Pain
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Possible role of inflammatory mediators in tactile hypersensitivity in rat models of mononeuropathy.
Peripheral hypersensitivity (hyperalgesia and allodynia) are common phenomena both in inflammatory and in neuropathic pain conditions. Several rat models of mononeuropathy (Bennett, Seltzer and Gazelius models) display such symptoms following partial injury to the sciatic nerve. Using immunohistochemistry and behavioral tests, we investigated inflammatory cell and cytokine responses in the sciatic nerve 14 days after injury created in these different models as well as after axotomy. ⋯ Our findings indicate that the considerable increase in monocytes/macrophages induced by a nerve injury results in a very high release of IL-6 and TNF-alpha. This may relate to the generation of tactile allodynia/hyperalgesia, since there was a clear correlation between the number of ED-1 and IL-6-positive cells and the degree of allodynia. It is possible that measures to reduce monocyte/macrophage recruitment and the release of pro-inflammatory interleukins after nerve damage could influence the development of neuropathic pain.
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We investigated the effects of acute and of chronic morphine treatment on T-lymphocyte function and natural killer (NK) cell activity in rats receiving chronic constriction injury (CCI) of the sciatic nerve. T-Lymphocyte function was evaluated based on concanavalin-A (ConA)- and phytohemagglutinin (PHA)-induced splenocyte proliferation. The effects of morphine on thermal hyperalgesia were also assessed by measuring paw withdrawal latency (PWL) in rats. ⋯ No tolerance to the suppression of NK cell activity and splenocyte proliferation was observed after chronic morphine treatment. These data suggest that both acute and chronic morphine treatment can cause a dose-dependent reversal of thermal hyperalgesia and inhibition of NK cell activity and splenocyte proliferation in rats with sciatic CCI, without concomitant development of tolerance. Opioid therapy for chronic neuropathic pain should be used cautiously, especially in immune-compromised cases.
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The hypothesis that the pain and allodynia associated with post-herpetic neuralgia (PHN) is maintained by a combination of input from preserved primary afferent nociceptors and sensitization of central pain transmitting neurons was examined in 17 subjects with PHN. Pain, allodynia, thermal sensory function, cutaneous innervation, and response to controlled application of 0.075% capsaicin were measured. ⋯ In three of the 'capsaicin responders' the area of allodynia expanded into previously non-allodynic and non-painful skin that had normal sensory function and cutaneous innervation. These observations support the hypothesis that allodynia in some PHN patients is a form of chronic secondary hyperalgesia maintained by input from intact and possibly 'irritable' primary afferent nociceptors to a sensitized CNS.
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Clinical Trial Controlled Clinical Trial
Effect of tonic muscle pain on short-latency jaw-stretch reflexes in humans.
The modulation of human jaw-stretch reflexes by experimental muscle pain was studied in three experiments. Short-latency reflex responses were evoked in the masseter and temporalis muscles by fast stretches (1 mm displacement, 10 ms ramp time) before, during and 15 min after a period with tonic pain. In Expt. ⋯ These results indicate that experimental jaw-muscle pain facilitates the short-latency (8-9 ms), probably monosynaptic, jaw-stretch reflex as revealed by both sEMG and imEMG. This effect could not be accounted for by variability in pre-stimulus EMG activity. An increased sensitivity of the fusimotor system at this level of static muscle excitation is suggested as a possible mechanism, which could contribute to an increased stiffness of the jaw-muscles during pain.