Compression trauma in the spinal cord and neural transplantation

Maureen S Riedl, Purdue University

Abstract

Adult, Long Evans hooded rats received a compression trauma at the T11-T12 level of the spinal cord extending 50% in the dorsoventral plane. The central hemorrhagic mass was removed from the lesion, resulting in a cavity. Control animals received no further surgery, while experimental animals received transplants of either 15-d neocortical tissue or 15-d spinal cord tissue injected intraparenchymally into the lesion site. Qualitative analysis of control animals showed the spread of hemorrhage and edema into the spinal cord over time. It was shown quantitatively that the degeneration that follows spinal cord injury can be divided into early and late components. Quantitative analysis also revealed an intense glial reaction involving both astrocytes and oligodendrocytes. A glial scar was not seen in control animals using light microscopic techniques. A matrix of blood vessels, connective tissue, astrocytes, macrophages, and endothelial cells filled the lesion site, but this was different from a glial scar. Some fine axonal fibers were seen near the lesion site and were probably collateral sprouts. Transplants of embryonic neural tissue can survive, grow, differentiate, and become integrated in the spinal cord following compression trauma. Transplants of 15-d neocortical tissue grew very large and readily became integrated, but poor growth and integration of 15-d spinal cord tissue was seen. The pathological reaction and glial reaction was similar to that of control animals. More axon collaterals were seen in regions of good integration than in regions of poor integration or in control animals, possibly because the transplant provided an environment suitable for viewing these collaterals. A glial scar was seen in 11% of the sections from spinal cords with 15-d neocortical tissues, which is less than has been previously reported in studies using laceration lesion. In most instances, the growth of the transplant did not provide the compaction to cause the glial scar. Usually, the growing transplant pushed into the host spinal cord in such a way that the diffuse arrangement of glia cells remained. Only rarely, and only in very limited regions did the transplant exert a compacting force sufficient to cause a glial scar, and only then in regions of the spinal cord that were not well integrated.

Degree

Ph.D.

Advisors

Vanable, Purdue University.

Subject Area

Neurology

COinS