Update on peripheral mechanisms of pain: beyond prostaglandins and cytokines

Schaible, Hans‐Georg; Ebersberger, Andrea; Natura, Gabriel

doi:10.1186/ar3305

Cited by 127 publications

(103 citation statements)

References 49 publications

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“…The clinical consequences are hyperalgesia (greater levels of perceived pain in response to painful stimuli) and allodynia (pain in response to stimuli such as touch which normally do not evoke pain) in tissues sensitized by this process. [29] Neuropathic pain is associated with damage to the nervous system. [30,31] a long-lasting increase in the excitability and responsiveness of neurons in the CNS that results in hyperalgesia and allodynia.…”

Section: Understanding Chronic Painmentioning

confidence: 99%

Rethinking chronic pain in a primary care setting

Stanos

Brodsky

Argoff

et al. 2016

Postgraduate Medicine

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Chronic pain substantially impacts patient function and quality of life and is a burden to society at large in terms of increased health care utilization and loss of productivity. As a result, there is an increasing recognition of chronic pain as a public health crisis. However, there remains wide variability in clinical practices related to the prevention, assessment, and treatment of chronic pain. Certain fundamental aspects of chronic pain are often neglected including the contribution of the psychological, social, and contextual factors associated with chronic pain. Also commonly overlooked is the importance of understanding the likely neurobiological mechanism(s) of the presenting pain and how they can guide treatment selection. Finally, physicians may not recognize the value of using electronic medical records to systematically capture data on pain and its impact on mood, function, and sleep. Such data can be used to monitor onset and maintenance of treatments effects at the patient level and evaluate costs at the systems level. In this review we explain how these factors play a critical role in the development of a coordinated, evidence-based treatment approach tailored to meet specific needs of the patient. We also discuss some practical approaches and techniques that can be implemented by clinicians in order to enhance the assessment and management of individuals with chronic pain in primary care settings. ARTICLE HISTORY

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Section: Understanding Chronic Painmentioning

confidence: 99%

Rethinking chronic pain in a primary care setting

Stanos

Brodsky

Argoff

et al. 2016

Postgraduate Medicine

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“…By binding to G protein-coupled receptors, prostaglandin E 2 increases cAMP which subsequently activates PKA in cells. This pathway enhances excitability of neurons by sensitizing ion channels in membranes such as TRPV1 receptors and Na þ channels (Schaible et al 2011). On the other hand, the mechanical hypernociception induced by bradykinin involves an indirect activation of PKA and a direct activation of B 2 receptor-mediated phospholipase C (PLC) which in turn leads to the production of PKC resulting in the sensitization of sensory ion channels which subsequently leads to hypernociception Linley et al 2010).…”

Section: Discussionmentioning

confidence: 99%

“…These mediators facilitate the electrical activity of the neuronal membrane by acting on neuronal receptors directly resulting in the activation of several molecular mechanisms which subsequently causes hypernociception (Linley et al 2010;Schaible et al 2011).…”

Section: Introductionmentioning

confidence: 99%

Possible mechanisms involved in the anti-nociceptive effects of hydro-ethanolic leaf extract of Ziziphus abyssinica

Boakye‐Gyasi

Henneh

Abotsi

et al. 2017

Pharmaceutical Biology

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Context: Various parts of Ziziphus abyssinica Hochst ex. A. Rich (Rhamnaceae) have been used in Ghanaian and African traditional medicine as an analgesic. However, there are little scientific data to support the anti-nociceptive effects of the hydro-ethanolic leaf extract of Ziziphus abyssinica (EthE) as well as the possible mechanisms involved in its anti-nociceptive effects. Purpose: To predict possible nociceptive pathways involved in the anti-nociceptive effects of EthE. Materials and methods: The effect of EthE (30, 100 and 300 mg/kg) on intraplantar injection of pain mediators such as interleukin-1b, tumour necrosis factor-a, prostaglandin E 2 and bradykinin was evaluated in male Sprague Dawley rats using Randall-Selitto test for 5 h. The effect of specific antagonists to the opioidergic, adenosinergic, ATP-sensitive K þ channels, nitric oxide, serotonergic, muscarinic, adrenergic and voltage-gated calcium channel on the anti-nociceptive effect of EthE (100 mg/kg) was evaluated using the formalin test in male imprinting control region (ICR) mice for 1 h. Results: Pretreatment of the rats with EthE significantly reversed the hypernociception induced by intraplantar injection of TNF-a (F 4,120 ¼ 10.86, p < 0.0001), IL-1b (F 4,120 ¼ 14.71, p < 0.0001), bradykinin (F 4,80 ¼ 12.52, p < 0.0001) and prostaglandin E 2 (F 5,144 ¼ 6.165, p ¼ 0.0001). The anti-nociceptive effect exhibited by EthE in the formalin test was reversed by systemic administration of N G -L-nitro-arginine methyl ester, naloxone, theophylline and glibenclamide. Conclusions: EthE inhibits hypernociception induced by TNF-a, IL-1b, bradykinin and prostaglandin E 2 . EthE exhibited anti-nociceptive effects possibly mediated through opioidergic, adenosinergic, ATP-sensitive potassium channels and nitric oxide cyclic GMP pathways. ARTICLE HISTORY

