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Placebo conditioning and placebo analgesia modulate a common brain network during pain anticipation and perception.

Watson A, El-Deredy W, Iannetti GD, Lloyd D, Tracey I, Vogt BA, Nadeau V, Jones AK - Pain (2009)

Bottom Line: The sham treatment group reported a significant reduction in pain rating (p=0.012).However, during altered pain experience only aMCC, post-central gyrus and posterior cingulate demonstrated altered activity.Our results suggest that the main effect of placebo arises from the reduction of anticipation of pain during placebo conditioning that is subsequently maintained during placebo analgesia.

View Article: PubMed Central - PubMed

Affiliation: Human Pain Research Group, University of Manchester Rheumatic Diseases Centre, Hope Hospital, Salford M6 8HD, UK. alison.watson@manchester.ac.uk

ABSTRACT
The neural mechanisms whereby placebo conditioning leads to placebo analgesia remain unclear. In this study we aimed to identify the brain structures activated during placebo conditioning and subsequent placebo analgesia. We induced placebo analgesia by associating a sham treatment with pain reduction and used fMRI to measure brain activity associated with three stages of the placebo response: before, during and after the sham treatment, while participants anticipated and experienced brief laser pain. In the control session participants were explicitly told that the treatment was inactive. The sham treatment group reported a significant reduction in pain rating (p=0.012). Anticipatory brain activity was modulated during placebo conditioning in a fronto-cingulate network involving the left dorsolateral prefrontal cortex (DLPFC), medial frontal cortex and the anterior mid-cingulate cortex (aMCC). Identical areas were modulated during anticipation in the placebo analgesia phase with the addition of the orbitofrontal cortex (OFC). However, during altered pain experience only aMCC, post-central gyrus and posterior cingulate demonstrated altered activity. The common frontal cortical areas modulated during anticipation in both the placebo conditioning and placebo analgesia phases have previously been implicated in placebo analgesia. Our results suggest that the main effect of placebo arises from the reduction of anticipation of pain during placebo conditioning that is subsequently maintained during placebo analgesia.

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Related in: MedlinePlus

(A and B) Sites of increased activation in brain regions that correlate with the intensity of pain stimulation, contrast between the painful (pre-conditioning scan) and non-painful (control conditioning scan) laser stimuli during the control session (Z > 1.8 p = 0.05 corrected for multiple comparisons). Significant activations were seen in areas of the “pain matrix” including; bilateral cerebellum, bilateral insula, left post-central gyrus, brainstem and ACC. (C and D) Sites of increased brain activation during placebo analgesia co-varied with measures of reported pain relief. The magnitude of reduction between control and sham treatment sessions co-varied with the magnitude of reduction in neural activity (control minus sham treatment scans for the post-conditioning blocks during painful stimulation). These structures included the following areas within the “pain matrix”; the left aMCC and PCC and left post-central gyrus (Z > 1.9 p = 0.05 corrected for multiple comparisons).
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fig3: (A and B) Sites of increased activation in brain regions that correlate with the intensity of pain stimulation, contrast between the painful (pre-conditioning scan) and non-painful (control conditioning scan) laser stimuli during the control session (Z > 1.8 p = 0.05 corrected for multiple comparisons). Significant activations were seen in areas of the “pain matrix” including; bilateral cerebellum, bilateral insula, left post-central gyrus, brainstem and ACC. (C and D) Sites of increased brain activation during placebo analgesia co-varied with measures of reported pain relief. The magnitude of reduction between control and sham treatment sessions co-varied with the magnitude of reduction in neural activity (control minus sham treatment scans for the post-conditioning blocks during painful stimulation). These structures included the following areas within the “pain matrix”; the left aMCC and PCC and left post-central gyrus (Z > 1.9 p = 0.05 corrected for multiple comparisons).

Mentions: To show the brain regions that correlate with the intensity of pain stimulation, we calculated a contrast between the painful (pre-conditioning scan) and non-painful (control conditioning scan) laser stimuli during the control session (Z > 1.8 p = 0.05 corrected). Significant activations were seen in areas of the “pain matrix” including; bilateral cerebellum, bilateral insula, left post-central gyrus, brainstem and ACC (Fig. 3A and B).


