The outcome of spinal cord injury depends on the extent of secondary damage
produced by a series of cellular and molecular events initiated by the pri
mary trauma. This article reviews the evidence that secondary spinal cord i
njury involves the apoptotic as well as necrotic death of neurons and glial
cells. Also discussed are the major factors that can contribute to cell de
ath, such as glutamatergic excitotoxicity, free radical damage, cytokines,
and inflammation. The development of innovative therapeutic strategies to r
educe secondary spinal cord injury depends on an increased understanding of
secondary injury mechanisms at the molecular and biochemical level. Such t
herapeutic interventions may include the use bf antiapoptotic drugs, free r
adical scavengers, and antiinflammatory agents. These could be targeted to
block key reactions on cellular and molecular injury cascades, thus reducin
g secondary tissue damage, minimizing side effects, and improving functiona
l recovery.