Articles: hyperalgesia.
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Physiological and pharmacological evidence both have demonstrated a critical role for voltage-gated sodium channels (VGSCs) in many types of chronic pain syndromes because these channels play a fundamental role in the excitability of neurons in the central and peripheral nervous systems. Alterations in function of these channels appear to be intimately linked to hyperexcitability of neurons. ⋯ This review focuses on the role of VGSCs in the hyperexcitability of sensory primary afferent neurons and their contribution to the inflammatory or neuropathic pain states. The discrete localization of the tetrodotoxin (TTX)-resistant channels, in particular NaV1.8, in the peripheral nerves may provide a novel opportunity for the development of a drug targeted at these channels to achieve efficacious pain relief with an acceptable safety profile.
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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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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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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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Referred muscle pain, resulting from algogenic conditions in viscera or other deep somatic structures (another muscle, a joint), is most often accompanied by secondary hyperalgesia and trophic changes (hypotrophy). Referred pain/ hyperalgesia from viscera is partly due to central sensitisation of viscero-somatic convergent neurons (triggered by the massive afferent visceral barrage) but also probably results from a reflex arc activation (the visceral input triggers reflex muscle contraction in turn responsible for sensitisation of muscle nociceptors). Referred pain/hyperalgesia from deep somatic structures is not explained by the mechanism of central sensitisation of convergent neurons in its original form, since there is little,convergence from deep tissues in the dorsal horn neurons. It has been proposed that these connections, not present from the beginning, are opened by nociceptive input from skeletal muscle, and that referral to myotomes outside the lesion results from the spread of central sensitisation to adjacent spinal segments.