Fig. 2

Pathophysiological processes in delayed cortical ischaemia. Key processes include angiographic vasospasm, microcirculatory constriction and formation of microthrombi, and waves of cortical spreading ischaemia, all of which can contribute to cerebral infarction. Delayed effects of the early brain injury such as neuronal and endothelial cell apoptosis, and systemic complications, can also occur. CPP cerebral perfusion pressure, ICP intracranial pressure, NO nitric oxide, SAH subarachnoid haemorrhage, TRP transient receptor potential. First published in Nature Reviews Neurology [95]