Intracarotid slow bolus injection of nimodipine during angiography for treatment of cerebral vasospasm after SAH. A preliminary report

Nimodipine was given as an intracarotid slow bolus injection in six patients with subarachnoid hemorrhage (SAH) due to rupture of a cerebral aneurysm, with angiographically demonstrated vasospasm. The patients were followed by serial angiograms for demonstration of the effect of nimodipine on vasospasm. After angiography, all patients were treated with a constant venous infusion of this new calcium antagonist. Although the therapeutic regimen was started only a few hours after onset of vasospasm, there was no change in cerebral vessel caliber detectable on angiograms following the intracarotid injection. Three patients died, two patients finally recovered with neurological deficits due to cerebral ischemia, and one patient with asymptomatic vasospasm remained symptom-free. Although nimodipine may act to prevent cerebral vasospasm after SAH, the authors believe that the intracarotid application is not effective after vasospasm has occurred.     

Effect of fasudil hydrochloride, a protein kinase inhibitor, on cerebral vasospasm and delayed cerebral ischemic symptoms after aneurysmal subarachnoid hemorrhage

The efficacy and safety of fasudil hydrochloride, a novel protein kinase inhibitor, were evaluated for the treatment of cerebral vasospasm and associated cerebral ischemic symptoms in patients with ruptured cerebral aneurysm. This randomized open trial with nimodipine as the control included 72 patients who underwent subarachnoid hemorrhage surgery for ruptured cerebral aneurysm of Hunt and Hess grades I to IV. For 14 days following surgery, patients were administered either 30 mg of fasudil hydrochloride by intravenous injection over a period of 30 minutes three times a day or 1 mg/hr of nimodipine by continuous intravenous infusion. Fasudil hydrochloride and nimodipine both showed inhibitory effects on cerebral vasospasm. The incidence of symptomatic vasospasm was five of 33 patients in the fasudil group and nine of 32 patients in the nimodipine group. Good recovery evaluated by the Glasgow Outcome Scale was achieved by 23 of 33 patients in the fasudil group and 19 of 34 patients in the nimodipine group. Both drugs significantly improved consciousness levels and neurological deficits such as aphasia. However, fasudil hydrochloride improved motor disturbance more than nimodipine. Adverse reactions occurred in 13 of 37 patients receiving fasudil hydrochloride and 15 of 35 patients receiving nimodipine. There were no serious adverse events in the fasudil group. The results of this clinical trial indicate that fasudil hydrochloride is a safe and efficient agent for suppressing cerebral vasospasm after subarachnoid hemorrhage surgery for ruptured cerebral aneurysm.     

Efficacy and safety of fasudil in patients with subarachnoid hemorrhage: final results of a randomized trial of fasudil versus nimodipine

Fasudil is believed to be at least equally effective as nimodipine for the prevention of cerebral vasospasm and subsequent ischemic injury in patients undergoing surgery for subarachnoid hemorrhage (SAH). We report the final results of a randomized, open trial to compare the efficacy and safety of fasudil with nimodipine. A total of 63 patients undergoing surgery for SAH received fasudil and 66 received nimodipine between 1998 and 2004. Symptomatic vasospasm, low density areas on computed tomography (CT), clinical outcomes, and adverse events were all recorded, and the results were compared between the fasudil and nimodipine groups. Absence of symptomatic vasospasm, occurrence of low density areas associated with vasospasm on CT, and occurrence of adverse events were similar between the two groups. The clinical outcomes were more favorable in the fasudil group than in the nimodipine group (p = 0.040). The proportion of patients with good clinical outcome was 74.5% (41/55) in the fasudil group and 61.7% (37/60) in the nimodipine group. There were no serious adverse events reported in the fasudil group. The present results suggest that fasudil is equally or more effective than nimodipine for the prevention of cerebral vasospasm and subsequent ischemic injury in patients undergoing surgery for SAH.     

