Articles: hyperalgesia.
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Trends Pharmacol. Sci. · Dec 2003
ReviewOpioid hyperalgesia and tolerance versus 5-HT1A receptor-mediated inverse tolerance.
In addition to analgesia, opioids also produce paradoxical hyperalgesic effects following acute and chronic treatment. In this article, we review the occurrence of this hyperalgesia under several conditions, and discuss the potential mechanisms and clinical implications. We also review recent evidence that paradoxical analgesia and inverse tolerance induced by stimulation of 5-HT(1A) receptors, which is a mirror image of opioid-induced hyperalgesia and tolerance, might achieve clinically significant analgesia in chronic pain.
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Curr Pain Headache Rep · Dec 2003
ReviewInduction and assessment of muscle pain, referred pain, and muscular hyperalgesia.
Muscle pain can be induced and assessed experimentally by a variety of methods. Ischemic and exercise-induced muscle pain are typical endogenous pain models; external stimulation with mechanical, electrical, and chemical modalities constitute the exogenous models. These models are a good basis to study the muscle sensitivity, muscle pain responses under normal and pathophysiologic conditions, and drug efficacy on specific muscle pain mechanisms. ⋯ The experimental test paradigm must include different stimulation modalities (multimodal) to obtain sufficiently advanced and differentiated information about the human nociceptive system under normal and pathophysiologic conditions because the different stimuli activate different receptors, pathways, and mechanisms. This may be a useful approach in future mechanism-based classification and treatment of muscle pain. Similarly, the multimodal approach is important in clinical studies to provide evidence for which specific muscle pain modalities and mechanisms are affected and how they are modulated by pharmacologic approaches.
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The aim of this review is to present research that has a bearing on the pathogenesis of hypersensitivity in muscle pain syndromes. Allodynia and hyperalgesia in these syndromes can be segmental or generalized and temporary or permanent. Hypersensitivity in muscle pain conditions in the clinic is best diagnosed by determining the pressure pain threshold. ⋯ Pathogenetic mechanisms for allodynia and hyperalgesia can be identified at several levels of the nociceptive system, from the nociceptors in the muscle to the cortex. Central sensitization of nociceptive neurons in the dorsal horn and a disturbed balance between inhibitory and facilitatory impulses in the descending tracts from the brain stem to the dorsal horn are the main mechanisms for pain hypersensitivity. Changes in function, biochemical make-up, and synaptic connections in the nociceptive neurons in the dorsal horn are considered to be caused by neuronal plasticity.
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Comparative Study
Spinal muscarinic receptors are activated during low or high frequency TENS-induced antihyperalgesia in rats.
Transcutaneous electrical nerve stimulation (TENS) is a non-pharmacological modality used clinically to relieve pain. Central involvement of serotonin and endogenous opioids are implicated in TENS-induced analgesia. Activation of spinal cholinergic receptors is antinociceptive and these receptors interact with opioid and serotonin receptors. ⋯ Atropine, pirenzepine and 4-DAMP significantly attenuated the antihyperalgesic effects of low and high frequency TENS while mecamylamine and methoctramine had no effects, compared to saline control. The results show that TENS-induced antihyperalgesia is mediated partially by activation of spinal muscarinic receptors but not spinal nicotinic receptors. Further, the results also indicate that spinal M1 and M3 muscarinic receptor subtypes mediate the muscarinic component of TENS antihyperalgesia.
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Nerve growth factor (NGF) is central to processes involved in an inflammatory hyperalgesia. Administration of exogenous NGF induces a hyperalgesia that is dependent on local neutrophil influx. The effects of administration of the cannabinoid anandamide and the cannabimimetic palmitoylethanolamide on an NGF-induced hyperalgesia and neutrophil accumulation were examined in this study. ⋯ NGF induced a thermal hyperalgesia that was attenuated by anandamide and palmitoylethanolamide. Only palmitoylethanolamide reduced neutrophil influx. Thus, cannabinoids show a neuronal CB1 receptor-mediated antihyperalgesic action and a separate inhibition of a proinflammatory neuroimmune process. Such a mechanism suggests a therapeutic site of analgesic action separable from central side effects.