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      Development and preliminary evaluation of a short self-report measure of generalized pain hypersensitivity

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          Generalized pain hypersensitivity is frequently observed in chronic pain conditions. Currently, identification is based on expert clinical opinion, and in very few cases combined with quantitative sensory testing. The objectives of this study were to develop and evaluate a short self-report measure of generalized pain hypersensitivity: a generalized pain questionnaire (GPQ).


          Items for the GPQ were developed based on a literature review, followed by an interview study with ten rheumatic patients with suspected pain hypersensitivity. We examined the psychometric properties of the preliminary items in a sample of 212 outpatients suffering from either fibromyalgia (FM; n=98) or rheumatoid arthritis (n=114). Additionally, self-reported data were gathered on sociodemographics, fibromyalgia-survey criteria, health status, and neuropathic-like pain features.


          Mokken-scale analyses demonstrated a unidimensional seven-item scale with strong homogeneity ( H=0.65) and high reliability ( r=0.90). Correlations between total GPQ scores and relevant external measures, such as the FM-survey criteria and neuropathic-like pain features, were consistent with a priori expectations, supporting its external construct validity. Furthermore, the GPQ had good accuracy in distinguishing between patients with FM (generally assumed to be the result of central nervous system hypersensitization) and patients with RA (assumed to result mostly in local nociceptive or inflammatory pain), with an area under the receiver-operating characteristic curve of 0.89. A cutoff value >10 had the highest combination of sensitivity (82.7%) and specificity (77.2%).


          The GPQ is psychometrically sound and appears promising for measuring the presence and severity of generalized pain hypersensitivity in chronic pain patients.

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          Most cited references 42

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          Index for rating diagnostic tests.

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            Neuronal plasticity: increasing the gain in pain.

            We describe those sensations that are unpleasant, intense, or distressing as painful. Pain is not homogeneous, however, and comprises three categories: physiological, inflammatory, and neuropathic pain. Multiple mechanisms contribute, each of which is subject to or an expression of neural plasticity-the capacity of neurons to change their function, chemical profile, or structure. Here, we develop a conceptual framework for the contribution of plasticity in primary sensory and dorsal horn neurons to the pathogenesis of pain, identifying distinct forms of plasticity, which we term activation, modulation, and modification, that by increasing gain, elicit pain hypersensitivity.
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                Author and article information

                J Pain Res
                J Pain Res
                Journal of Pain Research
                Journal of Pain Research
                Dove Medical Press
                17 January 2019
                : 12
                : 395-404
                [1 ]Department of Rheumatology, Medisch Spectrum Twente, Enschede, Netherlands
                [2 ]Department of Psychology, Health, and Technology, University of Twente, Enschede, Netherlands, P.M.tenKlooster@ 123456utwente.nl
                Author notes
                Correspondence: Peter M ten Klooster, Department of Psychology, Health, and Technology, University of Twente, PO Box 217, Enschede 7500 AE, Netherlands, Tel +31 53 489 6056, Email P.M.tenKlooster@ 123456utwente.nl
                © 2019 van Bemmel et al. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

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