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Objective: Exposure to repetitive head impacts (RHI) is associated with later‐life cognitive symptoms and neuropathologies, including chronic traumatic encephalopathy (CTE). Cognitive decline in community cohorts is often due to multiple pathologies; however, the frequency and contributions of these pathologies to cognitive impairment in people exposed to RHI are unknown. Here, we examined the relative contributions of 13 neuropathologies to cognitive symptoms and dementia in RHI‐exposed brain donors. Methods: Neuropathologists examined brain tissue from 571 RHI‐exposed donors and assessed for the presence of 13 neuropathologies, including CTE, Alzheimer disease (AD), Lewy body disease (LBD), and transactive response DNA‐binding protein 43 (TDP‐43) inclusions. Cognitive status was assessed by presence of dementia, Functional Activities Questionnaire, and Cognitive Difficulties Scale. Spearman rho was calculated to assess intercorrelation of pathologies. Additionally, frequencies of pathological co‐occurrence were compared to a simulated distribution assuming no intercorrelation. Logistic and linear regressions tested associations between neuropathologies and dementia status and cognitive scale scores. Results: The sample age range was 18–97 years (median = 65.0, interquartile range = 46.0–76.0). Of the donors, 77.2% had at least one moderate–severe neurodegenerative or cerebrovascular pathology. Stage III–IV CTE was the most common neurodegenerative disease (43.1%), followed by TDP‐43 pathology, AD, and hippocampal sclerosis. Neuropathologies were intercorrelated, and there were fewer unique combinations than expected if pathologies were independent (p < 0.001). The greatest contributors to dementia were AD, neocortical LBD, hippocampal sclerosis, cerebral amyloid angiopathy, and CTE. Interpretation: In this sample of RHI‐exposed brain donors with wide‐ranging ages, multiple neuropathologies were common and correlated. Mixed neuropathologies, including CTE, underlie cognitive impairment in contact sport athletes. ANN NEUROL 2024;95:314–324 [ABSTRACT FROM AUTHOR]

Chronic traumatic encephalopathy (CTE) is a neurodegenerative tauopathy associated with repetitive head impacts (RHI), but the components of RHI exposure underlying this relationship are unclear. We create a position exposure matrix (PEM), composed of American football helmet sensor data, summarized from literature review by player position and level of play. Using this PEM, we estimate measures of lifetime RHI exposure for a separate cohort of 631 football playing brain donors. Separate models examine the relationship between CTE pathology and players' concussion count, athletic positions, years of football, and PEM-derived measures, including estimated cumulative head impacts, linear accelerations, and rotational accelerations. Only duration of play and PEM-derived measures are significantly associated with CTE pathology. Models incorporating cumulative linear or rotational acceleration have better model fit and are better predictors of CTE pathology than duration of play or cumulative head impacts alone. These findings implicate cumulative head impact intensity in CTE pathogenesis. The relationship between the components of repetitive head impacts and chronic traumatic encephalopathy (CTE) remains unclear. Here, the authors use American football helmet sensor data to show that duration of play, cumulative head impacts and linear and rotational accelerations are significantly associated with CTE pathology. [ABSTRACT FROM AUTHOR]

Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease associated with a history of repetitive head impacts (RHI). CTE was described in boxers as early as the 1920s and by the 1950s it was widely accepted that hits to the head caused some boxers to become "punch drunk." However, the recent discovery of CTE in American and Australian-rules football, soccer, rugby, ice hockey, and other sports has resulted in renewed debate on whether the relationship between RHI and CTE is causal. Identifying the strength of the evidential relationship between CTE and RHI has implications for public health and medico-legal issues. From a public health perspective, environmentally caused diseases can be mitigated or prevented. Medico-legally, millions of children are exposed to RHI through sports participation; this demographic is too young to legally consent to any potential long-term risks associated with this exposure. To better understand the strength of evidence underlying the possible causal relationship between RHI and CTE, we examined the medical literature through the Bradford Hill criteria for causation. The Bradford Hill criteria, first proposed in 1965 by Sir Austin Bradford Hill, provide a framework to determine if one can justifiably move from an observed association to a verdict of causation. The Bradford Hill criteria include nine viewpoints by which to evaluate human epidemiologic evidence to determine if causation can be deduced: strength, consistency, specificity, temporality, biological gradient, plausibility, coherence, experiment, and analogy. We explored the question of causation by evaluating studies on CTE as it relates to RHI exposure. Through this lens, we found convincing evidence of a causal relationship between RHI and CTE, as well as an absence of evidence-based alternative explanations. By organizing the CTE literature through this framework, we hope to advance the global conversation on CTE mitigation efforts. [ABSTRACT FROM AUTHOR]

