• Masafumi Kubota, Shigeru Kobayashi, Tadayoshi Nonoyama, Seiichiro Shimada, Kenichi Takeno, Tsuyoshi Miyazaki, Guerrero Alexander Rodríguez AR, Hisao Iwamoto, and Hisatoshi Baba.
• Faculty of Medical Sciences, The University of Fukui , Department of Orthopaedics and Rehabilitation Medicine, Fukui, Japan.
• J. Neurotrauma. 2011 Mar 1; 28 (3): 459-67.

AbstractCervical myelopathy is caused by chronic segmental compression of the spinal cord because of degenerative changes of the spine. However, the exact mechanisms of chronic cervical cord compression are not fully understood. The purpose of this study was to validate a new animal model of chronic cervical cord compression capable of reproducing the clinical course without laminectomy in rats. A polyethylene line attached to a plastic plate was fastened with three turns around the vertebral body of C4 in 1-month-old rats. After surgery, the polyethylene line grows deeper into the dorsal wall of the spinal canal along with the growth of the spinal canal and vertebral body, producing a gradual compression of the spinal cord. The results show that this cervical canal stenosis (CCS) model in rats caused motor deficits and sensory disturbances 9 months after initiating CCS; however, no clinical manifestations took place until 6 months. The intramedullary high-intensity area on T2-weighted images was observed in 70% of the CCS model rats at 12 months after initiating CCS. In histological sections, the spinal cord was compressed along the entire circumference at 12 months after initiating CCS. The number of ventral neurons was decreased, and the white matter showed wallerian degeneration. This model might reproduce characteristic features of clinical chronic cervical cord compression, including progressive motor and sensory disturbances after a latency period and insidious neuronal loss, and represents chronic compression of the cervical spinal cord in humans.

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