Further verification by bootstrapped mediation analyses that pain catastrophizing modulates pain report but not spinal nociception: a reply to Lee, Hübscher, and McAuley.

We greatly appreciate that Lee et al. read our recently published article in PAIN that examined the influence of an experimental catastrophizing manipulation (ie, using cognitive behavioral techniques to reduce catastrophic thinking) on pain ratings and the nociceptive flexion reflex (NFR). In that article, we found that the experimental reduction in catastrophizing led to reductions in pain intensity, pain unpleasantness, and temporal summation of NFR (TS-NFR, ie, NFR responses to triple stimulations) but not NFRs to single stimulations. These data suggested that catastrophizing could play a causal role in modulating pain and also in modulating spinal sensitization (given that TS-NFR is believed to be a marker). However, after conducting formal mediation analyses according to Baron and Kenny followed by the traditional version of the Sobel test, we concluded that catastrophizing mediated the effect of the experimental manipulation on pain intensity and unpleasantness but not the effect of the experimental manipulation on temporal summation of NFR or NFRs to single stimulations. These results were in line with a number of previous correlational studies that found pain catastrophizing is associated with pain perception but not NFR. As Lee et al. noted in their PAIN editorial, there have been recent advances in mediation analyses that improve on the classic Baron and Kenny and Sobel approaches. For example, Preacher and Hayes argue for a bootstrapped Sobel test that provides a point estimate for the indirect effect and a bootstrapped confidence interval (CI) around the indirect effect. If the CI contains zero, then the indirect effect is not significantly different from zero, thus arguing against mediation. Not only does this quantify the indirect effect and provide a significance test for it but also overcomes the potential problem with the traditional Sobel test’s reliance on a normal distribution. Lee et al. encouraged us to use such an approach not only to test our conclusions but to also report the indirect effect and the bootstrapped test regardless of whether the total effect was significant (ie, regardless of whether the experimental manipulation had an effect on a dependent variable, [DV]). We gladly comply with their request to apply this more contemporary analysis to our data. We conducted bootstrapped Sobel tests using PROCESS designed by Hayes. This produced 95% CIs for the indirect effects that were generated from 1000 bootstrapped samples. The results are presented in Table 1. As can be seen, there was a significant indirect effect by pain catastrophizing on pain intensity and unpleasantness but not for TS-NFR or NFRs in response to single stimulations. Thus, these results support the conclusions of our original study and further support our conclusion that pain catastrophizing modulates pain report but not spinal nociception (as measured by NFR and TS-NFR). We thank Lee et al. for suggesting that we conduct these analyses so that we can have greater confidence in our results.