Drug treatment of cerebral vasospasm after subarachnoid hemorrhage following aneurysms

Abstract

Cerebral vasospasm (CVS) is a common and severe complication of aneurysmal subarachnoid hemorrhage (aSAH). Despite the improvement in treatment of aSAH, CVS complicating aSAH has remained the main cause of death. CVS begins most often on the third day after the ictal event and reaches the maximum on the 5th-7th postictal days. Several therapeutic modalities have been employed to prevent or reverse CVS. The aim of this review is to summate all the available drug treatment modalities for vasospasm.

Prevention and treatment of cerebral vasospasm after aneurysmalsubarachnoid hemorrhage

“…Oral Nimodipine lowers the incidence of vasospasm-caused brain ischemia by 34% and the rate of ASAH poor outcomes by 40% 6 . Its neuroprotectivefeatures most likely contribute to positive results in CVS 6,14 . Nimodipinehas a low complication rate, can diminish the risk of secondary DCI and may achieve positive angiographic and clinical results 14 .…”

“…Statins are here reviewed as another group of potential vasospasm preventing drugs. Some trials suggested that they boost cerebral vascular reactivity 6,14 .One meta-analysis showed beneficial effects of statins on incidence of delayed vasospasm, ischemic injury, and mortality, while another meta-analysis failed to show such results 16 . Recent meta-analysis showed higher number of complications with statin therapies than their favorable outcomes 17 .…”

“…As established vasospasm prophylaxis, CCB were investigated for their potential role in treatment 19 . Nimodipine, an L-type CCB, is currently the only pharmacologic agent showing an improvement in neurological outcomes when used for a period of 21 days, every 4 h after aneurysmal rupture, suggested by the current guidelines of the American Stroke Association 14,16 .Intravenous nicardipinedidn't show effect on outcomes after three months of use and verapamil is not selective to cerebral vasculature and its use requires more research 5,14 .…”

“…SAH induced vasospasm is a complex entity that contains delayed and reversible vasculopathy, damaged auto regulatory function, and hypovolemia 11,12,13 . DCI typically lasts the first 2 weeks after SAH, while CVS reaches maximal narrowing between day 5 and 14, and then gradual resolution over 2 to 4 weeks 5,14,15 . Almost 70% of ASAH patients haveangiographic manifestation of vasospasm, and circa 50% of these patients experience predominantlycloudingof consciousness and language impairments 3,6,11,15 .…”

“…Angiographic vasospasm can be illustrated as a narrowing of the contrast medium column in main arteries of the brain 15 . Proximal vessels, situated at the base of the brain, are preferentially affected 13 .In spite of continuous evolvement of endovascular gadgets and techniques, there are still hazards specific to this type of treatment 14 .…”