Neurofeedback of somatosensory alpha oscillations modulates sensory and affective pain through dissociable neurocognitive pathways

Abstract

Elevated somatosensory α-oscillations are associated with reduced pain sensitivity, motivating efforts to modulate these rhythms for analgesia. Neurofeedback enables voluntary regulation of neural activity through real-time feedback. Here, we examined whether neurofeedback targeting somatosensory α-oscillations modulates pain and explored the associated neurocognitive processes. In a double-blind, sham-controlled design, healthy participants ( n = 80) underwent neurofeedback training during capsaicin-induced tonic pain. Real neurofeedback provided feedback contingent on contralateral somatosensory α-power, whereas sham feedback was noncontingent. Pain intensity and unpleasantness were repeatedly assessed, and electroencephalography (EEG) analyses quantified α-power modulation and microstate dynamics. Compared with sham, real neurofeedback resulted in relatively higher α-power over the targeted somatosensory cortex during training. Behaviorally, real neurofeedback produced dissociable effects: pain unpleasantness showed an early and sustained reduction, whereas pain intensity exhibited a later-emerging, block-specific decrease. At the microstate level, real neurofeedback was associated with a shift in the relative appearance of EEG microstates D and E, indexed by an increased D/E time coverage ratio, previously linked to attentional control and salience-related processing. Mediation analyses suggested 2 associative pathways: an oscillation-to-network pathway linking α modulation and microstate dynamics to reductions in pain intensity, and a performance-to-affect pathway in which perceived training efficacy and positive affect were associated with reductions in pain unpleasantness. Together, these findings indicate that somatosensory α-neurofeedback preferentially modulates affective pain and, to a lesser extent, sensory pain through dissociable neurocognitive processes. This supports the potential of somatosensory α-neurofeedback as a mechanism-informed, nonpharmacological approach for pain modulation.