Cortical spreading depolarizations (CSD) are massive events which recently have been observed in many types of acute brain injury and likely lead to expansion of injury. These "brain tsunamis" are unlike any other type of brain electrical event (such as seizures or normal neuronal transmission) in that they progress very slowly across the surface of the brain (2-5mm/minute) and involve near complete depolarization of the neurons and other cells. The only similar event in neurophysiology is an anoxic depolarization, which is the final wave of loss of cell function preceding death in cells suffering severe, irreversible hypoxia or ischemia(1). In the case of CSD, the cell is able to recover function, however, at an enormous metabolic expense. Massive amounts of energy substrate (ATP, glucose, oxygen) as well as the delivery system to bring these substrates (blood flow) are required to restore the normal ionic gradient of the cell membrane and cell function. Because of this loss of function of cells, normal electrocortical (ECog) activity is transiently lost, resulting in a depression of the high frequency cortical activity, which is why the phenomenon is also frequently referred to as "cortical spreading depression." CSD has been definitively documented to occur after many types of acute brain injury including ischemic stroke, aneurysmal subarachnoid hemorrhage, intracerebral hemorrhage, and severe traumatic brain injury(2,3). The true incidence is, for the time being, unknown, in that the measurement technique requires placement of a small cortical electrode at the time of a surgical procedure. This limits the region of measurement to relatively small area in patients undergoing surgery, however even in this very small sample, the incidence of delayed SD after brain injury ranges from 53-88%(4). Efforts are underway to attempt to measure CSD less invasively(5) or non-invasively(6,7), however these techniques are currently under exploration and do not have the robust reliability of the cortical electrode system.