Pain
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Low back pain (LBP) is a leading cause of disability. However, the processes contributing to disability are not well understood. Therefore, this study (1) empirically derived LBP subgroups and (2) validated these subgroups using walking performance, pain, and disability measures. ⋯ The Maladaptive subgroup had reduced walking performance (slower self-selected walking speed, TUG completion, and obstacle approach and crossing speed) and worse clinical presentation (higher pain intensity, pain interference, and disability) (moderate to large effect sizes; P's < 0.05). Findings support the construct validity of this multidimensional subgrouping approach. Longitudinal studies are needed to determine whether the Maladaptive subgroup is predictive of poor outcomes, such as pain chronicity or persistent disability.
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Randomized Controlled Trial
Brief preoperative mind-body therapies for total joint arthroplasty patients: a randomized controlled trial.
Although knee and hip replacements are intended to relieve pain and improve function, up to 44% of knee replacement patients and 27% of hip replacement patients report persistent postoperative joint pain. Improving surgical pain management is essential. We conducted a single-site, 3-arm, parallel-group randomized clinical trial conducted at an orthopedic clinic, among patients undergoing total joint arthroplasty (TJA) of the hip or knee. ⋯ Moderation analysis revealed the surgery type did not differentially impact the 3 interventions. Thus, a single session of a simple, scripted MM intervention may be able to immediately decrease TJA patients' preoperative clinical symptomology and improve postoperative physical function. As such, embedding brief MM interventions in surgical care pathways has the potential to improve surgical outcomes for the millions of patients receiving TJA each year.
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Pain and depression are episodic conditions that might take a chronic course. They are clearly related, but information on how they influence each other in the process of chronification is limited. Pain catastrophizing is hypothesized to play a role in the development of depression and chronic pain, but few longitudinal studies have investigated their association over a longer term. ⋯ The number of years lived with chronic pain was associated with a chronic course of depression, with odds ratios increasing from 1.55 (95% CI [0.87-2.91]) to 14.19 (95% CI [8.99-22.41]) when reporting chronic pain on 2 vs 5 assessments compared with none. The results suggest that when pain intensity or catastrophizing change, depressive symptoms change in the same direction. When pain and catastrophizing become chronic, they seem to be mutually reinforcing determinants for chronic depression.
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Translational regulation permeates neuronal function. Nociceptors are sensory neurons responsible for the detection of harmful stimuli. Changes in their activity, termed plasticity, are intimately linked to the persistence of pain. ⋯ Injection of the peptide corresponding to the calcitonin gene-related peptide-encoded uORF resulted in pain-associated behavioral responses in vivo and nociceptor sensitization in vitro. An inhibitor of heterotrimeric G protein signaling blocks both effects. Collectively, the data suggest pervasive translation in regions of the transcriptome annotated as noncoding in dorsal root ganglion neurons and identify a specific uORF-encoded peptide that promotes pain sensitization through GPCR signaling.
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Small-fiber neuropathy (SFN), characterized by distal unmyelinated or thinly myelinated fiber loss, produces a combination of sensory dysfunction and neuropathic pain. Gain-of-function variants in the sodium channel Nav1.7 that produce dorsal root ganglion (DRG) neuron hyperexcitability are present in 5% to 10% of patients with idiopathic painful SFN. ⋯ Therefore, although these 2 Nav1.7 I228M knock-in mouse lines recapitulate the DRG neuron hyperexcitability associated with gain-of-function mutations in Nav1.7, they do not recapitulate the pain or neuropathy phenotypes seen in patients. We suggest that the relationship between hyperexcitability in sensory neurons and the pain experienced by these patients may be more complex than previously appreciated and highlights the challenges in modelling channelopathy pain disorders in mice.