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This study was aimed at evaluating the efficacy of glucosamine and potential mechanisms of actions in a neuropathic pain model in rats.
Learn More >Chronic pain with its comorbidities, such as depression, insomnia, and social deprivation, is a major cause of disability and health-economic burden. Insufficient response to pain medication and potentially serious adverse effects have led the majority of chronic pain patients to seek relief from non-pharmacological remedies. Along with this trend, pain research has paid increasing interest in critical evaluation of various complementary treatments. Music-based treatments have emerged as an efficacious and safe means to enhance the management of acute and chronic pain. We review the current position of music-based interventions in the treatment of chronic pain and present explanations for the analgesic effects of music through modulation of the primary nociception and discuss the contribution of the mesolimbic dopaminergic system to the affective component of pain perception. We propose ways to translate the novel theoretical understanding into clinical practice in different health care settings, primary health care in particular, and discuss the preconditions of successful implementation. We argue that music interventions provide low-cost, easily applicable complementary pain treatments not requiring heavy utilization of health care resources. Finally, we provide research and quality improvement frameworks and make suggestions to cover the gaps of existing evidence. PERSPECTIVE: This article addresses the current evidence for analgesic effects of music interventions, discusses its neurobiological basis and evaluates potential use of music in treating chronic pain patients in different health care settings. We also propose directions for future research to cover shortages in the currently published data.
Learn More >Bone marrow lesions (BMLs) are associated with pain in osteoarthritis (OA), but histological scores for OA focus on cartilage pathology. We developed a new scoring system, the Osteoarthritis Bone Score (OABS), to characterise OA-related BMLs.
Learn More >This study investigated the association between serological biomarkers at hospital admission with the development of long-term post-COVID pain symptoms in previously hospitalized COVID-19 survivors. A cohort study including patients hospitalised due to COVID-19 in one urban hospital of Madrid (Spain) during the first wave of the outbreak was conducted. Hospitalisation data, clinical data and eleven serological biomarkers were collected at hospital admission. Participants were scheduled for an individual telephone interview after hospital discharge for collecting data about post-COVID pain symptoms. A total of 412 (mean age: 62, SD: 15 years; 46.1% women) were assessed twice, a mean of 6.8 and 13.2 months after discharge. The prevalence of post-COVID pain symptoms was 42.7% (n=176) and 36.2% (n=149) at 6.8 and 13.2 months after hospital discharge. Patients reporting post-COVID pain exhibited a greater number of COVID-19 associated symptoms at hospital admission, more medical comorbidities, higher lymphocyte count, and lower glucose and creatine kinase (CK) levels (all, P<0.01) than those not reporting post-COVID pain. The multivariate analysis revealed that lower CK and glucose levels were significantly associated, but just explaining 6.9% of the variance of suffering post-COVID pain. In conclusion, the association between serological biomarkers associated with COVID-19 severity at hospital admission and the development of post-COVID pain is small. Other factors, e.g., higher number of COVID-19 onset symptoms (higher symptom load) could be more relevant for the development of post-COVID pain. As inflammatory biomarkers were not directly analyzed, they may have stronger predictive strengths for the development of post-COVID pain symptoms.
Learn More >Migraine affects over a billion individuals worldwide but its genetic underpinning remains largely unknown. Here, we performed a genome-wide association study of 102,084 migraine cases and 771,257 controls and identified 123 loci, of which 86 are previously unknown. These loci provide an opportunity to evaluate shared and distinct genetic components in the two main migraine subtypes: migraine with aura and migraine without aura. Stratification of the risk loci using 29,679 cases with subtype information indicated three risk variants that seem specific for migraine with aura (in HMOX2, CACNA1A and MPPED2), two that seem specific for migraine without aura (near SPINK2 and near FECH) and nine that increase susceptibility for migraine regardless of subtype. The new risk loci include genes encoding recent migraine-specific drug targets, namely calcitonin gene-related peptide (CALCA/CALCB) and serotonin 1F receptor (HTR1F). Overall, genomic annotations among migraine-associated variants were enriched in both vascular and central nervous system tissue/cell types, supporting unequivocally that neurovascular mechanisms underlie migraine pathophysiology.
Learn More >Both opioids and nonsteroidal anti-inflammatory drugs (NSAIDS) produce deleterious side effects and fail to provide sustained relief in patients with chronic inflammatory pain. Peripheral neuroinflammation (PN) is critical for initiation and development of inflammatory pain. A better understanding of molecular mechanisms underlying PN would facilitate the discovery of new analgesic targets and the development of new therapeutics. Emerging evidence suggests that peripheral sensory neurons are not only responders to painful stimuli, but are also actively engaged in inflammation and immunity, whereas the intrinsic regulatory mechanism is poorly understood. Here we report the expression of proton-selective ion channel Hv1 in peripheral sensory neurons in rodents and humans, which was previously shown as selectively expressed in microglia in mammalian central nervous system. Neuronal Hv1 was up-regulated by PN or depolarizing stimulation, which in turn aggravates inflammation and nociception. Inhibiting neuronal Hv1 genetically or by a newly discovered selective inhibitor YHV98-4 reduced intracellular alkalization and ROS production in inflammatory pain, mitigated the imbalance in downstream SHP-1-pAKT signaling, and also diminished pro-inflammatory chemokine release to alleviate nociception and morphine-induced hyperalgesia and tolerance. Thus, our data reveal neuronal Hv1 as a novel target in analgesia strategy and managing opioids-related side effects.
Learn More >Efficacy of monoclonal antibodies against calcitonin gene-related peptide (CGRP) or its receptor (calcitonin receptor-like receptor/receptor activity modifying protein-1, CLR/RAMP1) implicates peripherally-released CGRP in migraine pain. However, the site and mechanism of CGRP-evoked peripheral pain remain unclear. By cell-selective RAMP1 gene deletion, we reveal that CGRP released from mouse cutaneous trigeminal fibers targets CLR/RAMP1 on surrounding Schwann cells to evoke periorbital mechanical allodynia. CLR/RAMP1 activation in human and mouse Schwann cells generates long-lasting signals from endosomes that evoke cAMP-dependent formation of NO. NO, by gating Schwann cell transient receptor potential ankyrin 1 (TRPA1), releases ROS, which in a feed-forward manner sustain allodynia via nociceptor TRPA1. When encapsulated into nanoparticles that release cargo in acidified endosomes, a CLR/RAMP1 antagonist provides superior inhibition of CGRP signaling and allodynia in mice. Our data suggest that the CGRP-mediated neuronal/Schwann cell pathway mediates allodynia associated with neurogenic inflammation, contributing to the algesic action of CGRP in mice.
Learn More >To explore a protection motivation theory screening tool for predicting rehabilitation adherence.
Learn More >G protein coupled receptor kinase 2 (GRK2) has been demonstrated to play a crucial role in the development of chronic pain. Acupuncture is an alternative therapy widely used for pain management. In this study, we investigated the role of spinal neuronal GRK2 in electroacupuncture (EA) analgesia.
Learn More >A randomized controlled trial of a new type of Physiotherapy informed by Acceptance and Commitment Therapy (PACT), found that it improved functioning in people with chronic low back pain compared to usual physiotherapy care. Fidelity evaluation is necessary to understand trial processes and outcomes. This study evaluated PACT treatment fidelity including delivery, receipt, and enactment.
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