Pain
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Exercise and pain neuroscience education (PNE) have both been used as standalone treatments for chronic musculoskeletal pain. The evidence supporting PNE as an adjunct to exercise therapy is growing but remains unclear. The aim of this systematic review and meta-analysis was to evaluate the effect of combining PNE and exercise for patients with chronic musculoskeletal pain, when compared with exercise alone. ⋯ Long-term outcomes (>12 weeks) were only available for 2 studies and therefore were not suitable for meta-analysis. Meta-analysis revealed a significant difference in pain (weighted mean differences, -2.09/10; 95% confidence interval [CI], -3.38 to -0.80; low certainty), disability (standardized mean difference, -0.68; 95% CI, -1.17 to -0.20; low certainty), kinesiophobia (standardized mean difference, -1.20; CI, -1.84 to -0.57; moderate certainty), and pain catastrophizing (weighted mean differences, -7.72; 95% CI, -12.26 to -3.18; very low certainty) that favoured the combination of PNE and exercise. These findings suggest that combining PNE and exercise in the management of chronic musculoskeletal pain results in greater short-term improvements in pain, disability, kinesiophobia, and pain catastrophizing relative to exercise alone.
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Peripheral sensory neurons transduce physicochemical stimuli affecting somatic tissues into the firing of action potentials that are conveyed to the central nervous system. This results in conscious perception, adaptation, and survival, but alterations of the firing patterns can result in pain and hypersensitivity conditions. Thus, understanding the molecular mechanisms underlying action potential firing in peripheral sensory neurons is essential in sensory biology and pathophysiology. ⋯ They are proposed to have roles also in intercellular communication, ectopic firing, and responses to tonic and slow natural stimuli. We highlight how MPIs are of great interest for the study of sensory transduction physiology and how they may represent therapeutic targets for many pathological conditions, such as acute and chronic pain, itch, and altered sensory perceptions. We identify future research directions, including the elucidation of the underlying molecular determinants and modulation mechanisms, their relation to the encoding of natural stimuli and their implication in pain and hypersensitivity conditions.
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Opioids relieve acute pain, but there is little evidence to support the stability of the benefit over long-term treatment of chronic noncancer pain. Previous systematic reviews consider only group level published data which did not provide adequate detail. Our goal was to use patient-level data to explore the stability of pain, opioid dose, and either physical function or pain interference in patients treated for 12 months with abuse deterrent formulations of oxycodone and hydrocodone. ⋯ In a secondary analysis of 985 patients with a measured physical function, 338 (34.3%) maintained their physical function in addition to pain and opioid dose. Of 2040 patients with pain interference measured, 788 (38.6%) met criteria in addition. In a carefully controlled environment, about one-third of patients successfully titrated on opioids to treat chronic noncancer pain demonstrated continued benefit for up to 12 months.
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To understand a putative causal link for depression and pain, we retrieved summary statistics from genome-wide association studies conducted for pain at 7 different body sites (N = 151,922-226,683) and major depression disorder (MDD, Ncase/control = 246,363/561,190). We conducted a bidirectional Mendelian randomization analysis using distinct genome-wide association studies-identified single nucleotide polymorphisms for each trait as instrumental variables and performed several sensitivity analyses to verify Mendelian randomization assumptions. We also conducted functional annotation analysis using 396 tissue-specific annotations from the roadmap project. ⋯ In the reverse direction, genetically instrumented multisite chronic pain (OR = 1.78 per one increment in the number of pain site, 95% CI: 1.51-2.11) and headache (OR = 1.55 per one log-unit increase in headache risk, 95% CI = 1.13-2.10) were associated with MDD. Functional annotation analysis showed differential clustering patterns where depression clustered closely with headache and neck/shoulder pain, exhibiting substantial brain tissue enrichment. Our study indicates that depression is a causal risk factor for headache and pain localized at neck/shoulder, back, and abdominal/stomach, rather than pain at face, hip, and knee, and suggests common neurological pathologies underlying the development of depression, headache, and neck/shoulder pain.
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Clinical models of chronic low back pain (cLBP) highlight the role of excessive attention to pain and kinesiophobia on the origin of disability. At the motor control level, various mechanisms are involved in the impairments observed in patients with cLBP. We aimed to assess the role of maladaptative attentional behaviors by using a complex systems approach and a visual display as a distraction during walking. ⋯ Post hoc analysis showed that, without distraction, patients with cLBP had significantly lower ST complexity than controls, but when distracted, they regained gait complexity, recovering the level of controls. Our results suggest that excessive attention to pain causes loss of complexity and adaptability in cLBP and explain alterations of motor control with pain. Fractal analysis seems to be a promising method to explore movement variability and individual adaptability in musculoskeletal disorders.