Pain
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Individuals with chronic pain may experience negative responses from spouse, family, and friends. Responses such as overt criticism and hostility may be associated with worsening pain and function for chronic pain sufferers. We used a laboratory procedure to evaluate whether variability in spouse criticism/hostility exhibited toward chronic low back pain (CLBP) patients during a conflictual discussion predicted variability in patient pain and function during a subsequent pain-induction task. ⋯ Results support the hypothesis that spouse criticism and hostility-actually expressed or perceived-may worsen CLBP patient symptoms. Further, women patients and patients high in depressive symptoms appeared most vulnerable to spouse criticism/hostility. Thus, negative marital communication patterns may be appropriate targets for intervention, especially among these 2 at risk groups.
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Depression and musculoskeletal pain are associated, but long-term follow-up studies are rare. We aimed to examine the relationship of early depressive symptoms with developmental patterns of musculoskeletal pain from adolescence to middle age. Adolescents ending compulsory school (age 16) in Luleå, Northern Sweden, in 1981 (n = 1083) were studied and followed up in 1986, 1995, and 2008 (age 43) for musculoskeletal pain. ⋯ For severe pain, 2 trajectories were found: moderate-increasing (women 19%, men 9%) and low-stable. For each 0.1-point increase in the DSS, the odds ratio of membership in the moderate-increasing trajectory was 1.14 (1.04-1.25) in women and 1.17 (1.04-1.31) in men in the fully adjusted model. Thus, depressive symptoms at baseline are strongly associated with pain trajectory membership.
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Chronic pain conditions are highly comorbid with insufficient sleep. While the mechanistic relationships between the 2 are not understood, chronic insufficient sleep may be 1 pathway through which central pain-modulatory circuits deteriorate, thereby contributing to chronic pain vulnerability over time. To test this hypothesis, an in-laboratory model of 3 weeks of restricted sleep with limited recovery (5 nights of 4-hour sleep per night followed by 2 nights of 8-hour sleep per night) was compared with 3 weeks of 8-hour sleep per night (control protocol). ⋯ These changes may reflect abnormalities in central pain-modulatory processes. Limited recovery sleep did not completely resolve these alterations in pain-modulatory processes, indicating that more extensive recovery sleep is required. Results suggest that exposure to chronic insufficient sleep may increase vulnerability to chronic pain by altering processes of pain habituation and sensitization.
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To develop a simple, valid model to identify patients at high risk of opioid overdose-related hospitalization and mortality, Oregon prescription drug monitoring program, Vital Records, and Hospital Discharge data were linked to estimate 2 logistic models; a first model that included a broad range of risk factors from the literature and a second simplified model. Receiver operating characteristic curves, sensitivity, and specificity of the models were analyzed. Variables retained in the final model were categories such as older than 35 years, number of prescribers, number of pharmacies, and prescriptions for long-acting opioids, benzodiazepines or sedatives, or carisoprodol. ⋯ The positive predictive value of the model was low. Computationally simple models can identify high-risk patients based on prescription history alone, but improvement of the predictive value of models may require information from outside the prescription drug monitoring program. Patient or prescription features that predict opioid overdose may differ from those that predict diversion.
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There is an urgent need for better treatments for chronic pain, which affects more than 1 billion people worldwide. Antisense oligonucleotides (ASOs) have proven successful in treating children with spinal muscular atrophy, a severe infantile neurological disorder, and several ASOs are currently being tested in clinical trials for various neurological disorders. Here, we characterize the pharmacodynamic activity of ASOs in spinal cord and dorsal root ganglia (DRG), key tissues for pain signaling. ⋯ Furthermore, we confirm that ASOs are selective and do not modulate basal pain sensation. We also demonstrate that ASOs targeting the sodium channel Nav1.7 induce sustained analgesia up to 4 weeks. Taken together, our findings support the idea that ASOs possess the required pharmacodynamic properties, along with a long duration of action beneficial for treating pain.