In myelopathy, unilateral compression of the spinal cord in cases of disc herniation would be expected to produce Brown-Séquard syndrome. However, a transverse lesion syndrome occurs in most clinical cases. In order to reveal the mechanism by which unilateral compression induces transverse damage to the spinal cord, damage of the gray and white matter in each half of the spinal cord were evaluated quantitatively to determine the density of GFAP-positive astrocytes. The cervical spinal cord in rabbits was unilaterally compressed with a small screw. The area of each half of the damaged cord and the density of GFAP-positive astrocytes of the compressed and contralateral halves were investigated one week after the surgery. No apparent paralysis was observed during the period of observation. As the compression increased, the area of the compressed half of the spinal cord decreased significantly compared to the contralateral half. The densities of GFAP-positive astrocytes in the gray matter and the anterior funiculus increased significantly in the compressed half. There were no significant differences in the densities at the lateral and dorsal funiculi between the compressed and contralateral halves. The tissue damage in the gray matter of the compressed half was markedly higher. No significant difference between the two halves in damage was seen in the lateral funiculus, where in the lateral pyramidal and the dorsal spinocerebellar tracts are found. These findings provide evidence of the mechanistic basis for the spinal cord damage that leads to transverse lesion syndrome in unilateral compression myelopathy.
ASJC Scopus subject areas
- Clinical Neurology