Journal ArticleDOI
Mechanisms of sympathetic pain.
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TLDR
In some chronic pain states, notably causalgia and reflex sympathetic dystrophy, activity in sympathetic efferent neurones can exacerbate the pain and sympathectomies relieve it, and several specific hypotheses have been advanced as to the primary pathophysiological cause of pain in these patients.Abstract:
In some chronic pain states, notably causalgia and reflex sympathetic dystrophy, activity in sympathetic efferent neurones can exacerbate the pain and sympathectomies relieve it. These patients are said to have sympathetically maintained pain (SMP). In normal tissue, activity in postganglionic sympathetic efferents does not produce pain, nor is it capable of activating nociceptive sensory neurones. It can, however, induce modest firing in some mechanoreceptors. SMP is often held to result from a vicious circle of events which include changes in peripheral and central somatosensory processes, and most importantly a positive feedback element in the form of sympathetic efferent neurones which, by activating sensory neurones in the periphery, completes the vicious circle. Several specific hypotheses have been advanced as to the primary pathophysiological cause of pain in these patients. Suggestions, largely deriving from observations on animal models, include: ephaptic transmission, adrenergic receptors on sensory neurones, indirect coupling of sympathetic and sensory neurones, sensitization of nociceptive afferents, and, in the central nervous system, sensitization of dorsal horn neurones. All these suggestions have some supporting evidence, but none are able to adequately explain all the disturbances seen in patients with SMP.read more
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Journal ArticleDOI
Inflammatory mediators of pain.
TL;DR: While sensory fibres normally respond to a range of physical and chemical stimuli their activity and metabolism are profoundly altered by a variety of mediators generated by tissue injury and inflammation, which can profoundly affect the properties of nociceptors and their ability to transmit pain signals.
Journal ArticleDOI
Visceral and vascular complications resulting from anterior lumbar interbody fusion
Viswanathan Rajaraman,Roy D. Vingan,Patrick Roth,Robert F. Heary,Lisa Conklin,George B. Jacobs +5 more
TL;DR: Although many of these complications have been recognized in the literature, the significance of sympathetic dysfunction appears to have been underestimated and the high incidence of complications in this series likely reflects the strict criteria.
Journal ArticleDOI
Chronic pelvic pain and endometriosis: translational evidence of the relationship and implications
Pamela Stratton,Karen J. Berkley +1 more
TL;DR: Endometriotic lesions can develop their own nerve supply, thereby creating a direct and two-way interaction between lesions and the CNS that provides a mechanism by which the dynamic and hormonally responsive nervous system is brought directly into play to produce a variety of individual differences in pain.
Journal ArticleDOI
Pharmacology of chronic pain.
TL;DR: Current mechanistic aspects of chronic pain imposed by inflammation and peripheral neuropathy are focused on, and in particular the molecular changes involving the pharmacology of nociceptive pathways are reviewed since these have important implications for the management of pain.
Journal ArticleDOI
A unifying purinergic hypothesis for the initiation of pain.
TL;DR: In this paper, a hypothesis is put forward about the sources of ATP released to activate these receptors in three different pain conditions, as a cotransmitter from sympathetic nerves in causalgia and reflex sympathetic dystrophy, from endothelial cells in vascular pain, including migraine and angina; and from tumour cells in cancer.
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