Articles: hyperalgesia.
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Anesthesiology clinics · Jun 2011
ReviewNew concepts in acute pain management: strategies to prevent chronic postsurgical pain, opioid-induced hyperalgesia, and outcome measures.
Chronic postsurgical pain (CPSP) is a pain syndrome that has attracted attention for more than 10 years. CPSP is a pain syndrome that develops postoperatively and lasts for at least 2 months in the absence of other causes for pain (eg, recurrence of malignancy, chronic infection, and so forth). Pain continuing from a preexisting disease is not considered as CPSP. In this article, the authors discuss the etiopathogenesis of CPSP and interventions that can help prevent and treat this condition.
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Randomized Controlled Trial Comparative Study
[Clonidine for remifentanil-induced hyperalgesia: a double-blind randomized, placebo-controlled study of clonidine under intra-operative use of remifentanil in elective surgery of the shoulder].
In the postoperative period, α2-adrenergic agonists have an opioid sparing effect. In a previous, experimental study, it was also shown that clonidine attenuates remifentanil-induced hyperalgesia. In this study, we examined under clinical conditions whether early administration of a single dose of clonidine can inhibit remifentanil-induced hyperalgesia in patients undergoing elective surgery of the shoulder and with continuous intraoperative use of remifentanil. ⋯ An early single dose of 150 µg of clonidine did not reduce the postoperative morphine consumption and pain scores in patients undergoing elective surgery of the shoulder with remifentanil/propofol-based anaesthesia. After the effect of clonidine has presumably subsided the pain can even increase, therefore further studies with repetitive doses of clonidine should be carried out.
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To determine whether the local and referred pain from active myofascial trigger points (MTrPs) reproduce the overall spontaneous fibromyalgia syndrome (FMS) pain pattern and whether widespread pressure hypersensitivity is related to the presence of widespread active MTrPs in FMS. ⋯ The local and referred pain elicited from widespread active MTrPs fully reproduced the overall spontaneous clinical pain area in patients with FMS. Widespread mechanical pain hypersensitivity was related to a greater number of active MTrPs. This study suggests that nociceptive inputs from active MTrPs may contribute to central sensitization in FMS.
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Randomized Controlled Trial
Effects of COX inhibition on experimental pain and hyperalgesia during and after remifentanil infusion in humans.
Opioids may enhance pain sensitivity resulting in opioid-induced hyperalgesia (OIH). Activation of spinal cyclooxygenase may play a role in the development of OIH. The aim of this study was to demonstrate remifentanil-induced postinfusion hyperalgesia in an electrical pain and a cold pain model, and to investigate whether COX-2 (parecoxib) or COX-1 (ketorolac) inhibition could prevent hyperalgesia after remifentanil infusion. ⋯ These results demonstrated OIH in both models, and may suggest that COX-2 inhibition is more important than COX-1 inhibition in reducing hyperalgesia. Remifentanil-induced hyperalgesia was demonstrated for both electrically induced pain and cold-pressor pain. Both parecoxib and ketorolac prevented hyperalgesia in the electrical model, parecoxib to a larger extent.
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Glycine inhibitory dysfunction provides a useful experimental model for studying the mechanism of dynamic mechanical allodynia, a widespread and intractable symptom of neuropathic pain. In this model, allodynia expression relies on N-methyl-d-aspartate receptors (NMDARs), and it has been shown that astrocytes can regulate their activation through the release of the NMDAR coagonist d-serine. Recent studies also suggest that astrocytes potentially contribute to neuropathic pain. ⋯ These results suggest the following scenario: removal of glycine inhibition makes tactile stimuli able to activate astrocytes; activated astrocytes may provide d-serine to enable NMDAR activation and thus allodynia. Such a contribution of astrocytes to pathological pain fuels the emerging concept that astrocytes are critical players in pain signaling. Glycine disinhibition makes tactile stimuli able to activate astrocytes, which may provide d-serine to enable NMDA receptor activation and thus allodynia.