Pain
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The purpose of this systematic review was to summarize and critically appraise research developing or validating instruments to assess patient-reported safety, efficacy, and/or misuse in ongoing opioid therapy for chronic pain. Our search included the following datasets: OvidSP MEDLINE (1946-August 2012), OvidSP PsycINFO (1967-August 2012), Elsevier Scopus (1947-August 2012), OvidSP HaPI (1985-August 2012), and EBSCO CINAHL (1981-August 2012). Eligible studies were published in English and pertained to adult, nonsurgical/interventional populations. ⋯ The studies employed a wide variety of psychometric tests, with most demonstrating statistical significance, but several potential sources of bias and generalizability limitations were identified. Lack of testing in clinical practice limited assessment of feasibility. The dearth of safety and efficacy items and lack of testing in clinical practice demonstrates areas for further research.
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Bradykinin (BK) is an inflammatory mediator that can evoke oedema and vasodilatation, and is a potent algogen signalling via the B1 and B2 G-protein coupled receptors. In naïve skin, BK is effective via constitutively expressed B2 receptors (B2R), while B1 receptors (B1R) are purported to be upregulated by inflammation. The aim of this investigation was to optimise BK delivery to investigate the algesic effects of BK and how these are modulated by inflammation. ⋯ We have optimised a versatile experimental model by which BK and its analogues can be administered to human skin. We have found that there is an early phase of BK-induced pain which partly depends on the release of inflammatory mediators by MCs; however, subsequent hyperalgesia is not dependent on MC degranulation. In naïve skin, B2R signaling predominates, however, cutaneous inflammation results in enhanced B1R responses.
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The aim of the current study was to determine the course of back pain in older patients and identify prognostic factors for non-recovery at 3 months' follow-up. We conducted a prospective cohort study (the BACE study) of patients aged >55 years visiting a general practitioner (GP) with a new episode of back pain in the Netherlands. The course of back pain was described in terms of self-perceived recovery, pain severity, disability, pain medication, and GP visits at 6 weeks' and 3 months' follow-up. ⋯ At 3 months' follow-up 61% still reported non-recovery, but only 26% of these patients had revisited the GP. Longer duration of the back pain, severity of back pain, history of back pain, absence of radiating pain in the leg below the knee, number of comorbidities, patients' expectation of non-recovery, and a longer duration of the timed 'Up and Go' test were significantly associated with non-recovery in a multiple regression model (AUC 0.79). This information can help GPs identify older back pain patients at risk for non-recovery.
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Altered gray matter volume in the frontal pain modulation network in patients with cluster headache.
Previous functional imaging studies in episodic cluster headache (CH) patients revealed altered brain metabolism concentrated on the central descending pain control system. However, it remains unclear whether changes in brain metabolism during the "in bout" period are due to structural changes and whether these structural changes vary between the "in bout" and "out of bout" periods. To quantify brain structural changes in CH patients, the regional gray matter volume (GMV) was compared among 49 episodic CH patients during the "in bout" period and 49 age- and sex-matched controls. ⋯ Compared to "out of bout" scans, the "in bout" scans revealed significant GMV increases in the left anterior cingulate, insula, and fusiform gyrus. Additionally, compared to healthy controls, the "out of bout" scans revealed a trend of GMV reduction in the left middle frontal gyrus. These affected regions primarily belong to frontal pain modulation areas, and thus these GMV changes may reflect insufficient pain-modulating capacity in the frontal areas of CH patients.