An experimental animal model of spinal root compression syndrome: an analysis of morphological changes of myelinated axons during compression radiculopathy and after decompression.

The treatment of radicular pain is mainly empirical because there are only few experimental studies dealing with morphological changes during compression radiculopathy. The goal of the study was to investigate changes in the morphology of myelinated axons during spinal root compression and the influence of decompression in a new rat model. The number of myelinated axons and their diameter were measured at 1, 2, 5, and 8 weeks during compression of the dorsal spinal root. The same approach was applied for 1-week compression followed by decompression for 1 or 2 weeks and compression for 5 weeks followed by 3-week decompression. A decrease in the number of myelinated axons (particularly those of large diameters) occurred after compression for 1 week. Continued compression for up to 8 weeks resulted in centripetal increase in the number of myelinated axons and the persistence of a small fraction of large myelinated axons at the site of compression. After that time, a decreased number of axons and a reduced fraction of large myelinated axons occurred again. Decompression after 1-week compression caused a rapid increase in the number of both small and large myelinated axons within the spinal root including the site of compression. A small fraction of regenerated axons was found after 5-week compression followed by 3-week decompression. Finally, we investigated the time course of the temporary increase in the number of regenerated myelinated axons during dorsal root compression for up to 8 weeks. The efficacy of decompression was superior when applied one week after compression or after regress of the acute phase of aseptic inflammation associated with fragility of spinal root. The results of the study verify the need for early surgical decompression to prevent irreversible damage of the spinal roots.