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Child catastrophizing about parent chronic pain: A potential child vulnerability factor.

Objective Robust evidence suggests children's catastrophizing about their own pain is a risk factor for poor child pain-related outcomes. In children of parents with chronic pain, child catastrophizing about their parents' pain might be a unique predictor of child pain-related outcomes given their increased exposure to parental chronic pain and disability. The objective of this study was to examine associations between child and parent catastrophizing about their own and each other's pain and child and parent pain-related outcomes. Methods Seventy-two parents with chronic pain and their children (ages 8-15) completed questionnaires assessing their trait catastrophizing about their own and each other's pain, their own pain, and the child's internalizing symptoms. Children completed the cold pressor task (CPT) in the presence of their parent. Parents and children rated children's worst pain intensity and their own anxiety during the task. Analyses were guided by the Actor-Partner Interdependence Model. Results Greater child catastrophizing about parent pain was associated with children's and parents' increased catastrophizing about their own pain. Child catastrophizing about parent pain was associated with greater child- and parent-reported child internalizing symptoms and greater CPT pain intensity for the child, but not parent/child usual pain or CPT anxiety, over and above the influence of parent and child catastrophizing about their own pain. Conclusions Child catastrophizing about parent pain is a potential vulnerability factor associated with poor pain-related outcomes in children of parents with chronic pain that should be considered in future research and clinical settings. Statement of contribution What is already known on this subject? Higher rates of pain and internalizing symptoms are observed in offspring of parents with vs. without chronic pain. Greater child and parent pain catastrophizing are associated with poorer pain-related outcomes in children. Child catastrophizing about parent chronic pain and its association with child outcomes has not been examined. What does this study add? Greater child catastrophizing about parent chronic pain is associated with greater child internalizing and CPT pain. These effects were seen beyond the association of child and parent catastrophizing about their own pain.

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Pentraxin 3 (PTX3): A Molecular Marker of Endothelial Dysfunction in Chronic Migraine.

Even though endothelial dysfunction is known to play a role in migraine pathophysiology, studies regarding levels of endothelial biomarkers in migraine have controversial results. Our aim was to evaluate the role of pentraxin 3 (PTX3) and soluble tumour necrosis factor-like weak inducer of apoptosis (sTWEAK) as potential biomarkers of endothelial dysfunction in chronic migraine (CM). We performed a case-control study including 102 CM patients and 28 control subjects and measured serum levels of markers of endothelial dysfunction (PTX3 and sTWEAK) and inflammation [high-sensitivity C-reactive protein (hs-CRP)] as well as brachial artery flow-mediated dilation (FMD) during interictal periods. Interictal serum levels of PTX3 and sTWEAK were higher in CM patients than in controls (1350.6 ± 54.8 versus 476.1 ± 49.4 pg/mL, < 0.001 and 255.7 ± 21.1 versus 26.4 ± 2.6 pg/mL, < 0.0001; respectively). FMD was diminished in CM patients compared to controls (9.6 ± 0.6 versus 15.2 ± 0.9%, < 0.001). Both PTX3 and sTWEAK were negatively correlated with FMD (r = -0.508, < 0.001 and r = -0.188, = 0.033; respectively). After adjustment of confounders, PTX3 remained significantly correlated to FMD (r = -0.250, = 0.013). Diagnosis of CM was 68.4 times more likely in an individual with levels of PTX3 ≥ 832.5 pg/mL, suggesting that PTX3 could be a novel biomarker of endothelial dysfunction in CM.

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Placebo hypoalgesia: racial differences.

No large-cohort studies that examine racial effects on placebo hypoalgesic effects exist. To fill this void, we studied placebo effects in healthy and chronic pain participants self-identified as either African-American/Black (AA/Black) or White. We enrolled 372 study participants, 186 with a diagnosis of temporomandibular disorder (TMD) and 186 race, sex, and age matched healthy participants to participate in a placebo experiment. Using a well-established paradigm of classical conditioning with verbal suggestions, each individual pain sensitivity was measured to calibrate the temperatures for high- and low-pain stimuli in the conditioning protocol. These two temperatures were then paired with a red and green screen, respectively, and participants were told that the analgesic intervention would activate during the green screens to reduce pain. Participants then rated the painfulness of each stimulus on a Visual Analog Scale ranging from 0-100. Racial influences were tested on conditioning strength, reinforced expectations and placebo hypoalgesia. We found that White participants reported greater conditioning effects, reinforced relief expectations, and placebo effects when compared to their AA/Black counterparts. Racial effects on placebo were observed in TMD although negligible, short-lasting, and mediated by conditioning strength. Secondary analyses on the effect of experimenter-participant race and sex concordance indicated that same experimenter-participant race induced greater placebo hypoalgesia in TMDs while different sex induced greater placebo hypoalgesia in healthy participants. This is the largest study to analyze racial effects on placebo hypoalgesia and has implications for both clinical research and treatment outcomes.

