Stress elicits a variety of psychophysiological responses that show large interindividual variability. Determining the neural mechanisms that mediate individual differences in the emotional response to stress would provide new insight that would have important implications for understanding stress-related disorders. Therefore, the present study examined individual differences in the relationship between brain activity and the emotional response to stress. In the largest stress study to date, 239 participants completed the Montreal Imaging Stress Task (MIST) while heart rate, skin conductance response (SCR), cortisol, self-reported stress, and blood oxygen level dependent (BOLD) functional MRI (fMRI) signal responses were measured. The relationship between differential responses (heart rate, SCR, cortisol, and self-reported stress) and differential BOLD fMRI data was analyzed. Dorsolateral prefrontal cortex (PFC), dorsomedial PFC, ventromedial PFC, and amygdala activity varied with the behavioral response (i.e., SCR and self-reported stress). These results suggest the PFC and amygdala support processes that are important for the expression and regulation of the emotional response to stress, and that stress-related PFC and amygdala activity underlie interindividual variability in peripheral physiologic measures of the stress response.

This study suggests that endogenous pain modulatory processes are altered for cLBP patients, particularly TS of mechanical and heat stimuli. Pain catastrophizing and TS of mechanical pain may have important clinical relevance for cLBP, given associations with clinical pain and disability; however, future research is needed to replicate these findings.

Stress tasks performed during functional magnetic resonance imaging (fMRI) elicit a relatively small cortisol response compared to stress tasks completed in a traditional behavioral laboratory, which may be due to apprehension of fMRI that elicits an anticipatory stress response. The present study investigated whether anticipatory stress is greater prior to research completed in an MRI environment than in a traditional behavioral laboratory. Anticipatory stress (indexed by cortisol) was greater prior to testing in the MRI environment than traditional behavioral laboratory. Furthermore, anticipation of fMRI elicited a cortisol response commensurate with the response to the stress task in the behavioral laboratory. However, in the MRI environment, post-stress cortisol was significantly lower than baseline cortisol. Taken together, these findings suggest the stress elicited by anticipation of fMRI may lead to acute elevations in cortisol prior to scanning, which may in turn disrupt the cortisol response to stress tasks performed during scanning.

Background Racial differences in endogenous pain facilitatory processes have been previously reported. Evidence suggests that psychological and behavioral factors, including depressive symptoms and sleep, can alter endogenous pain facilitatory processes. Whether depressive symptoms and sleep might help explain racial differences in endogenous pain facilitatory processes has yet to be determined. Purpose This observational, microlongitudinal study examined whether depressive symptoms and sleep were sequential mediators of racial differences in endogenous pain facilitatory processes. Methods A total of 50 (26 African American and 24 non-Hispanic White) community-dwelling adults without chronic pain (mean 49.04 years; range 21–77) completed the Center for Epidemiological Studies Depression Scale prior to seven consecutive nights of sleep monitoring with actigraphy in the home environment. Participants subsequently returned to the laboratory for assessment of endogenous pain facilitation using a mechanical temporal summation protocol. Results Findings revealed greater depressive symptoms, poorer sleep efficiency, and greater temporal summation of mechanical pain in African Americans compared to non-Hispanic Whites. In a sequential mediation model, greater depressive symptoms predicted poorer sleep efficiency (t = −2.55, p = .014), and poorer sleep efficiency predicted enhanced temporal summation of mechanical pain (t = −4.11, p < .001), particularly for African Americans. Conclusions This study underscores the importance of examining the contribution of psychological and behavioral factors when addressing racial differences in pain processing. Additionally, it lends support for the deleterious impact of depressive symptoms on sleep efficiency, suggesting that both sequentially mediate racial differences in endogenous pain facilitation.

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