Delayed demyelination and macrophage invasion: a candidate for secondary cell damage in spinal cord injury.

Recent studies of the chronic morphology and physiology of experimental spinal cord injury (SCI) in the cat are reviewed and their conclusions outlined. In particular, variations in chronic dysmyelination of the lesion have been found to be largely independent of injury intensity, suggesting a secondary pathologic origin. New morphometric studies of the subacute development of contusion lesions are described. Using electron microscopy and light microscopic line-sampling of myelinated axons, it was found that demyelination of axons that survived the initial injury occurred largely between 2 and 7 days after contusion and did not accompany the much more rapid dissolution of myelin from those axons that degenerated within the first 2 days. The number of apparently intact axons at the center of the lesion declined by a factor of 2 or more in the same interval of 2-7 days. This secondary pathology was coincident with dense invasion of the lesion by macrophages and their phagocytosis of the membraneous debris remaining from the initial hemorrhagic necrosis. It is concluded that posttraumatic inflammation in the spinal cord should be investigated in more detail as a possible contributor to chronic deficits. In addition, these data emphasize the importance of defining the nature, time of occurrence, and proportional significance of secondary damage in order to evaluate those studies and hypotheses that attempt to differentiate acute secondary pathophysiology from primary degenerative processes.