Attempts by CLBP patients to suppress anger may aggravate pain related to their clinical condition through ironically increased feelings of anger.

Results support the notion that ethnic differences in pain treatment outcome exist. Further, ethnic minority groups appear to have greater levels of distress compared to Caucasians. However, African Americans, Latino/a's and Caucasians demonstrated similar improvements on all outcome measures, with exception of the use of prayer. Future studies should begin to explore the mechanisms to explain why ethnic group differences in pain treatment outcome occur.

We examined whether people who tend to catastrophize about pain and who also attempt to regulate negative thoughts and feelings through suppression may represent a distinct subgroup of individuals highly susceptible to pain and distress. Ninety-seven healthy normal participants underwent a 4-min ischemic pain task followed by a 2-min recovery period. Self-reported pain and distress was recorded during the task and every 20 s during recovery. Participants completed the Pain Catastrophizing Scale and the White Bear Suppression Inventory. Repeated measures multiple regression analysis (using General Linear Model procedures) revealed significant 3-way interactions such that participants scoring high on the rumination and/or helplessness subscales of the Pain Catastrophizing Scale and who scored high on the predisposition to suppress unwanted thoughts and feelings reported the greatest pain and distress during recovery. Results suggest that pain catastrophizers who attempt to regulate their substantial pain intensity and distress with maladaptive emotion regulation strategies, such as suppression, may be especially prone to experience prolonged recovery from episodes of acute pain. Thus, emotion regulation factors may represent critical variables needed to understand the full impact of catastrophic appraisals on long-term adjustment to pain.

This study used a placebo-controlled, between-subjects opioid blockade design to evaluate endogenous opioid involvement in the hypoalgesia associated with elevated resting blood pressure (BP) in 163 healthy individuals. Participants were randomly assigned to Drug condition (placebo, naltrexone) and Task Order (computerized maze task with harassment followed by an ischemic pain © Springer Science+Business Media, LLC 2009 Stephen.Bruehl@vanderbilt.edu . NIH Public Access NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript task or vice versa). Resting BP was assessed, followed by drug administration, and then the pain and maze tasks. A significant Drug × Systolic BP (SBP) interaction was observed on McGill Pain Questionnaire-Affective pain ratings (P < .01), indicating that BP-related hypoalgesia observed under placebo was absent under opioid blockade. A significant Gender × Drug × SBP × Task Order interaction was observed for VAS pain intensity (P < .02). Examination of simple effects comprising this interaction suggested that BP-related hypoalgesia occurred only in male participants who experienced the pain task in the absence of emotional arousal, and indicated that this hypoalgesia occurred under placebo but not under opioid-blockade. Results suggest that under some circumstance, BP-related hypoalgesia may have an endogenous opioid-mediated component in healthy individuals, particularly men.

Evidence suggests that anger and pain are related, yet it is not clear by what mechanisms anger may influence pain. We have proposed that effects of anger states and traits on pain sensitivity are partly opioid-mediated. In this study, we tested the extent to which analgesic effects of acute anger arousal on subsequent pain sensitivity were opioid-mediated by subjecting healthy participants to anger-induction and pain either under opioid blockade (oral naltrexone) or placebo. Participants were 160 healthy individuals. A double-blind, placebo-controlled, between-subjects opioid blockade design was used, with participants assigned randomly to one of two Drug conditions (placebo or naltrexone), and to one of two Task Orders (anger-induction followed by pain or vice versa). Results of ANOVAs showed significant Drug Condition × Task Order interactions for sensory pain ratings (MPQ-Sensory) and angry and nervous affect during pain-induction, such that participants who underwent anger-induction prior to pain while under opioid blockade (naltrexone) reported more pain, and anger and nervousness than those who underwent the tasks in the same order, but did so on placebo. Results suggest that for people with intact opioid systems, acute anger arousal may trigger endogenous opioid release that reduces subsequent responsiveness to pain. Conversely, impaired endogenous opioid function, such as that found among some chronic pain patients, may leave certain people without optimal buffering from the otherwise hyperalgesic affects of anger arousal, and so may lead to greater pain and suffering following upsetting or angry events.