Fear of pain and cortisol reactivity predict the strength of stress-induced hypoalgesia

I. Timmers, A. L. Kaas, Cwem Quaedflieg, E. E. Biggs, T. Smeets, J. R. de Jong

Research output: Contribution to journalArticleScientificpeer-review

19 Citations (Scopus)


Acute stress can have an effect on pain sensitivity, yet the direction of the effect – whether it is hypoalgesic or hyperalgesic – is mixed across studies. Moreover, which part of the stress response influences pain sensitivity is still unclear. In the current experimental study, we aim to examine the effect of acute stress on heat pain thresholds and pain tolerance levels in healthy participants, while taking into account individual differences in stress responses.

Forty‐two healthy participants were randomly assigned to either a well‐validated stress paradigm: the Maastricht Acute Stress Task (MAST; combining physical and psychological stressors) or to a nonstressful version of the task. Heat pain thresholds and tolerance levels were assessed at three times: prior to the MAST, immediately after the MAST during the presumed sympatho‐adrenal medullary (SAM) response, and 15 min after MAST to cover the presumed hypothalamus–pituitary–adrenal (HPA) axis response. Stress responses were assessed both subjectively and physiologically.

We observed that the acute stress induction led to increased heat pain thresholds, an effect that was present only in participants showing a cortisol response following stress induction and only in the presumed HPA axis time window. The strength of this hypoalgesic effect was further predicted by the change in cortisol and by fear of pain levels.

Our findings indicate that the HPA axis – and not the autonomic – stress response specifically underlies this stress‐induced hypoalgesic effect, having important implications for clinical states with HPA axis dysfunctions.
Original languageEnglish
Pages (from-to)1291-1303
JournalEuropean Journal of Pain
Issue number7
Publication statusPublished - 2018
Externally publishedYes


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