No abstract

The effect of opioid blockade on nociceptive flexion reflex (NFR) activity and subjective pain ratings was examined in 151 healthy young men and women. Using a within-subjects design, NFR threshold was assessed on two days after administration of either placebo or a 50 mg dose of naltrexone. Electrocutaneous pain threshold and tolerance levels were measured after NFR threshold assessment on each day. Results indicated that administration of naltrexone was consistently associated with hypoalgesic responding. Specifically, participants exhibited lower levels of NFR activity and reported lower pain ratings for electrocutaneous stimulation delivered at pain threshold and tolerance levels following administration of naltrexone as compared to placebo. These findings indicate that opiate blockade using the current standard dose may elicit hypoalgesia. A potential moderating effect of dose of opiate blockade medication and level of endogenous opioid activation should be carefully examined in future research.

This study explored possible gender moderation of previously reported associations between elevated trait anger-out and reduced endogenous opioid analgesia. One hundred forty-five healthy participants underwent acute electrocutaneous pain stimulation after placebo and oral opioid blockade in separate sessions. Blockade effects were derived reflecting changes in pain responses induced by opioid blockade. Hierarchical regressions revealed that elevated anger-out was associated with smaller pain threshold blockade effects (less opioid analgesia) in females, with opposite findings in males (interaction p < .001). Similar marginally significant interactions were noted for blockade effects derived for nociceptive flexion reflex threshold, pain tolerance, and pain ratings (p < .10). Anger-in was also associated negatively with pain threshold blockade effects in females but not males (interaction p < .05). Across genders, elevated anger-in was related to smaller pain tolerance blockade effects (p < .01). Overlap with negative affect did not account for these opioid effects. The anger-in/opioid association was partially due to overlap with anger-out, but the converse was not true. These findings provide additional evidence of an association between trait anger-out and endogenous opioid analgesia, but further suggest that gender may moderate these effects. In contrast to past work, anger-in was related to reduced opioid analgesia, although overlap with anger-out may contribute to this finding.

We examined the effects of baroreceptor stimulation on nociceptive responding in men and women with a positive or negative parental history of hypertension. The effects of three baroreceptor conditions (stimulation, inhibition, and control) on subjective pain and nociceptive responding were evaluated during electrocutaneous sural nerve stimulation. Pain ratings were lower in men with positive parental history relative to men with negative parental history, but this difference was not found in women. Both stimulatory and inhibitory baroreceptor conditions were associated with reduced pain reports compared to the control condition. There were no significant differences in nociceptive responding as a function of parental history of hypertension. Although this study confirms a link between hypoalgesia and risk for hypertension in men, it does not support the hypothesis that this attenuated pain perception is due to enhanced baroreceptor activity.

Previous work suggests possible relationships between offspring-reported parental history of chronic pain (CP) and offsprings' personal chronic pain experience. This study examined reliability of offsprings' reports of parental CP history based on direct comparison with confirmed parental reports. Participants included 108 male and female college students who completed a questionnaire assessing presence/absence and locations of any past or present CP lasting greater than 3 months. Information on maternal and paternal CP history was obtained using a similar questionnaire based both on offspring reports and on reports provided directly by offsprings' parents (for 75 participants). Results indicated relatively high sensitivity (0.79-0.94) but modest specificity (0.55-0.63) for offspring reports of parental CP history, and a tendency to overestimate the incidence of CP in both parents. Significant (Ps<0.001) but moderate inter-rater reliability was noted for judgments of parental CP history (kappas=0.41-0.53). Reliability generally decreased when offspring were asked to report on specific locations of parental CP. Offspring-reported parental CP history predicted (Ps<0.05) presence and number of locations at which offspring reported having personally experienced CP, consistent with previous studies. Results indicated that these relationships were not mediated by social desirability, negative affect, or catastrophizing cognitions. In contrast to results for offspring-reported data, confirmed parental CP history reports failed to predict offsprings' personal CP history. These results raise questions as to the validity of previous findings of relationships between family pain history and individuals' own experience of CP.