BackgroundMusic is sometimes used as an adjunct to pain management. However, there is limited understanding of by what means music modulates pain perception and how the brain responds to nociceptive inputs while listening to music, because clinical practice typically involves the coexistence of multiple therapeutic interventions. To address this challenge, laboratory studies with experimental and control conditions are needed.MethodsIn the present investigation, we delivered nociceptive laser stimuli on 30 participants under three conditions – participants were sitting in silence, listening to their preferred music, or listening to white noise. Differences among conditions were quantified by self-reports of pain intensity and unpleasantness, and brain activity sampled by electroencephalography (EEG).ResultsCompared with the noise and silence conditions, participants in the music condition reported lower ratings on pain unpleasantness, as reflected by reduced brain oscillations immediately prior to the nociceptive laser stimulus at frequencies of 4–15 Hz in EEG. In addition, participants showed smaller P2 amplitudes in laser-evoked potentials (LEPs) when they were listening to music or white noise in comparison to sitting in silence. These findings suggest that a general modulation effect of sounds on pain, with a specific reduction of pain unpleasantness induced by the positive emotional impact.ConclusionMusic may serve as a real-time regulator to modulate pain unpleasantness. Results are discussed in view of current understandings of music-induced analgesia.
Expectation interacting with nociceptive input can shape the perception of pain. It has been suggested that reward-related expectations are associated with the activation of the ventral tegmental area (VTA), which projects to the striatum (e.g., nucleus accumbens [NAc]) and prefrontal cortex (e.g., rostral anterior cingulate cortex [rACC]). However, the role of these projection pathways in encoding expectancy effects on pain remains unclear. In this study, we leveraged a visual cue conditioning paradigm with a long pain anticipation period and collected magnetic resonance imaging (MRI) data from 30 healthy human subjects (14 females). At the within-subject level, whole-brain functional connectivity (FC) analyses showed that the mesocortical pathway (VTA-rACC FC) and the mesolimbic pathway (VTA-NAc FC) were enhanced with positive expectation but inhibited with negative expectation during pain anticipation period. Mediation analyses revealed that cue-based expectancy effects on pain were mainly mediated by the VTA-NAc FC, and structural equation modeling showed that VTA-based FC influenced pain perception by modulating pain-evoked brain responses. At the between-subject level, multivariate pattern analyses demonstrated that gray matter volumes in the VTA, NAc, and rACC were able to predict the magnitudes of conditioned pain responses associated with positive and/or negative expectations across subjects. Our results therefore advance the current understanding of how the reward system is linked to the interaction between expectation and pain. Furthermore, they provide precise functional and structural information on mesocorticolimibic pathways that encode within-subject and between-subject variability of expectancy effects on pain. Significance StatementStudies have suggested that reward-related expectation is associated with the activation of the VTA, which projects to the striatum and prefrontal cortex. However, the role of these projection pathways in encoding expectancy effects on pain remains unclear. Using multimodality MRI and a visual cue conditioning paradigm, we found that the functional connectivity and gray matter volumes in key regions (the VTA, NAc, and rostral ACC) within the mesocorticolimbic pathways encoded expectancy effects on pain. Our results advance the current understanding of how the reward system is linked to the interaction between expectation and pain, and provide precise functional and structural information on mesocorticolimbic pathways that encode expectancy effects on pain.
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