Highlights
- •Pain was reduced by WM engagement and more so for high WM load.
- •This effect partly depended on descending pathways, as indicated by NFR inhibition.
- •Increasing WM load increased this effect, but only to a certain point.
- •Beyond this point, additional load was not more effective.
Abstract
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.
Key Words
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Article info
Publication history
Published online: February 09, 2021
Accepted:
February 7,
2021
Received in revised form:
January 27,
2021
Received:
December 9,
2020
Footnotes
Disclosures: This work was supported by a grant from the Natural Science and Engineering Research Council of Canada (MP: 06559). The contribution of MP was supported by the Fonds de recherche du Québec en Santé (FRQS). The contribution of Zoha Deldar was supported by the Department of Anatomy and the Center de Recherche en Neuropsychologie et Cognition (CERNEC) at Université de Montréal.
Conflicts of Interest: The authors declare no competing interests and no relationship that may lead to any conflict of interest.
Web: www.uqtr.ca/cognac.
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© 2021 by United States Association for the Study of Pain, Inc.
