Regional blood flow in the chronically compressed rat spinal cord

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Cervical myelopathy is a common cause of neurological disability among the elderly; however, the exact mechanism for the insidious and progressive deterioration remains to be elucidated. To study the pathophysiology, we developed a simple experimental model reproducing the course. In rats, a thin sheet of expanding polymer was implanted microsurgically underneath the C5-C6 laminae. In the control group, the polymer sheet was removed immediately. Changes in motor functions were monitored for 25 weeks after the operation, with voluntary exercise activity measured by odometer attached to revolving cages, and forced running capability measured by duration of exercise on a rotating treadmill. Motor neurons were counted stereologically in continuous sections. In the compression group, the forced running capability deteriorated after a latent period of 17 weeks and progressively thereafter. In the control group, it stayed unchanged throughout 25 weeks. Course of the voluntary exercise was comparable between the groups. Motor neuron density in the compression group decreased significantly in 9 weeks (-20.3%) and 25 weeks (-35.5%), but not in 1 or 3 weeks. This practical model properly reproduces characteristic features of the clinical cervical myelopathy, with progressive motor disturbance after a latency and insidious neuronal loss preceding the symptoms. These changes may be caused by decreased spinal cord blood flow measured by autoradiography