SPONTANEOUS LONG-TERM REMYELINATION AFTER TRAUMATIC SPINAL-CORD INJURY IN RATS

The capability of the central nervous system to remyelinate axons afte r a lesion has been well documented, even though it had been described as an abortive and incomplete process. At present there are no long-t erm morphometric studies to assess the spinal cord (SC) remyelinative capability. With the purpose to understand this phenomenon better, the SC of seven lesionless rats and the SC of 21 rats subjected to a seve re weight-drop contusion injury were evaluated at 1, 2, 4, 6, and 12 m onths after injury. The axonal diameter and the myelination index (MI = axolemmal perimeter divided by myelinated fiber perimeter) were regi stered in the outer rim of the cord at T9 SC level using a transmissio n electron microscope and a digitizing computer system. The average my elinated fiber loss was 95.1%, One month after the SC, 64% of the surv iving fibers were demyelinated while 12 months later, only 30% of the fibers had no myelin sheath. The MI in the control group was 0.72 +/- 0.07 (X +/- S.D.). In the experimental groups, the greatest demyelinat ion was observed two months after the lesion (MI = 0.90 +/- 0.03), whi le the greatest myelination was observed 12 months after the injury (M I = 0.83 +/- 0.02). There was a statistical difference (p < 0.02) in M I between 2 and 12 months which means that remyelination had taken pla ce. Remyelination was mainly achieved because of Schwann cells, The pr oportion of small fibers (diameter = 0.5 pm or less) considered as axo n collaterals, increased from 18.45% at 1 month to 27.66% a year after the contusion. Results suggest that remyelination is not an abortive phenomenon but in fact a slow process occurring parallel to other tiss ue plastic phenomena, such as the emission of axon collaterals. (C) 19 98 Elsevier Science B.V.