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Psychometric Validation of the Danish Version of the Oswestry Disability Index in Patients with Chronic Low Back Pain.

Registry based repeated-measures psychometric validation of the Danish Oswestry Disability Index (ODI) OBJECTIVE.: The goal was to use classical and modern psychometric validation methods to assess the measurement properties and the minimally clinical important difference (MCID) of the ODI in a Danish cohort of patients with chronic low back pain (LBP) being treated with spinal surgery.

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Xist attenuates acute inflammatory response by female cells.

Biological sex influences inflammatory response, as there is a greater incidence of acute inflammation in men and chronic inflammation in women. Here, we report that acute inflammation is attenuated by X-inactive specific transcript (Xist), a female cell-specific nuclear long noncoding RNA crucial for X-chromosome inactivation. Lipopolysaccharide-mediated acute inflammation increased Xist levels in the cytoplasm of female mouse J774A.1 macrophages and human AML193 monocytes. In both cell types, cytoplasmic Xist colocalizes with the p65 subunit of NF-κB. This interaction was associated with reduced NF-κB nuclear migration, suggesting a novel mechanism to suppress acute inflammation. Further supporting this hypothesis, expression of 5' XIST in male cells significantly reduced IL-6 and NF-κB activity. Adoptive transfer of male splenocytes expressing Xist reduced acute paw swelling in male mice indicating that Xist can have a protective anti-inflammatory effect. These findings show that XIST has functions beyond X chromosome inactivation and suggest that XIST can contribute to sex-specific differences underlying inflammatory response by attenuating acute inflammation in women.

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Characterisation of the effects of pulsed radio frequency treatment of the dorsal root ganglion on cerebrospinal fluid cellular and peptide constituents in patients with chronic radicular pain: A randomised, triple-blinded, controlled trial.

Chronic radicular neuropathic pain is a major clinical problem with a life time prevalence of more than 50%. Pulsed radiofrequency (PRF) treatment is a recognised therapy. However, the pathophysiology of chronic neuropathic pain (CNP) and the mechanism of action of PRF remains ill-defined. Improving our knowledge of the mechanisms of CNP and PRF action will enhance our ability to treat patients with this common debilitating problem more effectively. This study aims to characterise the CSF cellular and peptide constituents in patients with CNP and the effect of pulsed radiofrequency (PRF) on these constituents and reported pain.

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Self-reported traumatic etiology of pain and psychological function in tertiary care pain clinic patients: a collaborative health outcomes information registry (CHOIR) study.

Background and aims A sizable body of research has elucidated the significant role of psychological reactions to trauma on pain coping and outcomes. In order to best inform intervention development and clinical care for patients with both trauma and pain at the tertiary care level, greater clarity is needed regarding the magnitude of these effects and the specific pathways through which they may or may not function at the time of first presentation to such a treatment setting. To achieve this, the current study examined the cross-sectional relationships between traumatic etiology of pain, psychological distress (anger, depressive symptoms, and PTSD symptoms), and pain outcomes (pain catastrophizing, physical function, disability status). Methods Using a structural path modeling approach, analyses were conducted using a large sample of individuals with chronic pain (n = 637) seeking new medical evaluation at a tertiary pain management center, using the Collaborative Health Outcomes Information Registry (CHOIR). We hypothesized that the relationships between traumatic etiology of pain and poorer pain outcomes would be mediated by higher levels of psychological distress. Results Our analyses revealed modest relationships between self-reported traumatic etiology of pain and pain catastrophizing, physical function, and disability status. In comparison, there were stronger relationships between indices of psychological distress and pain catastrophizing, but a weaker pattern of associations between psychological distress and physical function and disability measures. Conclusions To the relatively small extent that self-reported traumatic etiology of pain correlates with pain-related outcomes, these relationships appear to be due primarily to the presence of psychiatric symptoms and manifest most notably in the context of psychological responses to pain (i.e. catastrophizing about pain). Implications Findings from this study highlight the need for early intervention for patients with traumatic onset of pain and for clinicians at tertiary pain centers to include more detailed assessments of psychological distress and trauma as a component of comprehensive chronic pain treatment.

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Appropriate referral and selection of patients with chronic pain for Spinal Cord Stimulation: European consensus recommendations and e-health tool.

Spinal cord stimulation (SCS) is an established treatment for chronic neuropathic, neuropathic-like and ischaemic pain. However, the heterogeneity of patients in daily clinical practice makes it often challenging to determine which patients are eligible for this treatment, resulting in undesirable practice variations. This study aimed to establish patient-specific recommendations for referral and selection of SCS in chronic pain.

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Necessary components of psychological treatment in pain management programs: A Delphi study.

There are various approaches to the psychological management of chronic pain and it is difficult to know which components of psychological therapies are necessary or desirable for the effective management of chronic pain.

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Co-prescribing of Opioids with Benzodiazepines and Other Hypnotics for Chronic Pain and Insomnia: Trends and Health Outcomes.

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