A psychophysical study of endogenous analgesia: The role of the conditioning pain in the induction and magnitude of conditioned pain modulation

Authors

  • Rony-Reuven Nirl,

    1. Department of Neurology, Rambam Health Care Campus, Haifa, Israel
    2. Laboratory of Clinical Neurophysiology, Faculty of Medicine, Technion—Israel Institute of Technology, Haifa, Israel
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  • Yelena Granovskyl,

    1. Department of Neurology, Rambam Health Care Campus, Haifa, Israel
    2. Laboratory of Clinical Neurophysiology, Faculty of Medicine, Technion—Israel Institute of Technology, Haifa, Israel
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  • David Yarnitskyl,

    Corresponding author
    1. Department of Neurology, Rambam Health Care Campus, Haifa, Israel
    2. Laboratory of Clinical Neurophysiology, Faculty of Medicine, Technion—Israel Institute of Technology, Haifa, Israel
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  • Elliot Sprecherl,

    1. Department of Neurology, Rambam Health Care Campus, Haifa, Israel
    2. Laboratory of Clinical Neurophysiology, Faculty of Medicine, Technion—Israel Institute of Technology, Haifa, Israel
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  • Michal Granotl

    1. Faculty of Social Welfare and Health Sciences, University of Haifa, Haifa, Israel
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Department of Neurology, Rambam Health Care Campus, P.O.B. 9602, Haifa 31096, Israel. Tel.: +972 4 854 2605; fax: +972 4 854 2944 davidy@tx.technion.ac.il.

Abstract

Endogenous analgesia (EA) can be examined experimentally using a conditioned pain modulation (CPM) paradigm. While noxious conditioning stimulation intensities (CSIs) are mainly used, it has not been fully investigated in the same experimental design whether the experienced conditioning pain level affects CPM responses. The principal goal of the present study was to characterize CPM induction and magnitudes evoked by various conditioning pain levels. Furthermore, we explored associations between conditioning pain reports and CPM responses across various CSIs. Thirty healthy, young, right-handed males were tested with a parallel CPM paradigm. Three different CSIs (hand water-immersion) induced mild, moderate and intense pain levels, rated 12.41±7.85, 31.57±9.56 and 58.1±11.43, respectively (0–100 numerical pain scale) (P<0.0001). Contact-heat ‘test-stimulus’ levels were compared before and during conditioning. Within the group, (i) CPM was induced only by the moderate and intense CSIs (Ps≤0.001); (ii) no difference was demonstrated between the magnitudes of these CPM responses. Regression analysis revealed that CPM induction was independent of the perceived conditioning pain level, but associated with the absolute CSI (P<0.0001). Conditioning pain levels were correlated across all CSIs, as were CPM magnitudes (Ps≤0.01). We conclude that among males, (i) once a CPM response is evoked by a required conditioning pain experience, its magnitude is not further affected by increasing conditioning pain and (ii) CPM magnitudes are inter-correlated, but unrelated to conditioning pain reports. These observations may suggest that CPM responses represent an intrinsic element of an individual's EA processes, which are not significantly affected by the experienced conditioning pain.

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