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- Wiebke Gandhi, Norma R Rosenek, Richard Harrison, and Tim V Salomons.
- Centre for Integrative Neuroscience & Neurodynamics, School of Psychology and Clinical Language Sciences, University of Reading, Reading, United Kingdom.
- Pain. 2020 Feb 1; 161 (2): 300-307.
AbstractThe amygdala is central to emotional processing of sensory stimuli, including pain. Because recent findings suggest that individual differences in emotional processes play a part in the development of chronic pain, a better understanding of the individual patterns of functional connectivity that makes individuals susceptible to emotionally modulated facilitation of pain is needed. We therefore investigated the neural correlates of individual differences in emotional pain facilitation using resting-state functional magnetic resonance imaging (rs-fMRI) with an amygdala seed. Thirty-seven participants took part in 3 separate sessions, during which pain sensitivity was tested (session 1), participants underwent rs-fMRI (session 2), and emotional pain modulation was assessed (session 3). The amygdala served as seed for the rs-fMRI analysis, and whole-brain voxel-wise connectivity was tested. Pain modulatory scores were entered as regressor for the group analysis. Stronger connectivity of the amygdala to S1/M1, S2/operculum, and posterior parietal cortex at rest characterized individuals who showed greater pain facilitation by negative emotions. When comparing the amygdala networks associated with pain unpleasantness and with pain-intensity modulation, most of the identified areas were equally related to either pain rating type; only amygdala connectivity to S1/M1 was found to predict pain-intensity modulation specifically. We demonstrate that trait-like patterns of functional connectivity between amygdala and cortical regions involved in sensory and motor responses are associated with the individual amplitude of pain facilitation by negative emotional states. Our results are an early step toward improved understanding of the mechanisms that give rise to individual differences in emotional pain modulation.
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