Pain
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Interoception is critical to health regulation and is often disrupted in individuals with chronic pain (ICPs). Interoceptive sensibility (IS)-the self-reported experience and relationship toward internal states-includes skills such as sensing, interpreting, and using bodily information for self-regulation. Current studies on IS and chronic pain (CP) adjustment are scarce, and how the interplay between different IS skills shapes CP adjustment remains unclear. ⋯ A cluster analysis identified 3 IS skills profiles: (1) high IS skills (n = 68), with the highest levels of attention regulation toward bodily sensations, body trust, listening for insight, and self-regulation; (2) low IS skills (n = 29), who distracted less and worried more about bodily sensations, and presented lower-body trust; and (3) mixed IS skills (n = 71), despite good body trust, attention regulation, and low worrying, showed lower awareness of body-mind connections. Interoceptive sensibility skills profiles differed in depression, vitality (fatigue), and psychological or behavioral processes, such as pain-related self-efficacy, catastrophizing, kinesiophobia, and activity pacing. These findings contribute to integrating body-mind connections more explicitly into current theoretical CP models and developing tailored interventions targeting specific IS skills to improve CP adjustment.
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Informing patients about potential side effects of pain treatment is a requirement that protects patients and aids decision making, but it increases the likelihood of unwanted nocebo side effects. If patients do not desire all side-effect information, it may be possible to ethically reduce nocebo effects through authorized concealment of side effects, whereby patients and clinicians engage in shared decision-making to regulate the disclosure of side-effect information. Currently, there is no experimental data clarifying the factors that causally influence desire for side-effect information in pain treatment. ⋯ Results were not moderated by participants' level of contact with the health care system, chronic health condition, or clinical pain history. Additional analyses indicated that low side-effect severity and frequency lessen desire for side-effect information because these variables reduce belief that side-effect information will be needed in the future and lower feelings of anticipated regret. The experiments identify situational and individual-difference factors that decrease the desire for side-effect information and provide evidence on when and for whom it may be useful for physicians to engage in shared medical decision-making with the goal of reducing nocebo side effects.
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Total knee arthroplasty (TKA) is the end-stage treatment of knee osteoarthritis (OA), and approximately 20% of patients experience chronic postoperative pain. Studies indicate that inflammatory biomarkers might be associated with pain in OA and potentially linked to the development of chronic postoperative pain after TKA. This study aimed to (1) evaluate preoperative serum levels of inflammatory biomarkers in patients with OA and healthy control subjects, (2) investigate preoperative differences of inflammatory biomarker profiles in subgroups of patients, and (3) compare subgroups of patients with and without postoperative pain 12 months after surgery. ⋯ The 12-months postoperative VAS and KOOS scores were significantly different between subgroups of patients ( P < 0.05). This study identified differences in specific inflammatory biomarker profiles when comparing patients with OA and control subjects. Cluster analysis identified 2 subgroups of patients with OA, with one subgroup demonstrating comparatively worse 12-month postoperative pain intensity and function scores.
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Dental pulp tissue is densely innervated by afferent fibers of the trigeminal ganglion. When bacteria cause dental decay near the pulpal tissue, a strong neuronal and immune response occurs, creating pulpitis, which is associated with severe pain and pulp tissue damage. Neuroimmune interactions have the potential to modulate both the pain and pathological outcome of pulpitis. ⋯ We found that the neuropeptide CGRP, facilitated the recruitment of myeloid cells into the pulp while also increasing spontaneous pain-like behavior 20% to 25% at an early time point. Moreover, when we depleted neutrophils and monocytes, we found that there was 20% to 30% more sensory afferent loss and increased presence of bacteria in deeper parts of the tissue, whereas there was a significant reduction in mechanical pain response scores compared with the control group at a later time point. Overall, we showed that there is a crosstalk between peptidergic neurons and neutrophils in the pulp, modulating the pain and inflammatory outcomes of the disease.