Articles: chronic.
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Observational Study
The long-term incidence of chronic post-surgical pain after coronary artery bypass surgery - A prospective observational study.
Chronic post-surgical pain (CPSP) represents a significant issue for many patients following surgery; however, the long-term incidence and impact have not been well described following cardiac surgery. Our aim was to characterize CPSP at least 5 years following coronary artery bypass grafting (CABG) surgery. ⋯ This study highlights the impact of CPSP 7 years following cardiac surgery and highlights the effect of surgical site, neuropathic pain and the importance of including pain assessment and management in the long-term follow-up of cardiac surgical patients. Strategies to address and prevent chronic pain following cardiac surgery should be further explored.
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To individually prescribe rehabilitation contents, it is of importance to know and quantify factors for rehabilitation success and the risk for a future healthcare use. The objective of our multivariable prediction model was to determine factors of rehabilitation success and the risk for a future healthcare use in patients with high-grade, chronic low back pain. We included members of the German pension fund who participated from 2012 to 2019 in multimodal medical rehabilitation with physical and psychological treatment strategies because of low back pain (ICD10:M54.5). ⋯ Many modifiable prognostic factors (such as duration of the rehabilitation [inverted u-shaped], type of the rehabilitation, and aftercare measure), nonmodifiable prognostic factors (such as sex and age), and disease-specific factors (such as sick leave days before the rehabilitation [linear positive] together with the pain grades) for rehabilitation success were identified. Inpatient medical rehabilitation programmes (3 weeks) may be more effective in preventing a second rehabilitation measure and/or early retirement because of low back pain compared with outpatient rehabilitation programs. Subsequent implementation of additional exercise programmes, cognitive behavioural aftercare treatment, and following scheduled aftercare are likely to be beneficial.
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Chronic pain associated with osteoarthritis (OA) remains an intractable problem with few effective treatment options. New approaches are needed to model the disease biology and to drive discovery of therapeutics. We present an in vitro model of OA pain, where dorsal root ganglion (DRG) sensory neurons were sensitized by a defined mixture of disease-relevant inflammatory mediators, here called Sensitizing PAin Reagent Composition or SPARC. ⋯ We screened ∼3000 approved drugs and mechanistically focused compounds, yielding data from over 1.2 million individual neurons with detailed assessment of functional OA-SPARC phenotype rescue and orthogonal "off-target" effects. Analysis of confirmed hits revealed diverse potential analgesic mechanisms including ion channel modulators and other mechanisms including MEK inhibitors and tyrosine kinase modulators. Our results suggest that the Raf-MEK-ERK axis in DRG neurons may integrate the inputs from multiple upstream inflammatory mediators found in osteoarthritis patient joints, and MAPK pathway activation in DRG neurons may contribute to chronic pain in patients with osteoarthritis.
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Neck pain is common among individuals with migraine, but there is a lack of information of how this comorbidity can be associated with cervical muscle function. This controlled cross-sectional study aimed to compare cervical muscle function, activity, and sensitization in women with migraine, neck pain, both, and neither. ⋯ The diagnosis of migraine and chronic neck pain is associated with altered function and activity of the cervical muscles. However, the test-induced pain had an important contribution to worse cervical muscle endurance. This suggests that the therapeutic approach should focus on de-sensitization of the trigeminal-cervical complex when dealing with the comorbidity of migraine and cervical pain.
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Localized provoked vulvodynia is characterized by chronic vulvar pain that disrupts every aspect of the patient's life. Pain is localized to the vulvar vestibule, a specialized ring of tissue immediately surrounding the vaginal opening involved in immune defense. In this article, we show inflammation is the critical first step necessary for the generation of pain signals in the vulva. ⋯ Activity is blocked by the TRPV4 antagonist HC067047, denoting specificity to TRPV4. Using lipidomics, we found pro-resolving lipids in the vulvar vestibule were dysregulated, characterized by a reduction in pro-resolving mediators and heightened production of inflammatory mediators. We demonstrate specialized pro-resolving mediators represent a potential new therapy for vulvar pain, acting on 2 key parts of the disease mechanism by limiting inflammation and acutely inhibiting TRPV4 signaling.