Working Memory Load-Dependent Cortical Mechanism of Distraction Analgesia in Healthy Individuals: An fNIRS Study.

Purpose: As a central element of executive function, working memory (WM) contributes to pain regulation by balancing cognitive resources between goal-directed attention and attention captured by nociceptive stimuli. Although WM load influences pain perception, its modulatory mechanism remains to be explored, particularly functional network interactions among pain-related brain regions during distraction. This study aims to investigate the effect of different-load WM tasks on pain perception via behavioral measures and functional near-infrared spectroscopy (fNIRS) data, and to explore the underlying cortical neural mechanism. Patients and Methods: Thirty-five healthy participants completed experiments under synchronized fNIRS. In the first part, participants completed a laser stimuli pain-rating task. In the second part, a 2 × 2 within-subject design was used to assess the distraction effect on pain perception. Participants performed an n-back task during two WM loads: high load (2-back) and low load (0-back), while receiving stimuli (with or without laser stimuli) to their right hand. All participants completed trials in five experimental conditions: pain task, 0-back task, 2-back task, 0-back with pain task, and 2-back with pain task. Pain intensity ratings and cognitive performance (accuracy and reaction time) were recorded. Results: High load WM significantly reduced both the perceived pain intensity and nociceptive neural activation in the primary sensorimotor cortex (SM1) and secondary somatosensory cortex (S2). In contrast to n-back task, n-back with pain task showed a significant reduction in functional connectivity between brain regions within the high load group, including RS2-anterior prefrontal cortex (aPFC), RSM1-right dorsolateral prefrontal cortex (RDLPFC), RSM1-aPFC, and LSM1-aPFC. Conclusion: This study provides evidence for load-dependent cortical mechanism of distraction analgesia in healthy individuals. We conclude that distraction analgesia effect of WM may result from suppression of sensorimotor cortical activity and decoupling of pain-processing networks.