The Factors Cause Vasospasm After Aneurysmal Subarachnoid Hemorrhage

Cerebral vasospasm remains a significant source of morbidity and mortality in patients with subarachnoid hemorrhage (SAH) after an aneurysmal rupture. Despite being a significant source of morbidity and mortality, death and disability from vasospasm have declined from approximately 35% in the early 1970's, to between 15% and 20% in the 1980's to <10% in the 1990's(1,2,3,4).Extensive research has shown that the big event that leads to the initiation of vasospasm is the release of oxyhemoglobin (blood breakdown product)(1,12,13). This mechanism appears to be a multifactorial process that involves the generation of free radicals, lipid peroxidation and activation of protein kinase C as well as phospholipase C and A2 with resultant accumulation of diacylglycerol and the release of endothelin-1(14,15,16,17,18). On the other hand, depletion of NO synthase (19,20,21) was also noted after SAH. Previous reports showed that shunting of CSF through a lumbar drain after an SAH markedly reduces the risk of clinically evident vasospasm and its sequelae, shortens hospital stay, and improves outcome. Its beneficial effects are probably mediated through the removal of spasmogens that exist in the CSF(22). In our preliminary data, we have demonstrated a case with severe vasospasm, CSF was collected both from EVD and lumbar drain. The ADMA level and amount of Nitrate was well correlate with vasospasm and the level was much higher in lumbar drain then EVD. So, we will compared the CSF from EVD and lumbar puncture to see which factor is correlate with vasospasm.