Background: Repetitive head impacts (RHI) from contact sports have been associated with cognitive and neuropsychiatric disorders. However, not all individuals exposed to RHI develop such disorders. This may be explained by the reserve hypothesis. It remains unclear if the reserve hypothesis accounts for the heterogenous symptom presentation in RHI-exposed individuals. Moreover, optimal measurement of reserve in this population is unclear and likely unique from non-athlete populations.Objective: We examined the association between metrics of reserve and cognitive and neuropsychiatric functioning in 89 symptomatic former National Football League players.Methods: Individual-level proxies (e.g., education) defined reserve. We additionally quantified reserve as remaining residual variance in 1) episodic memory and 2) executive functioning performance, after accounting for demographics and brain pathology. Associations between reserve metrics and cognitive and neuropsychiatric functioning were examined.Results: Higher reading ability was associated with better attention/information processing (β=0.25; 95% CI, 0.05-0.46), episodic memory (β=0.27; 95% CI, 0.06-0.48), semantic and phonemic fluency (β=0.24; 95% CI, 0.02-0.46; β=0.38; 95% CI, 0.17-0.59), and behavioral regulation (β=-0.26; 95% CI, -0.48, -0.03) performance. There were no effects for other individual-level proxies. Residual episodic memory variance was associated with better attention/information processing (β=0.45; 95% CI, 0.25, 0.65), executive functioning (β=0.36; 95% CI, 0.15, 0.57), and semantic fluency (β=0.38; 95% CI, 0.17, 0.59) performance. Residual executive functioning variance was associated with better attention/information processing (β=0.44; 95% CI, 0.24, 0.64) and episodic memory (β=0.37; 95% CI, 0.16, 0.58) performance.Conclusion: Traditional reserve proxies (e.g., years of education, occupational attainment) have limitations and may be unsuitable for use in elite athlete samples. Alternative approaches of reserve quantification may prove more suitable for this population. [ABSTRACT FROM AUTHOR]

Chronic traumatic encephalopathy (CTE) is a tauopathy associated with repetitive head impacts (RHI) that has been neuropathologically diagnosed in American football players and other contact sport athletes. In 2013, McKee and colleagues proposed a staging scheme for characterizing the severity of the hyperphosphorylated tau (p-tau) pathology, the McKee CTE staging scheme. The staging scheme defined four pathological stages of CTE, stages I(mild)–IV(severe), based on the density and regional deposition of p-tau. The objective of this study was to test the utility of the McKee CTE staging scheme, and provide a detailed examination of the regional distribution of p-tau in CTE. We examined the relationship between the McKee CTE staging scheme and semi-quantitative and quantitative assessments of regional p-tau pathology, age at death, dementia, and years of American football play among 366 male brain donors neuropathologically diagnosed with CTE (mean age 61.86, SD 18.90). Spearman's rho correlations showed that higher CTE stage was associated with higher scores on all semi-quantitative and quantitative assessments of p-tau severity and density (p's < 0.001). The severity and distribution of CTE p-tau followed an age-dependent progression: older age was associated with increased odds for having a higher CTE stage (p < 0.001). CTE stage was independently associated with increased odds for dementia (p < 0.001). K-medoids cluster analysis of the semi-quantitative scales of p-tau across 14 regions identified 5 clusters of p-tau that conformed to increasing CTE stage (stage IV had 2 slightly different clusters), age at death, dementia, and years of American football play. There was a predilection for p-tau pathology in five regions: dorsolateral frontal cortex (DLF), superior temporal cortex, entorhinal cortex, amygdala, and locus coeruleus (LC), with CTE in the youngest brain donors and lowest CTE stage restricted to DLF and LC. These findings support the usefulness of the McKee CTE staging scheme and demonstrate the regional distribution of p-tau in CTE. [ABSTRACT FROM AUTHOR]

