An Experimental Study Of The Pathogenesis Of Cervical Spondylotic Myelopathy

Objective: Cervical spondylosis myelopathy in the elderly is one of thecommon and frequently-occurring diseases. With the work and life stylechanges as well as the acceleration of the pace of life, the Morbidity rate of theCervical spondylosis myelopathy has showed an increasing trend, and the ageof onset becomes lower. Now,in China,the Morbidity rate of cervicalspondylosis myelopathy is about7.4%-13.8%and it keeps rising in the over50years old pepole.Today, cervical spondylosis myelopathy has more andmore serious threatened the health of people, affected the quality of people'slives. There are a lot sorts of reasons of cervical spondylosis myelopathy suchas cervical spine degeneration (including cervical disc and bone degeneration),bad body posture, cervical strain, trauma to cervical spine, deformity ofcervical vertebra and neck muscle diseases and so on. Degeneration changes isthe most important one in the clinical findings.The purpose of our experimentwas to explore the pathogenesis of cervical spondylosis myelopathy bybuilding a rabbit model that had implanted a radiopaque nail at the C3vertebral body causing compression of spinal cord,simulating the pathogenesisof human cervical spondylosis myelopathy. This experiment was to reveal theimportance of the apoptosis in the pathogenesis of cervical spondylosismyelopathy and suggest that anti-apoptotic treatment may become one of thesecondary treatment of cervical spondylotic myelopathy by observing thechanges in the degree of apoptosis with different time periods,in chroniccervical cord compression model.Methods:Choosing of the experimental animal:3months of age, male,30New Zealand rabbits, weight control in2to2.5Kg. Randomly divided into5groups.Each group contains6rabbits. Group A: control group.GroupB-Group E: model group. GroupB: spinal cord compression3months. GroupC: spinal cord compression4months. GroupD: spinal cord compression5months. GroupE: spinal cord compression6months.Building of the animalmodel: The24New Zealand rabbits were anesthetized by intraperitonealinjection of0.5ml of diazepam, then sumianxinII followed by0.1ml/kg.Ready for all the preoperative preparations. A5cm longitudinal incision wasmade in front of neck centering on a point about1cm inferior to the thyroidcartilage. Revealed to the vertebral body, identified the C3vertebralbody,made a hole (about3mm×3mm) until revealing the spinal cord in theC3vertebral body.Implanted a radiopaque nail into the hole,and then closedthe wound. Control group is the same with the model group in the surgicalprocedure except implanting the self-made spinal cord compression nail.Without acute spinal cord injury pattern change by counterchecking theCortical somatosensory evoked potentials(CSEP) after the surgery.Outcomemearures:⑴Evaluating the change of behavior using the modified Tarlovmotor scores;⑵Cortical somatosensory evoked potentials(CSEP) tomonitoring changes of the both lower extremities' somatosensery evokedpotential;⑶Observing the signal changes in spinal cord after spinal cordcompression by MRI imaging⑷Taking and fixing the compressive region ofthe spinal cord and undergoing HE staining and Bcl-2, Baximmunohistochemical staining, observe the degree of apoptosis in the spinalcord gray matter and white matter.Results:⑴Tarlov's motor scores showed that: With the extension of thetime of spinal cord compression the Tarlov's motor function score hadsignificant decreased compared with the control group.⑵The CSEP showedthat: With the extension of compression time, CSEP amplitude and latencywere significant changes.From group B to group E,the latency P15hadappeared to gradually extend.⑶M RI imaging studies: In T2-weighted imagesthe high signal can be seen in the rabbit spinal cord compression region of themodel group.⑷Histological examination: In the gray matter and white matterneurons and glial cells in the cell body shrinkage, structural disorder, tissueedema can be seen in the HE staining of the spinal cord of the model group, and with the oppression of time gradually increased the above characteristicshad aggravated. Bax immunohistochemical staining showed that:In the baxpositive cells the Bax staining was lighter in control group of spinal cord graymatter and white matter.In group B, In the bax positive cells the Bax stainingwas significantly deeper than control group..In group D, In the bax positivecells the Bax staining was the deepest compared with the other4groups.While,In group E, In the bax positive cells the depth of Bax staining was lighter thangroup D (p <0.05,statistically significant). Bcl-2immunohistochemicalstaining showed that:A small amount of expression of Bcl-2positive cells inthe control group. In group B, Bcl-2staining was the deepest, and thengradually decreased.Conclusions:(1) The rabbit model of chronic cervical spondylosismyelopathy that can better simulate the pathogenesis of human cervicalspondylosis myelopathy was successfully established by implanting aradiopaque nail in rabbits C3vertebral body and then compressing the spinalcord.(2) Suggesting that apoptosis may lead to one of the reasons for theincidence of cervical spondylotic myelopathy,and the relation between theextent of apoptosis and compression time and symptom of cervicalspondylotic myelopathy is nonlinear,by observing the changes of Spinal cordslices'HE, of Bax, Bcl-2staining in control group and model group.