Spatial aspects of pain modulation are not disrupted in adolescents with migraine.

OBJECTIVE: To compare spatial pain modulation capabilities between adolescents with and without migraine. BACKGROUND: Conditioned pain modulation (CPM) responses at the leg are similar in adolescents with versus without migraine. However, the anatomical region of testing may affect spatial pain modulation capabilities as differences in nociceptive processing between patients with migraine and healthy controls are found in local areas that are near the site of clinical pain but not in nonlocal areas. This study aimed to examine spatial pain modulation capabilities tested by the CPM paradigm using test stimulus applied to a local body area. METHODS: Nineteen adolescents with migraine (age 14.9 ± 2.3, mean ± SD; 16 female) and 20 healthy adolescents (age 13.8 ± 2.5, mean ± SD; 16 female) completed this case-control study at Cincinnati Children's Hospital Medical Center. Pressure pain thresholds (PPT) were assessed at the trapezius before and during immersion of the foot in a cold water bath (8°C). RESULTS: In the migraine group (146.0 ± 79.1, mean ± SD), compared to healthy controls (248.0 ± 145.5, mean ± SD), significantly lower PPT (kilopascal) values were found (estimate = 124.28, 95% CI: 58.98, 189.59, p < 0.001; effect size: d = 1.40). No differences between the groups were found for pain intensity and unpleasantness ratings of cold-water immersion nor the CPM response. CONCLUSIONS: This study found altered ascending nociceptive processing of mechanical stimuli at the neck in adolescents with migraine. However, endogenous pain modulatory mechanisms were functional and not altered. In light of other studies, impairments in inhibitory control may not be involved in migraine pathophysiology in pediatric patients regardless of stimulus location.

Weak Relationships Between Psychological Factors and Experimental Pain Outcomes in Pain-Free Individuals: An Aggregate Analysis of 8 Studies.

Although psychological factors such as anxiety, depression, and pain catastrophizing are known to influence pain outcomes in chronic pain populations, there are mixed results regarding whether they influence experimental pain outcomes in pain-free individuals. The objectives of this study were to determine the associations between psychological factors and experimental pain outcomes in pain-free adolescents and adults. Relationships between anxiety, depression, and pain catastrophizing and experimental pain outcomes across 8 different studies (total N = 595) were examined in different populations of pain-free adult and adolescent participants. Analyses were conducted with and without controlling for sex, age, and race. Studies were analyzed separately and as part of an aggregate analysis. Individual study analyses resulted in 136 regression models. Of these, only 8 models revealed a significant association between psychological factors and pain outcomes. The significant results were small and likely due to Type 1 error. Controlling for demographic factors had minimal effect on the results. The aggregate analyses revealed weak relationships between anxiety and pressure pain threshold (Fisher's z = -.10 [-.19, -.01]), anxiety and cold pain intensity ratings (Fisher's z = .18 [.04, .32]), and pain catastrophizing and pressure pain threshold (Fisher's z = -.14 [-.26, -.02]). Sample size calculations based on the aggregate analyses indicated that several hundred participants would be required to detect true relationships between these psychological factors and pain measures. The overall negative findings suggest that in pain-free individuals, anxiety, depression, and pain catastrophizing are not meaningfully related to experimental pain outcomes. PERSPECTIVE: Psychological variables have been shown to predict pain outcomes in chronic pain populations but these relationships may not generalize to pain-free populations. An analysis of 595 pain-free individuals across 8 studies in our lab revealed that anxiety, depression, and pain catastrophizing were not meaningfully related to experimental pain outcomes.

Associations of self-report and actigraphy sleep measures with experimental pain outcomes in patients with temporomandibular disorder and healthy controls.

OBJECTIVE: Discrepancies between self-reported and actigraphy sleep measures are common, producing ambiguity about which are better predictors of experimental pain outcomes. The current study tested if pain intensity during and situational pain catastrophizing following experimental pain were differentially predicted by self-reported or actigraphy sleep measures in patients with chronic temporomandibular disorder (TMJD) or healthy controls (HCs). METHODS: Forty patients with TMJD and 20 HCs completed self-report sleep measures (Pittsburgh Sleep Quality Index, PSQI; Insomnia Severity Index, ISI; PROMIS Sleep-Related Impairment [SRI] and Sleep Disruption [SD]), underwent an experimental pain induction consisting of four consecutive cold-water hand immersions, and provided pain intensity and situational pain catastrophizing ratings. Participants also wore an actigraphy watch and completed sleep diaries for seven days, which were averaged for actigraphic indices of total sleep time, sleep efficiency, wake after sleep onset, and self-reported sleep quality and restfulness. RESULTS: Individuals with TMJD reported higher pain intensity during experimental pain (M = 65.81 vs. 47.77, p = .007) and self-reported worse sleep compared to HCs (all p's < 0.02, Cohen's D = 0.73-1.25). No group differences emerged for actigraphy measures (all p's > 0.05, Cohen's D = 0.05-0.53). Sleep variables did not interact with group to predict responses to experimental pain (all p's > 0.05). Across groups, PROMIS-SRI predicted pain intensity (ß = 0.36, p = .008) and catastrophizing (ß = 0.36, p = .009) after controlling for multiple comparisons, smoking, medications, and age. CONCLUSION: Self-reported sleep (but not actigraphy) measures differentiate patients with TMJD from HCs. Sleep-related interference may place people at particular risk for higher pain intensity and catastrophizing following experimental pain.