The long-term effects of repetitive head impacts have been recognized for close to a century. What is now referred to as chronic traumatic encephalopathy (CTE) was first described by Martland in 1928 in a series of boxers. Over the years, several important articles were published, including Critchley's 1957 report where he introduced the term "chronic traumatic encephalopathy," Robert's study in 1969 which provided evidence of the prevalence of neurological impairment in retired fighters, and Corsellis' initial description of the pathology of CTE. However, what brought public attention to the issue of CTE in sports were the postmortem findings of CTE pathology in professional American football players, initially reported by Omalu and subsequently in a large series by McKee. There is now standardization of pathological criteria for CTE and recognition that it can be seen across all activities that involve repetitive head impacts. [ABSTRACT FROM AUTHOR]

Background: Factors of increased prevalence among individuals with Black racial identity (e.g., cardiovascular disease, CVD) may influence the association between exposure to repetitive head impacts (RHI) from American football and later-life neurological outcomes. Here, we tested the interaction between racial identity and RHI on neurobehavioral outcomes, brain volumetric measures, and cerebrospinal fluid (CSF) total tau (t-tau), phosphorylated tau (p-tau181), and Aβ1–42 in symptomatic former National Football League (NFL) players. Methods: 68 symptomatic male former NFL players (ages 40–69; n = 27 Black, n = 41 White) underwent neuropsychological testing, structural MRI, and lumbar puncture. FreeSurfer derived estimated intracranial volume (eICV), gray matter volume (GMV), white matter volume (WMV), subcortical GMV, hippocampal volume, and white matter (WM) hypointensities. Multivariate generalized linear models examined the main effects of racial identity and its interaction with a cumulative head impact index (CHII) on all outcomes. Age, years of education, Wide Range Achievement Test, Fourth Edition (WRAT-4) scores, CVD risk factors, and APOE ε4 were included as covariates; eICV was included for MRI models. P -values were false discovery rate adjusted. Results: Compared to White former NFL players, Black participants were 4 years younger (p = 0.04), had lower WRAT-4 scores (mean difference = 8.03, p = 0.002), and a higher BMI (mean difference = 3.09, p = 0.01) and systolic blood pressure (mean difference = 8.15, p = 0.03). With regards to group differences on the basis of racial identity, compared to White former NFL players, Black participants had lower GMV (mean adjusted difference = 45649.00, p = 0.001), lower right hippocampal volume (mean adjusted difference = 271.96, p = 0.02), and higher p-tau181/t-tau ratio (mean adjusted difference = −0.25, p = 0.01). There was not a statistically significant association between the CHII with GMV, right hippocampal volume, or p-tau181/t-tau ratio. However, there was a statistically significant Race x CHII interaction for GMV (b = 2206.29, p = 0.001), right hippocampal volume (b = 12.07, p = 0.04), and p-tau181/t-tau ratio concentrations (b = −0.01, p = 0.004). Conclusion: Continued research on racial neurological disparities could provide insight into risk factors for long-term neurological disorders associated with American football play. [ABSTRACT FROM AUTHOR]

