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.

This book examines cellular events following stroke, offering the first systematic discussion of metal ions, their function as co-factors in cellular and genetic signaling and their consequently important roles in biochemistry ranging from essential to toxic.