Placebo conditioning and placebo analgesia modulate a common brain network during pain anticipation and perception.

Watson A, El-Deredy W, Iannetti GD, Lloyd D, Tracey I, Vogt BA, Nadeau V, Jones AK - Pain (2009)

(A and B) Sites of increased activation in brain regions that correlate with the intensity of pain stimulation, contrast between the painful (pre-conditioning scan) and non-painful (control conditioning scan) laser stimuli during the control session (Z > 1.8 p = 0.05 corrected for multiple comparisons). Significant activations were seen in areas of the “pain matrix” including; bilateral cerebellum, bilateral insula, left post-central gyrus, brainstem and ACC. (C and D) Sites of increased brain activation during placebo analgesia co-varied with measures of reported pain relief. The magnitude of reduction between control and sham treatment sessions co-varied with the magnitude of reduction in neural activity (control minus sham treatment scans for the post-conditioning blocks during painful stimulation). These structures included the following areas within the “pain matrix”; the left aMCC and PCC and left post-central gyrus (Z > 1.9 p = 0.05 corrected for multiple comparisons).
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2743811&req=5

fig3: (A and B) Sites of increased activation in brain regions that correlate with the intensity of pain stimulation, contrast between the painful (pre-conditioning scan) and non-painful (control conditioning scan) laser stimuli during the control session (Z > 1.8 p = 0.05 corrected for multiple comparisons). Significant activations were seen in areas of the “pain matrix” including; bilateral cerebellum, bilateral insula, left post-central gyrus, brainstem and ACC. (C and D) Sites of increased brain activation during placebo analgesia co-varied with measures of reported pain relief. The magnitude of reduction between control and sham treatment sessions co-varied with the magnitude of reduction in neural activity (control minus sham treatment scans for the post-conditioning blocks during painful stimulation). These structures included the following areas within the “pain matrix”; the left aMCC and PCC and left post-central gyrus (Z > 1.9 p = 0.05 corrected for multiple comparisons).
Mentions: To show the brain regions that correlate with the intensity of pain stimulation, we calculated a contrast between the painful (pre-conditioning scan) and non-painful (control conditioning scan) laser stimuli during the control session (Z > 1.8 p = 0.05 corrected). Significant activations were seen in areas of the “pain matrix” including; bilateral cerebellum, bilateral insula, left post-central gyrus, brainstem and ACC (Fig. 3A and B).

Bottom Line: The sham treatment group reported a significant reduction in pain rating (p=0.012).However, during altered pain experience only aMCC, post-central gyrus and posterior cingulate demonstrated altered activity.Our results suggest that the main effect of placebo arises from the reduction of anticipation of pain during placebo conditioning that is subsequently maintained during placebo analgesia.

View Article: PubMed Central - PubMed

Affiliation: Human Pain Research Group, University of Manchester Rheumatic Diseases Centre, Hope Hospital, Salford M6 8HD, UK. alison.watson@manchester.ac.uk

ABSTRACT
The neural mechanisms whereby placebo conditioning leads to placebo analgesia remain unclear. In this study we aimed to identify the brain structures activated during placebo conditioning and subsequent placebo analgesia. We induced placebo analgesia by associating a sham treatment with pain reduction and used fMRI to measure brain activity associated with three stages of the placebo response: before, during and after the sham treatment, while participants anticipated and experienced brief laser pain. In the control session participants were explicitly told that the treatment was inactive. The sham treatment group reported a significant reduction in pain rating (p=0.012). Anticipatory brain activity was modulated during placebo conditioning in a fronto-cingulate network involving the left dorsolateral prefrontal cortex (DLPFC), medial frontal cortex and the anterior mid-cingulate cortex (aMCC). Identical areas were modulated during anticipation in the placebo analgesia phase with the addition of the orbitofrontal cortex (OFC). However, during altered pain experience only aMCC, post-central gyrus and posterior cingulate demonstrated altered activity. The common frontal cortical areas modulated during anticipation in both the placebo conditioning and placebo analgesia phases have previously been implicated in placebo analgesia. Our results suggest that the main effect of placebo arises from the reduction of anticipation of pain during placebo conditioning that is subsequently maintained during placebo analgesia.

Show MeSH
Related in: MedlinePlus