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Spinal Kyphosis Causes Demyelination and Neuronal Loss in the Spinal Cord: A New Model of Kyphotic Deformity Using Juvenile Japanese Small Game Fowls

Shimizu, Kentaro, MD*; Nakamura, Masaya, MD*; Nishikawa, Yuji, MD; Hijikata, Sadahisa, MD; Chiba, Kazuhiro, MD*; Toyama, Yoshiaki, MD*

doi: 10.1097/01.brs.0000184378.67465.5c
Basic Science

Study Design. Histologic changes in the spinal cord caused by progressive spinal kyphosis were assessed using a new animal model.

Objectives. To evaluate the effects of chronic compression associated with kyphotic deformity of the cervical spine on the spinal cord.

Summary of Background Data. The spinal cord has remarkable ability to resist chronic compression, however, delayed paralysis is sometimes seen following the development of spinal kyphosis. In the past, no animal model to clarify the mechanism of spinal cord damage due to spinal kyphotic deformity has been available.

Methods. Laminectomy and bilateral facetectomy at the C4–C5 level was performed in 52 Japanese small game fowls. Histologic changes in the spinal cord associated with progressive kyphotic deformity were examined at different time points after surgery in each animal. The degree of spinal cord flattening and the severity of demyelination in histologic sections were quantitatively evaluated using an image analyzer, and their association with the kyphotic angle was analyzed. Changes in the microvascular distribution in the spinal cord were also examined by microangiography.

Results. In all operated animals, progressive kyphosis developed reproducibly. The kyphotic angle increased gradually until 3 weeks after surgery and stabilized thereafter. There was a significant correlation between the kyphotic angle and the degree of spinal cord flattening. The spinal cord was compressed most intensely at the apex of the kyphosis, where demyelination of the anterior funiculus as well as neuronal loss and atrophy of the anterior horn were observed. Demyelination progressed as the kyphotic deformity became more severe, initially affecting the anterior funiculus and later extending to the lateral and then the posterior funiculus. Angiography revealed a decrease of the vascular distribution at the ventral side of the compressed spinal cord.

Conclusions. Progressive kyphosis of the cervical spine resulted in demyelination of nerve fibers in the funiculi and neuronal loss in the anterior horn due tochronic compression of the spinal cord. These histologic changes seem to be associated with both continuous mechanical compression and vascular changes in the spinal cord.

We have developed a new experimental model of chronic spinal cord compression using a bird. In this model, progressive and reproducible cord compression by kyphotic deformity was induced. The sequential radiologic, histologic, and microcirculatory changes in this model were evaluated.

From the *Department of Orthopaedic Surgery, School of Medicine, Keio University, Tokyo, Japan; and †Department of Orthopaedic Surgery, Tokyo Denryoku Hospital, Tokyo, Japan.

Acknowledgment date: December 22, 2004. First revision date: January 27, 2005. Acceptance date: January 31, 2005.

The manuscript submitted does not contain information about medical device(s)/drug(s).

Institutional, Foundation, and Other funds were received in support of this work. No benefits in any form have been or will be received from a commercial party related directly or indirectly to the subject of this manuscript.

Address correspondence and reprint requests to Masaya Nakamura, MD, 35 Shinanomachi, Shinjuku, Tokyo 160-8582, Japan; E-mail

© 2005 Lippincott Williams & Wilkins, Inc.