Background The onfield assessment of concussion in the adult athlete is challenging, given the elusiveness of injury, the sensitivity and specificity of the sideline assessment tools and the evolving nature of concussive injury. This paper reviews the evidence related to the onfield assessment and considers questions related to same day return to play, what to do when no physician is available onsite, as well as the benefit of remote notification of potential concussive events. Objective To review the evidence regarding the onfield assessment of concussion in the adult athlete. Additional key issues to consider include same day return to play for the adult athlete with concussion, what to do in a community setting when no doctor is present and whether there is any benefit with remote notification of potential concussive events that occur on the playing field. Data Sources Systematic literature review of concussion assessment and management. PubMed, MEDLINE, Psych Info and Cochrane Library databases were reviewed using the MeSH key words concussion and mild traumatic brain injury combined with athletic injuries. Each was refined by adding the key words 'adult', 'sideline assessment', 'onfield assessment' and 'return to play'. Results For the MEDLINE search, using 'concussion' and 'athletic injuries' as key words, there were 880 results, and refining by 'adult' there were 292 results. When 'traumatic brain injury' and 'athletic injuries' were combined, there were 210 results. When refining by 'adult', there were 89 results. Many of these results overlapped. Following an initial review, these articles form the basis of the discussion. Conclusions The onfield evaluation of sport-related concussion is often a challenge, given the elusiveness and variability of presentation, difficulty in making a timely diagnosis, specificity and sensitivity of the sideline assessment tools and the reliance on symptoms. Despite these challenges, the sideline evaluation is based on recognition of injury, assessment of symptoms, cognitive and cranial nerve function and balance. Serial assessments are often necessary and, since signs and symptoms may be delayed, erring on the side of caution (keeping an athlete out of participation when there is any suspicion for injury) is important. A standardised assessment of concussion is useful in the assessment of the athlete with suspected concussion but should not take the place of the clinician's judgement. [ABSTRACT FROM AUTHOR]

Background: Catastrophic head injuries in football are rare but tragic events. Purpose: To update the profile of catastrophic head injuries in high school and college football players and to describe relevant risk factors. Study Design: Case series; Level of evidence, 4. Methods: We reviewed 94 incidents of severe football head injuries reported to the National Center for Catastrophic Sports Injury Research during 13 academic years (September 1989 through June 2002). Results: In the study period there were an average of 7.23 (standard deviation = 2.05) direct high school and college catastrophic head injuries in scholastic football participants per year. There were 0.67 injuries per 100 000 (95% confidence interval: 0.54, 0.81 per 100 000) high school and 0.21 injuries per 100 000 (95% confidence interval: 0.0, 0.49 per 100 000) college participants for a risk ratio of 3.28 (95% confidence interval: 0.81, 13.3). The injuries resulted in subdural hematoma in 75 athletes, subdural hematoma with diffuse brain edema in 10 athletes, diffuse brain edema in 5 athletes, and arteriovenous malformation or aneurysm in 4 athletes. Fifty-nine percent of the contacts reported that the athlete had a history of a previous head injury, of which 71 % occurred within the same season as the catastrophic event. Thirty-nine percent of the athletes (21 of 54) were playing with residual neurologic symptoms from the prior head injury. There were 8 (9%) deaths as a result of the injury, 46 (51 %) permanent neurologic injuries, and 36 (40%) serious injuries with full recovery. Most players sustained a major impact to the head either from tackling or being tackled. Conclusion: The incidence of catastrophic head injuries in football has remained low since the advent of the modern day foot- ball helmet in the early 1970s. The incidence of catastrophic head injuries in football is dramatically higher at the high school level than at the college level. Although the reason for this discrepancy is unclear, an unacceptably high percentage of high school players were playing with residual symptoms from a prior head injury. Coaches, athletes, athletic trainers, and medical personnel need to adhere to the guideline that an athlete with any neurologic symptoms from a head injury should be strongly discouraged from returning to play. [ABSTRACT FROM AUTHOR]

Recently, it has become clear that head trauma can lead to a progressive neurodegeneration known as chronic traumatic encephalopathy. Although the medical literature also implicates head trauma as a risk factor for Alzheimer's disease, these findings are predominantly based on clinical diagnostic criteria that lack specificity. The dementia that follows head injuries or repetitive mild trauma may be caused by chronic traumatic encephalopathy, alone or in conjunction with other neurodegenerations (for example, Alzheimer's disease). Prospective longitudinal studies of head-injured individuals, with neuropathological verification, will not only improve understanding of head trauma as a risk factor for dementia but will also enhance treatment and prevention of a variety of neurodegenerative diseases. [ABSTRACT FROM AUTHOR]

