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Sequential events of secondary injury in TBI. This includes variety of processes such as depolarization, disruption of ionic homeostasis and release of neurotransmitters, lipid degradation, and oxidative stress. These events are a result of interaction between the excitatory amino acid released with an influx of oxygen-free radicals that ultimately set up NMDA, AMPA, α7, and nACR to sustain the unstable environment for cell injury and degenerative changes.
