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Noxious counterirritation in patients with advanced osteoarthritis of the knee reduces MCC but not SII pain generators: A combined use of MEG and EEG

DOI: http://dx.doi.org/10.2147/JPR.S3996

Keywords: counterirritation, DNIC, osteoarthritis, chronic pain, EEG, MEG

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Abstract:

xious counterirritation in patients with advanced osteoarthritis of the knee reduces MCC but not SII pain generators: A combined use of MEG and EEG Original Research (4462) Total Article Views Authors: Markus Quante, Stephanie Hille, Markus D Schofer, Jürgen Lorenz, Michael Hauck Published Date September 2008 Volume 2008:1 Pages 1 - 8 DOI: http://dx.doi.org/10.2147/JPR.S3996 Markus Quante1, Stephanie Hille2, Markus D Schofer3, Jürgen Lorenz4, Michael Hauck5 1Specialist Centre for Spinal Surgery, Hospital Neustadt, Neustadt in Holstein, Germany; 2Breast Care Center, Texas Medical Center, Huston, Texas, USA; 3Department of Orthopaedics and Rheumatology, University Hospital Giessen und Marburg GmbH, Marburg, Gemany; 4Department of Biomedical Engineering, Hamburg-University of Applied Sciences, Faculty of Life Sciences, Hamburg, Germany; 5Department of Neurophysiology and Pathophysiology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany Abstract: Chronic pain is mainly a result of two processes: peripheral and central sensitization, which can result in neuroplastic changes. Previous psychophysical studies suggested a decrease of the so-called pain-inhibiting-pain effect (DNIC) in chronic pain patients. We aimed to study the DNIC effect on the neuronal level using magnetoencephalography and electroencephalography in 12 patients suffering from advanced unilateral knee osteoarthritis (OA). DNIC was induced in patients by provoking the typical OA pain by a slightly hyperextended joint position, while they received short electrical pain stimuli. Although the patients did not report a reduction of electrical pain perception, the cingulate gyrus showed a decrease of activation during provoked OA pain, while activity in the secondary somatosensory cortex did not change. Based on much stronger DNIC induction at comparable intensities of an acute counterirritant pain in healthy subjects this result suggests a deficit of DNIC in OA patients. We suggest that the strength of DNIC is subject to neuronal plasticity of descending inhibitory pain systems and diminishes during the development of a chronic pain condition.

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