Stress-Induced Analgesia: An Evaluation of Effects on Pain Tolerance, Temporal Summation of Pain and the Role of Endogenous Opioid Mechanisms

Acute stress attenuates pain (stress-induced analgesia; SIA) but mechanisms remain debated. SIA effects on temporal summation of pain (TSP), a dynamic evoked pain measure indexing central sensitization, have been little studied. We tested whether acute laboratory stressors reduce pain perception and TSP and whether endogenous opioid (EO) mechanisms contributed. Participants (N=84) attended two laboratory sessions, receiving either oral naltrexone (50mg; opioid antagonist) or placebo (randomized, counterbalanced order). In each session, participants underwent two evoked pain stimuli (cold pressor test [CPT], heat pain) and a heat pain TSP protocol, once after extended rest and once after public speaking and mental arithmetic stressors. Stress attenuated pain perception (SIA) as indicated by significantly increased CPT tolerance; these SIA effects were abolished by opioid blockade. We observed significant SIA on initial pain ratings in the TSP protocol but not TSP slope (index of central sensitization). This SIA effect occurred in high stress responders only. Results demonstrate that endogenous opioids mediate effects of acute stress on static evoked pain responses, although this effect may be qualified by type of evoked pain stimulus. SIA does not influence central sensitization itself, but may exaggerate TSP values based on difference scores in TSP protocols by lowering initial ratings.