Pain
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Low back pain (LBP) follows different pain trajectories, and patients seem to recognize their trajectory. This allows self-reported visual pain trajectories (SRVTs) to support patient-provider communication. Pain trajectories appear stable over time for many patients, but the evidence is sparse. ⋯ The preference ORs indicated that transitions occurred mainly to similar SRVTs differing in only 1 subscale. Transitions to less or more intense SRVTs were associated with changes in clinical outcomes in the expected direction. Despite distinctly different SRVTs identified, individuals reported relatively stable LBP phenotypes but with potential for change.
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What are the care-seeking priorities of people living with chronic pain and carers and how can these shape interdisciplinary workforce training to improve high-value pain care? Phase 1: Australian people living with chronic pain (n = 206; 90% female) and carers (n = 10; 40% female) described their pain care priorities (eDelphi, round 1). A coding framework was inductively derived from 842 pain care priorities (9 categories, 52 priorities), including validation; communication; multidisciplinary approaches; holistic care; partnerships; practitioner knowledge; self-management; medicines; and diagnosis. Phase 2: In eDelphi round 2, panellists (n = 170; valid responses) rated the importance (1 = less important; 9 = more important) of the represented framework. ⋯ More than 74% of health professionals were fairly or extremely confident in their ability to support care priorities for 6 of 9 categories (66.7%). Phase 3: An interdisciplinary panel (n = 5) mapped an existing foundation-level workforce training program against the framework, identifying gaps and training targets. Recommendations were determined for framework adoption to genuinely shape, from a partnership perspective, Australian interdisciplinary pain training.
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The dominant view in the field of pain is that peripheral neuropathic pain is driven by microglia in the somatosensory processing region of the spinal dorsal horn. Here, to the contrary, we discovered a form of neuropathic pain that is independent of microglia. Mice in which the nucleus pulposus (NP) of the intervertebral disc was apposed to the sciatic nerve developed a constellation of neuropathic pain behaviours: hypersensitivity to mechanical, cold, and heat stimuli. ⋯ Pain hypersensitivity was also prevented by genetically disrupting the neurotrophin brain-derived neurotrophic factor selectively in macrophages. Moreover, the behavioural phenotypes as well as the molecular mechanisms of NP-induced pain hypersensitivity were not different between males and females. Our findings reveal a previously unappreciated mechanism for by which a discrete peripheral nerve lesion may produce pain hypersensitivity, which may help to explain the limited success of microglial inhibitors on neuropathic pain in human clinical trials.
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Adolescents with chronic pain (ACP) often experience impairments in their social functioning. Little is known about the consequences of these impairments on peer relationships of ACP. This study applied social network analysis to examine whether adolescents with more pain problems are less popular (RQ1), adolescents with similar pain problems name each other more often as being part of the same peer group (RQ2), dyads with an adolescent experiencing more pain problems report less positive (eg, support) and more negative (eg, conflict) friendship qualities (RQ3), and positive and negative friendship qualities moderate the relationship between pain and emotional distress (RQ4). ⋯ Finally, positive and negative friendship qualities moderated the relationship between pain and emotional distress. This study contributes to the literature on the importance of peer relationships of ACP. Clinical implications and directions for future research are discussed.
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The transient receptor potential ion channel TRPM3 is highly prevalent on nociceptive dorsal root ganglion (DRG) neurons, but its functions in neuronal plasticity of chronic pain remain obscure. In an animal model of nonspecific low back pain (LBP), latent spinal sensitization known as nociceptive priming is induced by nerve growth factor (NGF) injection. Here, we address the TRPM3-associated molecular basis of NGF-induced latent spinal sensitization at presynaptic level by studying TRPM3-mediated calcium transients in DRG neurons. ⋯ TRPM3 activation provokes an outbreak of pulsatile superoxide production (mitoflash) that comes in the form of a surge in frequency being tunable. We suggest that mitoflash pulsations downstream of TRPM3 activation might be an early signaling event initiating pain sensitization. Tuning of mitoflash activity would be a novel bottom-up therapeutic strategy for chronic pain conditions such as LBP and beyond.