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Chronic shoulder pain is a very prevalent condition causing disability and functional impairment. The purpose of the study was to evaluate the relationship between pain intensity, physical variables, psychological vulnerability, pronociceptive pain modulation profile and disability in older people with chronic shoulder pain.

The goal of this study is to evaluate the feasibility and efficacy of an auricular point acupressure smartphone app (mAPA) to self-manage chronic musculoskeletal pain.

Analgesic opioid (AO) misuse by patients ranges from 0% to 50%. General practitioners are the first prescribers of AO. Our objective was to validate the Prescription Opioid Misuse Index (POMI) in primary care. We conducted a psychometric study in patients with chronic pain who had been taking AOs for at least 3 months and were followed in general practice. Patients responded to the POMI at inclusion and after 2 weeks. The reference used was the DSM-V. Sixty-nine GPs included 160 patients (87 women, 54.4%), mean age 56.4 ± 15.2 years. The total POMI score was 1.50 ± 1.27, and 73/160 (45.6.0%) had a score ≥ 2 (misuse threshold). Internal validity was measured with the Kuder-Richardson coefficient, which was 0.44. Correlations between each item and the total score ranged from 0.06 to 0.35. Test-retest reliability was determined from 145 patients: Lin's concordance coefficient was 0.57 [0.46, 0.68]. Correlation with the DSM-V (Spearman's coefficient) was 0.52. The POMI does not have sufficient psychometric properties to be recommended as a tool to identify the misuse of AOs in primary care. This study clearly showed that there is a need to create a monitoring tool specific to primary care.

Pain is an important cause of disability and constitutes the main reason people seek medical care, especially in general practice. Nevertheless, nearly half of adult Europeans with chronic pain receive inadequate pain treatment. Limited knowledge about pain among physicians is recognized as a key barrier to treatment. This is due to the well-known insufficiency in pain education at both undergraduate and postgraduate levels. There is a scarcity of research exploring the perceptions of family medicine physicians on these issues. This study aims to evaluate the perceptions of these professionals concerning medical education, as well as their knowledge, skills, and preparedness to manage chronic pain and collect suggestions for improvement. A qualitative exploratory study will be performed using synchronous virtual focus groups and purposive sampling. Eligible participants will be 3rd- and 4th-year family medicine residents and family medicine specialists with at least five years of practice. Sample size and number of focus groups will depend on data saturation. A semi-structured guide will be used. A thematic categorical analysis will be conducted after verbatim transcription of the audiofiles. This protocol has been approved by the Health Ethics Committee.

The introduction of new drug classes for chronic migraine, such as monoclonal antibodies for calcitonin-gene-related peptide or its receptor (CGRPr), or antagonists of the same CGRP, have opened a new scenario in a selected population of individuals with migraine, and those presenting with chronic form of migraine in association with medication overuse. Medication overuse is now considered a complication of chronic migraine and, in fact, the treatment with CGRP(r)-MAbs of chronic migraine with medication overuse results in a clinical improvement of chronic migraine itself, accompanied by a parallel and obvious reduction in the intake of specific and non-specific acute migraine drugs. Education on the correct use of these drugs will be an essential tool to reduce the disability and costs of people suffering from CM complicated by MO, considering the long-term safety of the new therapies targeting the CGRP pathways. Only in this way can medication overuse risk can be reduced at its nadir in the scenario of chronicity of migraines.

