Association of Premorbid Anxiety and Depression Symptoms in Concussion Recovery in Collegiate Student-Athletes.

BACKGROUND: Mental health disorders are linked to prolonged concussion symptoms. However, the association of premorbid anxiety/depression symptoms with postconcussion return-to-play timelines and total symptom burden is unclear. OBJECTIVE: To examine the association of self-reported premorbid anxiety/depression symptoms in collegiate student-athletes with (1) recovery times until asymptomatic, (2) return-to-play, and (3) postconcussion symptom burden. STUDY DESIGN: Athletes in the Concussion Assessment, Research and Education Consortium completed baseline concussion assessments (Sport Concussion Assessment Tool [SCAT3] and Brief Symptom Inventory-18 [BSI-18]). Athletes were tested postinjury at <6 hours, 24 to 48 hours, time of asymptomatic and start of return-to-play protocol, unrestricted return-to-play, and 6 months after injury. Injured athletes were categorized into 4 groups based on BSI-18 scores: (1) B-ANX, elevated anxiety symptoms only; (2) B-DEP, elevated depression symptoms only; (3) B-ANX&DEP, elevated anxiety and depression symptoms; and (4) B-NEITHER, no elevated anxiety or depression symptoms. Relationship between age, sex, BSI-18 group, SCAT3 total symptom and severity scores, and time to asymptomatic status and return-to-play was assessed with Pearson's chi-squared test and robust analysis of variance. LEVEL OF EVIDENCE: Level 3. RESULTS: Among 1329 athletes with 1352 concussions, no respondents had a self-reported premorbid diagnosis of anxiety/depression. There was no difference in time until asymptomatic or time until return-to-play between BSI-18 groups (P = 0.15 and P = 0.11, respectively). B-ANX, B-DEP, and B-ANX&DEP groups did not have higher total symptom or severity scores postinjury compared with the B-NEITHER group. CONCLUSION: Baseline anxiety/depression symptoms in collegiate student-athletes without a mental health diagnosis are not associated with longer recovery times until asymptomatic, longer time to return-to-play, or higher postconcussion total symptom and severity scores compared with athletes without baseline symptoms. CLINICAL RELEVANCE: Anxiety and depression symptoms without a clear mental health diagnosis should be considered differently from other comorbidities when discussing prolonged recovery in collegiate student-athletes.

The Prevalence and Influence of New or Worsened Neck Pain After a Sport-Related Concussion in Collegiate Athletes: A Study From the CARE Consortium.

BACKGROUND: Neck pain in a concussion population is an emerging area of study that has been shown to have a negative influence on recovery. This effect has not yet been studied in collegiate athletes. HYPOTHESIS: New or worsened neck pain is common after a concussion (>30%), negatively influences recovery, and is associated with patient sex and level of contact in sport. STUDY DESIGN: Cohort study; Level of evidence, 2. METHODS: Varsity-level athletes from 29 National Collegiate Athletic Association member institutions as well as nonvarsity sport athletes at military service academies were eligible for enrollment. Participants completed a preseason baseline assessment and follow-up assessments at 6 and 24 to 48 hours after a concussion, when they were symptom-free, and when they returned to unrestricted play. Data collection occurred between January 2014 and September 2018. RESULTS: A total of 2163 injuries were studied. New or worsened neck pain was reported with 47.0% of injuries. New or worsened neck pain was associated with patient sex (higher in female athletes), an altered mental status after the injury, the mechanism of injury, and what the athlete collided with. The presence of new/worsened neck pain was associated with delayed recovery. Those with new or worsened neck pain had 11.1 days of symptoms versus 8.8 days in those without (P < .001). They were also less likely to have a resolution of self-reported symptoms in ≤7 days (P < .001). However, the mean duration of the return-to-play protocol was not significantly different for those with new or worsened neck pain (7.5 ± 7.7 days) than those without (7.4 ± 8.3 days) (P = .592). CONCLUSION: This novel study shows that neck pain was common in collegiate athletes sustaining a concussion, was influenced by many factors, and negatively affected recovery.

