APOPTOSIS AND DELAYED DEGENERATION AFTER SPINAL-CORD INJURY IN RATS AND MONKEYS

Apoptosis is a morphologically defined form of programmed cell death s een in a variety of circumstances, including immune cell selection, ca rcinogenesis and development(1,2). Apoptosis has very recently been se en after ischemic or traumatic injury to the central nervous system (C NS)(3-5), suggesting that active cell death as well as passive necrosi s may mediate damage after CNS injury. After spinal cord injury (SCI) in the rat, typical post-traumatic necrosis occurred, but in addition, apoptotic cells were found from 6 hours to 3 weeks after injury, espe cially in the spinal white matter. Apoptotic cells were positive for o ligodendrocyte markers. After SCI in monkeys, apoptotic cells were fou nd within remote degenerating fiber tracts. Both secondary degeneratio n at the site of SCI and the chronic demyelination of tracts away from the injury appear to be due in part to apoptosis. As cytokines have b een shown to mediate oligodendrocyte death in vitro(6), it seems likel y that chronic demyelination after CNS injury shares features with chr onic degenerative disorders like multiple sclerosis.