Injuries to the central nervous system cause biochemical changes, including neurotoxic as well as neuroprotective components. The balance between these 2 types of delayed reactions, which are remarkably stereotypic across categories of insult, substantially determines the ultimate extent of tissue damage and associated neurological dysfunction. Secondary injury factors are induced from seconds to weeks or months after trauma or ischemia, and may lead to either necrotic or apoptotic neural cell death. Blocking these delayed neurotoxic reactions or enhancing endogenous neuroprotective responses provide the theoretical basis for development of neuroprotective treatment strategies. Because various injury pathways may occur in parallel, and the blockade of one type of cell death pathway may shunt to another, the most effective neuroprotection approaches may require multidrug treatment or use of single agents with multipotential actions. Examples of promising multipotential drug treatment are discussed.
Faden A. Mechanisms of Cell Injury: Implications for Treating Neurological Disorders. Arch Neurol. 2003;60(2):296. doi:10.1001/archneur.60.2.296-a