Articles: hyperalgesia.
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Evidence suggests large diameter afferents, presumably in response to centrally mediated changes, augment the mechanical allodynia or hyperalgesia seen in delayed onset muscle soreness (DOMS) conditions. Healthy males aged 18 to 30 (n = 16) performed eccentric exercise eliciting DOMS in the tibialis anterior muscle of a randomly assigned exercised leg. The contralateral leg served as a control. Mechanosensitivity was assessed on the exercised and control legs prior to and 24 hours postexercise via pressure pain thresholds (PPTs). PPTs were assessed at the muscle site, and at a distant segmentally related site, either without vibration or with vibration concurrently applied to the distant muscle, segmentally related, or control extra-segmentally related site. Participants completed a 6-point Likert scale providing a subjective measure of DOMS 5 days postexercise. Baseline mechanosensitivity was not significantly different at any site between the exercised and control legs prior to the exercise. Soreness ratings were higher 24 to 48 hours postexercise (P < .05), and baseline PPTs at the exercised legs muscle site decreased postexercise (P < .001). On day 1 following exercise, segmentally related site PPTs reduced significantly when vibration was applied concurrently to the DOMS affected tibialis anterior muscle (P < .04) compared to baseline mechanosensitivity or extrasegmental control vibration. ⋯ Further evidence is presented by this article indicating that large diameter afferents, presumably via centrally mediated mechanisms, augment the mechanical hyperalgesia seen in DOMS conditions. Future research examining eccentric activity in individuals with likely centrally sensitized conditions may be warranted.
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Nitecapone reduces development and symptoms of neuropathic pain after spinal nerve ligation in rats.
Neuropathic pain is caused by damage or malfunctioning of the nervous system. It is fairly common and more resistant to treatment than other types of pain. Since nitecapone, an inhibitor of catechol-O-methyl-transferase (COMT), has decreased neuropathic symptoms in diabetic rats, we studied its effects in another model of neuropathic pain, the spinal nerve ligation (SNL) model. ⋯ In nitecapone-naïve animals a single dose of nitecapone also reduced mechanical allodynia on the 14th day after the surgery. Nitecapone reduced the symptoms of neuropathic pain after the SNL, which is in line with the earlier study. Our results suggest that nitecapone and other COMT inhibitors should be studied further in the treatment of neuropathic pain.
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Inflammatory pain represents an important unmet clinical need with important socioeconomic implications. Ceramide, a potent proinflammatory sphingolipid, has been shown to elicit mechanical hyperalgesia, but the mechanisms remain largely unknown. We now demonstrate that, in addition to mechanical hyperalgesia, intraplantar injection of ceramide (10 μg) led to the development of thermal hyperalgesia that was dependent on induction of the inducible cyclooxygenase (COX-2) and subsequent increase of prostaglandin E(2) (PGE(2)). ⋯ Our results further revealed that COX-2 induction is regulated by NF-κB and p38 kinase activation, since intraplantar injection of SC-514 (0.1-1 μg) or SB 203580 (1-10 μg), well-characterized inhibitors of NF-κB and p38 kinase activation, respectively, blocked COX-2 induction and increased formation of PGE(2) and thermal hyperalgesia in a dose-dependent manner. Moreover, activation of NF-κB was dependent on upstream activation of p38 MAPK, since SB 203580 (10 μg) blocked p65 phosphorylation, whereas p38 kinase phosphorylation was unaffected by NF-κB inhibition by SC-514 (1 μg). Our findings not only provide mechanistic insight into the signaling pathways engaged by ceramide in the development of hyperalgesia, but also provide a potential pharmacological basis for developing inhibitors targeting the ceramide metabolic-to-COX-2 pathway as novel analgesics.
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Opioid medications are commonly used to treat moderate-to-severe pain. While these medications are generally an effective means of pain control, they can, in rare cases, actually exacerbate the pain. This paradoxical reaction is called opioid-induced hyperalgesia (OIH). Patients experiencing OIH may benefit from decreasing or discontinuing the opioid, switching to an alternative opioid, and/or using a nonopioid medication for pain.
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Journal of endodontics · Aug 2011
Sex differences in neuropeptide content and release from rat dental pulp.
Studies to examine sex differences in response to pain have suggested that females exhibit lower threshold responses to painful stimuli and that threshold response varies greatly at different stages of the menstrual cycle. Additional studies suggest that sex differences may be caused by societal sex roles or differences in anxiety responses by men and women. ⋯ These data suggest that sex differences affect the role of NGF in the modulation of inflammation through the regulation of peripheral neuropeptide release and content.