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      Genetic and psychological factors interact to predict physical impairment phenotypes following exercise-induced shoulder injury

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          We investigated interactions between genetic and psychological factors in predicting shoulder impairment phenotypes. We hypothesized that pro-inflammatory genes would display stronger relationships compared with pain-related genes when combined with psychological factors for predicting phenotypic changes.

          Subjects and methods

          Altogether, 190 participants completed a 5-day experimental protocol. An experimental shoulder injury model was used to induce physical impairment, and a priori selected genetic (pain-related, pro-inflammatory) and psychological (anxiety, depressive symptoms, pain catastrophizing, fear of pain, kinesiophobia) factors were included as predictors of interest. Impairment phenotypes were injury-induced deficits in range of motion (ROM) and strength. After controlling for age, sex, and race, genetic and psychological predictors were entered separately as main effects and interaction terms in regression models for each phenotype.


          Strong statistical evidence was provided for interactions between: 1) IL-1β (rs1143634) and fear of pain for predicting loss of shoulder flexion and abduction, 2) IL-1β (rs1143634) and anxiety for predicting loss of flexion, and 3) IL-1β (rs1143634) and depressive symptoms for predicting loss of internal rotation. In addition, the interaction between OPRM1 (rs1799971) and fear of pain as well as COMT (rs4818) and pain catastrophizing provided strong statistical evidence for predicting strength loss.


          Pro-inflammatory gene variants contributed more to physical impairment with two single nucleotide polymorphisms (SNPs; IL-1β [rs1143634] and TNF/LTA [rs2229094]) interacting with psychological factors to predict six shoulder impairment phenotypes. In comparison, two pain-related gene SNPs (OPRM1 [rs1799971] and COMT [rs4818]) interacted with psychological factors to predict four shoulder impairment phenotypes (abduction: 5-day average loss; strength loss: 5-day average, peak, and relative loss).

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          Most cited references 34

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          Recent findings on how proinflammatory cytokines cause pain: peripheral mechanisms in inflammatory and neuropathic hyperalgesia.

          Numerous experimental studies provide evidence that proinflammatory cytokines induce or facilitate inflammatory as well as neuropathic pain and hyperalgesia. Direct receptor-mediated actions of cytokines on afferent nerve fibers have been reported as well as cytokine effects involving further mediators. The final outcome of cytokine action greatly depends on whether they act in the central of in the peripheral nervous system. Here we summarize recent findings on the peripheral mechanisms of action of three prototypic proinflammatory cytokines, interleukin-1beta, interleukin-6 and tumor necrosis factor-alpha, with regards to pain and hyperalgesia.
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            Psychometric properties of the TSK-11: a shortened version of the Tampa Scale for Kinesiophobia.

            The Tampa Scale for Kinesiophobia (TSK) is one of the most frequently employed measures for assessing pain-related fear in back pain patients. Despite its widespread use, there is relatively little data to support the psychometric properties of the English version of this scale. This study investigated the psychometric properties of the English version of the TSK in a sample of chronic low back pain patients. Item analysis revealed that four items possessed low item total correlations (4, 8, 12, 16) and four items had response trends that deviated from a pattern of normal distribution (4, 9, 12, 14). Consequently, we tested the psychometric properties of a shorter version of the TSK (TSK-11), having excluded the six psychometrically poor items. The psychometric properties of this measure were compared to those of the original TSK. Both measures demonstrated good internal consistency (TSK: alpha=0.76; TSK-11: alpha=0.79), test-retest reliability (TSK: ICC=0.82, SEM=3.16; TSK-11: ICC=0.81, SEM=2.54), responsiveness (TSK: SRM=-1.19; TSK-11: SRM=-1.11), concurrent validity and predictive validity. In respect of specific cut-off scores, a reduction of at least four points on both measures maximised the likelihood of correctly identifying an important reduction in fear of movement. Overall, the TSK-11 possessed similar psychometric properties to the original TSK and offered the advantage of brevity. Further research is warranted to investigate the utility of the new instrument and the cut-off scores in a wider group of chronic pain patients in different clinical settings.
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              Development of the Fear of Pain Questionnaire--III.

              Fear and/or anxiety about pain is a useful construct, in both theoretical and clinical terms. This article describes the development and refinement of the Fear of Pain Questionnaire (FPQ), which exists in its most current form as the FPQ-III. Factor analytic refinement resulted in a 30-item FPQ-III which consists of Severe Pain, Minor Pain, and Medical Pain subscales. Internal consistency and test-retest reliability of the FPQ-III were found to be good. Four studies are presented, including normative data for samples of inpatient chronic pain patients, general medical outpatients, and unselected undergraduates. High fear of pain individuals had greater avoidance/escape from a pain-relevant Behavioral Avoidance Test with Video, relative to their low fear counterparts, suggesting predictive validity. Chronic pain patients reported the greatest fear of severe pain. Directions for future research with the FPQ-III are discussed, along with general comments about the relation of fear and anxiety to pain.

                Author and article information

                J Pain Res
                J Pain Res
                Journal of Pain Research
                Journal of Pain Research
                Dove Medical Press
                23 October 2018
                : 11
                : 2497-2508
                [1 ]Department of Applied Physiology and Kinesiology, University of Florida, Gainesville, FL, USA, pborsa@ 123456hhp.ufl.edu
                [2 ]School of Health Professions, University of Southern Mississippi, Hattiesburg, MS, USA
                [3 ]Department of Molecular Genetics and Microbiology, Center for Epigenetics, UF Genetics Institute, University of Florida, Gainesville, FL, USA
                [4 ]Department of Biostatistics, University of Florida, Gainesville, FL, USA
                [5 ]Department of Community Dentistry and Behavioral Science, University of Florida, Gainesville, FL, USA
                [6 ]Duke Clinical Research Institute and Department of Orthopaedic Surgery, Duke University, Durham, NC, USA
                Author notes
                Correspondence: Paul A Borsa, Department of Applied Physiology and Kinesiology, University of Florida, 149 FLG, PO Box 118205, 1864 Stadium Road, Gainesville FL 32611, USA, Tel +1 352 294 1726, Fax +1 352 392 5262, Email pborsa@ 123456hhp.ufl.edu
                © 2018 Borsa 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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