English
 
Help Privacy Policy Disclaimer
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT

Released

Journal Article

A prefrontal non-opioid mechanism in placebo analgesia

MPS-Authors
/persons/resource/persons147

Petersson,  Karl Magnus
Neurobiology of Language Group, MPI for Psycholinguistics, Max Planck Society;
Cognitive Neurophysiology Research Group, Stockholm Brain Institute, Osher Center for Integrative Medicine, Karolinska Institutet, Stockholm, Sweden;
Cognitive Neuroscience Research Group, IBB/CBME, University of Algarve, Faro, Portugal;

External Resource
No external resources are shared
Fulltext (restricted access)
There are currently no full texts shared for your IP range.
Fulltext (public)
Supplementary Material (public)
There is no public supplementary material available
Citation

Petrovic, P., Kalso, E., Petersson, K. M., Andersson, J., Fransson, P., & Ingvar, M. (2010). A prefrontal non-opioid mechanism in placebo analgesia. Pain, 150, 59-65. doi:10.1016/j.pain.2010.03.011.


Cite as: https://hdl.handle.net/11858/00-001M-0000-0012-9D85-D
Abstract
ehavioral studies have suggested that placebo analgesia is partly mediated by the endogenous opioid system. Expanding on these results we have shown that the opioid-receptor-rich rostral anterior cingulate cortex (rACC) is activated in both placebo and opioid analgesia. However, there are also differences between the two treatments. While opioids have direct pharmacological effects, acting on the descending pain inhibitory system, placebo analgesia depends on neocortical top-down mechanisms. An important difference may be that expectations are met to a lesser extent in placebo treatment as compared with a specific treatment, yielding a larger error signal. As these processes previously have been shown to influence other types of perceptual experiences, we hypothesized that they also may drive placebo analgesia. Imaging studies suggest that lateral orbitofrontal cortex (lObfc) and ventrolateral prefrontal cortex (vlPFC) are involved in processing expectation and error signals. We re-analyzed two independent functional imaging experiments related to placebo analgesia and emotional placebo to probe for a differential processing in these regions during placebo treatment vs. opioid treatment and to test if this activity is associated with the placebo response. In the first dataset lObfc and vlPFC showed an enhanced activation in placebo analgesia vs. opioid analgesia. Furthermore, the rACC activity co-varied with the prefrontal regions in the placebo condition specifically. A similar correlation between rACC and vlPFC was reproduced in another dataset involving emotional placebo and correlated with the degree of the placebo effect. Our results thus support that placebo is different from specific treatment with a prefrontal top-down influence on rACC.