Articles: hyperalgesia.
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The role of serotonin (5-hydroxytrptamine, 5-HT) in the modulation of pain has been widely studied. Previous work led to the hypothesis that 5-hydroxyindolacetic acid (5-HIAA), a main metabolite of serotonin, might by itself influence pain thresholds. ⋯ Taken together, the present results suggest that 5-HIAA plays an important role in modulating peripheral thermal hyperalgesia in CFA induced inflammation, probably via a non-serotonin receptor mechanism.
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Spinal toll like receptor 3 is involved in chronic pancreatitis-induced mechanical allodynia of rat.
Mechanisms underlying pain in chronic pancreatitis (CP) are incompletely understood. Our previous data showed that astrocytes were actively involved. However, it was unclear how astrocytic activation was induced in CP conditions. In the present study, we hypothesized that toll-like receptors (TLRs) were involved in astrocytic activation and pain behavior in CP-induced pain. ⋯ These results suggest a probable "TLR3-astrocytes-IL-1β/MCP-1" pathway as a positive feedback loop in the spinal dorsal horn in CP conditions. TLR3-mediated neuroimmune interactions could be new targets for treating persistent pain in CP patients.
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Bmc Musculoskel Dis · Jan 2011
Analysis of deep tissue hypersensitivity to pressure pain in professional pianists with insidious mechanical neck pain.
The aim of this study was to investigate whether pressure pain hyperalgesia is a feature of professional pianists suffering from neck pain as their main playing-related musculoskeletal disorder. ⋯ Our findings revealed pressure pain hypersensitivity over distant non-symptomatic distant points but not over the symptomatic areas in pianists suffering from neck pain. In addition, pianists with neck pain also had smaller hand size than those without neck pain. Future studies are needed to further determine the relevance of these findings in the clinical course of neck pain as playing-related musculoskeletal disorder in professional pianists.
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Reproductive sciences · Jan 2011
Levo-tetrahydropalmatine retards the growth of ectopic endometrial implants and alleviates generalized hyperalgesia in experimentally induced endometriosis in rats.
One primary goal of medical treatment of endometriosis is to alleviate pain and there is a pressing need for new therapeutics for endometriosis with better efficacy and side-effect profiles. Levo-tetrahydropalmatine (l-THP) has been used as a sedative or analgesic for chronic pains in China since 1970s. In this study, we sought to evaluate the efficacy of l-THP, with or without valproic acid (VPA), in a rat model of endometriosis. ⋯ The treatment also significantly lowered immunoreactivity to all mediators involved in central sensitization and to HDAC2 in DRG, to TrkA and CGRP in ectopic endometrium, and to CGRP in eutopic endometrium. In summary, l-THP reduces lesion growth and generalized hyperalgesia. Thus, l-THP may be a promising therapeutics for endometriosis.
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Randomized Controlled Trial
The endogenous opioid system is not involved in modulation of opioid-induced hyperalgesia.
Some recent studies suggested a role of the endogenous opioid system in modulating opioid-induced hyperalgesia (OIH). In order to test this hypothesis, we conducted a prospective randomized, placebo-controlled, 2-way crossover study in healthy human volunteers. We utilized a well-established model of inducing OIH after a brief exposure to the μ-opioid agonist remifentanil using intradermal electrical stimulation. Patients were exposed to a randomized 90-minute infusion of remifentanil or saline placebo during 2 separate occasions. Development of OIH was quantified using changes in the average radius of the area of secondary hyperalgesia generated by electrical pain stimulation. A 23.6% (20.2) increase in area of secondary hyperalgesia over baseline was observed in the postinfusion period of the remifentanil session, demonstrating development of OIH (P = .03). In order to test endogenous opioid system modulation of OIH, patients were given a 1-time bolus of naloxone, which had no effect on the size of the hyperalgesic lesion in either the remifentinal or placebo session. These results suggested that the endogenous opioid system did not appear to modulate OIH. ⋯ Experimental evidence suggested that the endogenous opioid system did not significantly affect opioid-induced hyperalgesia. Consequently, this study suggested that alternative mechanisms such as pronociceptive stimulation and neuroplastic changes might be responsible for expression of OIH.