ENDOVASCULAR THERAPY FOR ANEURYSMAL VASOSPASM

Vasospasm of the cerebral vessels is a frequent occurrence after aneurysmal subarachnoid hemorrhage (SAH) and continues to be responsible for ischemic complications in a subset of patients. Greater understanding of the mechanisms responsible for cerebral vasospasm has been possible through the development of experimental models and pharmacologic investigations. Various medications have been evaluated in human clinical trials for their effect on reducing ischemic complications from vasospasm. Cerebroselective calcium channel blockers have been shown to be effective in improving outcome after SAH and are now routinely used. 2,11 These compounds may provide direct neuroprotection from ischemia as well as have a direct effect on vascular mechanisms. Large clinical trials have also evaluated the effect of 21 aminosteroids that have not been demonstrated to improve overall outcome in patients who have SAH. 14 Another therapy that is routinely employed for the prevention and treatment of ischemic deficits after SAH is triple-H therapy that denotes induced hypertension, hypervolemia, and hemodilution. 1 This treatment is accomplished with crystalloid and colloid solutions as well as with vasopressors to increase blood pressure. Despite the advantages offered by these medical therapies, they are not completely effective in eliminating delayed ischemic neurologic deficits (DINDs) from cerebral vasospasm. Endovascular therapy offers an additional modality for treatment in patients who continue to experience DINDs despite medical therapy.