TY - JOUR
T1 - Reduction of conditioned pain modulation in humans by naltrexone
T2 - An exploratory study of the effects of pain catastrophizing
AU - King, Christopher D.
AU - Goodin, Burel
AU - Kindler, Lindsay L.
AU - Caudle, Robert M.
AU - Edwards, Robert R.
AU - Gravenstein, Nikolaus
AU - Riley, Joseph L.
AU - Fillingim, Roger B.
N1 - Funding Information:
Acknowledgments This research was supported by a University of Florida College of Dentistry (UFCD) Student Summer Research Fellowship, UFCD Seed Grant (Riley), NIH-NIDCR grant T32 DE007200 (King), UF CTSI UL1TR000064/KL2TR000065 (King), American Pain Society Future Leaders in Pain Research Grant Program (King), AG033906-06S1 (Fillingim), and the UF Comprehensive Center for Pain Research (CCPR). The authors of this study have no conflict of interests. This material was also supported by the North Florida/South Georgia Veterans Health System, Gainesville, FL, USA.
PY - 2013/6
Y1 - 2013/6
N2 - 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.
AB - 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.
KW - Catastrophizing
KW - Conditioned pain modulation
KW - Diffuse noxious inhibitory control
KW - Endogenous opioids
KW - Heat pain
KW - Naltrexone
UR - http://www.scopus.com/inward/record.url?scp=84875344583&partnerID=8YFLogxK
U2 - 10.1007/s10865-012-9424-2
DO - 10.1007/s10865-012-9424-2
M3 - Article
C2 - 22534819
AN - SCOPUS:84875344583
SN - 0160-7715
VL - 36
SP - 315
EP - 327
JO - Journal of Behavioral Medicine
JF - Journal of Behavioral Medicine
IS - 3
ER -