Pain
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Recent studies highlight an interplay between pain perception and emotional responses. This necessitates a thorough investigation into how beliefs and motivational influences respond to visual stimuli of movements. Such an analysis is crucial for understanding the extent to which these factors contribute to disability levels associated with shoulder pain. ⋯ The perception of harm to shoulder movement (β = 0.11; P < 0.001; 95% confidence interval = 5.6-11.8) was significantly associated with the level of shoulder disability, whereas valence did not show a significant association (β = 0.26; P = 0.15; 95% confidence interval = 1.7-10.8). The perception of harm associated with shoulder movements images during daily activities was associated with disability. Individuals who believe that shoulder movements are harmful have greater disability.
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NCT02010281.
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Chronic pain is a serious and prevalent condition that can affect many facets of life. However, uncertainty remains regarding the strength of the association between chronic pain and death and whether the association is causal. We investigate the pain-mortality relationship using data from 19,971 participants aged 51+ years in the 1998 wave of the U. ⋯ This attenuation highlights the role of confounders of the pain-mortality relationship as potentially modifiable upstream risk factors for mortality. Posing the depressive symptoms variable as a mediator rather than a confounder of the pain-mortality relationship resulted in stronger evidence of a modest causal effect of pain on mortality (eg, HR: 1.08, 95% CI: 1.01-1.15). Future work is required to model exposure-confounder feedback loops and investigate the potentially cumulative causal effect of chronic pain at multiple time points on mortality.
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Research has indicated that the default mode network (DMN) is perturbated in patients with chronic pain when compared with healthy controls, and this perturbation is correlated with the duration of pain during the chronic pain stage. It remains unclear whether DMN adaptations manifest during the subacute pain stage and progress over time because of the duration of pain experience, rather than being a specific correlate of the chronic pain stage. Furthermore, information regarding whether these adaptations are related to cognitive processes of adaptation is lacking. ⋯ This was significantly mediated by coping attitudes towards pain. Default mode network perturbation may thus reflect neural adaptation processes to pain experience rather than a single correlate of the chronic pain stage and be modulated by cognitive adaption. This points to potentially underinvestigated significant adaptation processes that could enable more fine-grained patient stratification.
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Osteoarthritis (OA) is a highly prevalent and disabling joint disease, characterized by pathological progressive joint deformation and clinical symptoms of pain. Disease-modifying treatments remain unavailable, and pain-mitigation is often suboptimal, but recent studies suggest beneficial effects by inhibition of the voltage-gated sodium channel Na V 1.7. We previously identified compound 194 as an indirect inhibitor of Na V 1.7 by preventing SUMOylation of the Na V 1.7-trafficking protein, collapsin response mediator protein 2. ⋯ We found that the monoiodoacetate model induced (1) increased pain-like behaviors and calcium responses of glutamatergic neurons in the parabrachial nucleus after evoked cold and mechanical stimuli, (2) conditioned place aversion to mechanical stimulation, (3) functional weight bearing asymmetry, (4) increased sodium currents in dorsal root ganglia neurons, and (5) increased calcitonin gene-related peptide-release in the spinal cord. Crucially, administration of 194 improved all these pain-related outcomes. Collectively, these findings support indirect inhibition of Na V 1.7 as an effective treatment of OA-related pain through the inhibition of collapsin response mediator protein 2-SUMOylation via compound 194.