法舒地尔联用尼莫地平预防动脉瘤性蛛网膜下腔出血后迟发性脑血管痉挛的疗效观察

目的探讨法舒地尔联用尼莫地平对预防动脉瘤性蛛网膜下腔出血后脑血管痉挛的疗效及不良反应。方法在入院后即常规给予尼莫地平静脉持续泵入的同时,将50例动脉瘤性蛛网膜下腔出血患者在作动脉瘤栓塞治疗后,均给予腰大池引流及"3H"疗法,并随机分成2组,治疗组加用盐酸法舒地尔30mg静滴,3次/d,连用14d,观察2组血管痉挛的发生情况及不良反应。结果治疗组症状性脑血管痉挛1例,无症状性脑血管痉挛3例,对照组症状性脑血管痉挛3例,无症状性脑血管痉挛10例,2组间差异有统计学意义(P<0.05)。不良反应方面2组比较差异无统计学意义。结论法舒地尔联用尼莫地平在预防动脉瘤性蛛网膜下腔出血所致血管痉挛的疗效优于单用尼莫地平,安全性亦较高。     

Reversible cerebral vasoconstriction syndrome or primary angiitis of the central nervous system?

BACKGROUND: Reversible Cerebral Vasoconstriction Syndrome (RCVS) may present as thunderclap headache (TCH), accompanied by reversible cerebral vasospasm and focal neurological deficits, often without a clear precipitant. RCVS may be mistaken for Primary Angiitis of the Central Nervous System (PACNS) due to the presence of similar angiographic features of segmental narrowing of cerebral arteries. We discuss the clinical features of a young female migraine patient who developed TCH and was found to have RCVS following initial treatment with corticosteroids for PACNS, in the context of a systematic review of the available medical literature. METHODS: A Medline search was performed to identify all case reports since 1966 describing RCVS and PACNS that provide sufficient clinical detail to permit diagnostic classification according to published criteria. RCVS included case studies in which there was angiographic or transcranial Doppler ultrasound evidence of near-to-complete resolution of cerebral vasoconstriction in the absence of a well-recognized secondary cause. PACNS included reports of histologically confirmed PACNS either through biopsy or necropsy. RESULTS: Reversible Cerebral Vasoconstriction Syndrome occurs primarily in females and is characterized by sudden, severe headache at onset, normal CSF analysis, vasoconstriction involving the Circle of Willis and its immediate branches, and angiographic or TCD ultrasound evidence of near-to-complete vasospastic resolution within 1-4 weeks. It occurs typically in the context of vasoconstrictive drug use, the peripartum period, bathing, and physical exertion. CONCLUSION: Initial and follow-up (within 4 weeks) non-invasive angiographic studies are indicated in patients who present with TCH or who have clinical presentations that could be consistent with RCVS or PACNS in the absence of a well-recognized secondary cause, such as subarachnoid haemorrhage. Early reversibility of cerebral vasospasm is the key neuroradiological feature that supports the clinical diagnosis of RCVS.     

Poor Utilization of Nimodipine in Aneurysmal Subarachnoid Hemorrhage

Objective: To determine adherence to nimodipine administration in patients admitted with aneurysmal subarachnoid hemorrhage (aSAH). Background: Oral nimodipine (60 mg every 4 hours for 21 days) is recommended by the national guidelines for aSAH. A Cochrane systematic review has determined that nimodipine reduces the risk of cerebral ischemia and is currently the only effective drug for the prevention of vasospasm in aSAH patients. Design/Methods: We retrospectively analyzed 109 patients with aSAH admitted to the Neurosciences Intensive Care Unit (NICU) at a tertiary care medical center between 2010 and 2013. Nimodipine-prescribing patterns, days of therapy completed, and adverse effects were tabulated. Patients not initiated on nimodipine and reasons for prematurely stopping therapy were noted. Results: One hundred two (93%) patients with aSAH were started on oral nimodipine upon admission to the NICU. Early death (3%) and hypotension (1%) were reasons why patients were not started on nimodipine. Only 36 (33%) patients received nimodipine, 60 mg orally every 4 hours for 21 days. In 26 patients (39%), the dose of nimodipine was reduced because of excessive drops in blood pressure. Transient discontinuation occurred in 2 (2%) patients. Thirty one (47%) patients were discharged from the hospital before 21 days and nimodipine was not ordered to continue at home. Conclusion: We found that the majority of patients with aSAH in our practice did not complete 21 days of nimodipine. Hypotension was mostly responsible for dosing change or discontinuation.     

