Figure 1.

Multifactorial Pathophysiology of DCI. After aneurysmal subarachnoid hemorrhage, delayed cerebral ischemia can occur due to multifactorial pathophysiology. Vasospasm and microemboli, which can form as a result of a proinflammatory, hypercoagulable state after aneurysm rupture, produce regional hypoxia that can progress to infarction. Cortical spreading depressions, or waves of excitation propagating across the injured brain, can induce an inverse hemodynamic response wherein there is diminished blood flow to areas with increased metabolic demand. Persistent excitation leads to an increase in extracellular potassium and glutamate and an increase in intracellular calcium, which can lead to excitotoxic injury. When tissue at risk for infarction does not receive sufficient oxygen, DCI can result. Adapted from Leng, Fink, and Iadecola (2011).