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      Comparative Effectiveness of Botulinum Toxin Injection for Chronic Shoulder Pain: A Meta-Analysis of Randomized Controlled Trials

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          Abstract

          Botulinum toxin (BoNT) injection is regarded as a promising treatment for musculoskeletal pain. However, its efficacy for treating chronic shoulder pain remains unclear. We investigated the effectiveness of BoNT injections for chronic shoulder pain by conducting a systematic search of electronic databases up to March 2020 for randomized control trials (RCTs) that used BoNT injections for chronic shoulder pain treatment. The primary outcome was the between-group comparison of pain reduction, quantified by the standardized mean difference (SMD). Nine RCTs comprising 666 patients were included and divided into two groups: one group with shoulder joint pain ( n = 182) and the other group with shoulder myofascial pain ( n = 484). Regarding shoulder joint pain, the efficacy of BoNT injections was similar to that of the reference treatment (SMD: −0.605, 95% confidence level [CI]: −1.242 to 0.032 versus saline; SMD: −0.180, 95% CI: −0.514 to 0.153 versus corticosteroids) at one month post-intervention, and was superior (SMD: −0.648, 95% CI: −0.1071 to −0.225 versus corticosteroids) between one and three months. Likewise, in terms of shoulder myofascial pain, the effectiveness of BoNT injections did not differ from the reference treatment (SMD: −0.212, 95% CI: −0.551 to 0.127 versus saline; SMD: 0.665, 95% CI: −0.260 to 1.590 versus dry needling and SMD: 1.093; 95% CI: 0.128 to 2.058 versus lidocaine) at one month post- intervention, and appeared superior (SMD: −0.314, 95% CI: −0.516 to −0.111 versus saline) between one and three months. Our meta-analysis revealed that BoNT injections could be a safe and effective alternative for patients with chronic shoulder pain.

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          Most cited references 48

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          Regulation of calcitonin gene-related peptide secretion from trigeminal nerve cells by botulinum toxin type A: implications for migraine therapy.

          To determine the effect of botulinum toxin type A on calcitonin gene-related peptide secretion from cultured trigeminal ganglia neurons. The ability of botulinum toxins to cause muscle paralysis by blocking acetylcholine release at the neuromuscular junction is well known. Previous studies and clinical observations have failed to demonstrate sensory changes related to botulinum toxins or the disease of botulism. Recent studies, however, have suggested that botulinum toxin type A injected into pericranial muscles may have a prophylactic benefit in migraine. This observation has renewed the debate of a mechanism of sensory inhibition mediated by botulinum toxin type A. Primary cultures of rat trigeminal ganglia were utilized to determine whether botulinum toxin type A could directly decrease the release of calcitonin gene-related peptide, a neuropeptide involved in the underlying pathophysiology of migraine. Untreated cultures or cultures stimulated with a depolarizing stimulus (potassium chloride) or capsaicin, an agent known to activate sensory C fibers, were treated for 3, 6, or 24 hours with clinically effective doses of botulinum toxin type A or a control vehicle. The amount of calcitonin gene-related peptide secreted into the culture media following the various treatments was determined using a specific radioimmunoassay. A high percentage (greater than 90%) of the trigeminal ganglia neurons present in 1- to 3-day-old cultures was shown to express calcitonin gene-related peptide. Treatment with depolarizing stimuli (potassium chloride), a mixture of inflammatory agents, or capsaicin caused a marked increase (4- to 5-fold) in calcitonin gene-related peptide released from the trigeminal neurons. Interestingly, overnight treatment of trigeminal ganglia cultures with therapeutic concentrations of botulinum toxin type A (1.6 or 3.1 units) did not affect the amount of calcitonin gene-related peptide released from these neurons. The stimulated release of calcitonin gene-related peptide following chemical depolarization with potassium chloride or activation with capsaicin, however, was greatly repressed by the botulinum toxin, but not by the control vehicle. A similar inhibitory effect of overnight treatment with botulinum toxin type A was observed with 1.6 and 3.1 units. These concentrations of botulinum toxin type A are well within or below the range of tissue concentration easily achieved with a local injection. Incubation of the cultures with toxin for 24, 6, or even 3 hours was very effective at repressing stimulated calcitonin gene-related peptide secretion when compared to control values. These data provide the first evidence that botulinum toxin type A can directly decrease the amount of calcitonin gene-related peptide released from trigeminal neurons. The results suggest that the effectiveness of botulinum toxin type A in the treatment of migraine may be due, in part, to its ability to repress calcitonin gene-related peptide release from activated sensory neurons.
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            Comparison of lidocaine injection, botulinum toxin injection, and dry needling to trigger points in myofascial pain syndrome.

