Articles: chronic.
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Chronic postsurgical pain (CPSP) is a well-recognized potential complication with negative personal, social, and health care consequences. However, limited data exist on CPSP and on the course of pain over time after hysterectomy. Using data from a prospective cohort study on a consecutive sample assessed at 4 time points, presurgery (T1), 48 hours (T2), 4 months (T3), and 5 years postsurgery (T4), we sought to examine women's PSP trajectories using assessments of pain at T3 and T4. ⋯ Membership in PT2 and PT3 was predicted by presurgical anxiety (odds ratio [OR] = 1.131, P = 0.015; OR = 1.175, P = 0.009, respectively), emotional representation of the surgical disease (OR = 1.155, P = 0.034; OR = 1.213, P = 0.020, respectively), and pain catastrophizing (OR = 1.079, P = 0.043; OR = 1.143, P = 0.001, respectively). Furthermore, acute PSP intensity and frequency determined membership of women in PT3 (OR = 1.211, P = 0.033; OR = 3.000, P = 0.029, respectively), and postsurgical anxiety (OR = 1.182, P = 0.026) also played a key predictive role. This study identified factors that can be easily screened before and after surgery and are amenable to change through carefully designed timely and tailored interventions for women at risk of an unfavorable PSP trajectory posthysterectomy.
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Neglect-like symptoms (NLS) are frequently observed in complex regional pain syndrome (CRPS). The clinical meaning of NLS, however, is largely unknown. Therefore, this study sets out to assess the importance of NLS for patient outcome and to explore their clinical correlates. ⋯ Furthermore, high NLS scores had a negative impact on pain outcome after 6 months. Our results indicate that NLS have a different meaning in acute and chronic CRPS and might be of prognostic value. Possibly, treatment should focus on reducing NLS.
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Numerous preclinical studies support the role of spinal neuroimmune activation in the pathogenesis of chronic pain, and targeting glia (eg, microglia/astrocyte)- or macrophage-mediated neuroinflammatory responses effectively prevents or reverses the establishment of persistent nocifensive behaviors in laboratory animals. However, thus far, the translation of those findings into novel treatments for clinical use has been hindered by the scarcity of data supporting the role of neuroinflammation in human pain. ⋯ Furthermore, the neuroforaminal translocator protein signal was associated with responses to fluoroscopy-guided epidural steroid injections, supporting its role as an imaging marker of neuroinflammation, and highlighting the clinical significance of these observations. These results implicate immunoactivation at multiple levels of the nervous system as a potentially important and clinically relevant mechanism in human radicular pain, and suggest that therapies targeting immune cell activation may be beneficial for chronic pain patients.
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Resting-state functional connectivity (FC) has proven a powerful approach to understand the neural underpinnings of chronic pain, reporting altered connectivity in 3 main networks: the default mode network (DMN), central executive network, and the salience network (SN). The interrelation and possible mechanisms of these changes are less well understood in chronic pain. Based on emerging evidence of its role to drive switches between network states, the right anterior insula (rAI, an SN hub) may play a dominant role in network connectivity changes underpinning chronic pain. ⋯ Granger causality analysis revealed increased negative influence of the rAI on the posterior cingulate (DMN) in patients with OA in line with the observed enhanced anticorrelation. Moreover, dynamic FC was lower in the DMN of patients and thus more similar to temporal dynamics of the SN. Together, these findings evidence a widespread network disruption in patients with persistent OA pain and point toward a driving role of the rAI.
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Elevated N-methyl-D-aspartate receptor (NMDAR) activity is linked to central sensitization and chronic pain. However, NMDAR antagonists display limited therapeutic potential because of their adverse side effects. Novel approaches targeting the NR2B-PSD95-nNOS complex to disrupt signaling pathways downstream of NMDARs show efficacy in preclinical pain models. ⋯ Finally, TAT-GESV (i.t.) did not induce NMDAR-mediated motor ataxia in the rotarod test and did not alter basal nociceptive thresholds in the radiant heat tail-flick test. These observations support the hypothesis that antiallodynic efficacy of an nNOS-NOS1AP disruptor may result, at least in part, from blockade of p38 MAPK-mediated downstream effects. Our studies demonstrate, for the first time, that disrupting nNOS-NOS1AP protein-protein interactions attenuates mechanistically distinct forms of neuropathic pain without unwanted motor ataxic effects of NMDAR antagonists.