Reduction of Pain and Spinal Nociceptive Transmission by Working Memory is Load Dependant.

Working memory (WM) engagement produces pain inhibition. However, it remains unclear whether higher WM load increases this effect. The aim of this study was to investigate the interaction between WM load and pain inhibition by WM and examine the contribution of cerebrospinal mechanism. Thirty-eight healthy volunteers were assigned to one of 2 n-back groups for which WM load was different (2-back or 3-back). The experimental protocol comprised 5 counterbalanced conditions (0-back, n-back, pain, 0-back with pain, and n-back with pain). Pain and the nociceptive flexion reflex (NFR) were evoked by transcutaneous electrical stimulation of the sural nerve. Pain was significantly different between conditions, but not between n-back groups. Both the 0-back and n-back tasks reduced pain compared with pain alone, but the n-back task produced stronger pain inhibition compared with the 0-back task. NFR amplitude was significantly different between conditions but not between n-back groups. NFR was inhibited by the 0-back and n-back tasks, with no difference between the 2 tasks. These findings indicate that pain inhibition by WM is increased by WM load, but only to a certain point. NFR inhibition by WM suggests that inhibition of pain by WM depends, at least in part, on cerebrospinal mechanism. PERSPECTIVE: This behavioral and electrophysiological study shows that engaging in a cognitive task reduces pain by decreasing spinal nociceptive transmission, depending on task difficulty. These findings may yield better nonpharmacological pain therapies based on individual differences in working memory performance and capacity as well as several factors that regulate working memory.