Search

Clinical Scenario: Pain is a common symptom experienced by individuals who sustain an acute lateral ankle sprain and can continue to persist among those who develop chronic ankle instability. Most rehabilitation protocols for individuals with acute ankle sprains or chronic ankle instability focus on restoring physical impairments and have largely omitted any pain-relieving therapies. This impairment-based focus has led pain to be an understudied symptom among individuals with an ankle sprain history. Overlooking the role of pain has also left clinicians with little insight into whether pain experienced after an ankle sprain is local (i.e., peripheral sensitization) or widespread (i.e., central sensitization). Understanding the pain profiles for those with an ankle sprain history may represent an unexploited area for clinicians and future research to improve health outcomes for this patient population. Clinical Question: Is there evidence to suggest that pain mechanosensitivity levels are different between those with and without a history of lateral ankle sprain? Summary of Key Findings: The literature was systematically searched for Level 4 evidence or higher. The search yielded two cross-sectional case-control studies and one cross-sectional study that met the inclusion and exclusion criteria. Based on the available evidence, pain mechanosensitivity levels are lower across ligamentous stabilizers immediately after an acute ankle sprain and over lower extremity neuromuscular structures among individuals with chronic ankle instability. ClinicalBottom Line: There is weak evidence to support an ankle sprain history can affect local pain mechanosensitivity levels of structures surrounding the ankle but not at distant locations. Strength of Recommendation: Level 4 evidence is available according to the Center for Evidence-Based Medicine. [ABSTRACT FROM AUTHOR]

Background: Assessing sport-related concussions in athletes presents challenges due to symptom variability. This study aimed to explore the relationship between acute concussion symptoms and athlete fear avoidance, pain catastrophizing, depression, and anxiety. Anxiety and depression have previously been associated with the number of symptoms after a concussion, but no prior research has examined the possible link between athlete fear avoidance and acute concussion symptoms. Methods: Thirty-four collegiate athletes (mean age = 20.9 ± 1.8 years) were assessed within 48 h of a concussion using the Sport Concussion Assessment Tool 5, Athlete Fear Avoidance Questionnaire (AFAQ), Pain Catastrophizing Scale, and Hospital Anxiety and Depression Scale. Results: Results showed a significant association between the athlete fear avoidance and the number of concussion symptoms (r = 0.493, p = 0.003), as well as depression and anxiety measured by HADS (r = 0.686, p < 0.001). Athlete fear avoidance and HADS scores were predictors of symptom severity, explaining 41% of the variance (p = 0.001). Athletes with higher fear avoidance tended to report more symptoms post concussion. Conclusions: This study underscores the link between athlete fear avoidance, anxiety, depression, and the severity of concussion symptoms. Administering the AFAQ to assess athlete fear avoidance at the initial assessment of a concussion may be helpful in interpreting the symptoms of an acute concussion. [ABSTRACT FROM AUTHOR]

The purpose of this study was to determine whether high intensity interval training (HIIT) would lead to improvements in 1) maximal VO2, VE, VE/VCO2, and VE/MVV, and/or 2) resting salivary concentrations of pro-inflammatory markers Interleukin (IL-8), interferon-gamma-inducible-protein (CXCL10/IP-10)) and anti-inflammatory marker IL-1 receptor antagonist (IL-1ra) in adults with well-controlled asthma compared to non-asthma controls. Participants completed a maximal exercise test at the beginning (T1) and end (T2) of a 6-week HIIT intervention; saliva samples were obtained at the beginning and 30 min following the first (T1) and last (T2) exercise session. Adults with asthma (n = 20; age: 21.4 ± 2.4 years) and non-asthma controls (n = 12; age: 22.5 ± 3.4 years) completed the intervention. VO2max increased from T1 to T2 in both groups (asthma T1 32.9 ± 8, T2 38.6 ± 8.2 ml/kg/min; controls T1 34.5 ± 11.8, T2 38.9 ± 12.3 ml/kg/min). VEmax also increased in both groups (asthma T1 97.7, T2 110.8 units, p < 0.001, hp2 = <0.04; control T1 106.3, T2 118.1, p < 0.001, hp2 0.02). An increase in VE/VCO2 (F(1, 10)=22.11, p = 0.001) and VE/MVV (F(1, 10) = 111.30, p < 0.001) was observed in the control group; no differences were observed in the asthma group. No differences in IL-8 or IL-1ra were observed between groups. In the asthma group, resting salivary IP-10 concentrations significantly decreased from T1 (0.025 pg/ug protein) to T2 (0.015 pg/ug protein, p = 0.039, hp2= 0.3 (moderate effect)). A 6-week HIIT intervention led to a similar increase in VO2max and VEmax in those with and without asthma, and a decrease in resting salivary IP-10 levels among adults with asthma. [ABSTRACT FROM AUTHOR]