Pain
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Most theories of pain emphasize cognitive factors in the development of chronicity, but they have rarely been studied in the context of the transition from acute to chronic pain. The aim of the present study was to assess the role of interpretation bias, pain anxiety, and pain avoidance in acute and chronic pain and the transition from acute to chronic pain. Study 1 recruited a sample of N = 85 adults with chronic pain. ⋯ Pain anxiety was also associated with pain avoidance, but pain avoidance did not predict pain outcomes. This research provides further insight into the transition from acute to chronic pain, suggesting that interpretation bias in acute pain may play a role in pain-related anxiety that drives pain interference, thus maintaining chronic pain. These findings hold promise for further research into potential large-scale preventative interventions targeting interpretation bias and pain anxiety in acute 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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Postoperative pain is a major clinical problem imposing a significant burden on patients and society. In a survey 2 years after orthopedic surgery, 57% of patients reported persisting postoperative pain. However, only limited progress has been made in the development of safe and effective therapies to prevent the onset and chronification of pain after orthopedic surgery. ⋯ Percutaneous vagus nerve stimulation also improved locomotor coordination and accelerated bone healing. In the dorsal root ganglia, vagal stimulation inhibited the activation of glial fibrillary acidic protein-positive satellite cells but without affecting microglial activation. Overall, these data provide novel evidence supportive of the use of pVNS to prevent postoperative pain and inform translational studies to test antinociceptive effects of bioelectronic medicine in the clinic.
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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.