Neurofunctional change and its mechanism after decompression for chronic cervical myelopathy

English Keywords:Chronic spinal cord compression  Decompression  Moter evoked potential  Histology  Neurotrophic factors  Rat

English Abstract:

  【Abstract】 Objectives: To observe the neurofunctional recovery after decompression for chronic cervical myelopathy, and to investigate its mechanism. Methods: The rats were randomly divided into three groups: sham group (group A, n=10); compressive group(group B, n=10); decompressive group(group C, n=10). The expanding compression sheet made of a water-absorbing material was inserted underneath the C6-C7 laminae in rats of the compressive and decompressive groups. Laminectomy was performed after 4 weeks of compression. Moter evoked potential(MEP) was performed after 4 weeks and 12 weeks, and MRI was performed after 12 weeks. Then the rats were sacrificed, and gross specimens were processed for histological study. Luxol Fast Blue staining(LFB) was used to assess the myelin change. Immunofluorescence was performed to observe the number of neurons and the expression of brain-derived neurotrophic factor(BDNF) and vascular endothelial growth factor(VEGF). Results: For MEP at 4 weeks after injury, the latency and amplitude in group B and C showed significant difference compared with group A(P<0.05). There was no significant difference between group B and group C(P>0.05). At 12 weeks after injury, axial and sagittal MRI showed significant spinal cord compression and severe spinal canal stenosis in group B, while which were not noted in group A and B. For the latency and amplitude of MEP, there were significant differences among the three groups. For the latency, group Agroup C>group B. Gross specimens showed normal morphology in group A and obvious identation in group B, while the identation improved significantly in group C after 8 weeks of decompression. Immunofluorescence for neurons showed that a great number of healthy neurons was found in group A, with the number of neurons of 68.4±2.5. The majority of neurons disappeared and shrinked markedly in compressed level in group B, with the number of neurons of 35.2±3.1. The neurons shrinked slightly and the number of neurons increased in compressed level in group C compared with group B, with the number of neurons of 58.4±1.7. It showed significant differences among three groups(P<0.05). LFB staining revealed dense axon in group A, axonal demyelination in group B and significant recovery of demyelination in group C. For the immunofluorescence, a small amount of BDNF and VEGF expression was found in group A, with the number of BDNF and VEGF of 18.4±1.9 and 19.2±1.4 respectively. The expression of BDNF in group B was significantly up-regulated compared with group A, mainly located in the white matter of the compressed site, with the number of BDNF and VEGF of 37.2±3.5 and 17.4±2.1 respectively. The number of BDNF(68.4±2.7) and VEGF(51.7±3.1) in the white matter region increased significantly in group C after 8 weeks of decompression compared with group A and B. The number of BDNF and VEGF in group C was statistically upregulated than group A and B(P<0.05). Conclusions: The neurofunction improves after decompression, which may be contributed to inhibit neuronal damage and axonal demyelination as well as to increase the expression of BDNF and VEGF in the cervical spinal cord compression model.