Stroke is a major cause of death and disability in the U.S. and worldwide. A variety of pathophysiologic episodes or cellular medications occur following a stroke, and knowledge of these aftermath events can lead to potential therapeutic strategies that may reverse or attenuate stroke injury. Cellular events that occur following stroke include the excessive releases of excitatory amino acids, alterations in the genomic responses, mitochondrial injury producing reactive oxygen and nitrogen species (ROS), and secondary injury, often in the setting of reperfusion.