This book illustrates remarkable roles of metal ions in the neuropathophysiology of stroke, which is a major cause of death and disability worldwide. Metal ions have unique chemical properties that allow them to play diverse roles in the brain. They regulate excitability and function as co-factors in cellular and genetic signaling pathways and therefore, have important roles ranging from essential to toxic. For the first time, the dyshomeostasis and pathophysiological actions of these metals in stroke are discussed systematically in thirty-six chapters in one volume. Highlighted metal ions include: Aluminum (Al) Arsenic (As) Cadmium (Cd) Calcium (Ca) Copper (Cu) Iron (Fe) Magnesium (Mg) Manganese (Mn) Mercury (Hg) Nickel (Ni) Potassium (K) Selenium (Se) Sodium (Na) Zinc (Zn)

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.