            Myofascial pain syndrome (MPS) is one of the most common causes of chronic musculoskeletal pain. Several methods have been recommended for the inactivation of trigger points (TrP). This prospective, single-blind study was proposed to compare TrP injection with botulinum toxin type A (BTX-A) to dry needling and lidocaine injection in MPS. Eighty-seven trigger points (cervical and/or periscapular regions) in 23 female and six male patients with MPS were treated and randomly assigned to three groups: lidocaine injection (n=10, 32 TrP), dry needling (n=10, 33 TrP), and BTX-A injection (n=9, 22 TrP). Clinical assessment including cervical range of motion, TrP pain pressure threshold (PPT), pain scores (PS), and visual analog scales for pain, fatigue, and work disability were evaluated at entry and the end of the 4th week. Additionally, depression and anxiety were evaluated with the Hamilton depression and anxiety rating scales, and quality of life was assessed using the Nottingham health profile (NHP). The subjects were also asked to describe side effects. INJECTION PROCEDURE: One milliliter of 0.5% lidocaine was administered to each TrP in the lidocaine injection group, 10-20 IU of BTX-A to each TrP in the BTX-A group, and dry needling to each TrP in the last group, followed by stretching of the muscle groups involved. The patients were instructed to continue their home exercise programs. Pain pressure thresholds and PS significantly improved in all three groups. In the lidocaine group, PPT values were significantly higher than in the dry needle group, and PS were significantly lower than in both the BTX-A and dry needle groups. In all, visual analog scores significantly decreased in the lidocaine injection and BTX-A groups and did not significantly change in the dry needle group. Disturbance during the injection procedure was lowest in the lidocaine injection group. Quality of life scores assessed by NHP significantly improved in the lidocaine and BTX-A groups but not in the dry needle group. Depression and anxiety scores significantly improved only in the BTX-A-injected group. Injection is more practical and rapid, since it causes less disturbance than dry needling and is more cost effective than BTX-A injection, and seems the treatment of choice in MPS. On the other hand, BTX-A could be selectively used in MPS patients resistant to conventional treatments.
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              Activation of TRPV1 mediates calcitonin gene-related peptide release, which excites trigeminal sensory neurons and is attenuated by a retargeted botulinum toxin with anti-nociceptive potential.

              Excessive release of inflammatory/pain mediators from peripheral sensory afferents renders nerve endings hyper-responsive, causing central sensitization and chronic pain. Herein, the basal release of proinflammatory calcitonin gene-related peptide (CGRP) was shown to increase the excitability of trigeminal sensory neurons in brainstem slices via CGRP1 receptors because the effect was negated by an antagonist, CGRP8-37. This excitatory action could be prevented by cleaving synaptosomal-associated protein of M(r) 25,000 (SNAP-25) with botulinum neurotoxin (BoNT) type A, a potent inhibitor of exocytosis. Strikingly, BoNT/A proved unable to abolish the CGRP1 receptor-mediated effect of capsaicin, a nociceptive TRPV1 stimulant, or its elevation of CGRP release from trigeminal ganglionic neurons (TGNs) in culture. Although the latter was also not susceptible to BoNT/E, apparently attributable to a paucity of its acceptors (glycosylated synaptic vesicle protein 2 A/B), this was overcome by using a recombinant chimera (EA) of BoNT/A and BoNT/E. It bound effectively to the C isoform of SV2 abundantly expressed in TGNs and cleaved SNAP-25, indicating that its /A binding domain (H(C)) mediated uptake of the active /E protease. The efficacy of /EA is attributable to removal of 26 C-terminal residues from SNAP-25, precluding formation of SDS-resistant SNARE complexes. In contrast, exocytosis could be evoked after deleting nine of the SNAP-25 residues with /A but only on prolonged elevation of [Ca(2+)](i) with capsaicin. This successful targeting of /EA to nociceptive neurons and inhibition of CGRP release in vitro and in situ highlight its potential as a new therapy for sensory dysmodulation and chronic pain.
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                Author and article information

                Journal
                Toxins (Basel)
                Toxins (Basel)
                toxins
                Toxins
                MDPI
                2072-6651
                12 April 2020
                April 2020
                : 12
                : 4
                Affiliations
                [1 ]Department of Physical Medicine and Rehabilitation, National Taiwan University Hospital, Bei-Hu Branch, Taipei 10845, Taiwan; myronrbman@ 123456gmail.com (P.-C.H.); wwtaustin@ 123456yahoo.com.tw (W.-T.W.); dshan1121@ 123456yahoo.com (D.-S.H.)
                [2 ]Institute of Clinical Medicine, National Yang-Ming University, Taipei 11221, Taiwan
                [3 ]Department of Physical Medicine and Rehabilitation, National Taiwan University College of Medicine, Taipei 10048, Taiwan
                Author notes
                [* ]Correspondence: kvchang011@ 123456gmail.com ; Tel.: +886-2-2371-7101
                Article
                toxins-12-00251
                10.3390/toxins12040251
                7232231
                32290577
                © 2020 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                Categories
                Article

                Molecular medicine

                botulinum toxin, corticosteroid, joint, myofascial pain

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