- مبلغ: ۸۶,۰۰۰ تومان
- مبلغ: ۹۱,۰۰۰ تومان
The effect of acute stress on pain threshold and intolerance threshold are reported as producing either hypoalgesia or hyperalgesia. Yet, the contribution of individual stress reactivity in this respect has not been established. The aim was to test two pain modulation paradigms under acute stress manipulation, here for the first time, in order to study whether stress differentially affects pain modulation, and whether the effect is related to individual stress response. Participants were 31 healthy subjects. Conditioned pain modulation (CPM) and pain adaptation were measured before and after inducing an acute stress response using the Montreal Imaging Stress Task (MIST). Subjects' stress response was evaluated with salivary cortisol, autonomic function and perceived stress and anxiety. The MIST induced a validated stress response. On a group level, stress induced reduction in CPM magnitude and increase in pain adaptation compared to baseline. These responses correlated with stress reactivity. When the group was subdivided according to stress reactivity, only high stressresponders exhibited reduced CPM whereas only low stress-responders exhibited increased pain adaptation. The results suggest that acute stress may induce opposite effects on pain modulation, depending on individual stress reactivity magnitude, with an advantage to low stress-responders.
Limitations and Summary
Although the study provides new insights on the stress-pain interactions some reservations should be considered. First, the manipulation induced psychosocial stress that may differ from other types of stress. Additional studies are needed to allow for generalization of the results. Second, CPM was measured with two noxious contact heat stimuli. Although this paradigm was found reliable herein and by others ]25,32[, testing of additional CPM paradigms is recommended. Third, as all subjects were adult men, the results cannot be generalized to the entire population. In conclusion, this study demonstrates that acute psychosocial stress may induce opposite effects on pain modulation depending on individual stress reactivity; high stress-reactivity induces pronociception and low stressreactivity produces antinociception. The findings may have several implications. First, it is important to study stress effects not only on a group level but also considering individual differences in stress reactivity. With respect to pain management, since reduced CPM is associated with chronic pain [46,55], high stress-responders may be at higher risk for developing chronic pain. Therefore, identification of high vs. low stress-responders and closer monitoring of the former may enable individually tailored treatment with improved efficacy. In addition, interventions for stress management may improve pain modulation and reduce the risk of pain chronicity.