Cortical spreading depression, where clusters of neuronal depolarization produce an influx of calcium and sodium,

results in fluctuations in regional CBF (both hyperemia and ischemia) and brain oxygenation, with possible uncoupling of
flow and metabolism. Persistent or recurrent spreading depression may be a major factor associated with both early
and delayed cerebral ischemia.
Delayed arterial narrowing, or vasospasm, occurs in two-thirds of patients, beginning about 72 hours after SAH,
and may last for as long as 2 to 3 weeks. The most important risk factors for the development of vasospasm are the
amount of blood in the basal cisterns and the initial level of consciousness. The presence of vasospasm is a clear
predictor of neurological deterioration, delayed cerebral infarction, and worse outcomes. Some patients with radiographic
evidence of severe vasospasm do not become symptomatic. Conversely, some patients deteriorate neurologically despite
no more than mild radiographic vasospasm. Thus, the degree to which vasospasm is a direct cause of neurological decline,
rather than a coexisting process, has been questioned. The pathophysiology of DCI is undoubtedly more complex than
being attributable solely to vasospasm, and includes factors such as cortical spreading depression, inflammation, and
increased coagulation