Mechanisms of Injury Leading to Concussions in Collegiate Soccer Players: A CARE Consortium Study.

BACKGROUND: Few previous studies have investigated how different injury mechanisms leading to sport-related concussion (SRC) in soccer may affect outcomes. PURPOSE: To describe injury mechanisms and evaluate injury mechanisms as predictors of symptom severity, return to play (RTP) initiation, and unrestricted RTP (URTP) in a cohort of collegiate soccer players. STUDY DESIGN: Cohort study; Level of evidence, 2. METHODS: The Concussion Assessment, Research and Education (CARE) Consortium database was used. The mechanism of injury was categorized into head-to-ball, head-to-head, head-to-body, and head-to-ground/equipment. Baseline/acute injury characteristics-including Sports Concussion Assessment Tool-3 total symptom severity (TSS), loss of consciousness (LOC), and altered mental status (AMS); descriptive data; and recovery (RTP and URTP)-were compared. Multivariable regression and Weibull models were used to assess the predictive value of the mechanism of injury on TSS and RTP/URTP, respectively. RESULTS: Among 391 soccer SRCs, 32.7% were attributed to a head-to-ball mechanism, 27.9% to a head-to-body mechanism, 21.7% to a head-to-head mechanism, and 17.6% to a head-to-ground/equipment mechanism. Event type was significantly associated with injury mechanism [χ2(3) = 63; P < .001), such that more head-to-ball concussions occurred in practice sessions (n = 92 [51.1%] vs n = 36 [17.1%]) and more head-to-head (n = 65 [30.8%] vs n = 20 [11.1]) and head-to-body (n = 76 [36%] vs n = 33 [18.3%]) concussions occurred in competition. The primary position was significantly associated with injury mechanism [χ2(3) = 24; P < .004], with goalkeepers having no SRCs from the head-to-head mechanism (n = 0 [0%]) and forward players having the least head-to-body mechanism (n = 15 [19.2%]). LOC was also associated with injury mechanism (P = .034), with LOC being most prevalent in head-to-ground/equipment. Finally, AMS was most prevalent in head-to-ball (n = 54 [34.2%]) and head-to-body (n = 48 [30.4%]) mechanisms [χ2(3) = 9; P = .029]. In our multivariable models, the mechanism was not a predictor of TSS or RTP; however, it was associated with URTP (P = .044), with head-to-equipment/ground injuries resulting in the shortest mean number of days (14 ± 9.1 days) to URTP and the head-to-ball mechanism the longest (18.6 ± 21.6 days). CONCLUSION: The mechanism of injury differed by event type and primary position, and LOC and AMS were different across mechanisms. Even though the mechanism of injury was not a significant predictor of acute symptom burden or time until RTP initiation, those with head-to-equipment/ground injuries spent the shortest time until URTP, and those with head-to-ball injuries had the longest time until URTP.

Internal or External Training Load Metrics: Which Is Best for Tracking Autonomic Nervous System Recovery and Function in Collegiate American Football?

