• Kyle P Quinn, Ling Dong, Francis J Golder, and Beth A Winkelstein.
• Department of Bioengineering, University of Pennsylvania, Philadelphia, PA 19104-6321, USA.
• Pain. 2010 Nov 1;151(2):414-21.

AbstractExcessive cervical facet capsular ligament stretch has been implicated as a cause of whiplash-associated disorders following rear-end impacts, but the pathophysiological mechanisms that produce chronic pain in these cases remain unclear. Using a rat model of C6-C7 cervical facet joint capsule stretch that produces sustained mechanical hyperalgesia, the presence of neuronal hyperexcitability was characterized 7 days after joint loading. Extracellular recordings of spinal dorsal horn neuronal activity between C6 and C8 (117 neurons) were obtained from anesthetized rats, with both painful and non-painful behavioral outcomes established by the magnitude of capsule stretch. The frequency of neuronal firing during noxious pinch (p<0.0182) and von Frey filaments applications (4-26g) to the forepaw was increased (p<0.0156) in the painful group compared to the non-painful and sham groups. In addition, the incidence and frequency of spontaneous and after discharge firing were greater in the painful group (p<0.0307) relative to sham. The proportion of cells in the deep laminae that responded as wide dynamic range neurons also was increased in the painful group relative to non-painful or sham groups (p<0.0348). These findings suggest that excessive facet capsule stretch, while not producing visible tearing, can produce functional plasticity of dorsal horn neuronal activity. The increase in neuronal firing across a range of stimulus magnitudes observed at day 7 post-injury provides the first direct evidence of neuronal modulation in the spinal cord following facet joint loading, and suggests that facet-mediated chronic pain following whiplash injury is driven, at least in part, by central sensitization.Copyright © 2010 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.

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