Pain
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Complex regional pain syndrome (CRPS) is a disabling disease characterized by the classic symptoms and signs of inflammation. In this study we investigated the innate cytokine profile in patients with CRPS to determine a possible role of the immune system in the pathophysiology of CRPS. ⋯ Hence, our results do not support a role of genetic factors responsible for the cytokine profile in the pathophysiology of CRPS. These findings encourage further investigations of mechanisms responsible for neurogenic-induced inflammation.
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To investigate the roles of primary afferent fibers in development of the bee venom (BV)-induced persistent spontaneous nociception (PSN) and hyperalgesia (HA), the sciatic nerve or both the sciatic and saphenous nerves of rats were topically treated with capsaicin respectively under pentobarbital anesthesia to destroy the capsaicin-sensitive primary afferent (CSPA) fibers. Effect of the sciatic nerve capsaicin on the formalin-induced PSN was also evaluated. Destruction of the CSPA fibers of the sciatic nerve or both the sciatic and saphenous nerves only produced 34 or 69% inhibition of the mean total number of 1 h BV-induced paw flinches. ⋯ However, destruction of the CSPA fibers of both the sciatic and saphenous nerves was able to block development of both heat and mechanical HA in the whole BV-treated hind paw and heat hyperalgesia in the non-injected hind paw. Taken together, we conclude that: (1) the CSPA (C- and A delta-) fibers play a pivotal role in mediation of either the heat or the mechanical hyperalgesia induced by s.c. BV; (2) the CSPA fibers may play a crucial role in mediation of the formalin-induced PSN, but play a partial role in the BV-induced nociceptive process; (3) in addition to the sciatic nerve, the saphenous nerve is also involved in mediation of the BV-induced PSN as well as heat and mechanical hyperalgesia, while it is not likely to be involved in the formalin-induced nociception.
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Diffuse noxious inhibitory controls (DNIC), which involve supraspinal structures and modulate the transmission of nociceptive signals, were investigated in rats with chronic constriction injury of the sciatic nerve. Nerve-injured rats with increased sensitivity to mechanical and thermal stimulation on the operated side were anesthetized and recordings were made from trigeminal convergent neurons. Inhibitions of C-fiber-evoked neuronal responses during and after the application of nociceptive conditioning stimuli to the hindpaw, were measured to evaluate DNIC. ⋯ This was true regardless of the intensity and frequency of stimulation and regardless of whether the stimuli were applied transcutaneously or directly to the sciatic nerve. The clear-cut difference between the results obtained with natural and electrical conditioning stimuli suggests that the nociceptive neurons involved in the triggering of DNIC may not be sensitized at the central level. Peripheral mechanisms such as the sensitization of nerve injured fibers and/or sprouting of nerve terminals may thus be the main causes of DNIC increase in this model of neuropathic pain.