No abstract

Objectives: This systematic review examined studies that used mediation analysis to investigate the mechanisms of action of cognitivebehavioral, mind-body, and exercise-based interventions for pain and disability in people with chronic primary musculoskeletal pain.Materials and Methods: We searched 5 electronic databases for articles that conducted mediation analyses of randomized controlled trials to either test or estimate indirect effects. Results:We found 17 studies (n = 4423), including 90 mediation models examining the role of 22 putative mediators on pain or disability, of which 4 had partially mediated treatment effect; 8 had mixed results, and 10 did not mediate treatment effect. The conditions studied were chronic whiplash-associated pain, chronic low back pain, chronic knee pain, and mixed group of chronic primary musculoskeletal pain.Discussion: We observed that several of the studies included in our systematic review identified similar mechanisms of action, even between different interventions and conditions. However, methodological limitations were common. In conclusion, there are still substantial gaps with respect to understanding how cognitive-behavioral, mind-body, and exercise-based interventions work to reduce pain and disability in people with chronic primary musculoskeletal pain.

Background Clinicians commonly try to use mechanism-based knowledge to make sense of the complexity and uncertainty of chronic pain treatments to create a rationale for their clinical decision-making. Although this seems intuitive, there are some problems with this approach. Discussion The widespread use of mechanism-based knowledge in clinical practice can be a source of confusion for clinicians, especially when complex interventions with different proposed mechanisms of action are equally effective. Although the available mechanistic evidence is still of very poor quality, in choosing from various treatment options for people with chronic pain, an approach that correctly incorporates mechanistic reasoning might aid clinical thinking and practice. Conclusion By explaining that not all evidence of mechanism is the same and by making a proposal to start using mechanism-based knowledge in clinical practice properly, we hope to help clinicians to incorporate mechanistic reasoning to prioritize and start choosing what may best work for whom.

Experimental data suggest that associative learning can influence defensive avoidance behavior and pain perception in humans. However, whether voluntary movements can become conditioned stimuli (CSs) and influence pain responses is yet to be evaluated. Forty healthy volunteers participated in this study. Electrocutaneous stimuli applied to the shoulder at pain threshold level (UStest) and at pain tolerance level (US) were determined before a movement-conditioning paradigm. First, reaching movements to visual cues shown on one side of a computer screen were associated with the US (CS+ movements) on 80% of trials, whereas reaching movements to visual stimuli shown on the other side were never associated with the nociceptive-US (CS− movements). Next, participants underwent a test phase in which movements to visual cues on both sides were paired with the UStest on 50% of trials. During the test phase, participants were asked to evaluate whether the movement was painful (yes/no) and to rate pain intensity after each trial. Movement onset and duration as well as skin conductance responses were collected. The UStest stimuli were more likely to be perceived as painful and were also rated as more painful during CS+ movements. Movement onset latency and skin conductance responses were significantly higher in anticipation of the CS+ movement as compared to the CS− movement. These findings suggest that pain can be conditioned to voluntary movements.