Calcium antagonists and vasospasm

A critical review of the clinical data supports the conclusion that nimodipine decreases the severity of neurologic deficits and improves outcome after subarachnoid hemorrhage. The mechanisms by which mortality and morbidity are reduced are still controversial. First, the frequency of vasospasm is not altered (Figs. 5 and 6). Second, the consistent reversal of vasospasm once present has not been demonstrated either angiographically or by noninvasive cerebral blood flow studies. These observations suggest that there is either modification of microcirculatory flow (i.e., dilation of pial conducting vessels or decreased platelet aggregation) or a direct neuronal protective effect. As suggested previously, support for either mechanism is not resolute, and further investigation is necessary. Currently, nimodipine has been the most thoroughly investigated calcium antagonist both from an experimental and clinical perspective. Oral administration has had few reported complications. Therefore, the benefit/risk ratio clearly supports the prophylactic use of this calcium antagonist in patients of all clinical grades after subarachnoid hemorrhage. Evidence also indicates that starting nimodipine after the onset of delayed ischemic deficits is of benefit. Finally, it can be predicted that in the future additional calcium antagonists with more selective vascular or neuronal effects will be developed for use in neurologic disorders.     

Hypertensive encephalopathy as a complication of hyperdynamic therapy for vasospasm: report of two cases

OBJECTIVE AND IMPORTANCE: After developing subarachnoid hemorrhage, patients may deteriorate from a variety of well-known causes, including rebleeding, hydrocephalus, and vasospasm. Many patients now undergo empirical hyperdynamic vasospasm therapy with hypervolemia, induced hypertension, and nimodipine. CLINICAL PRESENTATION: We report two cases of iatrogenic hypertensive encephalopathy occurring during hyperdynamic therapy for cerebral vasospasm after subarachnoid hemorrhage. Hypertensive encephalopathy is a syndrome of rapidly evolving generalized or focal cerebral symptoms occurring in the setting of severe hypertension, which is reversible with antihypertensive therapy. INTERVENTION: The syndrome can be diagnosed in the appropriate clinical setting with computed tomographic or magnetic resonance imaging that demonstrates characteristic findings. In both cases, decreasing the blood pressure resulted in neurological improvement. CONCLUSION: In the setting of induced hypertensive/hypervolemic therapy for vasospasm, hypertensive encephalopathy should be considered as a potentially reversible cause of delayed neurological decline.     

Side effects of continuous intra-arterial infusion of nimodipine for management of resistant cerebral vasospasm in subarachnoid hemorrhage patients: A systematic review

BackgroundCerebral vasospasm is a common complication of subarachnoid hemorrhage. Nimodipine is the most frequently used drug for cerebral vasospasm management and is the only approved medication that has been demonstrated to reduce ischemic complications, infarct size and improve neurological outcome after aneurismal subarachnoid hemorrhage. The main purpose of this systematic review was to conduct a comprehensive analysis of the main cerebral and extracerebral side effects of continuous intra-arterial infusion of nimodipine in management of delayed cerebral ischemia in subarachnoid hemorrhage patients.Materials and methodsA protocol with the inclusion and exclusion criteria for matched cases and the method of analysis were established and agreed by all authors. We defined the scope of this review to include articles (prospective and retrospective) reporting the side effects of continuous intra-arterial infusion of nimodipine in human subjects. PRISMA guidelines were used to conduct this systematic review.ResultsA total of 8 articles reporting 136 patients were included in the review and analyzed. The side effects associated with continuous intra-arterial infusion of nimodipine were arterial hypotention, heparin-induced thrombocytopenia, atrial fibrillation or flutter, infections, acute kidney injury, hepatic and gastro-intestinal side effects.ConclusionThe most frequent side effects reported in the articles included in this systematic review associated with the continuous intra-arterial infusion of nimodipine were arterial hypotension and heparin-induced thrombocytopenia. Intracerebral hemorrhage, the elevation of ICP, heart rhythm disorders, infectious complications, and thrombosis of the catheter might be also associated with CIAN. Future prospective studies are warranted to establish the risks and incidence of procedure-related side effects.     

Controlled study of nimodipine in aneurysm patients treated early after subarachnoid hemorrhage

We enrolled 75 consecutive patients admitted with subarachnoid hemorrhages in a randomized, double-blind, placebo-controlled trial to determine the effect of early intervention with nimodipine on outcome and cerebral blood flow. The cardioprotective effect of nimodipine was assessed by measuring the electrocardiographic changes over the first 3 days of drug treatment. There was a mild lowering of the mean cerebral blood flow in the nimodipine-treated group over the 21-day period. Analysis of the continuous electrocardiographic traces showed no difference between the nimodipine and placebo groups in the frequency or type of abnormality detected. At 3 months, 4 of the 38 patients receiving nimodipine had died, compared with 10 of the 37 placebo-receiving patients. Of the 50 eligible patients who had a proven cerebral aneurysm, 1 patient (4%) on nimodipine died compared with 6 (24%) receiving placebo (0.01 less than P less than 0.05, chi 2 test; approximate 95% confidence interval for mortality difference, 0.4% to 39.6%). We conclude that nimodipine does not increase the cerebral blood flow or protect the heart after a subarachnoid hemorrhage. There were no side effects from nimodipine. The trend toward improved outcome should be verified in a larger series of patients.     

