Articles: hyperalgesia.
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Low back pain is a common problem, affecting approximately two-thirds of the adult population. Of these individuals, a significant percentage will exhibit symptoms of radicular pain or sciatica. The purpose of this study was to determine the effect of one systemic (2 mg/kg) or intrathecal (0.2 mg/kg) dose of a selective cyclooxygenase-2 inhibitor (SC-236) in decreasing existing mechanical allodynia in a rat model of radiculopathy. ⋯ The intrathecal drug route of administration produced greater attenuation in allodynia than the systemic dose, supporting a central mechanism of action of the cyclooxygenase-2 inhibitor (p = 0.002). The hypothesis that cyclooxygenase-2 is involved in spinal nociceptive processing after a nerve root injury was supported by this study. In addition, these data support continued basic science research to further elucidate central inflammatory processes that follow nerve root injury.
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Neuroscience letters · Oct 2000
Peripheral and spinal antihyperalgesic activity of SIB-1757, a metabotropic glutamate receptor (mGLUR(5)) antagonist, in experimental neuropathic pain in rats.
Recent studies suggest a role of Group 1 metabotropic glutamate receptors in mediating the development of spinal hypersensitivity in some pain states. Here, the possible role of mGluR(5) receptors in experimental neuropathic pain elicited by ligation of spinal nerves (L(5)/L(6) spinal nerve ligation, SNL) was explored with SIB-1757, a selective mGluR(5) antagonist. SNL-induced tactile allodynia was detected by decreased paw withdrawal thresholds to probing with von Frey filaments and thermal hyperalgesia by decreased paw withdrawal latencies to radiant heat applied to the plantar aspect of the hindpaw. ⋯ These data suggest a significant modulation of thermal hyperalgesia by mGluR(5) antagonists, consistent with reports that this receptor may be associated with afferent C-fibers. The less impressive effect seen on tactile allodynia, likely to be mediated by large fiber input, suggests that the observed modulation may be related to blockade of mGluR(5)-mediated spinal sensitization. These results do not support the involvement of these receptors in modulation of acute nociception but suggest the possibility of a role for Group I mGluRs in the mediation of aspects of neuropathic pain which may be associated with C-fiber inputs.
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Randomized Controlled Trial Comparative Study Clinical Trial
Peripheral lidocaine but not ketamine inhibits capsaicin-induced hyperalgesia in humans.
We examined the effect of the subcutaneous infiltration of ketamine, lidocaine and saline before injury on capsaicin-induced pain and hyperalgesia. Twelve healthy volunteers participated in two separate, randomized, double-blind, placebo-controlled crossover experiments. In experiment 1, 100 micrograms capsaicin was injected intradermally in one volar forearm 10 min after the skin had been pretreated with lidocaine 20.0 mg in 2.0 ml or 0.9% saline 2.0 ml at the capsaicin injection site. ⋯ Pain scores and areas of hyperalgesia were not affected when the contralateral site was infiltrated with ketamine or lidocaine. Lidocaine produced no side-effects, whereas ketamine produced paraesthesia, dizziness and sleepiness in six out of 24 (25%) cases. Blocking peripheral sodium channels with locally administered lidocaine reduces spontaneous pain and capsaicin-induced hyperalgesia but local block with the NMDA-type glutamate receptor antagonist ketamine has no effect on capsaicin-induced pain and hyperalgesia.
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Anesthesia and analgesia · Oct 2000
Randomized Controlled Trial Clinical TrialThe effect of systemic lidocaine on pain and secondary hyperalgesia associated with the heat/capsaicin sensitization model in healthy volunteers.
Although effective in neuropathic pain, the efficacy of systemic lidocaine in non-neuropathic pain remains uncertain. We investigated the analgesic effect of systemic lidocaine on the heat/capsaicin sensitization model of experimental pain in 24 volunteers. Sensitization was produced by heating the skin to 45 degrees C for 5 min, followed by a 30-min application of 0.075% capsaicin cream, and maintained by periodically reheating the sensitized skin. Subjects received IV lidocaine (bolus 2 mg/kg, then infusion 3 mg. kg. h), or saline for 85 min. Areas of secondary hyperalgesia, heat pain detection thresholds, and painfulness of stimulation with 45 degrees C for 1 min (long thermal stimulation) were quantified. Systemic lidocaine reduced the area of secondary hyperalgesia to brush, but not to von Frey hair stimulation. Lidocaine did not alter heat pain detection thresholds or painfulness of long thermal stimulation in normal skin. We conclude that, at infusion rates in the low- to mid-antiarrhythmic range, lidocaine has no effect on acute nociceptive pain but does have a limited and selective effect on secondary hyperalgesia. ⋯ The efficacy of systemic lidocaine in nonneuropathic pain remains uncertain. This study investigates the effect of systemic lidocaine on experimental-induced hyperalgesia in 25 volunteers. Hyperalgesia was induced by using an experimental pain model that uses heat and capsaicin in combination. Systemic lidocaine showed a selective effect on secondary hyperalgesia.
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Comment Letter
Can epidural fentanyl induce selective spinal hyperalgesia?