Rheumatoid arthritis (RA) is a chronic systemic disease of connective tissue with periods of exacerbation and remission. Fatigue is excessive strain throughout the body that is disproportionate or unrelated to an activity or lifestyle. Fatigue is an integral part of RA in most patients. The study aimed to assess the level of fatigue in RA patients and establish the relationship between fatigue and demographic and clinical factors. The study group consisted of 128 RA patients according to European League Against Rheumatism (EULAR) criteria. The Functional Assessment of Chronic Illness Therapy-Fatigue and -Medical Outcomes Study Short Form 36 (SF-36) vitality scores were used to assess the severity of fatigue symptoms. The analyzed variables were gender, age, disease duration, education, marital status, place of residence, work and residence status, pharmacological treatment, pain, morning stiffness, hemoglobin, C-reactive protein (CRP), rheumatoid factor (RF), compression soreness, Richie Articular Index, and DAS28 disease activity. The examined patients experience chronic fatigue-the mean value on the FACIT-F scale was 24.1 ± 9.1 points and on the SF-36 Vitality score was 14.2 ± 1.8 points. There is a relationship between the level of fatigue and pain, long-lasting morning stiffness, active disease, increased soreness of joints, and low hemoglobin values. When analyzing the symptom of fatigue, each patient should be approached individually, using the existing questionnaires or asking key questions to recognize the situation. The presence of fatigue symptoms should be considered during therapy and patient care by searching for and eliminating additional, intensifying stimuli and increasing its level.

Balneotherapy may be a relevant treatment for chronic low back pain (LBP) in individuals > 60 years old. This pilot study aimed to determine the effectiveness of balneotherapy for chronic LBP in people > 60 years old and to determine profiles of responders with trajectory model analysis. This was a pilot prospective open cohort study, with repeated measurements using validated questionnaires; participants were their own controls. The primary endpoint was the proportion of participants with a change in pain intensity between the start of treatment and 3 months after treatment assessed with a numeric scale (NS) from 0 to 100 mm, with an effect size (ES) > 0.5. The assessments involved questionnaires that were self-administered on days (D) 1 and 21 and at months 3 and 6. The secondary objective was to determine the profile of responders to balneotherapy. We included 78 patients (69.2% women), mean age 68.3 ± 5.3 years. The mean pain score on the NS was 48.8 ± 19.9 at D1 and 39.1 ± 20.5 at 3 months ( < 0.001). The ES was 0.47 [95% confidence interval [CI] 0.25 to 0.69] for the whole sample; 36% (28/78) had an ES > 0.5; 23% (18/78) had a moderate ES (0 to 0.5); and 41% (32/78) had an ES of zero (14/78) or < 0 (18/78), corresponding to increased pain intensity. The pain trajectory model showed that the change in pain between D1 and D21 for trajectory A (larger reduction in pain intensity) was -50% [95% CI -60 to -27], and for trajectory B (smaller reduction in pain intensity), it was -13% [-33 to 0] ( < 0.001). Between Day 1 and month 3, the change for trajectory A was -33% [-54; 0] and for trajectory B was -13% [-40 to 0] ( = 0.14). Finally, between D1 and month 6, the change for trajectory A was -50% [-60 to 0] and for trajectory B was -6% [-33 to 17] ( = 0.007). The patients in trajectory A reported performing more physical activity than those in trajectory B ( = 0.04). They were also less disabled, with a mean Oswestry Disability Index of 40.4 versus 45.7 for those in trajectory A and B, respectively, ( = 0.03) and had a higher total Arthritis Self-Efficacy Scale score. This real-life study of the effectiveness of balneotherapy on chronic LBP identified distinct pain trajectories and predictive variables for responders. These criteria could be used in decision-making regarding the prescription of balneotherapy, to ensure personalized management of chronic LBP.

Inflammatory arthritis is a severe joint disease that causes long-lasting pain that reduces a patient's quality of life. Several commercial medicines have been used to reduce the inflammation in arthritis. However, they have side effects that affect other organs and increase the infection rate in the patient. Therefore, searching for alternative medicines from natural herbs to use as a substitute for chemical drugs and reduce the side effects of drugs has become the focus of investigation. DC., known as andaliman, is an endemic spice that originates from Tapanuli, North Sumatera (Indonesia). Our previous study confirmed that andaliman exerts anti-inflammatory and xanthin oxidase enzymatic inhibitory activities. Unfortunately, there are no in vivo studies on the efficacy of andaliman in reducing inflammation in arthritis. This research aimed to produce an andaliman extract rich in essential oils, to formulate andaliman extract in a nanoemulsion product, and to test their anti-arthritic and anti-inflammatory effects on suppressing the gene expression of inflammatory arthritis in vivo. Several steps were used to conduct this experiment, including andaliman extraction, bioactive compound identification, nanoandaliman formulation, in vivo inflammatory arthritis mice modeling using complete Freund's adjuvant (CFA), and gene expression quantification using quantitative PCR (qPCR). Andaliman extract and nanoandaliman effectively reduced arthritic scores in CFA-induced arthritic mice. Both treatments also demonstrated anti-inflammatory potential via blocking several arthritic inflammatory gene expressions from cartilage tissue and brain in CFA-induced mice. Nanoandaliman at low dose (25 mg/kg bw) exerted a higher suppressive effect against the gene expression of and compared to that of andaliman extract. At high dose (100 mg/kg bw), andaliman extract effectively inhibited the expression of and genes in arthritic mice. These data suggest that nanoandaliman may be an alternative, natural anti-arthritic and anti-inflammatory candidate for the management of inflammatory arthritis.