Nimodipine in aneurysmal subarachnoid hemorrhage: a randomized study of intravenous or peroral administration

OBJECT: The calcium antagonist nimodipine has been shown to reduce the incidence of ischemic complications following aneurysmal subarachnoid hemorrhage (SAH). Although most randomized studies have been focused on the effect of the peroral administration of nimodipine, intravenous infusion is an alternative and the preferred mode of treatment in many centers. It is unknown whether the route of administration is of any importance for the clinical efficacy of the drug. METHODS: One hundred six patients with acute aneurysmal SAH were randomized to receive either peroral or intravenous nimodipine treatment. The patients were monitored for at least 10 days after bleeding in terms of delayed ischemic neurological deficits (DINDs) and with daily measurements of blood flow velocities in the middle cerebral arteries by using transcranial Doppler ultrasonography. Three months after SAH, clinical outcome and new cerebral infarctions according to MR imaging studies were recorded. RESULTS: Baseline characteristics (age, sex distribution, clinical status on admission, radiological findings, and aneurysm treatment) did not differ between the treatment groups. There was no significant difference in the incidence of DINDs (28 vs 30% in the peroral and intravenous groups, respectively) or middle cerebral artery blood flow velocities (> 120 cm/second, 50 vs 45%, respectively). Clinical outcome according to the Glasgow Outcome Scale was the same in both groups, and there was no difference in the number of patients with new infarctions on MR imaging. CONCLUSIONS: The results suggest that there is no clinically relevant difference in efficacy between peroral and intravenous administration of nimodipine in preventing DINDs or cerebral vasospasm following SAH.     

Effect of intraventricular sodium nitroprusside on cerebral hemodynamics and oxygenation in poor-grade aneurysm patients with severe, medically refractory vasospasm

OBJECTIVE: Sodium nitroprusside (SNP) was recently suggested as a treatment for cerebral ischemia in patients with severe, medically refractory vasospasm after subarachnoid hemorrhage. In this study, we sought to objectify the effect on cerebral hemodynamics and oxygenation (PbrO2) when using intraventricular SNP as a last resort therapy in poor-grade patients with subarachnoid hemorrhage; severe, medically refractory vasospasm; and compromised cerebral blood flow. METHODS: Thirteen of 185 consecutive patients with subarachnoid hemorrhage developed severe, medically refractory vasospasm and were treated with intraventricular SNP. All of these patients' neurological conditions were classified as Hunt and Hess Grade IV. SNP doses ranged from 10 to 40 mg with single-dose treatment and from 2 to 8 mg/h with continuous infusion. Angiography or PbrO2 measurement was used to assess the treatment effects. RESULTS: In 6 of the 13 patients, SNP improved cerebral hemodynamics, as demonstrated by increased PbrO2 or decreased cerebral circulation time. Only 1 patient showed increased diameter of the spastic vessel, however. Maximum increase in PbrO2 ranged from 5 to 52 mmHg. Adverse effects were hypertension in five patients, vomiting in three patients, and cardiac arrhythmia in one patient. Cerebral infarctions caused by vasospasm occurred in 6 (46%) of the 13 patients. No differences between SNP responders and SNP nonresponders were noted. CONCLUSION: In patients with severe, medically refractory vasospasm, intraventricular SNP may improve PbrO2 and cerebral blood flow, but the effect is highly variable. On the basis of the improvements we observed in 6 of 13 patients, intraventricular SNP administration is justified as a last resort therapy in patients with cerebral ischemia and impending infarction. Our findings suggest that SNP may be more effective when initiated early and administered continuously.     

