While extensive research points to mechanical injury of the cervical facet joint as a mechanism of whiplash injury, findings remain speculative regarding its potential for causing pain. The purpose of this study was to examine the relationship between facet joint distraction, capsular ligament strain, cellular nociceptive responses, and pain. A novel rat model of in viva facet joint injury was used to impose C6/C7 joint distraction in separate studies of subcatastrophic and physiologic vertebral distraction, as well as sham procedures. A common clinical measure of behavioral hypersensitivity (allodynia) was measured for 14 days after injury, as quantification of resulting pain symptoms. Also, on day 14, spinal activation of microglia and astrocytes was quantified to examine the potential role of glial activation as a physiologic mechanism of facet-mediated painful injury .Vertebral distractions of 0.90 ± 0.53 mm across the rat facet joint reliably produced symptoms of persistent pain. Allodynia results showed immediate and sustained behavioral sensitivity following subcatastrophic vertebral distractions; pain symptoms were significantly greater (p<0.008) than those for other injury groups. Further, spinal astrocytic activation was also greater (p=0.049) for subcatastrophic injuries compared to lower distraction magnitudes. The mean maximum principal strain in the capsular ligament for joint distractions of 0.57 ± 0.11 mm was 27.7 ± 11.9%. Findings suggest that facet capsule strains comparable to those previously reported for whiplash kinematics and subcatastrophic failures of this ligament have the potential to produce pain symptoms and alter one element of nociception. Results further suggest that a mechanical threshold likely exists for painful joint distraction, providing behavioral and physiologic evidence of the cervical facet joint's mechanical injury as a source of neck pain. Author/publisher)
Abstract