Introduction: Puberty is a critical developmental period during which changes in pain sensitivity are observed. Previous studies found that older and more mature adolescents have lower experimental pain sensitivity. However, it is unclear whether the differences in pain sensitivity are due to age or the pubertal maturation effect. Objectives: This observational study examined the relationships between the pubertal maturation stage, age, and experimental pain sensitivity in healthy girls. Methods: Healthy adolescent girls (n = 52, mean age 12.0 ± 1.4 years) completed the Pubertal Developmental Scale (PDS) to assess their pubertal stage. In addition, they completed a comprehensive quantitative sensory testing session, including pain thresholds, pain ratings to noxious stimuli, and pain modulation tests. Separate regression models were performed to assess the effect of pubertal maturation and age on experimental pain sensitivity as well as differences in experimental pain sensitivity between girls in different subjective self-perceived pubertal timing relative to peers. Results: No relationships were found between the PDS score and experimental pain sensitivity; however, age was significantly related to cold pain tolerance (P = 0.030). In addition, to differentiate between puberty and age, experimental pain sensitivity was compared in a subsample of girls of the same age but at different pubertal stages, and no differences in experimental pain sensitivity were observed. No differences were also found when comparing girls who mature early, same, or late relative to their peers. Conclusion: Puberty and age may have no effect on experimental pain sensitivity in healthy girls.

Background/Objectives: Variability in biopsychosocial factors can explain the interindividual variability in pain. One factor that can impact pain is the pain catastrophizing level. Interestingly, parental pain catastrophizing is related to the severity of the clinical pain of their children. This study explored whether parental pain catastrophizing is also associated with their children’s experimental pain sensitivity. Methods: Forty-five healthy girls (mean age 12.07 ± 1.47 years) and one of their parents participated in this study. Parents completed the Pain Catastrophizing Scale (PCS) about their child’s pain (PCS-Parent_child) as well as their pain (PCS-Parent). Children completed the PCS about their pain (PCS-Child) and the Pubertal Developmental Scale (PDS). Children underwent psychophysical tests, including paradigms of temporal summation, heat- and pressure-conditioned pain modulation, offset analgesia, and cold pain tolerance. Correlations and regression models were conducted to assess the relationships between parental pain catastrophizing scales (separately for PCS-Parent_child and PCS-Parent) and experimental pain sensitivity with and without controlling for PCS-Child and PDS. T-tests were used to compare pain sensitivity between participants with vs. without a family history of psychiatric disorder. Results: No significant relationships were found between the experimental pain sensitivity measures and either PCS-Parent_child or PCS-Parent with and without controlling for PCS-Child and PDS. No differences were found in experimental pain sensitivity between participants with and without a family history of psychiatric disorder. Conclusions: Parental pain catastrophizing may contribute minimally to the individual variability in experimental pain sensitivity of healthy adolescent girls.

Background/Objectives: Venipuncture is a painful and distress-inducing procedure, especially in adolescents. However, the effect of stress on venipuncture pain remains unclear. This study investigated the relationships between stress (venipuncture-related and general stress) and venipuncture pain intensity and unpleasantness, hypothesizing that higher stress levels would be associated with greater pain levels. Methods: Forty-two adolescents (five boys, mean age 12.2 ± 1.4) participated in the study, which included completing questionnaires and a blood draw. General stress was assessed using the Perceived Stress Scale. Before the blood draw, participants were asked to rate their venipuncture-related stress level using a Visual Analog Scale (VAS). Following venipuncture, participants rated their pain intensity and pain unpleasantness using the VAS. Nineteen participants returned for a similar study visit after 1 year. Regression models were used to assess the relationships between pain and stress. In addition, correlations were used to examine the relationships between baseline and 1-year follow-up stress and pain levels. Results: Only baseline venipuncture stress, but not general stress, was related to venipuncture pain intensity (estimate (SE) = 0.185 (0.046), t-ratio = 4.00, p < 0.001) and pain unpleasantness (estimate (SE) = 0.378 (0.116), t-ratio = 3.27, p = 0.002). Baseline stress levels were related to stress levels at 1-year follow-up. However, this was not found for pain levels. In addition, stress at baseline did not impact pain levels at 1-year follow-up. Conclusions: General stress may be different from venipuncture stress, with the latter having a greater influence on venipuncture pain. Developing interventions focused on reducing stress related to venipuncture in adolescents could assist in reducing pain and increase willingness to undergo needle procedures.

Introduction: Adolescence is a period of drastic biopsychosocial change that affects the trajectory of health into adulthood. Cross-sectional studies have reported that older youth typically exhibit lower experimental pain sensitivity than younger youth, but only one study thus far has directly examined this longitudinally. The factors contributing to changes in pain sensitivity remain unclear, but sex hormones, which dramatically fluctuate during adolescence, could play a key role. Objectives: This longitudinal study aimed to examine changes in experimental pain sensitivity/modulation and their relationship to changes in sex hormone levels. Methods: Healthy girls (n = 35, 9–16 years old) completed quantitative sensory testing (QST) at baseline and 1-year follow-up including thermal/pressure pain threshold; heat/cold pain intensity; cold pain tolerance; mechanical temporal summation; offset analgesia; and heat/pressure conditioned pain modulation. Serum blood samples were analyzed for total testosterone, dihydrotestosterone (DHT), dehydroepiandrosterone (DHEA), DHEA-sulfate (DHEA-S), and androstenedione (A4). Pain measures that significantly differed from baseline to follow-up were dependent variables in bootstrapped linear regression models with sex hormones as individual predictors in separate models. Additional regressions included baseline age and changes in pubertal stage and menstrual phase as covariates. Results: Cold pain threshold (CPT) increased over 1 year (baseline = 11.93°C, follow-up = 15.72°C, P = 0.012). Increased ΔDHT predicted increased ΔCPT after controlling baseline age, Δpubertal stage, and Δmenstrual phase ( ΔR ² = 0.294, ΔF _1,18 = 9.49, P = 0.006, β = 0.583), but no other relationships between ΔQST measures and Δsex hormones were significant. Conclusion: These findings suggest that during puberty, changes in sex hormone levels may have minor contributions to changes in experimental pain sensitivity in healthy girls.