Articles: hyperalgesia.
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Human subjects infected with herpes or varicella-zoster viruses complain of pain, such as allodynia, in or near the region with vesicles. However, the mechanisms of the pain are unclear. We show for the first time that infection with herpes simplex virus type-1 (HSV-1) induces allodynia and hyperalgesia in mice. ⋯ In contrast, when started from days 5 or 6, acyclovir treatment slightly inhibited the development of skin lesions and the viral proliferation, but not allodynia and hyperalgesia. These results suggest that the propagation of HSV-1 in the dorsal root ganglia produces allodynia and hyperalgesia as a result of functional abnormality of the sensory neurons in mice. This may be a useful model for studying the mechanisms of herpetic pain.
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Randomized Controlled Trial Clinical Trial
Spatial mapping of the zone of secondary hyperalgesia reveals a gradual decline of pain with distance but sharp borders.
The purpose of this study was to examine how pain to punctate mechanical stimuli varies with position within the zone of secondary hyperalgesia. Secondary hyperalgesia was produced by an intradermal injection of capsaicin (50 microg) into the volar forearm of human volunteers (n=9). Before and at 20, 60 and 100 min after the capsaicin injection, a computer-controlled electromechanical stimulator was used to deliver controlled-force stimuli to the skin via a 12-mm wide, 100-microm thick blade probe. ⋯ This finding unlikely reflects a ceiling effect because pain ratings within the zone of secondary hyperalgesia increased linearly with force. The relatively uniform pain ratings to the blade stimuli within the zone of secondary hyperalgesia and the sharp border that delimits the zone of hyperalgesia indicate that this sensory disturbance approaches being an 'all-or-nothing' phenomenon. Thus, a two-state model for central plasticity is needed to explain secondary hyperalgesia.
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We have examined the participation of NK1 receptors in neuropathic pain by comparing behavioural responses after partial sciatic nerve ligation in wild-type (WT) and NK1 receptor knockout (KO) mice. Mechanical responses were tested with von Frey hairs, and cooling responses with acetone. ⋯ Mechanical (mean threshold 20 +/- vs 9 +/- 1 mN) and cold allodynia (61 +/- vs 14 +/- 2 behaviours evoked by acetone) were significantly greater than in sham animals, but similar in WT and KO mice. We conclude that NK1 receptors are not essential for mechanical and cold allodynia evoked by partial nerve ligation.
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The perception of pain sensation (threshold), whether local or central, is altered by inflammatory processes. Anti-inflammatory drugs block this by raising the pain threshold and by reducing the inflammatory process. Melatonin is claimed to have anti-inflammatory activity in animal models of acute and chronic inflammation. ⋯ The attenuation of lipopolysaccharides-induced hyperalgesia by melatonin was not reversed by naltrexone (4 mg/kg). In vitro studies showed that melatonin, in concentrations ranging from 100 to 1000 nM, suppressed tumor necrosis factor-alpha (TNF-alpha) without affecting the nitric oxide (NO) release in lipopolysaccharides-activated murine peritoneal macrophages. Taken together, the present results demonstrated that melatonin reverses lipopolysaccharides-induced hyperalgesia.
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Neuroscience letters · Apr 2000
Contralateral heat hyperalgesia induced by unilaterally intraplantar bee venom injection is produced by central changes: a behavioral study in the conscious rat.
In a previous study, we found that subcutaneous (s.c.) intraplantar injection of bee venom unilaterally could produce bilateral heat hyperalgesia. However, the bee venom-induced heat hyperalgesia identified in the injection site was presumed to be different from that identified in the contralateral hindpaw, since the former co-existed with the mechanical hyperalgesia while the latter did not. The aim of the present study was to testify whether the contralateral heat hyperalgesia identified in the bee venom model was a consequence of central changes. ⋯ After axotomy, the bee venom-induced heat hyperalgesia in the non-injected hindpaw was not altered at all compared with that prior to axotomy. Moreover, intrathecal pre-treatment with either N-methyl-D-aspartate (NMDA) or non-NMDA receptor antagonist could prevent the development of the contralateral heat hyperalgesia. The present results suggest that central sensitization contributes to development of the bee venom-induced contralateral heat hyperalgesia and activation of both NMDA and non-NMDA receptors in the spinal cord is involved in the processing.