Response of pathological ischaemic muscle pain to analgesics.

Sacchetti, G; Lampugnani, R; Battistini, Carolina; Mandelli, V.

doi:10.1111/j.1365-2125.1980.tb05828.x

Cited by 13 publications

(10 citation statements)

References 23 publications

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“…While skin afferents provide detailed information about the external environment and transmit pain-related information in response to external sources of injury, muscle afferents are sensitive to the capacity of the muscle to function as a force-generating organ with intermittent periods of high metabolic demand. In addition to mechanical forces, muscle afferents appear to be attuned to byproducts released during muscle contraction or accumulated under ischemic conditions, as ischemia itself is sufficient to elicit pain (Sacchetti et al 1980). This fits with the clinical description of muscle pain as diffuse and hard to localize.…”

Section: Sensory Transductionsupporting

confidence: 70%

Behavioral Neurobiology of Chronic Pain

Taylor¹,

Finn²

2014

Current Topics in Behavioral Neurosciences

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Current Topics in Behavioral Neurosciences provides critical and comprehensive discussions of the most significant areas of behavioral neuroscience research, written by leading international authorities. Each volume offers an informative and contemporary account of its subject, making it an unrivalled reference source. Titles in this series are available in both print and electronic formats.With the development of new methodologies for brain imaging, genetic and genomic analyses, molecular engineering of mutant animals, novel routes for drug delivery, and sophisticated cross-species behavioral assessments, it is now possible to study behavior relevant to psychiatric and neurological diseases and disorders on the physiological level. The Behavioral Neurosciences series focuses on ''translational medicine'' and cutting-edge technologies. Preclinical and clinical trials for the development of new diagnostics and therapeutics as well as prevention efforts are covered whenever possible.More information about this series at

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Section: Sensory Transductionsupporting

confidence: 70%

Behavioral Neurobiology of Chronic Pain

Taylor¹,

Finn²

2014

Current Topics in Behavioral Neurosciences

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“…the change in membrane potential. This is relevant to physiopathology as NSAIDs are known to physiologically block the experimentally-induced acidosis in human skin [24,25] and to relieve from muscle pain [68,69]. As this action of NSAIDs on acidic pain can occur even in the absence of inflammation, it clearly shows that it is completely independent of the COX pathways.…”

Section: Nsaids Directly Inhibit Asic Activitymentioning

confidence: 95%

Acid-Sensing Ion Channels (ASICs): New Targets for the Analgesic Effects of Non-Steroid Anti-Inflammatory Drugs (NSAIDs)

Voilley

2004

CDTIA

155

111

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Non-steroid anti-inflammatory drugs (NSAIDs) are major drugs used in the treatment of inflammation and pain in a wide variety of disorders. NSAIDs constitute a diverse group of chemicals, categorized according to their chemical structures that share the same therapeutic properties. Among the main compounds are aspirin and salicylate, diclofenac and flurbiprofen. The best-known mechanism of action of NSAIDs is the inhibition of prostaglandin synthesis secondary to their action on cyclooxygenases (COXs). However, data have been accumulating through the years indicating that NSAIDs also act on other targets to counteract pain. Their analgesic effects are not necessarily the consequence of their anti-inflammatory action. Administration of NSAIDs reduces cutaneous and corneal pain induced by acidic pH in the absence of inflammation. Tissue acidosis, which is a dominant factor in inflammation, tumors and ischemia, has an important contribution in pain and hyperalgesia. This is due to direct excitation of the nociceptive sensory neurons by protons-gated depolarizing currents. Actually, these neurons bear a major category of ion channels that are sensitive to extracellular pH changes, the acid-sensing ion channels (ASICs). ASIC channels are able to induce action potential triggering on sensory neurons after a moderate extracellular pH decrease. They undergo transcriptional induction and post-translational regulation during inflammation and thus participate in the hypersensitization of the nociceptive system in this physiopathological condition. One specific ASIC isoform is also thought to mediate cardiac ischemic pain. COX-independent direct inhibition of their activity by different NSAIDs has been shown to occur at therapeutic doses of these compounds, on native ASIC currents on sensory neurons, as well as on ASIC channels expressed in heterologous systems. Moreover, NSAIDs also prevent the large inflammation-induced increase of their expression. These two effects are thus proposed to play an important role in the analgesic effects of NSAIDs in addition to their well-known action through COXs, and particularly in case of inflammation.

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“…Patients often report mild muscle pain at rest that is acutely worsened by either pressure or use of injured muscle. In addition to mechanical forces, muscle afferents appear to be attuned to by-products released during muscle contraction or accumulated under ischemic conditions, as ischemia itself is sufficient to elicit pain (Sacchetti et al 1980). Thermal sensitive fibers, activated by cool or warm temperatures, are also present in muscle (Hertel et al 1976; Kumazawa and Mizumura 1977), but muscles do not reach noxious levels of heat under physiological conditions (Saltin et al 1968; Brooks et al 1971).…”

Section: Sensory Transductionmentioning

confidence: 99%

Anatomical and Physiological Factors Contributing to Chronic Muscle Pain

Gregory

Sluka

2014

Behavioral Neurobiology of Chronic Pain

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Chronic muscle pain remains a significant source of suffering and disability despite the adoption of pharmacologic and physical therapies. Muscle pain is mediated by free nerve endings distributed through the muscle along arteries. These nerves project to the superficial dorsal horn and are transmitted primarily through the spinothalamic tract to several cortical and subcortical structures, some of which are more active during the processing of muscle pain than other painful conditions. Mechanical forces, ischemia, and inflammation are the primary stimuli for muscle pain, which is reflected in the array of peripheral receptors contributing to muscle pain-ASIC, P2X, and TRP channels. Sensitization of peripheral receptors and of central pain processing structures are both critical for the development and maintenance of chronic muscle pain. Further, variations in peripheral receptors and central structures contribute to the significantly greater prevalence of chronic muscle pain in females.

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Response of pathological ischaemic muscle pain to analgesics.

Cited by 13 publications

References 23 publications

Behavioral Neurobiology of Chronic Pain

Behavioral Neurobiology of Chronic Pain

Acid-Sensing Ion Channels (ASICs): New Targets for the Analgesic Effects of Non-Steroid Anti-Inflammatory Drugs (NSAIDs)

Anatomical and Physiological Factors Contributing to Chronic Muscle Pain

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