Abstract
The current study tested the hypothesis that conditioned pain modulation is mediated by the release of endogenous opioids
with a placebo-controlled (sugar pill) study of naltrexone (50 mg) in 33 healthy volunteers over two counter-balanced sessions.
Pain modulation consisted of rating of heat pain (palm) during concurrent cold water immersion (foot). Compared to baseline
heat pain ratings, concurrent foot immersion lowered pain intensity ratings, which suggests an inhibitory effect, was reduced
with naltrexone, suggesting at least partial dependence of inhibition on endogenous opioids. An exploratory analysis revealed
that individual differences in catastrophizing moderated the effects of naltrexone; endogenous opioid blockade abolished modulation
in subjects lower in catastrophizing while modulation was unaffected by naltrexone among high catastrophizers. The results
suggest a role of endogenous opioids in endogenous analgesia, but hint that multiple systems might contribute to conditioned
pain modulation, and that these systems might be differentially activated as a function of individual differences in responses
to pain.
with a placebo-controlled (sugar pill) study of naltrexone (50 mg) in 33 healthy volunteers over two counter-balanced sessions.
Pain modulation consisted of rating of heat pain (palm) during concurrent cold water immersion (foot). Compared to baseline
heat pain ratings, concurrent foot immersion lowered pain intensity ratings, which suggests an inhibitory effect, was reduced
with naltrexone, suggesting at least partial dependence of inhibition on endogenous opioids. An exploratory analysis revealed
that individual differences in catastrophizing moderated the effects of naltrexone; endogenous opioid blockade abolished modulation
in subjects lower in catastrophizing while modulation was unaffected by naltrexone among high catastrophizers. The results
suggest a role of endogenous opioids in endogenous analgesia, but hint that multiple systems might contribute to conditioned
pain modulation, and that these systems might be differentially activated as a function of individual differences in responses
to pain.
- Content Type Journal Article
- Pages 1-13
- DOI 10.1007/s10865-012-9424-2
- Authors
- Christopher D. King, Department of Community Dentistry and Behavioral Science, College of Dentistry, University of Florida, 1329 SW 16th St, Suite 5180, PO Box 103628, Gainesville, FL 32610-3628, USA
- Burel Goodin, Department of Community Dentistry and Behavioral Science, College of Dentistry, University of Florida, 1329 SW 16th St, Suite 5180, PO Box 103628, Gainesville, FL 32610-3628, USA
- Lindsay L. Kindler, Department of Community Dentistry and Behavioral Science, College of Dentistry, University of Florida, 1329 SW 16th St, Suite 5180, PO Box 103628, Gainesville, FL 32610-3628, USA
- Robert M. Caudle, Department of Oral and Maxillary Surgery, College of Dentistry, University of Florida, Gainesville, FL, USA
- Robert R. Edwards, Department of Anesthesiology, Brigham and Women’s Hospital and Harvard Medical School, Chestnut Hill, MA, USA
- Nikolaus Gravenstein, Department of Anesthesiology, College of Medicine, University of Florida, Gainesville, FL, USA
- Joseph L. Riley, Department of Community Dentistry and Behavioral Science, College of Dentistry, University of Florida, 1329 SW 16th St, Suite 5180, PO Box 103628, Gainesville, FL 32610-3628, USA
- Roger B. Fillingim, Department of Community Dentistry and Behavioral Science, College of Dentistry, University of Florida, 1329 SW 16th St, Suite 5180, PO Box 103628, Gainesville, FL 32610-3628, USA
- Journal Journal of Behavioral Medicine
- Online ISSN 1573-3521
- Print ISSN 0160-7715