Citation

Guest JD, Hiester ED, Bunge RP. Exp. Neurol. 2005; 192(2): 384-393.

Affiliation

Department of Neurological Surgery and the Miami Project to Cure Paralysis, University of Miami, Lois Pope LIFE Center, 1095 NW 14th Terrace, Miami, FL 33136, USA. jguest@med.miami.edu

Copyright

(Copyright © 2005, Elsevier Publishing)

DOI

10.1016/j.expneurol.2004.11.033

PMID

15755556

Abstract

The natural history of post-traumatic demyelination and myelin repair in the human spinal cord is largely unknown and has remained a matter of speculation. A wealth of experimental studies indicate that mild to moderate contusive injuries to the mammalian spinal cord evolve into a cavity with a preserved rim of white matter in which a population of segmentally demyelinated axons persists. It is believed that such injured axons have abnormal conduction properties. Theoretically, such axons might show improved function if myelin repair occurred. Schwann cells can remyelinate axons affected by multiple sclerosis, but little evidence exists that such repair can occur spontaneously following traumatic human SCI. Therefore, it is important to determine if chronic demyelination is present following human spinal cord injury. There are no previous reports that have conclusively demonstrated demyelination in the human spinal cord following traumatic spinal cord injury using immunohistochemical techniques. Immunohistochemical methods were used to study the distribution of peripheral and central myelin proteins as well as axonal neurofilament at the injury epicenter in 13 postmortem chronically injured human spinal cords 1-22 years following injury. Of these seven could be assessed by our methods. We found that some axonal demyelination can be detected even a decade following human SCI and indirect evidence that invading Schwann cells contributed to restoration of myelin sheaths around some spinal axons.

Language: en