Background: There is a lack of injury data for the new Olympic sport of Rugby-7s, particularly for involved youth. Objective: To determine injury rates and characteristics for players participating in U.S. Rugby-7s U19 (under 19 years of age) tournaments. Methods: Injury data were collected, using the Rugby Injury Survey & Evaluation report methodology, at 24 U.S. Rugby-7 s U19 tournaments over 30 tournament days (2010–2014). Tournament medical-attention injuries and time-loss injuries (days absent before return to training/competition including post tournament) were recorded. Results: During the 2101 playing hours (3072 males, aged 17.2 ± 1.5 years; 732 females, 16.6 ± 1.3 years of age), there were 173 tournament injuries with an overall injury incidence of 82.4/1000 player-match-hours (ph) (CI 70.5–95.6). Acute injuries (79.5/1000 ph) occurred during tackling (56.2/1000 ph) and involved joints/ligaments (32.8/1000 ph) of lower extremities (31.9/1000 ph). Head and neck injuries, including concussions, were common (males 21.9/1000 ph; females 22.0/1000 ph). Medical-attention injury incidences (49.5/1000 ph; n = 104; 95% CI 40.5–60.0) were higher than time loss (32.8/1000 ph; n = 69; 95% CI 25.5–41.6). Overall, injury incidences found no difference between sex (RR 0.78; p = 0.369). Time-loss injuries resulted in an average of 35.5 d to return to sport. Discussion: This study is the first to report match injury incidences for U19 participants in Rugby-7s. Overall, match injury incidence among U.S. U19 Rugby-7s tournaments was similar compared to adult U.S. community Rugby-7s. Recurrent injury risk was notable in this population. Community injury surveillance studies are essential to understand risk from participation in amateur sports. Knowledge of these injury patterns in U19 Rugby-7s will help identify areas to direct resources to enable growth of Rugby-7s in youths and emerging countries being exposed to Rugby-7 s. Age-based injury frequency and patterns in rugby and its various formats are needed for the development of evidence-based, sport-specific, and population-specific injury prevention initiatives. Conclusions: The match injury incidence of U19 participants in U.S. Rugby-7s was similar to the incidence among adult participants. Recurrent match injury risk was high at 23%. There were no significant differences in injury incidences between males and females. The first three matches of a tournament day result in the most injuries. [ABSTRACT FROM AUTHOR]

Repetitive head impacts (RHIs) from football are associated with the neurodegenerative tauopathy chronic traumatic encephalopathy (CTE). It is unclear whether a history of traumatic brain injury (TBI) is sufficient to precipitate CTE neuropathology. We examined the association between TBI and CTE neuropathology in 580 deceased individuals exposed to RHIs from football. TBI history was assessed using a modified version of the Ohio State University TBI Identification Method Short Form administered to informants. There were 22 donors who had no TBI, 213 who had at least one TBI without loss of consciousness (LOC), 345 who had TBI with LOC, and, of those with a history of TBI with LOC, 36 who had at least one moderate-to-severe TBI (msTBI, LOC >30 min). CTE neuropathology was diagnosed in 405. There was no association between CTE neuropathology status or severity and TBI with LOC (odds ratio [OR] = 0.95, 95% confidence interval [CI] = 0.64–1.41; OR = 1.22, 95% CI = 0.71–2.09) or msTBI (OR = 0.70, 95% CI = 0.33–1.50; OR = 1.01, 95% CI = 0.30–3.41). There were no associations with other neurodegenerative or cerebrovascular pathologies examined. TBI with LOC and msTBI were not associated with CTE neuropathology in this sample of brain donors exposed to RHIs from American football. [ABSTRACT FROM AUTHOR]

Provides information on the management of sport-related concussion recommended for certified athletic trainers (ATC), physicians and other medical professionals caring for athletes as detailed under the position statement of the National Athletic Trainers' Association of the U.S. Factors that attributed to the decrease in number of incidence of fatalities and nonfatal catastrophic injuries among high school and collegiate football players between 1976 and 1980 in the country; Mechanisms and presentation of traumatic brain injury; Action that should be taken by ATC to detect deteriorating signs and symptoms that may indicate a more serious head injury.

