The key players and the complex interrelationships involved in the secondary cascade of events occurring during the first minutes, hours, and days after traumatic CNS injury are shown in Figure 1.1-5 Most of the players involved in ischemic and hemorrhagic CNS insults are the same as for traumatic injury. For TBI and SCI the most immediate event is mechanically induced depolarization and the consequent opening of voltage-dependent ion channels (i.e., Na +, K +, Ca2 +). Similarly, the onset of ischemia is quickly followed by loss of ionic homeostasis in the affected tissue. In the case of intracerebral hemorrhage or SAH, this loss of normal ion distribution is more insidious, requiring time for the secondary ischemic events to manifest themselves. The depolarization leads to massive release of a variety of neurotransmitters, including glutamate, which can cause the opening of glutamate-receptor-operated ion channels (e.g., NMDA and AMPA). The most important consequence of these rapidly evolving ionic disturbances is the accumulation of intracellular Ca2 + (i.e., Ca2 + overload), which initiates several damaging effects. The first is mitochondrial dysfunction, leading to a failure of aerobic energy metabolism, shift to glycolytic (i.e., anaerobic)
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