(427) Negative affect and functional status predict opioid analgesic effects on chronic pain: evidence for endogenous opioid mediation

Abstract

Negative affect may be associated with opioid analgesic effectiveness. Studies in the acute post-operative pain context consistently report that elevated negative affect is linked to greater opioid analgesic requirements. Virtually no work has examined these issues in the chronic pain context, and possible underlying mechanisms have not previously been explored. We evaluated whether negative affect and functional status are associated with subsequent analgesic responsiveness to morphine, and whether endogenous opioid mechanisms mediate these associations. Participants included 81 individuals with chronic low back pain (LBP), all using no opioid analgesics. Participants attended 3 identical laboratory sessions during which they received either intravenous naloxone (8mg), morphine sulfate (0.08mg/kg), or saline placebo. Low back pain intensity was evaluated pre- and post-drug in each condition. Pre-post drug changes in low back pain under placebo compared to naloxone and morphine condition changes were derived as indices of endogenous opioid inhibition of back pain and morphine analgesia, respectively. Elevated scores on the BDI, STAI, Trait Anger Scale, Pain Catastrophizing Scale (PCS), and Pain Disability Index (PDI), and lower scores on total SF-36 function, were significantly associated with greater morphine-related reductions in back pain (relative to placebo). Effects of BDI, PCS, PDI, and SF-36 function on morphine analgesia were partially mediated by differences in endogenous opioid function. Individuals reporting greater negative affect and lower functional status exhibited greater morphine-related reductions in low back pain. This effect is opposite in direction to post-operative acute pain studies using indirect measures of opioid effectiveness (i.e., morphine requirements), and extends this literature to the context of opioid analgesic therapy for chronic pain. Furthermore, this study suggests that deficits in endogenous opioid function may link negative affect and functional status to opioid analgesic responsiveness. Consideration of negative affect and functional measures as predictors in personalized medicine protocols appears warranted. Negative affect may be associated with opioid analgesic effectiveness. Studies in the acute post-operative pain context consistently report that elevated negative affect is linked to greater opioid analgesic requirements. Virtually no work has examined these issues in the chronic pain context, and possible underlying mechanisms have not previously been explored. We evaluated whether negative affect and functional status are associated with subsequent analgesic responsiveness to morphine, and whether endogenous opioid mechanisms mediate these associations. Participants included 81 individuals with chronic low back pain (LBP), all using no opioid analgesics. Participants attended 3 identical laboratory sessions during which they received either intravenous naloxone (8mg), morphine sulfate (0.08mg/kg), or saline placebo. Low back pain intensity was evaluated pre- and post-drug in each condition. Pre-post drug changes in low back pain under placebo compared to naloxone and morphine condition changes were derived as indices of endogenous opioid inhibition of back pain and morphine analgesia, respectively. Elevated scores on the BDI, STAI, Trait Anger Scale, Pain Catastrophizing Scale (PCS), and Pain Disability Index (PDI), and lower scores on total SF-36 function, were significantly associated with greater morphine-related reductions in back pain (relative to placebo). Effects of BDI, PCS, PDI, and SF-36 function on morphine analgesia were partially mediated by differences in endogenous opioid function. Individuals reporting greater negative affect and lower functional status exhibited greater morphine-related reductions in low back pain. This effect is opposite in direction to post-operative acute pain studies using indirect measures of opioid effectiveness (i.e., morphine requirements), and extends this literature to the context of opioid analgesic therapy for chronic pain. Furthermore, this study suggests that deficits in endogenous opioid function may link negative affect and functional status to opioid analgesic responsiveness. Consideration of negative affect and functional measures as predictors in personalized medicine protocols appears warranted.