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. 2023 Jun 21;4:1145934. doi: 10.3389/fpain.2023.1145934

Figure 3.

Figure 3

VmPFC, stress, and pain. (A) High Stress group (N = 25) show greater limbic-striatal (amygdala, hippocampus, insula and striatum) responses during acute stress exposure compared to the Low Stress (N = 25), but lower, more hypoactive VmPFC response to stress in the high vs. low stress groups (105). (B) The ROI of the hypoactive VmPFC response was entered in a mediation analysis to assess whether VmPFC functional response during acute stress mediated the effects of chronic stress on greater self reported pain symptoms (N = 50). Mediational analysis indicated that high chronic stress was associated with lower stress-induced VmPFC response (a process: −0.03, p < .01) and lower the VmPFC response, higher the reported pain symptoms (b process: −7.37, p < .05), and that the direct significant effect of high chronic stress associated with high pain symptoms (c = 0.52, p < .05) was fully accounted by the stress-induced VmPFC functional response (indirect effect c′: a × b = .22, p < .05, 95% CI = .01–.74), such that the direct effect of chronic stress on pain symptoms was no longer significant once the stress-related VmPFC response was included in the mediational mode (Direct effect c/c′ = 0.52/0.30, p = ns). *p < .05, **p < .01.