Neurorestoratology evidence in an animal model with cervical spondylotic myelopathy

Abstract

Background: Cervical spondylotic myelopathy (CSM) is a chronic compression injury of the spinal cord, with potentially reversible conditions after surgical decompression, and a unique model of incomplete spinal cord injury. Several animal studies showed pathological changes of demyelination, axon loss and neuron apoptosis in rats with chronic spinal cord compression. However, there is a limited understanding of the neurological change in the spinal cord after surgical decompression. The aim of this study was to validate the neurorestoratology of myelopathic lesions in the spinal cord in a rat model. Materials and methods: A total of 16 adult Sprague-Dawley rats were divided into four groups: sham control (group 1); CSM model with 4-week chronic compression (group 2), 2 weeks (group 3) and 4 weeks (group 4) after surgical decompression of CSM model. The compression and decompression were verified by magnetic resonance imaging (MRI) test. Neurological function was evaluated by Basso, Beattie, and Bresnahan (BBB) locomotor rating scale, ladder rung walking test and somatosensory-evoked potentials (SEPs). Neuropathological change was evaluated by histological examinations. Results: MRI confirmed the compression of the cervical spinal cord as well as the reshaping of cord morphology after decompression. After decompression, significant changes of neurological function were observed in BBB scores (p < 0.01, F = 10.52), ladder rung walking test (p < 0.05, F = 14.21) and latencies (p < 0.05, F = 5.76) and amplitudes (p < 0.05, F = 3.8) of SEP. Neuronal degeneration was obvious in the ventral horn with gradual restoration. After decompression, the motor neuron number in the ventral horn did not show significant changes (p > 0.05). However, increasing trend of myelin area and staining intensity were observed in all columns of the white matter (p < 0.05) after decompression, especially in the compressed lateral column. Conclusion: The established rat model is able to simulate histopathological characteristics of cervical myelopathy in human beings. The neuropathological change demonstrated that neurorestoratology in the myelopathic spinal cord would probably attribute to axonal remyelination of the white matter, but there would be an incapability of neuronal regeneration.

Different Time-Frequency Distribution Patterns of Somatosensory Evoked Potentials in Dual- and Single-Level Spinal Cord Compression

“…Thus, various lesion sites along the spinal cord may influence the mediation effect and thereby lead to differing morphological changes of SEPs. With mild neurological deficits in this study, the pathological changes evaluated by H&E staining are located in the injury level of the cervical cord in two weeks after injury as reported in previous study [20], [28], [38], [40]- [42], [47], the results were consistent with other semi-quantitative or quantitative analysis methods like the LFB staining [28], [40], MRI [28], [30], [40], micro-CT [38], [41], it inferred that the injury took place in the condition of chronic spinal cord compression.…”

Biomechanics of a novel artificial cervical vertebra from an in vivo caprine cervical spine non-fusion model

“…Although ACCF has been reported to exhibit good neurologic recovery [ 9 ], and restoration of cervical alignment in patients with CSM, the long-segment solid fusion inevitably sacrifices partial motor function of the cervical spine. The loss of motion at the operative levels can lead to an increased range of motion (ROM) of the adjacent intervertebral space [ 10 , 11 ], which can possibly lead to adjacent segment disease and resulting in CSM in those patients [ [12] , [13] , [14] ].…”