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Subconcussive Impact in Sports: A New Era of Awareness

Sports concussion is a form of mild traumatic brain injury (mTBI) caused by an impulsive force transmitted to the head. While concussion is recognized as a complex pathophysiological process affecting the brain at multiple scales, the causal link between external load and cellular, molecular level damage in mTBI remains elusive. The present study proposes a multiscale framework to analyze concussion and demonstrates its applicability with a real-life concussion case. The multiscale analysis starts from inputting mouth guard-recorded head kinematic into a detailed finite element (FE) head model tailored to the subject's head and white matter (WM) tract morphology. The resulting WM tract-oriented strains are then extracted and input to histology-informed micromechanical models of corpus callosum subregions with axonal detail to obtain axolemma strains at a subcellular level. By comparing axolemma strains against mechanoporation thresholds obtained via molecular dynamics (MD) simulations, axonal damage is inferred corresponding to a likelihood of concussion, in line with clinical observation. This novel multiscale framework bridges the organ-to-molecule length scales and accounts both inter- and intra-subject regional variability, providing a new way of non-invasively predicting axonal damage and real-life concussion analysis. The framework may contribute to a better understanding of the mechanistic causes behind concussion.

This study reports a multiscale computational framework for concussion, for the first time revealing a picture of how a global impact to the head measured on the field transfers to the cellular level of axons and finally down to the molecular level. Demonstrated with a real-life concussion case using a detailed and subject-specific head model, the results show molecular level damage corresponds to a likelihood of concussion, in line with clinical observation. An insight into the multiscale mechanical consequences is critical for a better understanding of the complex pathophysiological process affecting the brain at impact, which today are still poorly understood. Analyzing the concussive injury mechanisms the whole way from brains to molecules may also have significant clinical relevance. We show that in a typical injury scenario, the axolemma sustains large enough strains to entail pore formation in the adjoining lipid bilayer. Proration is found to occur in bilayer regions lacking ganglioside lipids, which provides important implications for the treatment of brain injury and other related neurodegenerative diseases.

To determine the magnitude of translational and rotational head accelerations during downhill mountain biking.

Observational study.

Sixteen male downhill cyclists (age 26.4 ± 8.4 years; stature 179.4 ± 7.2 cm; mass 75.3 ± 5.9 kg) were monitored during two rounds of the British Downhill Series. Riders performed two runs on each course wearing a triaxial accelerometer behind the right ear. The means of the two runs for each course were used to determine differences between courses for mean and maximum peak translational (g) and rotational accelerations (rad/s²) and impact duration for each course.

Significant differences (p < 0.05) were revealed for the mean number of impacts (>10 g), FW = 12.5 ± 7.6, RYF = 42.8 ± 27.4 (t_(22.96) = −4.70; p < 0.001; 95% CI = 17.00 to 43.64); maximum peak rotational acceleration, FW = 6805.4 ± 3073.8 rad/s², RYF = 9799.9 ± 3381.7 rad/s² (t₍₃₂₎ = −2.636; p = 0.01; 95% CI = 680.31 to 5308.38); mean acceleration duration FW = 4.7 ± 1.2 ms, RYF = 6.5 ± 1.4 ms (t₍₃₂₎ = −4.05; p < 0.001; 95% CI = 0.91 to 2.76) and maximum acceleration duration, FW = 11.6 ± 4.5 ms, RYF = 21.2 ± 9.1 (t_(29.51) = −4.06; p = 0.001; 95% CI = 4.21 to 14.94). No other significant differences were found.

Findings indicate that downhill riders may be at risk of sustaining traumatic brain injuries and course design influences the number and magnitude of accelerations.

Every year an estimated 42 million people worldwide suffer a mild traumatic brain injury (MTBI) or concussion. More severe traumatic brain injury (TBI) is a well-established risk factor for a variety of neurodegenerative diseases including Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis (ALS). Recently, large epidemiological studies have additionally identified MTBI as a risk factor for dementia. The role of MTBI in risk of PD or ALS is less well established. Repetitive MTBI and repetitive sub-concussive head trauma have been linked to increased risk for a variety of neurodegenerative diseases including chronic traumatic encephalopathy (CTE). CTE is a unique neurodegenerative tauopathy first described in boxers but more recently described in a variety of contact sport athletes, military veterans, and civilians exposed to repetitive MTBI. Studies of repetitive MTBI and CTE have been limited by referral bias, lack of consensus clinical criteria for CTE, challenges of quantifying MTBI exposure, and potential for confounding. The prevalence of CTE is unknown and the amount of MTBI or sub-concussive trauma exposure necessary to produce CTE is unclear. This review will summarize the current literature regarding the epidemiology of MTBI, post-TBI dementia and Parkinson's disease, and CTE while highlighting methodological challenges and critical future directions of research in this field. This article is part of a Special Issue entitled SI:Traumatic Brain Injury.

Concussive and subconcussive head injury is a global phenomenon that affects millions of people each year. Concussive injury has been extensively studied in sport, which has led to a greater understanding of the biomechanical forces involved and guidelines aimed at preventing athletes from playing while concussed. Subconcussive forces by definition do not meet the threshold for concussion but nonetheless may have significant long term consequences due to the repetitive pattern of injury to the head. Quantifying these impact forces using a forensic head model provides the groundwork for future studies by establishing a range or threshold of subconcussive impact forces that could be correlated with clinical assessments. The use of a forensic head model has distinct advantages in terms of ethics and safety.

To determine whether the King–Devick (K–D) test used as a sideline test in junior rugby league players over 12 matches in a domestic competition season could identify witnessed and incidentally identified episodes of concussion.

A prospective observational cohort study of a club level junior rugby league team (n = 19) during the 2014 New Zealand competition season involved every player completing two pre-competition season baseline trials of the K–D test. Players removed from match participation, or who reported any signs or symptoms of concussion were assessed on the sideline with the K–D test and referred for further medical assessment. Players with a pre- to post-match K–D test difference > 3 s were referred for physician evaluation.

The baseline test–retest reliability of the K–D test was high (r_s = 0.86; p < 0.0001). Seven concussions were medically identified in six players who recorded pre- to post-match K–D test times greater than 3 s (mean change of 7.4 s). Post-season testing of players demonstrated improvement of K–D time scores consistent with learning effects of using the K–D test (67.7 s vs. 62.2 s).

Although no witnessed concussions occurred during rugby play, six players recorded pre- to post-match changes with a mean delay of 4 s resulting in seven concussions being subsequently confirmed post-match by health practitioners. All players were medically managed for a return to sports participation.

The K–D test was quickly and easily administered making it a practical sideline tool as part of the continuum of concussion assessment tools for junior rugby league players.