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Articles, Behavioral/Systems/Cognitive

Brain Mechanisms Supporting the Modulation of Pain by Mindfulness Meditation

Fadel Zeidan, Katherine T. Martucci, Robert A. Kraft, Nakia S. Gordon, John G. McHaffie and Robert C. Coghill
Journal of Neuroscience 6 April 2011, 31 (14) 5540-5548; https://doi.org/10.1523/JNEUROSCI.5791-10.2011
Fadel Zeidan
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Katherine T. Martucci
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Robert A. Kraft
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Nakia S. Gordon
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John G. McHaffie
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Robert C. Coghill
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  • Figure 1.
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    Figure 1.

    Experimental procedures across time. First column, Psychophysical training session: Subjects first came in for psychophysical training. In this session, subjects were familiarized with visual analog scales, the range of thermal stimulation, and thermal stimulation paradigm used in the subsequent MRI sessions. Second column, MRI session 1: In the first two blocks, subjects were asked to reduce movement and keep eyes closed (rest). A heat (49°C) and neutral (35°) series were randomly presented in one of two blocks. Before anatomical acquisition, subjects were instructed to “begin meditating by focusing on the sensations of the breath.” Subjects continued to attend to the breath during a block of noxious stimulation (49°C) or neutral (35°). Pain ratings were assessed after each block. Third column: The 4 d (20 min/d) meditation intervention. Subjects were taught to focus on the changing sensations of the breath. They were taught that discursive thoughts were to be acknowledged without affective reaction and “let go” by redirecting their focus back on breath sensations. In sessions 3 and 4, sounds of the MRI scanner were introduced to familiarize subjects with the MRI environment. The fourth column describes the MRI session 2 (after meditation training). In the first four blocks, subjects were instructed to reduce movement and close their eyes (rest). Two heat (49°C) and two neutral (35°C) blocks were randomly administered. Before anatomical acquisition, subjects were instructed to “begin meditating by focusing on the sensations of the breath.” Subjects continued to meditate across two blocks of noxious stimulation (49°C) and neutral (35°C). Pain ratings were assessed after each block.

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    Figure 2.

    Mean (SEM) psychophysical pain ratings across each session. Meditation, after training, significantly reduced pain intensity ratings and pain unpleasantness ratings when compared with rest *p < 0.05.

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    Figure 3.

    Brain activations and deactivations illustrate the main effects of ATB and pain in the MRI session before training. In the main effect of pain, there was greater activation in SI corresponding to the stimulation site, ACC, SII, left putamen, and bilateral insula. There was no ATB-related brain activity, but the deactivations for the main effect of meditation were found in the medial PFC, posterior cingulate cortex, thalamus, and paracingulate gyrus. Slice locations correspond to standard stereotaxic space.

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    Figure 4.

    Brain activations and deactivations illustrate the main effects of pain and meditation, as well as the overlap between pain and meditation in MRI session 2 (after training). Noxious stimulation activated the ACC, bilateral anterior insula, and posterior insula/SII. Meditation activated bilateral ACC, OFC, ventral striatum, anterior insula, SI, and SII. Moreover, meditation was associated with deactivations in the medial PFC and posterior cingulate cortex, consistent with default mode network activation. There was significant overlap between meditation and pain in the ACC and anterior insula, suggesting that these areas serve as a possible substrate for pain modulation. Slice locations correspond to standard stereotaxic space.

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    Figure 5.

    Interaction between meditation and pain-related brain activation in MRI session 2. General linear modeling analyses detected a significant interaction in SI (z = 68) between meditation and rest in the presence of noxious stimulation. There was a significant activation of the contralateral SI during heat stimulation while subjects were not meditating. Meditation significantly reduced activation in SI during noxious heat stimulation. Slice locations correspond to standard stereotaxic space.

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    Figure 6.

    Relationship between meditation-induced decreases in psychophysical pain ratings and pain-related brain activation. Subjects reporting the greatest decrease in pain intensity ratings also exhibited the largest increase in the ACC and right anterior insula activation. Top, Similarly, subjects reporting the greatest activation in the OFC exhibited the greatest decreases in pain unpleasantness. In contrast, greater deactivation in the thalamus was related to larger decreases in pain unpleasantness ratings. Bottom, Slice locations correspond to standard stereotaxic space.

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    Figure 7.

