The mechanisms behind development of chronic pain are still not fully understood. Over the last years, evidence has emerged connecting sensitization in the peripheral and the central nervous system to amplification of pain experiences in osteoarthritis. However, few studies have tried to assess the contribution of these mechanisms directly to pain in the clinical situation.In this issue of the Scandinavian Journal of Pain, Søren T. Skou and co-workers in Lars Arendt-Nielsen’s research group report on their study of patients with unilateral knee osteoarthritis (OA) causing long duration knee pain. They explored relationship between experimentally assessed pain mechanisms and clinical measures of OA pain.The authors induce temporal summation by computer controlled pressure algometry, spatial summation by cuff-algometer, and conditioning pain modulation by ischemic compression of the arm. Based on the multiple-regression model, they found that 55% of variance of the perceived maximal pain intensity in the osteoarthritic knee could be explained by quantitative experimental pain measures reflecting central pain mechanisms, in particular spreading sensitization and temporal summation. Conditioning pain modulation using ischemic arm pain as conditional pain stimuli, often termed top down pain regulation , was not associated with clinical OA-pain in these patients.1Peripheral and central pain mechanisms in knee
Scandinavian Journal of Pain – de Gruyter
Published: Apr 1, 2013
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