Evaluation of the calcium-antagonist nimodipine for the prevention of vasospasm after aneurysmal subarachnoid haemorrhage

Summary 70 consecutive patients admitted within four days after the first aneurysmal subarachnoid haemorrhage (SAH) were evaluated by daily transcranial Doppler ultrasound (TCD) measurement of the blood flow velocities (BFVs) of both middle cerebral arteries (MCAs) and by daily recordings of their clinical grade (Hunt and Hess). Patients with no or only little subarachnoid blood in the first CT after admission were classified as low-risk for the development of symptomatic vasospasm (VSP), and patients with big subarachnoid clots or thick layers of subarachnoid blood were graded as high-risk patients for symptomatic VSP. The first series of 33 patients received no nimodipine whereas the second series of 37 patients were treated with nimodipine 2 mg/h intravenously, starting within 24 hours after the SAH in the majority of patients. 7–14 days postoperatively, the intravenous dose was changed to oral nimodipine 60 mg/q4h for one week and then discontinued. A mean BFV curve of the side with the higher flow velocities correlated with the mean clinical status (Hunt and Hess) was calculated by computer analysis for the patients treated without nimodipine and for those receiving nimodipine in each risk group. The mean BFV curves of the same risk groups were compared in order to evaluate the effect of nimodipine for the prevention of vasospasm following SAH. The delayed neurological deficits (DIND) and the functional outcome six months after the SAH were recorded in each group and compared.Nimodipine given within four days after the SAH did not prevent vasospasm evaluated by TCD, but it significantly reduced the severity of the vasoconstriction, especially in high-risk patients. It reduced significantly the incidence of DIND in high-risk patients and improved their functional outcome. Although nimodipine may have a reduced efficacy in preventing vasospasm after early operation of high-risk patients, it probably protects the brain by increasing its tolerance to focal ischaemia.     

Two patients treated with intra-aortic balloon pump counterpulsation after subarachnoid hemorrhage

Intra-aortic balloon pump counterpulsation (IABP) was used to treat two patients with symptomatic vasospasm after subarachnoid hemorrhage. One could not tolerate triple H therapy (hypertensive hypervolemic hemodilution) because of poor cardiac function and another suffered acute myocardial infarction after aneurysm surgery followed by cardiac failure. IABP increased cerebral blood flow and prevented cerebral infarction in the former case but this could not reverse cerebral ischemia in the latter. IABP may be one choice for patients with vasospasm after subarachnoid hemorrhage.     

Prophylactic hyperdynamic postoperative fluid therapy after aneurysmal subarachnoid hemorrhage: a clinical, prospective, randomized, controlled study

OBJECTIVE: To investigate the role of prophylactic hyperdynamic postoperative fluid therapy in preventing delayed ischemic neurological deficits attributable to cerebral vasospasm. METHODS: We designed a prospected, randomized, controlled study and included 32 patients with subarachnoid hemorrhage. Sixteen patients received hypervolemic hypertensive hemodilution fluid therapy; the other 16 patients received normovolemic fluid therapy. All patients were monitored for at least 12 days, with clinical assessments, transcranial Doppler recordings, single-photon emission computed tomographic (SPECT) scanning, and routine computed tomographic scanning. For fluid balance monitoring, a number of blood samples were obtained on a daily basis and continuous central venous pressure and mean arterial blood pressure measurements were performed for both groups. All patients received intravenous nimodipine infusions between Day 1 and Day 12. End points of this study were clinical outcomes, clinically evident and transcranial Doppler sonography-evident vasospasm, SPECT findings, complications, and costs. Clinical examinations (using the Glasgow Outcome Scale) performed 1 year after discharge, together with neuropsychological assessments and SPECT scanning, were the basis for the evaluation of clinical outcomes. RESULTS: No differences were observed between the two groups with respect to cerebral vasospasm (as observed clinically or on transcranial Doppler recordings). When regional cerebral blood flow was evaluated by means of SPECT analysis performed on Day 12 after subarachnoid hemorrhage, no differences were revealed. One-year clinical follow-up assessments (with the Glasgow Outcome Scale), including SPECT findings and neuropsychological function results, did not demonstrate any significant group differences. Costs were higher and complications were more frequent for the hyperdynamic therapy group. CONCLUSION: Neither early nor late outcome measures revealed any significant differences between the two subarachnoid hemorrhage treatment models.     