    Paired t test illustrating differences in brain activation between the main effects of pain and meditation across MRI sessions. Top, Noxious stimulation activated significantly greater SI corresponding to the stimulation site, bilateral SII, and bilateral insula before training when compared with after training. After training, noxious stimulation activated greater medial PFC, frontal pole, thalamus, and ACC when compared with before training. Bottom, There was greater superior temporal gyrus activation during the ATB condition before training compared with meditation after training. However, there was greater OFC, ACC, and right anterior insula meditation-related activation after training when compared with ATB before training. Slice locations correspond to standard stereotaxic space.

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    Table 1.

    Cerebral blood flow, respiration rate, and heart rate means (SEM) across conditions and sessions

    CBFRespiration rateHeart rate
    Session 1
        Rest: neutral74.12 (3.01)19.97 (1.29)72.53 (2.33)
        Rest: heat71.51 (2.93)20.45 (1.11)74.79 (2.39)
        ATB: neutral70.69 (3.56)17.05 (1.00)70.46 (1.79)
        ATB: heat67.90 (3.08)19.32 (1.33)74.07 (2.19)
    Session 2
        Rest: neutral68.57 (3.17)16.72 (0.82)74.82 (3.08)
        Rest: heat66.82 (2.59)17.12 (0.93)77.32 (2.95)
        Meditation: neutral65.09 (3.59)11.55 (0.74)73.62 (2.77)
        Meditation: heat65.47 (3.86)9.47 (0.67)a75.38 (2.70)
    • CBF was lower when subjects were instructed to attend to the breath (n = 15). However, there were no differences between rest and ATB in session 1 or between rest and meditation in session 2.

    • ↵aRespiration rate during heat stimulation and meditation was significantly lower than all other conditions (n = 10). Heat stimulation increased heart rate when compared with neutral stimulation (n = 9).

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The Journal of Neuroscience: 31 (14)
Journal of Neuroscience
Vol. 31, Issue 14
6 Apr 2011
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Brain Mechanisms Supporting the Modulation of Pain by Mindfulness Meditation
Fadel Zeidan, Katherine T. Martucci, Robert A. Kraft, Nakia S. Gordon, John G. McHaffie, Robert C. Coghill
Journal of Neuroscience 6 April 2011, 31 (14) 5540-5548; DOI: 10.1523/JNEUROSCI.5791-10.2011

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Brain Mechanisms Supporting the Modulation of Pain by Mindfulness Meditation
Fadel Zeidan, Katherine T. Martucci, Robert A. Kraft, Nakia S. Gordon, John G. McHaffie, Robert C. Coghill
Journal of Neuroscience 6 April 2011, 31 (14) 5540-5548; DOI: 10.1523/JNEUROSCI.5791-10.2011
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  • Meditation Increases DHEA more than the Placebo Effect
    James M Howard
    Published on: 19 November 2015
  • Published on: (19 November 2015)
    Page navigation anchor for Meditation Increases DHEA more than the Placebo Effect
    Meditation Increases DHEA more than the Placebo Effect
    • James M Howard, Biologist

    The basis of the results in this report might be increased dehydroepiandrosterone (DHEA). It is known that mindfulness / meditation increases DHEA (Glaser et al., 1992; Manzaneque et al., 2011).

    It is my hypothesis that the placebo effect results from increased DHEA. Possible Explanation of Failure to Thrive Infants May Have a Reduced Melatonin -- DHEA Cycle"...a basis of the placebo effect. at: http://anthropo...

    Show More

    The basis of the results in this report might be increased dehydroepiandrosterone (DHEA). It is known that mindfulness / meditation increases DHEA (Glaser et al., 1992; Manzaneque et al., 2011).

    It is my hypothesis that the placebo effect results from increased DHEA. Possible Explanation of Failure to Thrive Infants May Have a Reduced Melatonin -- DHEA Cycle"...a basis of the placebo effect. at: http://anthropogeny.com/Failure%20to%20Thrive.htm.

    Meditation may simply produce more DHEA than the placebo effect because meditation is a targeted, practiced method of specifically increasing dehydroepiandrosterone.

    References

    Glaser JL, Brind JL, Vogelman JH, Eisner MJ, Dillbeck MC, Wallace RK, Chopra D, Orentreich N. Elevated serum dehydroepiandrosterone sulfate levels in practitioners of the Transcendental Meditation (TM) and TM-Sidhi programs. J Behav Med. 1992 Aug;15(4):327-41.

    Manzaneque, J. M., Vera, F. M., Ramos, N. S., Godoy, Y. A., Rodriguez, F. M., Blanca, M. J., Fernandez, A. and Enguix, A. (2011), Psychobiological modulation in anxious and depressed patients after a mindfulness meditation programme: a pilot study. Stress and Health, 27: 216???222

    Conflict of Interest:

    None declared

    Show Less
    Competing Interests: None declared.

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