STUDY DESIGN: Investigation of intraradicular inflammation induced by mechanical compression. OBJECTIVE: To investigate the mechanism of nerve root pain, this study used a lumbar nerve root compression model. SUMMARY OF BACKGROUND DATA: The manifestation of pain at sites of inflammation has a close relationship with the release of mediators from macrophages. However, the mediators involved in inflammation of nerve roots as a result of mechanical compression remain almost unknown. METHODS: In this study, the seventh lumbar nerve root of dogs was compressed with a clip for 3 weeks to observe the changes caused by compression. Immunohistochemistry was performed using the avidin-biotin-peroxidase complex method to observe the changes of T cells (CD45) and macrophages (Mac-1) after compression. Antibodies against as interleukin-1 (IL-1), tumor necrosis factor-alpha (TNF-alpha), inducible nitric oxide synthase (i-NOS), and cyclooxygenase (COX)-1 and 2 were used to examine the localization and changes of these mediators caused by nerve root compression. RESULTS: In control animals, resident T cells were detected, but there were no macrophages. IL-1beta and COX-2 were positive in the Schwann cells and vascular endothelial cells, while COX-1 was detected in the vascular endothelial cells. However, no cells showed TNF-alpha or i-NOS positively. After nerve root compression, numerous T cells and macrophages appeared among the demyelinized nerve fibers. The macrophages were positive for IL-1beta, TNF-alpha, i-NOS, and COX-2. CONCLUSION: Inflammatory cytokines, NO, and COX-2 may be deeply involved in radiculitis caused by mechanical compression, and these mediators seem to be important in the manifestation of root pain.
STUDY DESIGN: Investigation of intraradicular inflammation induced by mechanical compression. OBJECTIVE: To investigate the mechanism of nerve root pain, this study used a lumbar nerve root compression model. SUMMARY OF BACKGROUND DATA: The manifestation of pain at sites of inflammation has a close relationship with the release of mediators from macrophages. However, the mediators involved in inflammation of nerve roots as a result of mechanical compression remain almost unknown. METHODS: In this study, the seventh lumbar nerve root of dogs was compressed with a clip for 3 weeks to observe the changes caused by compression. Immunohistochemistry was performed using the avidin-biotin-peroxidase complex method to observe the changes of T cells (CD45) and macrophages (Mac-1) after compression. Antibodies against as interleukin-1 (IL-1), tumor necrosis factor-alpha (TNF-alpha), inducible nitric oxide synthase (i-NOS), and cyclooxygenase (COX)-1 and 2 were used to examine the localization and changes of these mediators caused by nerve root compression. RESULTS: In control animals, resident T cells were detected, but there were no macrophages. IL-1beta and COX-2 were positive in the Schwann cells and vascular endothelial cells, while COX-1 was detected in the vascular endothelial cells. However, no cells showed TNF-alpha or i-NOS positively. After nerve root compression, numerous T cells and macrophages appeared among the demyelinized nerve fibers. The macrophages were positive for IL-1beta, TNF-alpha, i-NOS, and COX-2. CONCLUSION: Inflammatory cytokines, NO, and COX-2 may be deeply involved in radiculitis caused by mechanical compression, and these mediators seem to be important in the manifestation of root pain.
Authors: W Teske; J Krämer; T Lichtinger; O Köster; C Schulze-Pellengahr; T Theodoridis; J Ludwig Journal: Eur Spine J Date: 2012-08 Impact factor: 3.134
Authors: Harley Goldberg; William Firtch; Mark Tyburski; Alice Pressman; Lynn Ackerson; Luisa Hamilton; Wayne Smith; Ryan Carver; Annu Maratukulam; Lawrence A Won; Eugene Carragee; Andrew L Avins Journal: JAMA Date: 2015-05-19 Impact factor: 56.272
Authors: J T Wald; T P Maus; J R Geske; F E Diehn; T J Kaufmann; N S Murthy; K R Thielen; S Watson Journal: AJNR Am J Neuroradiol Date: 2013-02-28 Impact factor: 3.825
Authors: Seong Soo Choi; Eun Young Joo; Beom Sang Hwang; Jong Hyuk Lee; Gunn Lee; Jeong Hun Suh; Jeong Gill Leem; Jin Woo Shin Journal: Korean J Pain Date: 2014-03-28