This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Investigations of pain use protocols that induce pain and/or sample participants with naturally occurring pain. Research examining experimentally induced pain is limited in its applicability to naturally occurring pain because experimentally induced pain is more predictable and controllable without the same meaning and emotional consequences. Patients with fibromyalgia syndrome (FMS) show evidence of tonic nociceptive impulse input, which is at least partially responsible for their hyperalgesia/allodynia and central sensitization. We hypothesize that intermittent bouts of inflammatory pain are instrumental in triggering signal cascades that increase peripheral and central sensitization in these patients. One of these possible inflammatory bouts is related to muscle injury from activity or exertion. Our proposed method of addressing the role of inflammation for pain in FMS is to study inflammatory mediators and/or acute phase reactants. We will study these inflammatory markers in delayed-onset muscle soreness (DOMS). Eccentric muscle contractions can reliably induce temporary muscle soreness and pain that occur after the performance of the DOMS protocol. In addition, there is convincing evidence of a dose-response relationship between the intensity of the eccentric muscle contractions and subsequent muscle soreness. We plan to examine central/peripheral sensitization or desensitization to thermal/mechanical stimuli before and after DOMS has been induced. In addition, we will test well validated markers of inflammation, that are also known to be involved in pain signaling, including acute phase reactants (ESR, CRP, neopterin), cytokines, and other inflammatory mediators like MARCKS (myristolated alanine rich protein kinase C substrate) in plasma and urine to investigate their close relationship with central sensitization in FMS.
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