Effects of conditioned pain modulation on Capsaicin-induced spreading muscle hyperalgesia in humans

Author:

Schliessbach Jürg12ORCID,Siegenthaler Andreas3,Graven-Nielsen Thomas4,Arendt-Nielsen Lars4,Curatolo Michele45ORCID

Affiliation:

1. Institute of Interventional Pain Medicine Zurich, IISZ , Zurich , Switzerland

2. Department of Anesthesiology and Pain Medicine, Inselspital , Bern University Hospital, University of Bern , Bern , Switzerland

3. Chronic Pain Management , Lindenhof Hospital, Lindenhof Group Bern , Bern , Switzerland

4. Center for Neuroplasticity and Pain (CNAP) , SMI, Aalborg University , Aalborg , Denmark

5. Department of Anesthesiology and Pain Medicine , University of Washington , Seattle WA , USA

Abstract

Abstract Objectives Muscle pain can be associated with hyperalgesia that may spread outside the area of primary injury due to both peripheral and central sensitization. However, the influence of endogenous pain inhibition is yet unknown. This study investigated how endogenous pain inhibition might influence spreading hyperalgesia in experimental muscle pain. Methods Conditioned pain modulation (CPM) was assessed in 30 male volunteers by cold pressor test at the non-dominant hand as conditioning and pressure pain thresholds (PPT) at the dominant 2nd toe as test stimuli. Subjects were classified as having inhibitory or facilitating CPM based on published reference values. Subsequently, muscle pain and hyperalgesia were induced by capsaicin injection into the non-dominant supraspinatus muscle. Before and 5, 10, 15, 20, 30, 40, 50 and 60 min later, PPTs were recorded at the supraspinatus, infraspinatus and deltoid muscle, ring finger and toe. Results Compared to baseline, PPTs decreased at the supraspinatus, infraspinatus and deltoid muscle (p≤0.03), and increased at the finger and toe (p<0.001). In facilitating CPM (n=10), hyperalgesia occurred at 5, 10, 15, 20 and 40 min (p≤0.026). In inhibitory CPM (n=20), hyperalgesia only occurred after 10 and 15 min (p≤0.03). At the infraspinatus muscle, groups differed after 5 and 40 min (p≤0.008). Conclusions The results suggest that facilitating CPM is associated with more spreading hyperalgesia than inhibitory CPM. This implies that poor endogenous pain modulation may predispose to muscle pain and spreading hyperalgesia after injury, and suggest that strategies to enhance endogenous pain modulation may provide clinical benefits.

Publisher

Walter de Gruyter GmbH

Subject

Anesthesiology and Pain Medicine,Neurology (clinical)

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