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  • 1.
    Bergman, Stefan
    et al.
    Research and Development Centre, Spenshult, Oskarström, Sweden.
    Jacobsson, Lennart T.H.
    Herrström, Per
    Petersson, Ingemar F.
    Health status as measured by SF‐36 reflects changes and predicts outcome in chronic musculoskeletal pain: a 3‐year follow up study in the general population2004In: Pain, ISSN 0304-3959, E-ISSN 1872-6623, Vol. 108, no 1-2, p. 115-123Article in journal (Refereed)
    Abstract [en]

    The SF-36 is a well-validated health status instrument measuring eight different health concepts. One aim of this study was to compare health status as measured by SF-36 in subjects from the general population with no chronic pain (NCP), chronic regional pain (CRP), and chronic widespread pain (CWP). A second aim was to assess if SF-36 could reflect changes in pain status over time. A third aim was to study if health status at baseline, measured by SF-36, could predict pain status 3 years later. The study was designed as a 3-year follow up with a postal questionnaire, including the SF-36 health survey, to 2357 subjects from the general population aged 20-74 years. The results were controlled for age, sex, co-morbidity, and socio-economic status. At baseline, all eight health concepts of SF-36 discriminated between subgroups with NCP, CRP and CWP. Changes in SF-36 over the 3-year follow up time coincided with improvement or deterioration of pain status. Baseline SF-36 scores predicted pain outcome 3 years later. These results support that both physical and mental aspects of health status as measured by SF-36 are affected by the burden of musculoskeletal pain, are sensitive to changes in pain status, and also predict the further development of pain. Published by Elsevier B.V. All rights reserved.

  • 2.
    Namer, Barbara
    et al.
    University of Erlangen, Nürnberg, Germany.
    Hilliges, Marita
    Halmstad University, School of Business and Engineering (SET), Biological and Environmental Systems (BLESS), Biomechanics and Biomedicine.
    Ørstavik, Kristin
    Rikshospitalet University Hospital, Oslo, Norway.
    Schmidt, Roland
    University Hospital, Uppsala, Sweden.
    Weidner, Christian
    University of Erlangen, Nürnberg, Germany.
    Torebjörk, Erik
    University Hospital, Uppsala, Sweden.
    Handwerker, Hermann
    University of Erlangen, Nürnberg, Germany.
    Schmelz, Martin
    University Heidelberg, Germany.
    Endothelin1 activates and sensitizes human C-nociceptors2007In: Pain, ISSN 0304-3959, E-ISSN 1872-6623, Vol. 137, no 1, p. 41-49Article in journal (Refereed)
    Abstract [en]

    Microneurography was used to record action potentials from afferent C-fibers in cutaneous fascicles of the peroneal nerve in healthy volunteers. Afferent fibers were classified according to their mechanical responsiveness to von Frey stimulation (75 g) into mechano-responsive and mechano-insensitive nociceptors. Various concentrations of Endothelin1 (ET1) and Histamine were injected into the receptive fields of C-fibers. Activation and heat sensitization were monitored. Axon reflex flare and psychophysical ratings were assessed after injection of ET1 and codeine into the forearms after pre-treatment with an H1 blocker or sodium chloride. 65% of mechanosensitive nociceptors were activated by ET1. One-third showed long lasting responses (>15 min). In contrast, none of thirteen mechano-insensitive fibers were activated. Sensitization to heat was observed in 62% of mechanosensitive and in 46% of mechano-insensitive fibers. Injection of ET1 produced a widespread axon reflex flare, which was suppressed by pre-treatment with an H1 receptor blocker. In addition, pain sensations were induced more often than itching by ET1 in contrast to codeine. No wheal was observed after injection of ET1. Both itching and pain were decreased after H1 blocker treatment. In summary: (1) In humans ET1 activates mechanosensitive, but not mechano-insensitive, nociceptors. (2) Histamine released from mast cells is not responsible for all effects of ET1 on C-nociceptors. (3) ET1 could have a differential role in pain compared to other chemical algogens which activate additionally or even predominantly mechano-insensitive fibers.

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