Human mesenchymal stem cell (hMSC) and extracellular vesicle (EV) therapy is a promising treatment for discogenic low back pain (LBP). Although promising, major obstacles remain to be overcome. Cellular senescence reduces self-renewal and multipotent potentials, and the senescence-associated secretory phenotype creates an inflammatory environment negatively affecting tissue homeostasis. Reducing senescence could therefore improve regenerative approaches. Ortho-Vanillin (o-Vanillin) has senolytic activity and anti-inflammatory properties and could be a valuable supplement to MSC and EV therapy. Here, we used direct co-culture experiments to evaluate proteoglycan synthesis, inflammatory mediators, and senescent cells in the presence or absence of o-Vanillin. EV release and transfer between hMSCs and intervertebral disc cells (DCs) was examined, and the effect on hMSC differentiation and DC phenotype was evaluated in the presence and absence of o-Vanillin. This study demonstrates that o-Vanillin affects cell communication, enhances hMSC differentiation and improves DC phenotype. Co-cultures of DCs and hMSCs resulted in increased proteoglycan synthesis, a decreased number of senescent cells and decreased release of the cytokines IL6 and 8. Effects that were further enhanced by o-Vanillin. o-Vanillin profoundly increased EV release and/or uptake by hMSCs and DCs. DC markers were significantly upregulated in both cell types in response to conditioned media of o-Vanillin treated donor cells. Collectively, this study demonstrates that o-Vanillin affects hMSC and DC crosstalk and suggests that combining hMSCs and senolytic compounds may improve the outcome of cell supplementation and EV therapy for LBP.

Chemotherapy-induced neuropathic pain is a debilitating and dose-limiting side effect. Oxaliplatin is a third-generation platinum and antineoplastic compound that is commonly used to treat colorectal cancer and commonly yields neuropathic side effects. Available drugs such as duloxetine provide only modest benefits against oxaliplatin-induced neuropathy. A particularly disruptive symptom of oxaliplatin is painful cold sensitivity, known as cold allodynia. Previous studies of the peptide, RgIA, and its analogs have demonstrated relief from oxaliplatin-induced cold allodynia, yielding improvement that persists even after treatment cessation. Moreover, underlying inflammatory and neuronal protection were shown at the cellular level in chronic constriction nerve injury models, consistent with disease-modifying effects. Despite these promising preclinical outcomes, the underlying molecular mechanism of action of RgIA4 remains an area of active investigation. This study aimed to determine the necessity of the α9 nAChR subunit and potential T-cell mechanisms in RgIA4 efficacy against acute oxaliplatin-induced cold allodynia. A single dose of oxaliplatin (10 mg/kg) was utilized followed by four daily doses of RgIA4. Subcutaneous administration of RgIA4 (40 µg/kg) prevented cold allodynia in wildtype mice but not in mice lacking the α9 nAChR-encoding gene, . RgIA4 also failed to reverse allodynia in mice depleted of CD3 T-cells. In wildtype mice treated with oxaliplatin, quantitated circulating T-cells remained unaffected by RgIA4. Together, these results show that RgIA4 requires both and CD3 T-cells to exert its protective effects against acute cold-allodynia produced by oxaliplatin.