Articles: chronic-pain.
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Controlled Clinical Trial
Suppression of Emotion Expression Mediates the Effects of Negative Affect on Pain Catastrophizing: A Cross-Sectional Analysis.
Negative affect is associated with individual differences in pain catastrophizing (PC). Research suggests that variations in emotion regulation may modify negative affect on PC. Using the process model of emotion regulation, this study examined the relationships of 2 emotion regulatory strategies, cognitive reappraisal and expressive suppression, with negative affect and PC. ⋯ These preliminary findings suggest that expressive suppression of emotion plays a mediating role in PC and subsequent pain adjustment outcomes. More research is needed to further examine other types of negative emotions and different emotion regulatory strategies used in chronic pain adjustment.
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Comparative Study
Hypogonadism in Men With Chronic Pain Linked to the Use of Long-acting Rather Than Short-acting Opioids.
There is a need to elucidate the variables associated with testosterone suppression among men on daily opioid therapy for chronic pain. ⋯ Among a contemporary sample of men receiving chronic daily opioids, we found a high prevalence of hypogonadism associated with duration of action, but not with total daily dose of the opioid.
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The management of chronic noncancer pain (CNCP) involves trade-offs between immediate and delayed consequences of various treatments. Temporal trade-offs may be particularly salient for older adults because of age-related differences in prognosis and perceptions of future time. This study examined how perceptions of time influence the management of CNCP among patients and providers with particular emphasis on age differences. ⋯ Time horizons have practical implications for the quality of the patient-provider relationship and self-management of CNCP. A better understanding of the underlying mechanisms could inform interventions to reduce age disparities in pain care.
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Few studies have described patterns and determinants of health services utilization (HSU) in chronic pain (CP) subjects. We aimed to describe these, in particular, regarding medical consultations (MCs), diagnostic tests (DTs), pain medicines (PMs) and nonpharmacologic treatment methods (NTM) utilization. ⋯ The main drivers behind HSU are pain severity, psychological distress, and socio-economic determinants. An important set of benchmarks are presented regarding HSU in CP subjects, comprising useful tools for public health policy and decision-making. Results presented may suggest possible inequalities in the access to NTM, and interventions to improve access are encouraged. Moreover, possible indirect evidence of imaging DT overuse is presented, and it is recommended that their use in CP subjects should more closely follow existing guidelines.
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Pain catastrophizing regularly occurs in chronic pain patients. It has been suggested that pain catastrophizing is a stable, person-based construct. These findings highlight the importance of investigating catastrophizing in conceptualizing specific approaches for pain management. One important area of investigation is the mechanism underlying pain catastrophizing. Therefore, this study explored the relationship between a neurophysiological marker of cortical excitability, as assessed by transcranial magnetic stimulation, and catastrophizing, as assessed by the Brazilian Portuguese Pain Catastrophizing Scale, in patients with chronic myofascial pain syndrome. The Pain Catastrophizing Scale is a robust questionnaire used to examine rumination, magnification and helplessness that are associated with the experience of pain. We include 24 women with myofascial pain syndrome. The Brazilian Portuguese Pain Catastrophizing Scale and cortical excitability were assessed. Functional and behavioral aspects of pain were evaluated with a version of the Profile of Chronic Pain scale and by multiple pain measurements (eg, pain intensity, pressure pain threshold, and other quantitative sensory measurements). Intracortical facilitation was found to be significantly associated with pain catastrophizing (β = .63, P = .001). Our results did not suggest that these findings were influenced by other factors, such as age or medication use. Furthermore, short intracortical inhibition showed a significant association with pressure pain threshold (β = .44, P = .04). This study elaborates on previous findings indicating a relationship between cortical excitability and catastrophizing. The present findings suggest that glutamatergic activity may be associated with mechanisms underlying pain catastrophizing; thus, the results highlight the need to further investigate the neurophysiological mechanisms associated with pain and catastrophizing. ⋯ This study highlights the relationship between cortical excitability and catastrophizing. Cortical measures may illuminate how catastrophizing responses may be related to neurophysiological mechanisms associated with chronic pain.