Pain
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Child and parent pain catastrophizing are reported preoperative risk factors for children's acute and persistent postsurgical pain. This study examined dyadic relations between child and parent pain catastrophizing and child and parent ratings of child pain prior to (M = 4.01 days; "baseline") and following surgery (M = 6.5 weeks; "acute follow-up"), as well changes in pain catastrophizing during this time in 167 youth (86% female; Mage = 14.55 years) undergoing spinal fusion surgery and 1 parent (89% mothers). Actor-partner interdependence models assessed cross-sectional and longitudinal intra- and interpersonal effects. ⋯ Baseline child and parent pain catastrophizing did not predict child pain at acute follow-up. In conclusion, child, not parent, pain catastrophizing was associated with children's pre- and postsurgical pain, and showed significantly less stability over time. There is a need to better understand contributors to the stability or changeability of pain catastrophizing, the prospective relation of catastrophizing to pain, and contexts in which child vs parent pain catastrophizing is most influential for pediatric postsurgical pain.
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Multicenter Study
Brain signature and functional impact of centralized pain: a Multidisciplinary Approach to the Study of Chronic Pelvic Pain (MAPP) Network Study.
Chronic pain is often measured with a severity score that overlooks its spatial distribution across the body. This widespread pain is believed to be a marker of centralization, a central nervous system process that decouples pain perception from nociceptive input. Here, we investigated whether centralization is manifested at the level of the brain using data from 1079 participants in the Multidisciplinary Approach to the Study of Chronic Pelvic Pain Research Network (MAPP) study. ⋯ Widespread pain was also associated with reduced physical and mental function independent of pain severity. Brain pathology in patients with centralized pain is related to pain distribution throughout the body. These patients may benefit from interventions targeting the central nervous system.
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Fibromyalgia syndrome (FMS) is a central sensitization syndrome; however, peripheral pain sources potentially exacerbate its symptoms of chronic diffuse musculoskeletal pain and hyperalgesia. This prospective study evaluated visceral pain as a possible triggering factor for FMS pain and hyperalgesia in comorbid patients. Women with (1) FMS + irritable bowel syndrome (IBS); (2) FMS + primary dysmenorrhea (Dys); (3) FMS + Dys secondary to endometriosis (Endo); (4) FMS + colon diverticulosis (Div) were compared with FMS-only women, for fibromyalgia pain (number and intensity of episodes and analgesic consumption) over comparable periods and for somatic hyperalgesia (electrical and pressure pain thresholds) in painful (tender points) and control areas (trapezius, deltoid, quadriceps muscles, and overlying subcutis and skin). ⋯ Fibromyalgia syndrome pain and hyperalgesia in all tissues and all sites significantly decreased in patients after visceral comorbidity treatment (dietary for 6 months [IBS], hormonal for 6 months [dysmenorrhea], laser [endometriosis], and surgery [diverticulosis]) (0.05 < P < 0.0001) vs no change in untreated patients. Visceral pain enhances FMS symptoms, probably augmenting the level of central sensitization typical of the syndrome. Systematic assessment and treatment of visceral pain comorbidities should be a part of FMS management strategy.
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Pain-related social support has been shown to be directly associated with pain-related disability, depending on whether it promotes functional autonomy or dependence. However, previous studies mostly relied on cross-sectional methods, precluding conclusions on the temporal relationship between pain-related social support and disability. Also, research on the behavioral and psychological processes that account for such a relationship is scarce. ⋯ Moderated mediation analyses showed that formal social support for functional dependence (T1) predicted an increase in pain-related disability (T3), that was mediated by self-reported physical functioning (T2) and by pain-related self-efficacy (T2) at short to moderate pain duration and at low to moderate pain intensity, but not at higher levels. Findings emphasized that social support for functional dependence is a risk factor for pain-related disability and uncovered the "why" and "when" of this relationship. Implications for the design of social support interventions aiming at promoting older adults' healthy aging despite chronic pain are drawn.