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

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.

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.

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.

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.