Pain
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A substantial evidence-practice gap exists between healthcare professionals learning about the biopsychosocial model of pain and adopting this model in clinical practice. This review aimed to explore the barriers and enablers that influence the application of a biopsychosocial approach to musculoskeletal pain in practice, from the clinicians' perspective. Qualitative evidence synthesis was used. ⋯ Three metathemes were identified that impact the adoption of the biopsychosocial model across the whole of health: (1) at the microlevel, healthcare professionals' personal factors, knowledge and skills, and their misconceptions of clinical practice guidelines, perception of patients' factors, and time; (2) at the mesolevel, clinical practice guideline formulation, community factors, funding models, health service provision, resourcing issues, and workforce training issues; and (3) at the macrolevel, health policy, organizational, and social factors. Synthesized data revealed multilevel (whole-of-health) barriers and enablers to health professionals adopting a biopsychosocial model of pain into practice. Awareness of these multilevel factors may help inform preimplementation preparedness and support more effective implementation of the biopsychosocial model of musculoskeletal pain into clinical practice.
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Pain is a ubiquitous experience encompassing perceptual, autonomic, and motor responses. Expectancy is known to amplify the perceived and autonomic components of pain, but its effects on motor responses are poorly understood. Understanding expectancy modulation of corticospinal excitability has important implications regarding deployment of adaptive and maladaptive protective behaviours in anticipation of pain. ⋯ These results demonstrate that merely expecting pain influenced all pain components. Findings shed new light on the aetiology of expectancy-modulated pain, whereby expecting pain mobilises the motor system to protect the body from harm by a protective withdrawal reflex, associated with reduced corticospinal excitability, and activates similar processes as increased nociceptive stimulation. This has significant practical implications for the treatment of pain, particularly in scenarios where avoidance of pain-related movement contributes to its maintenance.
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Identifying genetic risk factors for lumbar spine disorders may lead to knowledge regarding underlying mechanisms and the development of new treatments. We conducted a genome-wide association study involving 100,811 participants with genotypes and longitudinal electronic health record data from the Electronic Medical Records and Genomics Network and Geisinger Health. Cases and controls were defined using validated algorithms and clinical diagnostic codes. ⋯ Another locus on chromosome 2 spanning GFPT1, NFU1, and AAK1 was associated with LSS (lead variant rs13427243:G>A, OR = 1.10 for A, P = 4.3 × 10-8) and replicated in UK Biobank (OR = 1.11, P = 5.4 × 10-5). This was the first genome-wide association study meta-analysis of lumbar spinal disorders using electronic health record data. We identified 2 novel associations with LSRS and LSS; the latter was replicated in an independent sample.
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Migraine is highly prevalent and is the sixth leading cause worldwide for years lost to disability. Therapeutic options specifically targeting migraine are limited, and delta opioid receptor (DOP) agonists were recently identified as a promising pharmacotherapy. The mechanisms by which DOPs regulate migraine are currently unclear. ⋯ Immunohistochemical analysis of the trigeminal ganglia revealed coexpression of DOP with CGRP as well as with a primary component of the CGRPR, RAMP1. In the trigeminal nucleus caudalis, DOP was not coexpressed with CGRP but was highly coexpressed with RAMP1 and calcitonin receptor-like receptor. These results suggest that DOP agonists inhibit migraine-associated pain by attenuating CGRP release and blocking pronociceptive signaling of the CGRPR.
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To better understand the mechanisms underpinning work-related neck pain, this cross-sectional and single-blinded study compared somatosensory profiles among sonographers with varied neck disability levels. Based on K-mean cluster analysis of scores on the neck disability index (NDI), participants were classified into no (NDI ≤ 8%, n = 31, reference group), mild (NDI = 10%-20%, n = 43), or moderate/severe (NDI ≥ 22%, n = 18) disability groups. Data were collected on bodily pain distribution and severity and psychological measures including depression, anxiety, pain-catastrophizing, and fear-avoidance beliefs using validated scales. ⋯ Group differences were not found for conditioned pain modulation or exercise-induced analgesia. These findings suggest that heightened pain facilitation, rather than impaired pain inhibition may underpin nociplastic pain in participants with moderate/severe disability, and it may be associated with depression and anxiety. Clinicians should be aware that individuals with work-related neck pain presenting with moderate/severe disability display distinct somatosensory features and tailor management strategies accordingly.