, gait, and speech similar to Parkinson's disease often accompany CTE.
Despite the wealth of symptoms identified, these psychological factors need to be integrated with genetic susceptibility, chemical analysis of blood and cerebrospinal fluid, and brain imaging in order to accurately diagnose CTE in living patients. Possible chemical markers and genetic predispositions for CTE have been identified from research on Alzheimer's disease, and pilot studies show promise for diagnostic MRI and MRS scans as brain imaging technology improves. Late last year, Boston University CSTE began a study of NFL players and non-contact athletes to begin integrating these parts and develop methods to diagnose CTE before death. Some knowledge needed for such a diagnosis still evades researchers, but scientific advancement creeps closer to this goal every day.
Over the last 7 years, the exponential eruption of public interest and outrage around chronic traumatic encephalopathy has dwarfed the incremental advancements in research. Tremendous holes remain in what we know about how and why CTE develops in battered brains. These questions should not serve as grounds for the public health hazard's dismissal, but should instead prompt caution with a still unfamiliar threat.
We want to hear what you think about this article. Submit a letter to the editor or write to email@example.com.