Articles: hyperalgesia.
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Opioid-induced hyperalgesia (OIH) refers to a phenomenon whereby opioid administration results in a lowering of pain threshold, clinically manifest as apparent opioid tolerance, worsening pain despite accelerating opioid doses, and abnormal pain symptoms such as allodynia. ⋯ Despite initial skepticism and reservations, the phenomenon of OIH in humans is now accepted a clinical reality and a challenge faced by anesthesiologists, intensivists, pain specialists, and other workers in a diverse range of settings from perioperative care to palliative care medicine.
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Migraine is known to be associated to particular psychological features. Cutaneous allodynia is a painful sensation or discomfort induced by a non-noxious stimulus, and is a frequent complaint during migraine attacks. The aim of this study was to compare the personality profile of allodynic and non-allodynic migraineurs to identify possible relationships between psychological aspects and the presence of allodynia. ⋯ No significant difference was found between the two groups in any area of the personality profile. The psychological profile seems not to affect the presence/absence of cutaneous allodynia in migraine patients. This reinforces the hypothesis that allodynia is a "somatic" symptom, not modified by psychological aspects.
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Reg Anesth Pain Med · May 2008
Comparative StudyThe effect of opioid dose and treatment duration on the perception of a painful standardized clinical stimulus.
The concept of opioid-induced hyperalgesia has recently gained prominence as a contributing factor for opioid tolerance and long-term treatment failure. But whereas the preclinical data for this phenomenon are strong, the mixed clinical data derive primarily from experimental pain models conducted in volunteers and heroin addicts, and nonstandardized clinical stimuli, e.g., surgery. The primary objective of this study is to delineate the effect of opioid dose and treatment duration on pain intensity and unpleasantness ratings following a standardized clinical pain stimulus. ⋯ The results of this study bolster preclinical and experimental pain models demonstrating enhanced pain perception in subjects receiving opioid therapy. This simple clinical model may provide a useful tool in examining opioid-induced hyperalgesia.
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Acta Anaesthesiol Scand · May 2008
Comparative StudyKetamine blocks enhancement of spinal long-term potentiation in chronic opioid treated rats.
Long-term opioid treatment is associated with the development of hyperalgesia. In a rat model we wanted to study if chronic opioid treatment changed the induction and maintenance of spinal long-term potentiation (LTP), a form of hyperexcitability in the spinal cord. We also wanted to investigate if the clinically available NMDA receptor antagonist ketamine inhibited the effect of chronic opioid treatment on LTP. ⋯ Our results indicate that animals treated with long-term opioid show amplification of stimulus-induced central sensitisation compared to opioid naïve animals. Ketamine inhibited the morphine-induced enhancement of LTP, supporting the role of ketamine in prevention of opioid induced hyperalgesia.
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It has been demonstrated that spontaneous nociceptive behaviors, cutaneous hyperalgesia and paw edema can be induced by intraplantar injection of scorpion Buthus martensi Karch (BmK) venom in rats. In the present study, activation of spinal extracellular signal-regulated kinase (ERK) signaling pathway and its contribution to pain-related responses induced by scorpion BmK venom were investigated. It was found that ERK was activated not only in the superficial layers but also in deep layers of L4-L5 spinal cord dorsal horn, which started at 2 min, peaked at 30-60 min and almost disappeared at 4h following intraplantar injection of BmK venom. ⋯ In addition, BmK venom-induced spinal c-Fos expression could be inhibited by U0126 dose-dependently. Intrathecal delivery of NMDA receptor antagonist (5R, 10S)-(+)-5-methyl-10, 11-dihydro-5H-dibenzo [a,d]-cyclohepten-5-10-imine hydrogen maleate (MK-801) and the non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) could partially inhibit activation of spinal ERK induced by BmK venom at 30 min. Thus, activation of ERK in spinal cord dorsal horn, partially mediated by NMDA and non-NMDA receptor, potentially contributes to BmK venom-induced pain-related behaviors.