Introduction: An International Symposium: Cellular and Molecular Correlates of Central Nervous System Trauma

An international symposium on the "Cellular and Molecular Correlates of Central Nervous System Trauma" was held on April 21–24, 1988, at the University of North Texas in Denton, Texas. The symposium focused on the mechanisms of cellular injury and death, secondary injury mechanisms, recovery mechanisms, strategies to increase neuronal survival and recovery, regeneration, and grafting. This article summarizes the discussions at the symposium and reviews these subjects. Recent literature is cited. On the cellular level, emphasis was placed on the role and mechanisms of neuronal injury mediated by calcium ions (Ca+2) in both in vivo and in vitro trauma and ischemia models, Ca+2-activated neutral proteases, how neurons protect themselves against excessive Ca+2 entry, excitotoxic neurotransmitters, free radicals, nerve growth factor, and brain magnesium. On the molecular level, the discussion centered on heat shock (stress) proteins induced by injury, DNA strand breaks, injury-induced changes in sodium channel subtypes, and resealing of injured axons. Axonal pathology in head trauma and physiology of injured spinal axons were reviewed. Data relating to ganglioside and polyamine effects in neural trauma were presented. The effects of neuronal and astrocytic grafts on host neurons were assessed, both in vitro and in vivo. It is concluded that the field is rapidly developing, progress is being made in developing treatments that prolong cell survival after injury, that the study of secondary injury mechanisms provide a rich source of insights concerning how neurons protect themselves against injury, and that both environment and genetic factors play major roles in determining the ability of neurons to reconstitute themselves after injury.