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      Unpredictable stress delays recovery from exercise-induced muscle pain: contribution of the sympathoadrenal axis

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          Abstract

          Introduction:

          Although stress is a well-establish risk factor for the development of chronic musculoskeletal pain, the underlying mechanisms, specifically the contribution of neuroendocrine stress axes, remain poorly understood.

          Objective:

          To evaluate the hypothesis that psychological stress-induced activation of the sympathoadrenal stress axis prolongs the muscle pain observed after strenuous exercise.

          Methods:

          Adult male Sprague-Dawley rats were exposed to unpredictable sound stress and eccentric exercise. The involvement of the sympathoadrenal stress axis was evaluated by means of surgical interventions, systemic administration of epinephrine, and intrathecal β 2-adrenergic receptor antisense.

          Results:

          Although sound stress alone did not modify nociceptive threshold, it prolonged eccentric exercise-induced mechanical hyperalgesia. Adrenal medullectomy (ADMdX) attenuated, and administration of stress levels of epinephrine to ADMdX rats mimicked this effect of sound stress. Knockdown of β 2-adrenergic receptors by intrathecal antisense also attenuated sound stress-induced prolongation of eccentric exercise-induced hyperalgesia.

          Conclusion:

          Together, these results indicate that sympathoadrenal activation, by unpredictable sound stress, disrupts the capacity of nociceptors to sense recovery from eccentric exercise, leading to the prolongation of muscle hyperalgesia. This prolonged recovery from ergonomic pain is due, at least in part, to the activation of β 2-adrenergic receptors on muscle nociceptors.

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          Most cited references 57

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          Enhanced central pain processing of fibromyalgia patients is maintained by muscle afferent input: a randomized, double-blind, placebo-controlled study.

          Fibromyalgia (FM) syndrome is characterized by pain and widespread hyperalgesia to mechanical, thermal, and electrical stimuli. Despite convincing evidence for central sensitization of nociceptive pain pathways, the role of peripheral tissue impulse input in the initiation and maintenance of FM is unclear. Therefore this randomized, double-blind, placebo-controlled trial of 22 female normal controls (NCs) and 28 female FM subjects tested the effects of trapezius muscle (TrapM) tender point injections with 1% lidocaine on local pain thresholds as well as on remote heat hyperalgesia at the forearm. Prior to muscle injections shoulder pain was standardized by tonic mechanical muscle stimulation, resulting in local pain ratings of 4.0+/-0.5 VAS units. Tonic muscle stimulation was interrupted for the TrapM injections but was continued afterwards at the same level. NC as well as FM subjects experienced significant increases of TrapM pressure pain thresholds from lidocaine injections but not from placebo injections (p<0.001). Additionally, heat hyperalgesia of FM participants was significantly reduced at areas remote from the injection site (forearm) by lidocaine but not by placebo (p=0.02). Neither lidocaine nor saline injections significantly affected clinical FM pain ratings, a result most likely due to the very low dose of lidocaine (50mg) used in this trial. Lidocaine injections increased local pain thresholds and decreased remote secondary heat hyperalgesia in FM patients, emphasizing the important role of peripheral impulse input in maintaining central sensitization in this chronic pain syndrome; similar to other persistent pain conditions such as irritable bowel syndrome and complex regional pain syndrome.
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            Dysfunctional endogenous analgesia during exercise in patients with chronic pain: to exercise or not to exercise?

            Exercise is an effective treatment for various chronic pain disorders, including fibromyalgia, chronic neck pain, osteoarthritis, rheumatoid arthritis, and chronic low back pain. Although the clinical benefits of exercise therapy in these populations are well established (i.e. evidence based), it is currently unclear whether exercise has positive effects on the processes involved in chronic pain (e.g. central pain modulation). Reviewing the available evidence addressing the effects of exercise on central pain modulation in patients with chronic pain. Narrative review. Exercise activates endogenous analgesia in healthy individuals. The increased pain threshold following exercise is due to the release of endogenous opioids and activation of (supra)spinal nociceptive inhibitory mechanisms orchestrated by the brain. Exercise triggers the release of beta-endorphins from the pituitary (peripherally) and the hypothalamus (centrally), which in turn enables analgesic effects by activating μ-opioid receptors peripherally and centrally, respectively. The hypothalamus, through its projections on the periaqueductal grey, has the capacity to activate descending nociceptive inhibitory mechanisms. However, several groups have shown dysfunctioning of endogenous analgesia in response to exercise in patients with chronic pain. Muscle contractions activate generalized endogenous analgesia in healthy, pain-free humans and patients with either osteoarthritis or rheumatoid arthritis, but result in increased generalised pain sensitivity in fibromyalgia patients. In patients having local muscular pain (e.g. shoulder myalgia), exercising non-painful muscles activates generalized endogenous analgesia. However, exercising painful muscles does not change pain sensitivity either in the exercising muscle or at distant locations. The reviewed studies examined acute effects of exercise rather than long-term effects of exercise therapy. A dysfunctional response of patients with chronic pain and aberrations in central pain modulation to exercise has been shown, indicating that exercise therapy should be individually tailored with emphasis on prevention of symptom flares. The paper discusses the translation of these findings to rehabilitation practice together with future research avenues.
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              Review of pharmacological therapies in fibromyalgia syndrome

              This review addresses the current status of drug therapy for the management of fibromyalgia syndrome (FMS) and is based on interdisciplinary FMS management guidelines, meta-analyses of drug trial data, and observational studies. In the absence of a single gold-standard medication, patients are treated with a variety of drugs from different categories, often with limited evidence. Drug therapy is not mandatory for the management of FMS. Pregabalin, duloxetine, milnacipran, and amitriptyline are the current first-line prescribed agents but have had a mostly modest effect. With only a minority of patients expected to experience substantial benefit, most will discontinue therapy because of either a lack of efficacy or tolerability problems. Many drug treatments have undergone limited study and have had negative results. It is unlikely that these failed pilot trials will undergo future study. However, medications, though imperfect, will continue to be a component of treatment strategy for these patients. Both the potential for medication therapy to relieve symptoms and the potential to cause harm should be carefully considered in their administration.
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                Author and article information

                Journal
                Pain Rep
                Pain Rep
                PAIREP
                Painreports
                Pain Reports
                Wolters Kluwer (Philadelphia, PA )
                2471-2531
                Sep-Oct 2019
                18 September 2019
                : 4
                : 5
                Affiliations
                [a ]Department of Oral and Maxillofacial Surgery, University of California, San Francisco, CA, USA
                [b ]Department of Preventive and Restorative Dental Sciences, University of California, San Francisco, CA, USA
                [c ]Department of Medicine, University of California, San Francisco, CA, USA
                Author notes
                [* ]Corresponding author. Address: University of California San Francisco, 513 Parnassus Ave, Room S709, San Francisco, CA 94143-0440. Tel.: +1 415 476 5108; fax: +1 415 476 6305. E-mail address: jon.levine@ 123456ucsf.edu (J.D. Levine).
                Article
                PAINREPORTS-D-19-0088 00005
                10.1097/PR9.0000000000000782
                6882572
                Copyright © 2019 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of The International Association for the Study of Pain.

                This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal.

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