Pain
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We tested whether aerobic exercise training altered morphine analgesic responses or reduced morphine dosages necessary for adequate analgesia. Patients with chronic back pain were randomized to an 18-session aerobic exercise intervention (n = 38) or usual activity control (n = 45). Before and after the intervention, participants underwent 3 laboratory sessions (double-blinded, crossover) to assess effects of saline placebo, i.v. morphine (0.09 mg/kg), and i.v. naloxone (12 mg) on low back pain and evoked heat pain responses. ⋯ Of clinical significance were findings that relative to the control group, aerobic exercise produced analgesia more similar to that observed after receiving ≈7 mg morphine preintervention (P < 0.045). Greater pre-post intervention increases in endogenous opioid function (from any source) were significantly associated with larger pre-post intervention decreases in morphine analgesia (P < 0.046). The overall pattern of findings suggests that regular aerobic exercise has limited direct effects on morphine responsiveness, reducing morphine analgesia in males only.
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Widespread or ectopic sensitization is a hallmark symptom of chronic pain, characterized by aberrantly enhanced pain sensitivity in multiple body regions remote from the site of original injury or inflammation. The central mechanism underlying widespread sensitization remains unidentified. The central nucleus of the amygdala (also called the central amygdala, CeA) is well situated for this role because it receives nociceptive information from diverse body sites and modulates pain sensitivity in various body regions. ⋯ Furthermore, chemogenetic excitation of gamma-aminobutyric acid-ergic neurons in the right CeA induced de novo bilateral hind paw sensitization in the rats without inflammation. These results indicate that the CeA neuronal activity determines hind paw tactile sensitivity in rats with remote inflammatory pain. They also suggest that the hind paw sensitization used in a large number of preclinical studies might not be simply a sign of the pain at the site of injury but rather a representation of the augmented CeA activity resulting from inflammation/pain in any part of the body or from activities of other brain regions, which has an active role of promoting defensive/protective behaviors to avoid further bodily damage.
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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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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.