Nimodipine treatment of ischemic neurological deficits due to cerebral vasospasm after subarachnoid hemorrhage: Clinical results of a multicenter study

Abstract

Intravenous Nimodipine was administered to 109 patients (65 female and 44 male) with either pre- or post-operative progressive neurological deterioration from cerebral vasospasm following subarachnoid hemorrhage from a ruptured aneurysm. In 91 of the patients the efficacy of Nimodipine in relieving ischemic symptoms was assessed and in all of the 109 patients the tolerance was evaluated. The aneurysms were related to following arteries: anterior communicating artery (41%), middle cerebral artery (24%), internal carotid artery (10%), vertebro-basilar arteries (4%) and others (5.5%); 11% of the patients had multiple aneurysms. On 16 of the 91 patients no surgery was performed. On 16% of the remaining 75 patients surgery was performed within 72 hours after the hemorrhage, 57% were operated between day 4 and day 15 and 29% after day 16. The ischemic neurological deficits occurred preoperatively in 67% of the patients and post-operatively in 23%. At the beginning of treatment 84% of the patients were graded III-V according to the Hunt and Hess grading system. Most of the patients received doses of 24-48 mg Nimodipine daily as constant i.v. infusion for 7-10 days. The grade of neurological deficit at the end of the treatment was evaluated according to the Glasgow Outcome Scale. 59 (65%) of the patients showed complete recovery or marked improvement of the ischemic symptoms while 22% remained unchanged and 11% died due to severe vasospasm. Administration of Nimodipine seemed to be more efficient in cases where treatment was started within 24 hours. In the patient group which was treated pre-operatively, recurrent hemorrhage was recorded in 8% of the patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Survey of clinical experience with nimodipine in patients with subarachnoid hemorrhage

“…In a placebo-controlled double-blind study [14] mortality due to vasospasm alone was 2.7% in the nimodipine group and 16.7% in the placebo group. Similar results were found in an open therapeutic study [25]. Clinical improvement was associated in other studies with changes in objective parameters such as cerebral blood flow and central conduction time [12,15,27].…”

“…Koos et al [25] administered nimodipine to 91 patients with either pre-or postoperative progressive neurological deterioration from cerebral vasospasm in a prospective, open trial. 84% of all patients were in poor grades (Hunt & Hess III-V) at the begin of nimodipine treatment (1-2 mg/hour constant infusion followed by oral doses of 240 mg per day).…”

Nimodipine

“…However, comparing their findings with those of previous studies involving surgery only, it appears likely that the combination of surgery and nimo-273 dipine does result in better outcomes. In some studies nimodipine (about 10 mg/L) was also applied directly to the artery during surgery (Auer 1984;Ljunggren et al 1984), and some patients received oral nimodipine for varying periods (7 to 18 days) after intravenous therapy (Auer 1984;Koos et al 1985;Ljunggren et al 1984). In another study of 100 patients of all grades treated with early surgery and 7 to 12 days of intravenous nimodipine 30 ,.,.g/kg/ h, only 5 (none of the 61 with internal carotid or middle cerebral artery aneurysms) developed permanent neurological dysfunction due to delayed ischaemia (Saveland et al 1986) [ fig.…”

“…In another study of 100 patients of all grades treated with early surgery and 7 to 12 days of intravenous nimodipine 30 ,.,.g/kg/ h, only 5 (none of the 61 with internal carotid or middle cerebral artery aneurysms) developed permanent neurological dysfunction due to delayed ischaemia (Saveland et al 1986) [ fig. 1990;Gilsbach & Harders 1989;Koos et at. Surgery was performed within 72 hours of haemorrhage in most studies.…”

Spontaneous Subarachnoid Hemorrhage: Assessment of Prognosis and Initial Management in the Intensive Care Unit

“…Other efforts to treat symptomatic vasospasm have been disappointing [116]. Recently, treatment of ischemic deficits from vasospasm with nimodipine, a calcium antagonist, has successfully been tried in some patients [117], but evaluation of benefits and possible risks (e.g., adverse effect on raised ICP, risk of rebleeding) in larger samples is needed. Measures to reduce an increased ICP from diffuse or focal cerebral edema associated with symptomatic vasospasm include controlled hyperventilation and osmodiuretics [6,116,118].…”