Acute operation and preventive nimodipine improve outcome in patients with ruptured cerebral aneurysms

Sixty-five patients with ruptured aneurysms were operated upon within 48 to 72 hours after subarachnoid hemorrhage (SAH) and were treated with a regimen of intra- and postoperative nimodipine for the prevention of symptomatic vasospasm. The clinical grading (Hunt and Hess) was I to III in 49 patients and IV or V in 16. The SAH was mild in 15 patients, moderate in 27, and severe in 23; 12 patients harbored an intracerebral hematoma, and 6 had intraventricular bleeding. Acute hydrocephalus was observed on preoperative computed tomography (CT) in 19 patients. On CT 3 days postoperatively (i.e., Day 3-4 after SAH), 30 of 65 patients still had subarachnoid blood; however, severe symptomatic vasospasm as the deciding threatening event during the delayed postoperative period was not encountered in this series. Transient symptoms of ischemia were noted in 2 patients (3%) and were accompanied by angiographic spasm in 1. Irreversible neurological deficit occurred in 2 patients (3%); in 1 of these, it was a complication of postoperative control angiography. Of the patients preoperatively graded I or II, 96% had an excellent to fair outcome 6 months postoperatively, and 1 patient (4%) had died because of a surgical complication. Among patients preoperatively graded III or IV, 86% had an excellent to fair outcome, and the remaining 14% had a poor outcome. Shunt-dependent hydrocephalus developed in 7% of the patients. Acute surgical repair of ruptured cerebral aneurysms and preventive topical and intravenous administration of nimodipine reduce management complications and improve outcome; above all, ischemic lesions from symptomatic vasospasm are reduced to a minimum.     

Intrathecal nimodipine therapy in a primate model of chronic cerebral vasospasm

The safety, prevention, and treatment of chronic vasospasm by repeated administration of intrathecally applied nimodipine was evaluated in a primate model of chronic cerebral vasospasm. Twenty-four female cynomolgous monkeys were randomized into three groups of 8: sham, clot, and clot + intrathecal nimodipine. All animals underwent a subarachnoid hemorrhage (SAH) induction operative procedure after base line angiography. Nimodipine was administered postoperatively by subcutaneous injection of 1 ml/0.2 mg tid for 6 days through an Ommaya reservoir with the catheter placed in the subarachnoid basal cisterns. Angiography was performed on Day 7 post-SAH induction. Intrathecally applied nimodipine was not effective in the prevention of angiographic vasospasm. It also did not seem to decrease the degree of pathological change when compared to controls. One animal in the nimodipine group died 2 hours after an intrathecal injection secondary to a respiratory arrest. Transient sedation and hypoventilation were common. No adverse pathological effects were noted. Intrathecal nimodipine did not produce a significant dilation of vessels in moderate or severe spasm when assessed by angiography 2 hours after intrathecal injection. Only 1 animal in 8 showed diffuse dilation of vasospastic cerebral vessels after an intrathecal nimodipine injection. Three other animals in this group developed dilation only of the basilar artery, which was in mild spasm.     

Chronic cerebral vasospasm: effect of calcium antagonists

The efficacy of the calcium antagonists nifedipine and nimodipine was evaluated in a multiinjection canine model of severe chronic cerebral vasospasm. Each of 21 adult mongrel dogs (15 to 20 kg) was assigned to one of four experimental groups. All animals received a total of 15 ml of fresh, unheparinized arterial blood via three cisterna magna injections. Selective left vertebral arteriography was performed 1 week before and exactly 7 days after the simulated subarachnoid hemorrhage. Treatment with calcium antagonists was initiated at 24 hours and continued for 7 consecutive days. Comparisons were based on the percentage of reduction in basilar artery diameter. On a milligram/kilogram basis, we used the manufacturer's maximal recommended daily dosages of nifedipine, whereas the dosages of nimodipine used were 3 to 7 times greater than that reported to be therapeutically effective in reducing the incidence of severe deficits from vasospasm in patients with aneurysmal subarachnoid hemorrhage. In this laboratory trial, systemic treatment with calcium antagonists did not prevent or significantly reduce chronic arterial narrowing. In the control group, spasm reduced basilar artery diameter an average of 71% +/- 11 (SD). In the group treated with nifedipine, 10 mg orally every 6 hours, vessel diameter was reduced an average of 58% +/- 13%. In those animals treated with nimodipine, 20 or 40 mg orally every 4 hours, the basilar artery diameter was decreased an average of 59% +/- 8 and 56% +/- 7, respectively. A preliminary trial using direct intracisternal administration of these agents demonstrated increased vessel diameter within 20 minutes in four of six animals, supporting other reports that this route of administration may prove more efficacious in the treatment of chronic cerebral vasospasm.     

