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Dynamic Quantitative Sensory Testing to Characterize Central Pain Processing
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Temporal changes in cortical activation during conditioned pain modulation (CPM), a LORETA study.

Ruth Moont1, Yonatan Crispel, Rina Lev

  • 1The Rappaport Faculty of Medicine, Technion - Israel Institute of Technology, Haifa, Israel Faculty of Social Welfare and Health Sciences, University of Haifa, Israel Department of Neurology, Rambam Health Care Campus, Haifa, Israel.

Pain
|February 23, 2011
PubMed
Summary
This summary is machine-generated.

Conditioned pain modulation (CPM) involves cortical control, with the orbitofrontal cortex (OFC) and amygdala showing increased activity before pain sensory areas decrease theirs, leading to pain reduction.

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Area of Science:

  • Neuroscience
  • Pain Perception
  • Neuroimaging

Background:

  • Conditioned pain modulation (CPM) attenuates pain perception and evoked potentials in healthy individuals.
  • While CPM is spinal-bulbar, it is influenced by cortical control.
  • Previous research has not detailed the temporal and spatial cortical changes during CPM.

Purpose of the Study:

  • To investigate the interplay between pain perception/processing areas and descending pain inhibition control under CPM.
  • To identify dynamic changes in cortical activations during CPM using high temporal resolution.
  • To explore the role of specific prefrontal cortical areas in CPM-induced analgesia.

Main Methods:

  • Utilized source localization (sLORETA) on pain-evoked potentials to identify cortical generators.
  • Examined brief, consecutive 50 ms poststimulus time windows.
  • Applied phasic noxious heat stimuli to the forearm with and without conditioning heat pain to the hand in healthy males.

Main Results:

  • CPM induced an initial increase in orbitofrontal cortex (OFC) and amygdala activation (250-300 ms poststimulus), correlated with pain reduction.
  • Subsequently, reduced activations were observed in somatosensory cortices, supplementary motor area, insula, and anterior cingulate cortex (from 400 ms).
  • Prefrontal areas (OFC, amygdala) increased activity before sensory pain areas decreased theirs.

Conclusions:

  • CPM-induced pain inhibition is under the control of the OFC and amygdala.
  • These prefrontal areas play a crucial role in initiating descending pain modulation.
  • The findings elucidate the temporal dynamics of cortical involvement in CPM.