Cervical spondylotic myelopathy (CSM) is the most common cause of neurological disability in worldwide, which is caused by chronic compression of the spinal cord. Mainstay of treatment is surgical decompression, conservative treatment, or symptomatic analgesics. However, many patients end up with substantial residual disability. Disabilities of motor and sensory function are caused by neuronal damage and axonal loss. Therefore, we supposed that accomplishment of axonal growth is the most critical therapeutic strategy for CSM. Since our previous study suggested acteoside as a facilitator of axonal growth in spinal cord injury, this study aimed to investigate effects of acteoside on functional disability in CSM model mice.
The animal models of CSM reported so far have experimental disadvantages, such as difficulties of controlling compressive intensity, and unstable and too long time-course for appearance of motor dysfunction. First, we established a new mouse model of CSM to solve the problems. After laminectomy at C3-C5, the cervical cord was compressed by a mini screw. Motor functions of forelimbs and hind limbs decreased depth-dependently of the compression. The dysfunction was obvious at least 9 days after the compression. At the compressed center, GFAP-positive astrocytes increased, and NF-H positive axonal density decreased compared to sham mice. Since we succeeded establishing CSM model, acteoside was administered orally from 7 days after compression. Motor and sensory functions and histological evaluation are now under investigation.