Cardiorespiratory problems in the use of calcium antagonists for vasospasm prophylaxis in subarachnoid hemorrhage

Since studies by Allen et al. [1] calcium antagonists have been commonly used for prevention of cerebral vasospasm in patients suffering from acute subarachnoid hemorrhage (SAH). Vasodilatation-induced hypotension, increase of cardiac output and intrapulmonary shunting (Qs/Qt) are wellknown cardiovascular effects. These problems are discussed in light of previous reports and present case study of a 34-year-old woman treated with the calcium antagonist nimodipine after SAH. Reproducible results from invasive haemodynamic monitoring (Swan-Ganz-thermodilution catheter) indicated correlation between nimodipine application and increased intrapulmonary shunting. This effect can be hazardous for SAH patients because preexisting cerebral ischemic hypoxia makes them particularly susceptible to additional decrease in oxygen supply.     

Cerebral vasospasm with subarachnoid hemorrhage from cerebral arteriovenous malformations

The angiograms and clinical records of 12 patients with subarachnoid hemorrhage from cerebral arteriovenous malformations were reviewed. Of these 12 patients, cerebral vasospasm was confirmed in 1 patient. The case of a 28-year-old man who showed angiographic evidence of cerebral vasospasm is reported, and the rarity of vasospasm associated with subarachnoid hemorrhage from cerebral arteriovenous malformations is discussed.     

Effect of early operation on cerebral vasospasm

The effect of early operation on cerebral vasospasm was studied in 150 patients with aneurysmal subarachnoid hemorrhages who fulfilled all of the following criteria: admission by day 2 after subarachnoid hemorrhage, no rebleeding, clinical grades I to IV on admission, subarachnoid hemorrhage alone on computed tomography scan, not operated on between days 4 and 20, and availability of bilateral carotid angiograms done by day 2 and redone between days 7 and 9. The patients were divided into two groups: those operated on by day 3 (group 1: 116 patients) and those operated on after day 20 or not operated on (group 2: 34 patients). Severity of both subarachnoid hemorrhage on computed tomography scan and angiographic vasospasm were graded into 0-IV. Angiographic vasospasm was observed in 95% of group 1 and in 88% of group 2 patients. A significant difference could not be found between groups 1 and 2 in the angiographic vasospasm grades. The incidence of symptomatic vasospasm in group 1 was 18%, which was significantly lower than the 44% in group 2. In group 1 patients with subarachnoid hemorrhage grades II to III, the incidences of symptomatic vasospasm and low density area on computed tomography scan were 13% and 10%, respectively. Both of these rates were significantly lower than those in group 2, which were 50% and 36%, respectively. However, in patients with subarachnoid hemorrhage grade IV, no differences could be found between groups 1 and 2. There was a close correlation between the angiographic vasospasm grades and the incidence of symptomatic vasospasm in group 1. However, in group 1, no correlation could be observed between the site of ruptured aneurysms or the timing of operations and vasospasm. Although there is still a limit to the effect of early operation on cerebral vasospasm in patients with subarachnoid hemorrhage grade IV, symptomatic vasospasm after subarachnoid hemorrhage may be ameliorated by early operation in patients with subarachnoid hemorrhage grades II to III.     

Implications of nimodipine prophylaxis of cerebral vasospasm on anesthetic management during intracranial aneurysm clipping

Nimodipine, a calcium entry blocking agent similar in structure to nifedipine but with selective cerebrovascular dilating effects, has potential use in the therapy and prevention of cerebral vasospasm after intracranial hemorrhage. The authors summarize the effects of calcium entry blockers, review the pharmacology of nimodipine, and discuss both the known and possible interactions of oral nimodipine with physical and pharmacological interventions that neuroanesthesiologists employ for patients with cerebral vasospasm during craniotomy for aneurysm clipping. In a series of 26 patients undergoing aneurysm clipping, the authors found that intraoperative blood pressure tended to be reduced by nimodipine. Although the number of patients was limited by the fact that they were enrolled in a multi-center nimodipine aneurysm study and thus had to meet the criteria for that study, it is concluded that prophylaxis of cerebral vasospasm with nimodipine in patients with ruptured intracranial aneurysm results only in a favorable tendency toward lower systemic blood pressure during craniotomy.