Abstract
Background
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.
Methods
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.
Results
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.
Conclusions
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.
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.
Methods
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.
Results
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.
Conclusions
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 language | English |
|---|---|
| Pages (from-to) | 1291-1303 |
| Journal | European Journal of Pain |
| Volume | 22 |
| Issue number | 7 |
| DOIs | |
| Publication status | Published - 2018 |
| Externally published | Yes |