Articles: hyperalgesia.
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Anesthesia and analgesia · Oct 2009
Activation of extracellular signal-regulated kinase in sciatic nerve contributes to neuropathic pain after partial sciatic nerve ligation in mice.
The mitogen-activated protein kinase family plays an important role in several types of pain. However, the detailed role of phosphorylated extracellular signal-regulated kinase (pERK) in the region of injured peripheral nerve is poorly understood. In this study, we investigated whether pERK in injured sciatic nerve contributes to neuropathic pain induced by partial sciatic nerve ligation (PSL) in mice. ⋯ Activation of ERK in Schwann cells of the injured peripheral nervous system may play an important role in the development of neuropathic pain. Our results suggest that pERK itself and ERK-related mediators are potential therapeutic targets for the treatment of neuropathic pain.
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Randomized Controlled Trial
[The effects of lornoxicam in preventing remifentanil-induced postoperative hyperalgesia].
Intraoperative remifentanil administration results in acute opioid tolerance that is manifested by increased postoperative pain, opioid requirement and specifically peri-incisional hyperalgesia. The aim of this study was to investigate the effect of lornoxicam in preventing remifentanil-induced hyperalgesia. ⋯ Lornoxicam administered preemptively prevented remifentanil-induced hyperalgesia.
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J Neurosurg Anesthesiol · Oct 2009
Systemic lidocaine inhibits remifentanil-induced hyperalgesia via the inhibition of cPKCgamma membrane translocation in spinal dorsal horn of rats.
Remifentanil is being used increasingly as one component of total intravenous anesthesia. Severe postoperative pain has occasionally been reported with discontinuation of remifentanil. This study was designed to determine the involvement of conventional protein kinase Cgamma (cPKCgamma) in the inhibitory action of lidocaine on remifentanil-induced hyperalgesia of rats after propofol-remifentanil-based anesthesia. ⋯ After plantar incision, the withdrawal threshold on both the contralateral and the ipsilaeral side at 30, 120, and 300 minutes postanesthesia in group R was significantly lower than in groups P, RL, and L (P<0.05). Both immunoblotting and immunofluorescence showed that cPKCgamma membrane translocation increased in dorsal horn neurons of propofol-remifentanil-based anesthetized rats, which could be inhibited by systemic lidocaine. These results suggested that increased cPKCgamma membrane translocation was involved in remifentanil-induced hyperalgesia, which was inhibited by systemic lidocaine and may contribute to reduced postoperative pain in rats after propofol-remifentanil-based anesthesia.
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Central sensitization, caused either by tissue inflammation or peripheral nerve injury, plays an important role in persistent pain. An animal model of capsaicin-induced pain has well-defined peripheral and central sensitization components, thus is useful for studying the analgesic effect on two separate components. The focus of this study is to examine the analgesic effects of electroacupuncture (EA) on capsaicin-induced secondary hyperalgesia, which represents central sensitization. ⋯ EA analgesic effect was inhibited by a systemic non-specific opioid receptor (OR) antagonist or an intrathecal mu- or delta-OR antagonist. EA analgesic effect was not affected by an intrathecal kappa-OR antagonist or systemic adrenergic receptor antagonist. This study demonstrates that EA produces a stimulation point-specific analgesic effect on capsaicin-induced secondary hyperalgesia (central sensitization), mediated by activating endogenous spinal mu- and delta-opioid receptors.
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Clinical Trial
Homotopic stimulation can reduce the area of allodynia in patients with neuropathic pain.
Allodynia is a common, troublesome feature of neuropathic pain conditions. In a previous study of postherpetic neuralgia we observed that repeated tactile stimulation appeared to reduce the size of the area of allodynia in some patients. We have undertaken a pragmatic clinical study to characterise this phenomenon in neuropathic pain patients with a range of different aetiologies. ⋯ There was no change in heat pain threshold at a distant site following allodynic stimulation, suggesting no activation of diffuse noxious inhibitory control. Repeated thermal noxious stimulation (median NRS 7) could also elicit changes (>30%) in the area of allodynia in some patients (reductions in 7/20, increases in 3/20). Thus, we have found that a brief period of homotopic painful stimulation can reduce the area of allodynia in around half of patients with established neuropathic pains.