European journal of pain : EJP
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Review Meta Analysis
A Meta-analysis of the Associations of Elements of the Fear-Avoidance Model of Chronic Pain with Negative Affect, Depression, Anxiety, Pain-related Disability and Pain Intensity.
Biopsychosocial conceptualizations of clinical pain conditions recognize the multi-faceted nature of pain experience and its intersection with mental health. A primary cognitive-behavioural framework is the Fear-Avoidance Model, which posits that pain catastrophizing and fear of pain (including avoidance, cognitions and physiological reactivity) are key antecedents to, and drivers of, pain intensity and disability, in addition to pain-related psychological distress. This study aimed to provide a comprehensive analysis of the magnitude of the cross-sectional association between the primary components of the Fear-Avoidance Model (pain catastrophizing, fear of pain, pain vigilance) with negative affect, anxiety, depression, pain intensity and disabilities in studies of clinical pain. ⋯ This meta-analysis reveals that, among individuals with various pain conditions, pain catastrophizing, fear of pain, and pain vigilance have medium to large associations with pain- related negative affect, anxiety, and depression, pain intensity and disability. Differences in the strength of the associations depend on the type of self-report tool used to assess fear of pain.
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Randomized Controlled Trial
Neuropathic-like pain symptoms in inflammatory hand osteoarthritis lower quality of life and may not decrease under prednisolone treatment.
Pain is common in hand osteoarthritis (OA) and multiple types may occur. We investigated the prevalence, associated patient characteristics, influence on health-related quality of life (HR-QoL) and response to anti-inflammatory treatment of neuropathic-like pain in inflammatory hand OA. ⋯ Pain is the dominant symptom in hand OA, with an unclear aetiology. In this study, we found that neuropathic-like pain may play a role in hand OA, that it showed associations with female sex, younger age and more comorbidities and that it lowered health-related quality of life in hand OA. Neuropathic-like pain in hand OA seems resistant to prednisolone therapy but did not seem to interfere with the treatment of inflammatory pain with prednisolone.
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Identifying predictors of poor postoperative outcomes is crucial for planning personalized pain treatments. The aim of this study was to examine pain outcomes using cluster analysis in N = 2678 patients from the PAIN-OUT registry at first postoperative day. ⋯ Improvement of postoperative pain requires assessment methods that go beyond pain intensity scores. We perform a cluster analysis among PAIN-OUT patients that revealed a cluster of vulnerable postoperative patients, using a novel composite measure of postoperative outcomes: the factor scores of the International Pain Outcomes Questionnaire. By changing the focus from pain intensity to multidimensional pain outcomes, male gender and number of comorbidities appeared as new risk factors for worse postoperative outcomes. The study also identified procedures that require urgent quality improvements.
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We previously established a macaque model of central post-stroke pain (CPSP) and confirmed the involvement of increased activity of the posterior insular cortex (PIC) and secondary somatosensory cortex (SII) to somatosensory stimuli in mechanical allodynia by a combination of imaging techniques with local pharmacological inactivation. However, it is unclear whether the same intervention would be effective for thermal hyperalgesia. Therefore, using the macaque model, we examined behavioural responses to thermal stimuli following pharmacological inactivation of the PIC/SII. ⋯ CPSP is caused by stroke lesions in the sensory system and characterized by mechanical allodynia or thermal hyperalgesia. Inactivation of the PIC/SII has an analgesic effect on mechanical allodynia; however, it is not clear whether the same intervention could reduce thermal hyperalgesia. Here, using the macaque model, we demonstrated that inactivation of these cortices reduces hypersensitivity to thermal stimuli. This result emphasizes that increased PIC/SII activity can contribute to abnormal pain of multiple modalities.