Chronic traumatic encephalopathy and athletes

Abstract

Recent case reports have described athletes previously exposed to repetitive head trauma while participating in contact sports who later in life developed mood disorders, headaches, cognitive difficulties, suicidal ideation, difficulties with speech, and aggressive behavior. Postmortem discoveries show that some of these athletes have pathologic findings that are collectively termed chronic traumatic encephalopathy (CTE). Current hypotheses suggest that concussions or perhaps blows to the head that do not cause the signs and symptoms necessary for making the diagnosis of concussion, so-called subconcussive blows, cause both the clinical and pathologic findings. There are, however, some athletes who participate in contact sports who do not develop the findings ascribed to CTE. Furthermore, there are people who have headaches, mood disorders, cognitive difficulties, suicidal ideation, and other clinical problems who have neither been exposed to repeated head trauma nor possessed the pathologic postmortem findings of those currently diagnosed with CTE. The current lack of prospective data and properly designed case-control studies limits the current understanding of CTE, leading to debate about the causes of the neuropathologic findings and the clinical observations. Given the potential for referral and recall bias in available studies, it remains unclear whether or not the pathologic findings made postmortem cause the presumed neurobehavioral sequela and whether the presumed risk factors, such as sports activity, cerebral concussions, and subconcussive blows, are solely causative of the clinical signs and symptoms. This article discusses the current evidence and the associated limitations. Recent case reports have described athletes previously exposed to repetitive head trauma while participating in contact sports who later in life developed mood disorders, headaches, cognitive difficulties, suicidal ideation, difficulties with speech, and aggressive behavior.

Football Players' Head-Impact Exposure After Limiting of Full-Contact Practices

“…potential for long-term neurodegeneration. [21][22][23][24] Despite a lack of evidence to account for other conditions with similar clinical presentations, bias in the sample populations, and lack of control data, [25][26][27][28][29][30][31][32][33] sporting organizations have sought to reduce head-impact frequency during football participation. The number of full contact days for football has been restricted at the professional level and to a lesser extent at the collegiate and interscholastic levels, but no studies have directly measured the effect of such rule changes.…”

If You're Not Measuring, You're Guessing: The Advent of Objective Concussion Assessments

“…Additionally, numerous publications counter the speculation of widespread long-term declines. [78][79][80][81][82][83][84][85][86] Indeed, contactand collision-sport athletes live longer than the general population; have no increased risk for dementia, Parkinson disease, or amyotrophic lateral sclerosis 87 ; and have a suicide rate that is half the expected rate in the general population. 88 Despite these findings, science continues to catch up with the misinformation communicated through the media regarding possible relationships.…”

Sports-related brain injuries: connecting pathology to diagnosis

“…91 Case reports and series started to appear several decades later, during the 1950s and 1960s, describing pathological features associated with this condition such as cerebral atrophy, neuronal loss, gliosis, and argyrophilic neurofibrillary tangles. 18,27,81,102,123 Over time, investigators began to realize that the neurocognitive deficits seen in dementia pugilistica also affected men and women subjected to a broad range of brain trauma including physical abuse, head banging, poorly controlled epilepsy, and rugby.…”

“…26,131 Up to the turn of the 21st century, many studies were published noting similar symptoms among boxers, although no prospective longitudinal studies were performed to track progression of their symptoms. 91 Interest in CTE spiked during the early 21st century when Omalu and colleagues ascribed this condition to an American football player 108 and a professional wrestler. 109 Subsequently, this disease has also been identified in soccer, baseball, ice hockey, and rugby players, in addition to military personnel.…”

“…107 Beta (b)-amyloid deposition remains a controversial characteristic of CTE because it occurs inconsistently and is not as strongly associated with CTE as other pathological findings. 88,91,109,110 In 1 study of 68 patients with CTE diagnosed by history and presence of NFTs, 50% of cases showed signs of diffuse b-amyloid plaques, and 30% of cases had classic neuritic plaques seen in AD. 90 However, b-amyloid plaques in this cohort were associated with increasing age, which may be attributed to comorbid AD or other neurodegenerative conditions.…”