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      Efficacy of neural prolotherapy versus local corticosteroid soft tissue injection for treatment of chronic anserine bursitis: a prospective randomized clinical trial

      Ain-Shams Journal of Anesthesiology
      Springer Science and Business Media LLC

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          Abstract

          Background

          Anserine bursitis is characterized by the presence of spontaneous pain with tenderness at the inferomedial aspect of the knee joint. Neural prolotherapy aims to relieve pain of a variety of chronic musculoskeletal disorders. The study aim was to explore the short-term efficacy of neural prolotherapy (subcutaneous perineural injection of dextrose 5% solution) versus local corticosteroid injection for pain relief and improvement of function in patients with chronic anserine bursitis. The enrolled patients were randomly assigned to receive neural prolotherapy (subcutaneous perineural injection of dextrose 5% solution) (neural prolotherapy group) or a single local soft tissue injection of corticosteroid (corticosteroid group). Outcome measures included Western Ontario McMasters Universities osteoarthritis index, assessment of overall anserine bursitis pain severity using the visual analogue scale, patient’s global assessment of anserine bursitis severity using the visual analogue scale, and clinical assessment for the presence of tenderness on the anserine bursa region. Patients were evaluated before injection and after intervention by 4 weeks.

          Results

          The study included 67 lower limbs from 43 patients with chronic anserine bursitis. No significant differences were found between both treatment groups regarding all assessed parameters at the start of the study. After 4 weeks, within-group analysis showed that there was a statistically significant improvement in Western Ontario McMasters Universities osteoarthritis index and its subscales ( P ≤ 0.0001), overall anserine bursitis pain severity ( P ≤ 0.0001), and patient’s global assessment of anserine bursitis severity ( P ≤ 0.0001), as well as there was significant improvement regarding the presence of tenderness at the anserine bursa region in both groups in comparison to the preinjection assessment. At the postinjection assessment, between-group analysis showed that there were no significant differences regarding all assessed outcome parameters. All patients in both groups tolerated the injection procedure and were satisfied with the procedure. There was no significant difference between the two groups regarding patients’ satisfaction to the procedure results. Improvement was achieved in 86.4% of patients included in the neural prolotherapy group versus 95.2% of patients included in the corticosteroid group.

          Conclusions

          Neural prolotherapy was effective in relieving pain, improving local tenderness and function in patients with chronic anserine bursitis similar to local corticosteroid injection.

          Trial registration

          ClinicalTrials.gov, registration number: NCT04509440. Registered 12 August 2020—Retrospectively registered,

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          Most cited references27

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          How to Calculate Sample Size for Different Study Designs in Medical Research?

          Calculation of exact sample size is an important part of research design. It is very important to understand that different study design need different method of sample size calculation and one formula cannot be used in all designs. In this short review we tried to educate researcher regarding various method of sample size calculation available for different study designs. In this review sample size calculation for most frequently used study designs are mentioned. For genetic and microbiological studies readers are requested to read other sources.
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            Neuroinflammation and Central Sensitization in Chronic and Widespread Pain.

            Chronic pain is maintained in part by central sensitization, a phenomenon of synaptic plasticity, and increased neuronal responsiveness in central pain pathways after painful insults. Accumulating evidence suggests that central sensitization is also driven by neuroinflammation in the peripheral and central nervous system. A characteristic feature of neuroinflammation is the activation of glial cells, such as microglia and astrocytes, in the spinal cord and brain, leading to the release of proinflammatory cytokines and chemokines. Recent studies suggest that central cytokines and chemokines are powerful neuromodulators and play a sufficient role in inducing hyperalgesia and allodynia after central nervous system administration. Sustained increase of cytokines and chemokines in the central nervous system also promotes chronic widespread pain that affects multiple body sites. Thus, neuroinflammation drives widespread chronic pain via central sensitization. We also discuss sex-dependent glial/immune signaling in chronic pain and new therapeutic approaches that control neuroinflammation for the resolution of chronic pain.
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              TRPV1 receptors in the CNS play a key role in broad-spectrum analgesia of TRPV1 antagonists.

              Vanilloid receptor type 1 (TRPV1) is a ligand-gated nonselective cation channel that is considered to be an important integrator of various pain stimuli such as endogenous lipids, capsaicin, heat, and low pH. In addition to expression in primary afferents, TRPV1 is also expressed in the CNS. To test the hypothesis that the CNS plays a differential role in the effect of TRPV1 antagonists in various types of pain, the analgesic effects of two TRPV1 antagonists with similar in vitro potency but different CNS penetration were compared in vivo. Oral administration of either A-784168 (1-[3-(trifluoromethyl)pyridin-2-yl]-N-[4-(trifluoromethylsulfonyl)phenyl]-1,2,3,6-tetrahydropyridine-4-carboxamide) (good CNS penetration) or A-795614 (N-1H-indazol-4-yl-N'-[(1R)-5-piperidin-1-yl-2,3-dihydro-1H-inden-1-yl]urea) (poor CNS penetration) blocked capsaicin-induced acute pain with the same potency. In complete Freund's adjuvant (CFA)-induced chronic inflammatory pain, oral administration of either compound blocked thermal hyperalgesia with similar potency. Furthermore, intraplantar or intrathecal administration of A-784168 blocked CFA-induced thermal hyperalgesia, suggesting that both peripheral and CNS TRPV1 receptors may play a role in inflammatory thermal hyperalgesia. The effects of the two TRPV1 antagonists were further assessed in models presumably mediated by central sensitization, including CFA- and capsaicin-induced mechanical allodynia and osteoarthritic pain. In these models, the potency of the two compounds was similar after intrathecal administration. However, when administered orally, A-784168, with good CNS penetration, was much more potent than A-795614. Together, these results demonstrate that TRPV1 receptors in the CNS play an important role in pain mediated by central sensitization. In addition, these results demonstrate that significant CNS penetration is necessary for a TRPV1 antagonist to produce broad-spectrum analgesia.
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                Author and article information

                Contributors
                (View ORCID Profile)
                Journal
                Ain-Shams Journal of Anesthesiology
                Ain-Shams J Anesthesiol
                Springer Science and Business Media LLC
                2090-925X
                December 2022
                January 08 2022
                December 2022
                : 14
                : 1
                Article
                10.1186/s42077-021-00198-8
                1bec4f27-6f03-475a-b63a-9f8af9bf14f3
                © 2022

                https://creativecommons.org/licenses/by/4.0

                https://creativecommons.org/licenses/by/4.0


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