Exposure to nucleus pulposus and displacement of intraspinal nervous structures with assessment of spontaneous behavioral changes in rats.
To develop a controlled, experimental model for nerve root injury.
There are a number of experimental models presented for studies on radiculopathies. One frequently used model is based on exposure to nucleus pulposus and displacement of the dorsal root ganglion (DRG). However, it is clinically more common that the nerve roots are displaced/compressed than the DRG. In this study, we developed a model for displacement of the nerve root by modifying the DRG model.
After removing the left L3–L4 facet joint, the underlying disc was punctured, and the L4 nerve root was displaced laterally by an injection needle (n = 10). In sham experiments, the same procedure was performed without disc puncture and displacement (n = 10). In 10 rats, the left L4–L5 facet joint was removed. The underlying disc was punctured and the L4 DRG was displaced medially by an injection needle. Assessment of spontaneous behavioral changes was performed on days 1, 3, 7, 14, and 21, postsurgery.
There was a clear increase in duration of the behavior “unloading of the paw” after displacement of the DRG that was most pronounced on day 1 and then gradually declined. There was a similar pattern for this behavior induced by nerve root displacement, although the duration was higher than that for the DRG displacement. No apparent trends in behavioral changes were observed for the other behaviors studied.
Displacement of the nerve root induced more changes in the pain behavior than displacement of the DRG, but only for the behavior unloading of the paw. Because nerve root injury is more common than DRG injury, this model may be more clinically relevant than the DRG model.
Level of Evidence: N/A
A model for nerve root injury in the rat was developed. The model induced more behavioral changes than a similar model on dorsal root ganglion injury. Because the nerve root is more commonly injured than the dorsal root ganglion this may be a more clinically relevant model.
*Musculoskeletal Research, Department of Medical Chemistry and Cell Biology, Institute of Biomedicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden; and
†Department of Orthopaedic Surgery, Graduate School of Biomedical Sciences, Hiroshima University, Hiroshima, Japan.
Address correspondence and reprint requests to Kjell Olmarker MD, PhD, Musculoskeletal Research, Department of Medical Chemistry and Cell Biology, Institute of Biomedicine, Sahlgrenska Academy, University of Gothenburg, SE-405 30 Gothenburg, Sweden; E-mail: email@example.com
Acknowledgment date: November 7, 2012. First revision date: April 2, 2013. Second revision date: June 10, 2013. Acceptance date: June 13, 2013.
The manuscript submitted does not contain information about medical device(s)/drug(s).
AFA Insurance, Stiftelsen Olle Engkvist Byggmästare and the Spine Society of Europe Task Force on Research grant funds were received to support this work.
Relevant financial activities outside the submitted work: grants, board membership, royalties, stock/stock options and travel/accommodations/meeting expenses.