Key Mechanisms of Secondary Neuronal Damage After Brain Trauma

摘要: Progress in the successful application of novel therapies treatment severe traumatic brain injury (TBI) humans has been disappointing [1]. Currently, is limited to field stabilization and supportive neurointensive care, clinically accepted strategies control intracranial hypertension, surgical resection mass lesions [2]. A number have shown promise contemporary experimental models TBI [3], but none successfully translated clinical use via a randomized controlled trial demonstrating beneficial effect on outcome. Examples important failures include trials two agents targeting oxidative injury, tirilazad [4] Superoxide dismutase (SOD) [5], one excitotoxicity, Selfotel [6]. Both excitotoxicity are felt represent mechanisms secondary damage laboratory condition [3, 7]. Even mild hypothermia (32-34°C), most promising therapy as applied [8, 9, 10, 11] preliminary investigation [12, 13, 14, 15], failed demonstrate unequivocal efficacy recent multicenter TBI. Some these may reflect considerable difficulties encountered conducting setting acute such lack knowledge temporal therapeutic windows opportunity for any inability select appropriate patients during phase [1, 4, 16]. For example, Shiozaki et al. [16] reported that hypothermia, after adults was ineffective absence hypertension. However, delaying until hypertension developed would very likely diminish its [17, 18].