Sport coaches increasingly rely on external load metrics for designing effective training programs. However, their accuracy in estimating internal load is inconsistent, and their ability to predict autonomic nervous system (ANS) deterioration is unknown. This study aimed to evaluate the relationships between internal and external training load metrics and ANS recovery and function in college football players. Football athletes were recruited from a D1 college in the southeastern US and prospectively followed for 27 weeks. Internal load was estimated via exercise cardiac load (ECL; average training heartrate (HR) × session duration) and measured with an armband monitor equipped with electrocardiographic capabilities (Warfighter MonitorTM (WFM), Tiger Tech Solutions, Miami, FL, USA). External load was estimated via the summation and rate of acceleration and decelerations as measured by a triaxial accelerometer using the WFM and an accelerometer-based (ACCEL) device (Catapult Player Load, Catapult Sports, Melbourne, Australia) worn on the mid-upper back. Baseline HR, HR variability (HRV) and HR recovery served as the indicators for ANS recovery and function, respectively. For HRV, two, time-domain metrics were measured: the standard deviation of the NN interval (SDNN) and root mean square of the standard deviation of the NN interval (rMSSD). Linear regression models evaluated the associations between ECL, ACCEL, and the indicators of ANS recovery and function acutely (24 h) and cumulatively (one- and two-week). Athletes (n = 71) were male and, on average, 21.3 ± 1.4 years of age. Acute ECL elicited stronger associations for 24 h baseline HR (R2 0.19 vs. 0.03), HR recovery (R2 0.38 vs. 0.07), SDNN (R2 0.19 vs. 0.02) and rMSSD (R2 0.19 vs. 0.02) compared to ACCEL. Similar results were found for one-week: 24 h baseline HR (R2 0.48 vs. 0.05), HR recovery (R2 0.55 vs. 0.05), SDNN (R2 0.47 vs. 0.05) and rMSSD (R2 0.47 vs. 0.05) and two-week cumulative exposures: 24 h baseline HR (R2 0.52 vs. 0.003), HR recovery (R2 0.57 vs. 0.05), SDNN (R2 0.52 vs. 0.003) and rMSSD (R2 0.52 vs. 0.002). Lastly, the ACCEL devices weakly correlated with ECL (rho = 0.47 and 0.43, p < 0.005). Our findings demonstrate that ACCEL poorly predicted ANS deterioration and underestimated internal training load. ACCEL devices may "miss" the finite window for preventing ANS deterioration by potentially misestimating training loads acutely and cumulatively.

Exposures to Elevated Core Temperatures during Football Training: The Impact on Autonomic Nervous System Recovery and Function.

Exercising with elevated core temperatures may negatively affect autonomic nervous system (ANS) function. Additionally, longer training duration under higher core temperatures may augment these negative effects. This study evaluated the relationship between exercise training duration and 24 h ANS recovery and function at ≥37 °C, ≥38 °C and ≥39 °C core temperature thresholds in a sample of male Division I (D1) collegiate American football athletes. Fifty athletes were followed over their 25-week season. Using armband monitors (Warfighter MonitorTM, Tiger Tech Solutions, Inc., Miami, FL, USA), core temperature (°C) and 24 h post-exercise baseline heart rate (HR), HR recovery and heart rate variability (HRV) were measured. For HRV, two time-domain indices were measured: the root mean square of the standard deviation of the NN interval (rMSSD) and the standard deviation of the NN interval (SDNN). Linear regression models were performed to evaluate the associations between exercise training duration and ANS recovery (baseline HR and HRV) and function (HR recovery) at ≥37 °C, ≥38 °C and ≥39 °C core temperature thresholds. On average, the athletes were 21.3 (± 1.4) years old, weighed 103.0 (±20.2) kg and had a body fat percentage of 15.4% (±7.8%, 3.0% to 36.0%). The duration of training sessions was, on average, 161.1 (±40.6) min and they ranged from 90.1 to 339.6 min. Statistically significant associations between training duration and 24 h ANS recovery and function were observed at both the ≥38.0 °C (baseline HR: ß = 0.10 ± 0.02, R2 = 0.26, p < 0.0000; HR recovery: ß = -0.06 ± 0.02, R2 = 0.21, p = 0.0002; rMSSD: ß = -0.11 ± 0.02, R2 = 0.24, p < 0.0000; and SDNN: ß = -0.16 ± 0.04, R2 = 0.22, p < 0.0000) and ≥39.0 °C thresholds (ß = 0.39 ± 0.05, R2 = 0.62, p < 0.0000; HR recovery: ß = -0.26 ± 0.04, R2 = 0.52, p < 0.0000; rMSSD: ß = -0.37 ± 0.05, R2 = 0.58, p < 0.0000; and SDNN: ß = -0.67 ± 0.09, R2 = 0.59, p < 0.0000). With increasing core temperatures, increases in slope steepness and strengths of the associations were observed, indicating accelerated ANS deterioration. These findings demonstrate that exercise training under elevated core temperatures (≥38 °C) may negatively influence ANS recovery and function 24 h post exercise and progressively worsen.