. After the initial aneurysm hemorrhage, multiple pathological mechanisms account for neuronal injury including: hydrocephalus,
apoptosis, cerebral edema, loss of blood–brain barrier, abnormal cerebral autoregulation, microthrombosis, cortical spreading depression
and vasospasm.
. Current treatment of delayed cerebral ischemia (DCI) involves nimodipine, maintenance of euvolemia, induced hypertension for
symptomatic DCI and possible endovascular treatment for patients with DCI symptoms refractory to induced hypertension.
. Cortical spreading depolarization is the latest mechanisms targeted for in DCI after aneurysmal subarachnoid hemorrhage and future
trials will use ketamine to suppress cortical spreading depolarizations.
. Other future therapy for DCI will include agents to block apoptotic pathways, agents to prevent smooth muscle cell contraction and
proliferation and low-dose anticoagulation to prevent microthrombosis.