Brain damage induced by blunt head trauma is multifactorial in that the initial injury both induces extensive depolarization and damages tissue through transient sheer forces that mechanically deform tissue components, especially axons and microvessels. Furthermore, although there is little evidence for initial energy depletion, subsequent tissue edema and microvascular perfusion shunting may result in areas of focal ischemia. This review suggests that these events lead to a final common pathway of neuronal death that involves loss of cellular calcium homeostasis, production of injurious free radicals, and tissue acidosis.