Exploration of conditioned pain modulation effect on long-term potentiation-like pain amplification in humans
Peer reviewed, Journal article
Published version
Date
2017Metadata
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Abstract
Background This study aimed to explore conditioned pain modulation (CPM) effect on long‐term potentiation (LTP)‐like pain amplification induced by cutaneous 10‐Hz conditioning electrical stimulation (CES). Methods Conditioned pain modulation was induced by cold pressor conditioning stimulus (CPCS) (4 °C) which was applied immediately before CES in the active session. In the control session, water with a temperature of 32 °C was used. Twenty subjects participated in two sessions in a randomized crossover design with at least 1‐week interval. Perceptual intensity ratings to single electrical stimulation (SES) at the conditioned skin site and to pinprick and light‐stroking stimuli in the immediate vicinity of the CES electrodes were measured . Superficial blood flow (SBF), skin temperature (ST) and heat pain threshold (HPT) were measured covering both homotopic and heterotopic skin. The pain intensities during CES process were measured and short‐form McGill Pain Questionnaire (SF‐MPQ) was used for assessing CES pain experience. Results Cold pressor conditioning stimulus reduced pain perception increments to weak pinprick and light‐stroking stimuli after 10‐Hz CES compared with the control session. Moreover, CPCS resulted in lower pain intensity ratings during CES process but without affecting the SF‐MPQ scores between two sessions. The SBF and ST increased after CES and then gradually declined but without differences between CPCS and control sessions. CPM did not affect HPT and pain intensity increments to SES. Conclusions The CPCS inhibited heterotopic perception amplification to weak mechanical stimuli after CES. The results indicate that endogenous descending inhibitory systems might play a role against development of non‐nociceptive perception amplificatory states (e.g. allodynia). Exploration of conditioned pain modulation effect on long-term potentiation-like pain amplification in humans