Clinical Trials

Because oral calcium channel blockers appear to reduce the severity of cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH), interest in their application intraarterially has emerged for cases in which noninvasive means of alleviating vasospasm are unsuccessful. Studies to date have been limited to the administration of low intraarterial doses because of concerns about hemodynamic stability and changes in intracranial pressure. These doses, although effective in cases of milder vasospasm, were inadequate in severe cases. The authors present a series of 10 patients with cerebral vasospasm who underwent 12 procedures in which they received > or = 20 mg of intraarterial verapamil per procedure. Read More on PubMed

Attempts to reverse cerebral vasospasm (CVS) after aneurysmal subarachnoid hemorrhage (aSAH) rely on a limited number of treatments. Calcium channel blockers have proven a benefit but their vasodilating effect on spastic cerebral arteries is relatively modest. Milrinone, a phosphodiesterase inhibitor, combines vasodilating and inotropic properties, but limited data exist to support its use for the treatment of CVS. We assessed the efficacy and tolerance of milrinone in patients with CVS secondary to aSAH. Read More on PubMed

Papaverine is the primary intra-arterial (IA) treatment for vasospasm after aneurysmal subarachnoid hemorrhage (SAH); however, is it limited in effect and by adverse effects. We prospectively studied the use of IA nicardipine as a treatment for vasospasm. Read More on PubMed

There is uncertainty about the efficacy of hypertension, hypervolemia, and hemodilution (triple-H) therapy in reducing the occurrence of delayed ischemic neurological deficits (DINDs) and death after subarachnoid hemorrhage. The authors therefore conducted a systematic review to evaluate the efficacy of triple-H prevention in decreasing the rate of clinical vasospasm, DINDs, and death. Read More on PubMed

Delayed ischaemia due to cerebral 'vasospasm' is a significant cause of morbidity and mortality after aneurysm haemorrhage. In a literature review more than 30 000 cases were found where vasospasm after subarachnoid haemorrhage (SAH) was discussed. The incidence of angiographic vasospasm was 43.3% overall, and 67.3% where angiography was done at a time of maximum expected spasm. Symptomatic vasospasm or delayed ischaemic deficit (DID) occurred in 32.5%. There was no difference in incidence and time course between preoperative and postoperative cases. 30% of those with DID died, and permanent neurological deficits occurred in 34%. A fatal outcome was much more likely in the presence of vasospasm, and a satisfactory outcome one third less likely. Vasospasm is thus the cause of death in about 10%, and of disability in slightly more cases of aneurysmal SAH. The extent of the problem has not changed significantly over three decades. Read More on PubMed

Cerebral vasospasm following aneurysmal subarachnoid hemorrhage is one of the most important causes of cerebral ischemia, and is the leading cause of death and disability after aneurysm rupture. There are two definitions of cerebral vasospasm: angiographic and clinical. Care must be exercised to be certain that it is clear which entity is being addressed. The diagnosis of the clinical syndrome is one of exclusion and can rarely be made with absolute certainty. The pathogenesis of cerebral vasospasm is poorly understood. Most current theories focus on the release of factors from the subarachnoid clot. More attention must be given to the role of endothelial damage and alterations in the blood-arterial wall barrier. The application of modern techniques for studying vascular smooth muscle which have been developed as a result of research in the areas of hypertension and atherosclerosis must be applied to the problem of cerebral vasospasm. A stress test to select patients with angiographic arterial narrowing who have adequate cerebral vascular reserve to undergo surgery should be developed. The optimal treatment of vasospasm awaits development of agents for blocking or inactivating spasmogenic substances or blocking arterial smooth muscle contraction. Rheological or hemodynamic manipulations to prevent or reverse ischemic consequences of vasospasm are relatively effective, but complicated and hazardous, and should be viewed principally as interim measures awaiting development of more specific therapies for the arterial narrowing. Read More on PubMed