Articles: hyperalgesia.
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The aim of the present study was to examine the effect of intrathecal (i.t.) injection of pertussis toxin (PTX) on the nociceptive threshold and protein kinase C (PKC) expression in the rat spinal cord. The role of N-methyl-D-aspartic acid (NMDA) receptors in these changes was also examined. Male Wistar rats were implanted with two i.t. catheters, one of which was connected to a mini-osmotic pump and used to infuse saline or D-2-amino-5-phosphonopentanoic acid (D-AP5) (2 microg/h) starting on day 3 after i.t. catheter insertion. ⋯ Infusion of the NMDA antagonist, D-AP5, prevented both the thermal hyperalgesia and the increase in PKCgamma isoform expression in PTX-treated rats, and had no effect on these values in nai;ve rats. Intrathecal injection of the PKC inhibitor, chelerythrine (10 microg), significantly inhibited the thermal hyperalgesia observed in PTX-treated rats. These results show that i.t. injection of PTX induced thermal hyperalgesia accompanied by a selective increase in PKCgamma expression in both the synaptosomal membrane and cytosolic fractions of the dorsal horn of the rat lumbar spinal cord, and both effects were inhibited by the NMDA receptor antagonist, D-AP5.
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Neuroscience letters · Feb 2003
Comparative StudyA comparison of hyperalgesia and neurogenic inflammation induced by melittin and capsaicin in humans.
Melittin (a main compound of bee venom) and capsaicin were injected intradermally in healthy human volunteers: (1) to study secondary mechanical hyperalgesia (static hyperalgesia and dynamic hyperalgesia) around the injection site; and (2) to correlate the sensory changes to the neurogenic inflammation assessed by laser-doppler blood flowmetry. Melittin 50 microg and capsaicin 10 microg induced comparable spontaneous pain and increased blood flow (neurogenic inflammation). ⋯ This is the first report studying mechanical hyperalgesia induced by melittin in humans, and the results were in agreement with the previous observations in rats. Melittin seems to be a valuable model to study a possible contribution of neurogenic inflammation to hyperalgesia in humans.
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Journal of neurology · Feb 2003
Botulinum Toxin A reduces neurogenic flare but has almost no effect on pain and hyperalgesia in human skin.
Botulinum toxin A (BoNT/A) has been used therapeutically to treat muscular hypercontractions and sudomotor hyperactivity. There is increasing evidence that BoNT/A might also have analgesic properties, in particular in headache. In the present investigation we tested the often cited hypothesis that BoNT/A-induced analgesia can be attributed to inhibition of neuropeptide release from nociceptive nerve fibers. ⋯ In conclusion our results indicate that peripheral neuropeptide release is attenuated by BoNT/A. In contrast, the analgesic effect of BoNT/A was very limited. Therefore we assume that other than neuropeptide mechanisms must be important for BoNT/A induced pain relief in clinical pain syndromes.
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Randomized Controlled Trial Comparative Study Clinical Trial
Cold allodynia and hyperalgesia in neuropathic pain: the effect of N-methyl-D-aspartate (NMDA) receptor antagonist ketamine--a double-blind, cross-over comparison with alfentanil and placebo.
Cold allodynia and hyperalgesia are frequent clinical findings in patients with neuropathic pain. While there have been several clinical studies showing the involvement of central sensitization mechanisms and N-methyl-D-aspartate (NMDA) receptor activation in mechanical allodynia/hyperalgesia and ongoing pain, the mechanisms of thermal allodynia and hyperalgesia have received less attention. The aim of the present study was to examine the effect of the NMDA-receptor antagonist ketamine on thermal allodynia/hyperalgesia, ongoing pain and mechanical allodynia/hyperalgesia in patients with neuropathic pain (11 patients with post-traumatic neuralgia and one patient with post-herpetic neuralgia). ⋯ Significant and marked reductions of hyperalgesia to cold (visual analogue score at threshold value) were seen following both alfentanil (4.5 before, 1.4 after, median value) and ketamine (6.8 before, 0.4 after, median value). Alfentanil and ketamine also significantly reduced ongoing pain and mechanical hyperalgesia. It is concluded that NMDA-receptor mediated central sensitization is involved in cold hyperalgesia, but since CPDT remained unaltered, it is likely that other mechanisms are present.
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Mirror-image allodynia is a mysterious phenomenon that occurs in association with many clinical pain syndromes. Allodynia refers to pain in response to light touch/pressure stimuli, which normally are perceived as innocuous. Mirror-image allodynia arises from the healthy body region contralateral to the actual site of trauma/inflammation. ⋯ The present studies demonstrate that both ipsilateral and mirror-image SIN-induced allodynias are (1) reversed by intrathecal (peri-spinal) delivery of fluorocitrate, a glial metabolic inhibitor; (2) prevented and reversed by intrathecal CNI-1493, an inhibitor of p38 mitogen-activated kinases implicated in proinflammatory cytokine production and signaling; and (3) prevented or reversed by intrathecal proinflammatory cytokine antagonists specific for interleukin-1, tumor necrosis factor, or interleukin-6. Reversal of ipsilateral and mirror-image allodynias was rapid and complete even when SIN was maintained constantly for 2 weeks before proinflammatory cytokine antagonist administration. These results provide the first evidence that ipsilateral and mirror-image inflammatory neuropathy pain are created both acutely and chronically through glial and proinflammatory cytokine actions.