Articles: hyperalgesia.
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The Visual Analogue Scale (VAS), Numerical Rating Scale (NRS), Verbal Rating Scale (VRS), and the Faces Pain Scale-Revised (FPS-R) are among the most commonly used measures of pain intensity in clinical and research settings. Although evidence supports their validity as measures of pain intensity, few studies have compared them with respect to the critical validity criteria of responsivity, and no experiment has directly compared all 4 measures in the same study. The current study compared the relative validity of VAS, NRS, VRS, and FPS-R for detecting differences in painful stimulus intensity and differences between men and women in response to experimentally induced pain. ⋯ The findings are consistent with previous studies supporting the validity of each scale. The most support emerged for the NRS as being both (1) most responsive and (2) able to detect sex differences in pain intensity. The results also provide support for the validity of the scales for use in Portuguese samples.
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Randomized Controlled Trial
Effect of transdermal opioids in experimentally induced superficial, deep and hyperalgesic pain.
Chronic pain and hyperalgesia can be difficult to treat with classical opioids acting predominately at the µ-opioid receptor. Buprenorphine and its active metabolite are believed to act through µ-, κ- and δ-receptors and may therefore possess different analgesic and anti-hyperalgesic effects compared with pure µ-receptor agonists, for example, fentanyl. Here, we have compared the analgesic and anti-hyperalgesic effects of buprenorphine and fentanyl. ⋯ Buprenorphine, but not fentanyl, showed analgesic effects against experimentally induced, bone-associated pain and primary hyperalgesia compared with placebo. These tissue- and modality-differentiated properties may reflect the variable effects of opioid drugs observed in individual patients.
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The perception of pain is initiated by the transduction of noxious stimuli through specialized ion channels and receptors expressed by primary nociceptive neurons. The molecular mechanisms that orchestrate the expression and function of ion channels relevant for pain processing are poorly understood. We demonstrate here a central role of the transcription factor Smad-interacting protein 1 (Sip1/Zfhx1b/Zeb2), a 2-handed zinc finger DNA-binding protein with essential functions in neural crest and forebrain development, in controlling nociceptive neuron excitability and pain sensitivity. ⋯ Analysis of the voltage-gated currents underlying repetitive firing revealed a significant increase in persistent sodium currents and a reduction in delayed rectifier potassium currents. Modeling experiments in conjunction with experimental results suggest that these changes cause a depolarization-induced block of action potential propagation past the DRG axon T-junction. These data suggest that Sip1 controls the transduction properties of heat-sensitive primary sensory neurons and thus thermal pain sensitivity in a novel manner via coordinated changes in DRG-neuron voltage-gated ion channels.
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Acid-sensing ion channels (ASICs) are activated by acidic pH and may play a significant role in the development of hyperalgesia. Earlier studies show ASIC3 is important for induction of hyperalgesia after muscle insult using ASIC3-/- mice. ASIC3-/- mice lack ASIC3 throughout the body, and the distribution and composition of ASICs could be different from wild-type mice. ⋯ ASIC3 mRNA in DRG and protein levels in muscle were decreased in vivo by miR-ASIC3. In CHO-K1 cells co-transfected with ASIC1a and ASIC3, miR-ASIC3 reduced the amplitude of acidic pH-evoked currents, suggesting an overall inhibition in the surface expression of heteromeric ASIC3-containing channels. Our results show, for the first time, that reducing ASIC3 in vivo in primary afferent fibers innervating muscle prevents the development of inflammatory hyperalgesia in wild-type mice, and thus, may have applications in the treatment of musculoskeletal pain in humans.
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Myofascial pain syndrome (MPS) is an important clinical condition characterized by chronic muscle pain and a myofascial trigger point (MTrP) located in a taut band (TB). However, its pathogenic mechanism is still unclear. We developed an animal model relevant to conditions of MPS, and analyzed the mechanism of the muscle pain in this model. We applied eccentric contraction (EC) to a rat's gastrocnemius muscle (GM) for 2 weeks, and examined the mechanical withdrawal thresholds, histological changes, and expressions and contents of nerve growth factor (NGF). The mechanical withdrawal threshold decreased significantly at the next day of first EC and continued up to 9 days after EC. TBs were palpable at 3 to 8 days after initiation of EC. In EC animals, necrotic and regenerating muscle cells were found significantly more than in control animals. In EC animals, NGF expressions in regenerating muscle cells and NGF contents of GM were significantly higher than control animals. Administration of NGF receptor (TrkA) inhibitor K252a showed significant suppression of mechanical hyperalgesia in EC animals. Repeated EC induced persistent mechanical muscle hyperalgesia associated with TB. NGF expressed in regenerating muscle cells may have an important role in persistent mechanical muscle hyperalgesia which might be relevant to pathogenesis of MPS. ⋯ The present study shows that NGF expressed in regenerating muscle cells is involved in persistent muscular mechanical hyperalgesia. NGF-TrkA signaling in primary muscle afferent neurons may be one of the most important and promising targets for MPS.