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“…Studies have shown elevated intraneuronal NGF levels during inflammatory processes. These increased levels are associated with increased BDNF expression, which, although not contributing to the processing of nociceptive information in normal circumstances, contributes to inflammatory hypersensitivity 30 . It has been reported that the use of a receptor-inactivating protein (TrkA-IgG) to block the effects of endogenous NGF resulted in a reduction in sensitivity to thermal stimuli but no change in sensitivity to mechanical stimuli, showing that peripheral sensitivity can be regulated by NGFs 31 .…”

Section: Neurotrophic Factorsmentioning

confidence: 99%

Neurotrophic factors and tension-type headache: another brick in the wall?

Folchini

Kowacs

2015

Arq. Neuro-Psiquiatr.

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T ension-type headache (TTH) is the most prevalent primary headache and the second most prevalent disorder in the world 1 . However, despite the great progress made in understanding the putative physiological and biological abnormalities of migraines in recent decades 2 , the same cannot be said for their counterpart, TTH, which has been relegated to the background by most investigators 3 and, now neglected 4 , can be considered the "ugly duckling" of headache disorders classified by the International Headache Society (IHS). In what is perhaps a vicious circle, few initiatives have been taken by independent academic or industry-financed researchers to change this situation.The physiological basis of TTH was explored in the 1990s 5, and the findings allowed hypotheses for putative biochemical mechanisms associated with this type of headache to be drawn up 6 . Nevertheless, these hypothetical mechanisms have yet to be confirmed and, with few exceptions, the studies that have been carried out did not use animal models or test these mechanisms to the same level of detail as in migraine studies 2 . It is against this background that the paper in this edition by Domingues et al., who studied the role of neurotrophic factors in TTH down to the molecular level, acquires particular importance 7 . In a well-designed and carefully conducted cross-sectional study, Domingues et al. determined serum levels of brain-derived neurotrophic factor (BDNF), nerve-growth factor (NGF), neurotrophin-3 (NT-3) and neurotrophin-4/5 (NT-4/5) in forty-eight TTH patients and forty-eight age and gender-matched controls. The authors searched for a correlation between these neurotrophic factors and TTH (both episodic and chronic) as well as other measurable psychosocial variables 7 . Early studies of the pathophysiology of TTH supported the muscle-contraction theory, although TTH can occur with or without pericranial tenderness. The widespread acceptance this theory gained can be observed in a review by Maekawa et al. 8 , who discussed the factors supporting and refuting the putative role of adrenergic receptors and muscle hypoperfusion in myofascial pain.Following a different line of investigation, and probably considering the similarities between migraine and TTH, such as their sharing of common triggers 3,9 , Ashina et al. searched unsuccessfully for changes in neuropeptides such as substance P, neuropeptide Y and vasoactive intestinal polypeptide (VIP) in peripheral blood of patients with chronic tension-type headache (CTTH) 10,11 . Their findings may have in fact been anticipated by Bach et al., who found normal levels of calcitonin gene-related peptide (CGRP) in the cerebrospinal fluid of patients with TTH 12,13 . To date, the most consistent finding in the pathophysiology of CTTH has been the evidence that glyceryl-nitrate (GNT) infusion can induce late-onset tension-type-like headache in CTTH sufferers 14,15 . These findings prompted a cross-over trial, which showed that NG-monomethyl-L-arginine hydrochloride (L-NMMA), an NOS inhib...

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Update on peripheral mechanisms of pain: beyond prostaglandins and cytokines

Cited by 127 publications

References 49 publications

Rethinking chronic pain in a primary care setting

Rethinking chronic pain in a primary care setting

Possible mechanisms involved in the anti-nociceptive effects of hydro-ethanolic leaf extract of Ziziphus abyssinica

Neurotrophic factors and tension-type headache: another brick in the wall?

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