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Experimental Study On The Animal Model Of Cervical Spinal Cord Injury Without Fracture And Dislocation

Posted on:2009-12-20Degree:DoctorType:Dissertation
Country:ChinaCandidate:H F JiangFull Text:PDF
GTID:1114360245463453Subject:Surgery
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Objective:The purpose of the research was to show a good animal model of cervical spinal cord injury without fracture and dislocation , was to evaluation the function of the spinal cord, was to realize the pathology and nerve functional changes of the spinal codr during compression, was to qualitative quantitatively record and analysis weighting spinal cord function, was to research the relatively of spinal cord injury and nerve dysfunction. The cervical spinal cord injury without fracture and dislocation refers to the acute cervical spinal cord injury induced by cervical trauma without radiographic abnormality. The mechanisms underlying the injury are unclear. The clinical manifestations were different widely , and the most common injury pattern was the central cord syndrome. Various animal experiments on spinal cord injury have been conducted to deepen the understanding on the pathology of compressed lesions. However, these experiments usually used the models of acute or chronic symptoms produced by weight bearing and/or clamps, and there have been a few studies on chronic compression from the front side with acute compression from the dorsal side. Major symptom of cervical spinal cord injury without fracture and dislocation is spinal paralysis which is generated by the osteoarthropathic changes of the spine, and the spine presents such morphological characteristics as cervical disk degeneration, osteophyte formation , hypertrophic yellow ligament, cervical spinal stenosis, and abnormal mobility of the cervical spine. On these basis, the mechanism of injury is probably acute stretching of the cord as in flexion and torsional strain. However pathology of cervical spinal cord injury without fracture and dislocation has remained unclear because of the absence of an appropriate animal model for the studies. In the present study, we tried to establish an animal model with typical clinical characteristics of cervical spinal cord injury without fracture and dislocation, in which disk and facet were maintained to preserve mobility of the cervical spine, and compression was given to a single intervertebral space using a screw from the front side and a catheter with balloon from the dorsal side. In this model, spinal cord anterior-posterior compression is produced at the same level. With MRI, electrophysiological test, and histological examination, we confirmed that this model efficiently produces cervical spinal cord injury without fracture and dislocation. Method: In our model, surgical treatment is not performed on intervertebral disks and facets, and compression is given to a single intervertebral space. This maintains a wide range of vertebral motions. In our model, the spinal cord is thought to be compressed from the front and dorsal sides and this produces conditions similar to cervical spinal cord injury without fracture and dislocation. Gradually increased anterior compression using a metal screw, and observed the compression group showed certain disturbance of limb function during compression of the spinal canal. In our model, compression is given to one intervertebral space, and the disk and facet are maintained; the catheter with balloon posterior compression is inserted through C5,6 intervertebal foramen. The antero-posterior compression produces the condition of spinal canal stenosis. Therefore, in our model, antero-posterior spinal cord compression is thought to be efficiently produced during the operation and this would be the mechanism of paralysis in this model.Eighteen 4-6 ages goat (body weights: 18-23kg) were used in this study. The goat were divide into foure groups randomly (A:control Grup, B:chronic Compression group, C:aute Compression group, D:anterior-posterior Compression group).In this study, cortical somatosensory evoked potential (CSEP) was used as a parameter for the spinal cord function. CSEP were recorded by stimulating the posterior tibial nerve at the ankle. A recording needle electrode was placed in the scaple of forehead. A ground electrode was placed into the right forelimb. The latency of a CSEP positive peak was measured from the onset of the stimulus to the peak. The amplitude of a positive peak was measured from the positive peak to the immediately preceding negative peak. The evoked potentials were recorded at 5 min,30min,1wek,2 weeks post decompression and before spinal cord injury in each group.Motor function behaviour score was performed before surgery and after surgery. Histologic studies were performed on part of animals. Pathological samples were observed by light and electron microscope. 3D-CT and MRI were performed to observe spinal cord deforms after the pressure. Statistical analysis was conducted using Student's t-test, and P values less than 0.01 or 0.05 were considered statistically significant.Result:CSEP recorded before spinal cord compression showed a stable pattern. Spianl cord compression result in a gradual decrement in the peak latency and significant increment in the peak amplitude. In the control group, the waveform, latency and amplitude of evoked potentials remained stable throughout the whole experiment. In the C group, a decrease in amplitude and an increase in latency of CSEP were observed immediately after decompression, the amplitude and the latency recovered after 2 weeks. In the B group the results showed apprently decrease of amplitude and increse of latency. In the D group, after severe spinal cord compression, the waves deformed further, the latency and amplitude did not reached preinjury level after 2 weeks.Histologic studies showed the compression cause different pathological changes, including nerve cell in gray matter and auxiliary fibers in white matter, such as disappear of the Nissl body and nucleolus, chromation margination, demyelination. The most difference among the groups was the numbers of hemorrhagic focus in spinal cord. Pathological changes also confirmed increased severity of injury with increasing power of compression. Conclusion: Compared with the previous experiment model, this modelhas its own advantages as follows:simple to perform, saft to carry out, successful rate is higher. Pathologic histology and spinal cord function changes were similar to the characteristics of clinical cervical spinal cord injury without fracture and dislocation. This model ideally simulated the pathological procedure of the cervical spinal cord injury without fracture and dislocation.
Keywords/Search Tags:cervical spinal cord injury without fracture and dislocation, animal model, cortical somatosensory evoked potential
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