Background & Aims
Experimentally induced sensitization of nociceptive pathways in healthy participants is regularly used as an experimental model of persistent pain. Such experimental sensitization does indeed lead to a nociceptive mechanical hypersensitivity reminiscent of the one observed in chronic pain. Interestingly, effects on the processing of non-nociceptive stimuli are also reported. This makes the model particularly interesting for studying the bidirectional relationship between persistent pain and non-nociceptive changes, whose underlying mechanisms remain unclear. Previous data has also shown that such experimental sensitization induces changes at the autonomic level, and it has been proposed that increases in arousal would not only influence the development of mechanical hypersensitivity but potentially also affect the co-occurrence of non-nociceptive effects. However, the role of arousal in the development of mechanical hypersensitivity has actually never been tested systematically.
Methods
In a between-subject design (N=40), we used two different electrical stimulation intensities to induce sensitization on one forearm, and we measured arousal (skin conductance level/SCL; heart rate variability/HRV) at several time points before, during and after the sensitization, as well as mechanical sensitivity (self-reported intensity of pinprick stimulation) on both forearms before (T0) and after the sensitization (T1= directly after, T2= 20 min after sensitization). We tested whether higher intensity electrical stimulation, as compared to lower intensity electrical stimulation, leads to both higher mechanical hypersensitivity on the sensitized arm and higher arousal (repeated measures ANOVA), as well as whether there is a relationship between arousal and mechanical hypersensitivity (multiple regression). For both mechanical sensitivity and arousal measures, difference scores to baseline (i.e. before the sensitization) were computed.
Results
Results showed a significant interaction between arm and group for mechanical sensitivity, indicating that after the sensitization procedure, the difference in mechanical sensitivity between the sensitized and the non-sensitized arm was bigger in the higher as compared to the lower intensity stimulation group (p=0.022, partial eta2= 0.128). Regarding SCL and HRV, we did not observe any significant difference between the groups, at none of the time points. There was however a significant relationship between mechanical sensitivity and arousal measured directly after the sensitization procedure: while SCL significantly predicted mechanical sensitivity assessed at T1 (r2=0.173, p=0.007, ?=1.999), HRV significantly predicted the sensitivity developed at T2 (r2=0.218, p=0.002, ?=-0.327).
Conclusions
The results suggest that autonomic changes are associated with the development of mechanical hypersensitivity after the sensitization of nociceptive pathways in healthy participants. Furthermore, they open up an avenue for studying such changes as a potential common mechanism in both the described nociceptive but also non-nociceptive effects that have been observed after sensitization.
References
None
Presenting Author
Lieve Filbrich
Poster Authors
Topics
- Mechanisms: Biological-Systems (Physiology/Anatomy)