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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Anesthesia and analgesia · Oct 2011
Lidocaine attenuates the development of diabetic-induced tactile allodynia by inhibiting microglial activation.
Lidocaine is used clinically for tactile allodynia associated with diabetes-induced neuropathy. Although the analgesic effect of lidocaine through suppression of microglial activation has been implicated in the development of injury-induced neuropathic pain, its mechanism of action in diabetes-induced tactile allodynia has not yet been completely elucidated. ⋯ Lidocaine alleviates STZ-induced tactile allodynia, possibly by modulating the p38 pathway in spinal microglial cells. Inhibiting microglial activation by lidocaine treatment early in the course of diabetes-induced neuropathy represents a potential therapeutic strategy for tactile allodynia.
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Pain is a common and debilitating accompaniment of neuropathy that occurs as a complication of diabetes. In the current study, we examined the effect of continuous release of gamma amino butyric acid (GABA), achieved by gene transfer of glutamic acid decarboxylase (GAD67) to dorsal root ganglia (DRG) in vivo using a non-replicating herpes simplex virus (HSV)-based vector (vG) in a rat model of painful diabetic neuropathy (PDN). Subcutaneous inoculation of vG reduced mechanical hyperalgesia, thermal hyperalgesia and cold allodynia in rats with PDN. ⋯ In vitro, infection of primary DRG neurons with vG prevented the increase in Na(V)1.7 resulting from exposure to hyperglycemia. The effect of vector-mediated GABA on Na(V)1.7 levels in vitro was blocked by phaclofen but not by bicuculline, a GABA(B) receptor effect that was blocked by pertussis toxin-(PTX) interference with Gα((i/o)) function. Taken in conjunction with our previous observation that continuous activation of delta opioid receptors by vector-mediated release of enkephalin also prevents the increase in Na(V)1.7 in DRG exposed to hyperglycemia in vitro or in vivo, the observations in this report suggest a novel common mechanism through which activation of G protein coupled receptors (GPCR) in DRG neurons regulate the phenotype of the primary afferent.
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Anesthesia and analgesia · Oct 2011
Cannabidiol prevents the development of cold and mechanical allodynia in paclitaxel-treated female C57Bl6 mice.
The taxane chemotherapeutic paclitaxel frequently produces peripheral neuropathy in humans. Rodent models to investigate mechanisms and treatments are largely restricted to male rats, whereas female mouse studies are lacking. ⋯ Paclitaxel produced allodynia that was largely dose independent and more robust in female mice, and this effect was prevented by treatment with cannabidiol. Our preliminary findings therefore indicate that cannabidiol may prevent the development of paclitaxel-induced allodynia in mice and therefore be effective at preventing dose-limiting paclitaxel-induced peripheral neuropathy in humans.
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Comparative Study
Genotype-selective phenotypic switch in primary afferent neurons contributes to neuropathic pain.
Pain is normally mediated by nociceptive Aδ and C fibers, while Aβ fibers signal touch. However, after nerve injury, Aβ fibers may signal pain. Using a genetic model, we tested the hypothesis that phenotypic switching in neurotransmitters expressed by Aβ afferents might account for heritable differences in neuropathic pain behavior. ⋯ Substance P immunoreactivity was also upregulated in large-diameter neurons, but this change was similar in the 2 lines. Our findings suggest that phenotypic switching contributes to the heritable difference in pain behavior in HA vs LA rats. Specifically, we propose that in HA rats, but less so in LA rats, injured, spontaneously active Aβ afferents both directly drive CGRP-sensitive central nervous system pain-signaling neurons and also trigger and maintain central sensitization, hence generating spontaneous pain and tactile allodynia.