Introduction:Acute stress reduces responses to static evoked pain stimuli (stress-induced analgesia [SIA]). Whether SIA inhibits temporal summation of pain, a dynamic evoked pain measure indexing central sensitization, has been little studied and mechanisms were not evaluated.Objectives:We tested whether acute laboratory stressors reduce temporal summation and whether endogenous opioid (EO) mechanisms contributed.Methods:Participants were 72 healthy individuals who attended 2 laboratory sessions, receiving either oral naltrexone (50 mg; opioid antagonist) or placebo (randomized, counterbalanced order). In each session, participants underwent a temporal summation protocol with evoked heat pain stimuli, once after extended rest and once after experiencing 2 acute stressors (public speaking and mental arithmetic challenge). Reduced temporal summation in the stress/pain relative to rest/pain condition indexed SIA.Results:Analyses in the placebo condition indicated significant SIA on initial pain ratings but not temporal summation slope (index of central sensitization). This SIA effect was moderated by stress reactivity, with SIA only observed in high stress responders. Analyses comparing SIA across the drug conditions did not reveal any evidence of stress-related EO inhibition of temporal summation outcomes. Moderation analyses revealed that high, but not low, stress responders exhibited paradoxical analgesic effects of naltrexone on initial pain ratings but not temporal summation slopes. Independent of stress effects, significant EO inhibition of temporal summation slopes was observed, but only in females.Conclusions:Results suggest that acute stress may reduce initial ratings in temporal summation protocols via nonopioid mechanisms but does not alter the temporal summation slope commonly used to index central sensitization.
Bibliographical noteFunding Information:
This work was supported by grants R01AG048915 (S.B.), R01DA050334 (S.B.), R01DA16351 (M.A.), and R01DA027232 (M.A.) from the National Institutes of Health, and an AHA-Grant-in-Aid (M.A.) from the American Heart Association—Minnesota. The authors would like to express their appreciation to Motohiro Nakajma, Deanna Ellestad, and Angie Harju for their assistance on data collection and management of this study.
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- Central sensitization
- Endogenous opioid
- Stress-induced analgesia
- Temporal summation