Former American football players are at risk for chronic traumatic encephalopathy (CTE) which may have parkinsonism as a clinical feature. Former football players were prospectively assessed for parkinsonism. 120 former professional football players, 58 former college football players, and 60 same-age asymptomatic men without repetitive head impacts, 45–74 years, were studied using the MDS-UPDRS to assess for parkinsonism, and the Timed Up and Go (TUG). Traumatic encephalopathy syndrome (TES), the clinical syndrome of CTE, was adjudicated and includes parkinsonism diagnosis. Fisher's Exact Test compared groups on parkinsonism due to small cell sizes; analysis of covariance or linear regressions controlling for age and body mass index were used otherwise. Twenty-two (12.4%) football players (13.3% professional, 10.3% college) met parkinsonism criteria compared with two (3.3%) in the unexposed group. Parkinsonism was higher in professional (p = 0.037) but not college players (p = 0.16). There were no differences on the MDS-UPDRS Part III total scores. Scores on the individual MDS-UPDRS items were low. TUG times were longer in former professional but not college players compared with unexposed men (13.09 versus 11.35 s, p < 0.01). There were no associations between years of football, age of first exposure, position or level of play on motor outcomes. TES status was not associated with motor outcomes. Parkinsonism rates in this sample of football players was low and highest in the professional football players. The association between football and parkinsonism is inconclusive and depends on factors related to sample selection, comparison groups, and exposure characteristics. • Parkinsonism/motor finding prevalence did not differ in former American football players compared to asymptomatic unexposed men. • Former players did have slowness on the Timed Up and Go (TUG) compared to the asymptomatic unexposed men. • TUG times were slower in former football players with TES-CTE probable compared to those with no TES and TES-CTE possible. [ABSTRACT FROM AUTHOR]

Purpose: There is a comparative lack of concussion incidence data on the new Olympic sport Rugby 7s. This study aimed to determine the incidence (number of concussions per 1000 playing hours [ph]), mean and median severity (days absence), and cause of concussive injuries. Methods: This is a prospective epidemiology study, amateur to elite/national candidate, male (9768) and female (3876) players in USA Rugby sanctioned tournaments, compliant with the international consensus statement for studies in rugby union. Results: Concussions in US Rugby 7s were 7.7/1000 ph (n = 67). Women encountered concussions at 8.1/1000 ph, and men at 7.6/1000 ph (risk ratio [RR] = 1.10, P = 0.593). Elite/national-level players encountered concussions at higher rates (18.3/1000 ph) than lower levels (6.4/1000 ph; RR = 5.48, P < 0.001). Nonelite backs had higher concussive injury rates compared with forwards (7.7/1000 ph; 3.6/1000 ph; RR = 1.28, P = 0.024). Women missed 36.7 d absence from play, meanwhile men missed 27.9 d (P = 0.245). Retrospective history recall reflected previous concussive injuries occurred in 43% of the current study's cohort; of these, 57% encountered multiple concussions within 1 yr. The incidence of repetitive concussions was not statistically different between genders (RR = 1.09, P = 0.754). Most concussions occurred from tackles (63%) and collisions (24%) (P = 0.056). Conclusions: Sports-related concussions occurred with frequency among US amateur Rugby 7s players. US Elite tournament players sustained concussions at much higher rates than international male Rugby 7s counterparts. A substantial portion of US players who sustained a concussion had previous concussion injuries. Given the high rate of concussion, including repetitive concussive injuries, US Rugby 7s may benefit from concussion prevention measures similar to other contact sports such as instruction on proper tackling techniques, in-game and postgame medical assessment, and a standardized return-to-play protocol. [ABSTRACT FROM AUTHOR]