Pain catastrophizing is associated with enhanced pain; however, the mechanisms by which it modulates pain are poorly understood. Evidence suggests that catastrophizing modulates supraspinal processing of pain but does not modulate spinal nociception (as assessed by nociceptive flexion reflex [NFR]). Unfortunately, most NFR studies have been correlational. To address this, this study experimentally reduced catastrophizing to determine whether it modulates spinal nociception (NFR). Healthy pain-free participants (N = 113) were randomly assigned to a brief 30-minute catastrophizing reduction manipulation or a control group that received pain education. Before and after manipulations, 2 types of painful stimuli were delivered to elicit (1) NFR (single trains of stimuli) and (2) temporal summation of NFR (3 stimulations at 2 Hz). After each set of stimuli, participants were asked to report their pain intensity and unpleasantness, as well as their situation-specific catastrophizing. Manipulation checks verified that catastrophizing was effectively reduced. Furthermore, pain intensity and unpleasantness to both stimulation types were reduced by the catastrophizing manipulation, effects that were mediated by catastrophizing. Although NFRs were not affected by the catastrophizing manipulation, temporal summation of NFR was reduced. However, this effect was not mediated by catastrophizing. These results indicate that reductions in catastrophizing lead to reductions in pain perception but do not modulate spinal nociception and provides further evidence that catastrophizing modulates pain at the supraspinal, not the spinal, level.

This study suggests that an optimistic outlook may beneficially impact clinical pain severity by altering endogenous pain modulatory capacity. Furthermore, individuals with low optimism (ie, pessimists) may be more adept at engaging resources that promote psychological resilience, which in turn, enhances endogenous pain modulatory capacity. Therefore, this study supports consideration of psychological resilience factors when evaluating experimental and clinical pain outcomes.

ObjectiveRacial/ethnic disparities in pain are well‐recognized, with non‐Hispanic blacks (NHBs) experiencing greater pain severity and pain‐related disability than non‐Hispanic whites (NHWs). Although numerous risk factors are posited as contributors to these disparities, there is limited research addressing how resilience differentially influences pain and functioning across race/ethnicity. Therefore, this study examined associations between measures of psychosocial resilience, clinical pain, and functional performance among adults with knee osteoarthritis (OA), and assessed the moderating role of race/ethnicity on these relationships.MethodsIn a secondary analysis of the Understanding Pain and Limitations in Osteoarthritic Disease (UPLOAD‐2) study, 201 individuals with knee OA (NHB = 105, NHW = 96) completed measures of resilience (ie, trait resilience, optimism, positive well‐being, social support, positive affect) and clinical pain, as well as a performance‐based measure assessing lower‐extremity function and movement‐evoked pain.ResultsBivariate analyses showed that higher levels of psychosocial resilience were associated with lower clinical pain and disability and more optimal physical functioning. NHBs reported greater pain and disability, poorer lower‐extremity function, and higher movement‐evoked pain compared with NHWs; however, measures of psychosocial resilience were similar across race/ethnicity. In moderation analyses, higher optimism and positive well‐being were protective against movement‐evoked pain in NHBs, whereas higher levels of positive affect were associated with greater movement‐evoked pain in NHWs.ConclusionOur findings underscore the importance of psychosocial resilience on OA‐related pain and function and highlight the influence of race/ethnicity on the resilience‐pain relationship. Treatments aimed at targeting resilience may help mitigate racial/ethnic disparities in pain.

Unpredictable threat amplifies pain and spinal nociception (as measured by the nociceptive flexion reflex, NFR), but it is unknown whether pain catastrophizing mediates this threat-related amplification. To examine this, the present study experimentally reduced catastrophizing and examined the effect on threat-evoked pain/NFR facilitation. Healthy pain-free participants (N 5 113) were randomly assigned to a brief 30-minute intervention designed to reduce catastrophic thoughts or a control intervention that involved education about pain neurobiology. Before the interventions, participants underwent a block of 8 pseudorandomly ordered periods of safe (no abdominal shock) and threat (abdominal shock possible) during which pain and NFR were evoked by electric stimulations to the ankle. After the safe/threat periods, participants rated pain intensity, pain unpleasantness, and situation-specific pain catastrophizing. The same test block was delivered after the intervention to examine changes in catastrophizing and threat-evoked pain/NFR facilitation. As expected, pain catastrophizing was reduced by the catastrophizing reduction intervention, relative to the control group. Furthermore, pain intensity, unpleasantness, and NFR magnitudes were higher during threat periods than safe. However, this threat-related pain/NFR amplification was not attenuated by the catastrophizing reduction intervention at the group level, although the intervention generally led to lower pain ratings (but not reduced NFR), regardless of the context. Nonetheless, bootstrapped mediation analyses found that reductions in catastrophizing mediated reductions in threat-related amplification of pain, but not NFR. This suggests that catastrophizing is partly responsible for threat-evoked pain amplification and provides further evidence that catastrophizing does not amplify pain at the spinal level.