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Effects of Conditioned Pain Modulation on Spread of Hyperalgesia after Intramuscular Capsaicin in Humans

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      Muscle pain can be associated with altered central pain processing, leading to hyperalgesia both locally and at distant body sites. The role of endogenous inhibitory mechanisms in hyperalgesia associated with muscle pain remains unclear. This study investigated the influence of conditioned pain modulation (CPM) on hyperalgesia at multiple body sites induced by intramuscular injection of capsaicin in the supraspinatus muscle. Thirty healthy males underwent CPM testing using the cold pressor test as conditioning stimulus and pressure pain threshold (PPT) as test stimulus. Muscle pain and hyperalgesia were induced by injection of capsaicin into the non-dominant supraspinatus muscle. Before and 5, 10, 15, 20, 30, 40, 50 and 60 min later, PPTs were recorded bilaterally at the supraspinatus, infraspinatus and deltoid muscles, ring finger and toe. Subjects were classified as inhibitory vs. facilitating CPM based on published reference values. Compared to baseline, PPTs decreased significantly at the supraspinatus, infraspinatus and deltoid muscle (p<0.001, p<0.001 and p=0.03), and increased at the finger and toe bilaterally (P<0.001). In the facilitating CPM group, significant hyperalgesia occurred at 5, 10, 15, 20 and 40 minutes (p=0.001, p=0.001, p=0.005, p=0.026 and p=0.001, respectively). In the inhibitory group, it only occurred after 10 and 15 minutes (p=0.01 and p=0.03). Hyperalgesia outside the injected supraspinatus muscle was more pronounced and longer lasting in the infraspinatus muscle of subjects with facilitating CPM than in subjects with inhibitory CPM (p=0.008 and =0.001 after 5 and 40 minutes, respectively). Impaired endogenous pain modulation may be a predisposing factor for spread of hyperalgesia after induction of muscle pain. Therefore, impaired endogenous modulation can be one explanation for the variability of the clinical manifestations among patients having the same primary nociceptive trigger. Strategies to enhance endogenous pain modulation may provide clinical benefits. The study was funded by a grant from the University Hospital of Bern, Inselspital, intended to promote the career of young physicians (grant recipient: J.S.). The Center for Neuroplasticity and Pain (CNAP) is supported by the Danish National Research Foundation (DNRF121).
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