• Markus Quante, Stephanie Hille, Markus D Schofer, Jürgen Lorenz, and Michael Hauck.
• Specialist Centre for Spinal Surgery, Hospital Neustadt, Neustadt in Holstein, Germany.
• J Pain Res. 2008 Jan 1; 1: 1-8.

AbstractCHRONIC 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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