Unpredictable threat amplifies pain and spinal nociception (as measured by the nociceptive flexion reflex, NFR), but it is unknown whether pain catastrophizing mediates this threat-related amplification. To examine this, the present study experimentally reduced catastrophizing and examined the effect on threat-evoked pain/NFR facilitation. Healthy pain-free participants (N = 113) were randomly assigned to a brief 30-minute intervention designed to reduce catastrophic thoughts or a control intervention that involved education about pain neurobiology. Before the interventions, participants underwent a block of 8 pseudorandomly ordered periods of safe (no abdominal shock) and threat (abdominal shock possible) during which pain and NFR were evoked by electric stimulations to the ankle. After the safe/threat periods, participants rated pain intensity, pain unpleasantness, and situation-specific pain catastrophizing. The same test block was delivered after the intervention to examine changes in catastrophizing and threat-evoked pain/NFR facilitation. As expected, pain catastrophizing was reduced by the catastrophizing reduction intervention, relative to the control group. Furthermore, pain intensity, unpleasantness, and NFR magnitudes were higher during threat periods than safe. However, this threat-related pain/NFR amplification was not attenuated by the catastrophizing reduction intervention at the group level, although the intervention generally led to lower pain ratings (but not reduced NFR), regardless of the context. Nonetheless, bootstrapped mediation analyses found that reductions in catastrophizing mediated reductions in threat-related amplification of pain, but not NFR. This suggests that catastrophizing is partly responsible for threat-evoked pain amplification and provides further evidence that catastrophizing does not amplify pain at the spinal level.
Pain catastrophizing partially mediates threat-evoked amplification of pain, but not threat-evoked amplification of spinal nociception.
Department of Psychology, The University of Tulsa, Tulsa, OK, USA
Corresponding author. Address: Department of Psychology, The University of Tulsa, 800 South Tucker Dr, Tulsa, OK 74104, USA. Tel.: (918) 631-2839; fax: (918) 631-2833. E-mail address: email@example.com (J. L. Rhudy).
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Received May 29, 2015
Received in revised form September 10, 2015
Accepted October 12, 2015