Mechanism of myelopathy and neuronal loss caused, by chronic spinal cord compression in a novel rat model.

点击翻译按钮获取中文摘要

A novel experimental model was developed in the rat to reproduce chronic cervical myelopathy. A thin expanding polymer was installed underneath the cervical laminae without causing immediate injury to the spinal cord. After the operation, motor functions were monitored for 25 weeks; voluntary exercise by cumulative count of revolving cages, and locomotion capability by maximal duration on a rotating treadmill.Immediately after surgery, the two parameters decreased but recovered in two weeks in the compression and in the control (undergoing sham operation) groups. Capability of forced locomotion deteriorated in the compression group with a latency of 17 weeks and progressively thereafter. In the control group, the parameter stayed unchanged throughout 25 weeks. In both groups, amount of voluntary exercise declined gradually in a comparable manner during the observation period.Motor neurons were counted stereologically in continuous sections (thickness and interval :5 μm, 300 slices) at 1,3,9,and 25 weeks after surgery. The neuron count decreased significantly in 9 weeks (-20.3%) and 25 weeks (-35.5%) after compression. Cross sectional area of the cord was reduced by 11.3 % (25 weeks).The model successfully reproduces important characteristics of clinical spondylotic myelopathy, namely, progressive course with an insidious onset, and association of motor neuron loss that precedes the symptoms.