Transcranial Doppler findings in a population with clinical probable reversible cerebral vasoconstriction syndrome

ObjectiveTo describe transcranial Doppler (TCD) findings in a population with clinical probable RCVS. Exploratory objectives included the study of clinical characteristics of probable RCVS patients with and without spasm detected by TCD.MethodsCross-sectional cohort study of patients with thunderclap headache (TCH) without subarachnoid hemorrhage (SAH) of our neurology and headache center between 2010 and 2019, selecting patients with clinical diagnosis of probable RCVS (negative angiography study) by ICHD-3 criteria and with at least two TCD studies.ResultsFrom 114 TCH patients, 36/114 had probable RCVS by ICHD-3 criteria and had at least two TCD studies available. The mean age at RCVS onset was 42.9 years (21–72 years); 29/36 (80.6%) were female, 7/28 (25%) had cardiovascular risk factors and 20/36 (55.6%) had history of migraine. Most common triggers were stressful emotion, drugs, valsalva maneuvers and sexual activity. Five/36 (13.9%) had complications and 3/36 (8.3%) had late recurrence. Initial TCD was performed on average of 16 (6–26) days after headache onset. Twenty-nine had vasospasm on TCD, presenting mean flow velocity of MCA (VMCA) of 135.7 ± 17.0 cm/s and mean maximum VMCA of 138.3 ± 17.2. Vasospasm was mild in 21/29 patients (72.4%) and moderate in 8/29 (27.6%). Complete VMCA normalization occurred on average 41 (30–70) days after headache onset and 24 (11–47) days after initial TCD. The group of patients with vasospasm detected by TCD had more female patients (26/29, 89.7% vs. 3/7, 42.8%, P = 0.016), and more TCH attacks (mean of 3.6 vs. 2.14, P = 0.049).ConclusionTCD may be a useful tool in the identification of vasospasm in patients with probable RCVS, supporting the diagnosis of RCVS in patients presenting with recurrent TCH without SAH.     

Cisternal sustained release dihydropyridines for subarachnoid hemorrhage

Nimodipine improved outcome in patients with subarachnoid hemorrhage (SAH) although hypotension limited the dose that could be administered systemically. Subarachnoid delivery of nicardipine or nimodipine may be more efficacious. We tested the efficacy of cisternal application of sustained release nicardipine and nimodipine in SAH in monkeys and dogs, respectively. SAH was created in 13 cynomolgus macaques by placement of autologous blood clot around right middle cerebral, anterior cerebral, and internal carotid arteries. Placebo poly-D,L-lactide coglycolide (PLGA), nicardipine PLGA or mibefradil PLGA was inserted in the clots. Catheter and computed tomography angiography (CTA) were performed at baseline and 7 days later (day 7). Cerebral infarction was assessed on day 7 by magnetic resonance imaging. Six dogs underwent baseline angiography and injection of autologous blood plus PLGA or nimodipine-loaded PLGA microparticles into the cisterna magna. Blood injection was repeated 2 days later and angiography 7 and 14 days later. Animals were euthanized and brains were examined histologically. Cerebrospinal fluid and serum nimodipine concentrations were measured. Nicardipine, but not mibefradil PLGA decreased vasospasm in monkeys (paired t-tests) although there was no significant effect on infarctions see on MRI. In dogs, nimodipine-PLGA produced high local concentrations of nimodipine that were associated with reduced basilar artery vasospasm. No untoward histological effects were observed. There was no reduction in microthrombi in animals treated with nimodipine PLGA compared to placebo PLGA. Site-specific, sustained release formulations of dihydropyridines can deliver high concentrations to the cerebrospinal fluid without causing systemic side effects, and may reduce angiographic vasospasm after SAH. Since nimodipine improves outcome in patients with SAH without necessarily preventing vasospasm, further studies are warranted.     

Feasibility and safety of intrathecal nimodipine on posthaemorrhagic cerebral vasospasm refractory to medical and endovascular therapy

OBJECTIVE: The effectiveness of balloon angioplasty and intra-arterial infusion of vasodilating agents for patients suffering from severe vasospasm following aneurysmal subarachnoid haemorrhage (SAH) is often unsatisfying and there is still demand for further last resort treatment strategies. In the current prospective study, we attempted the intrathecal lavage administration of nimodipine in cases of severe cerebral vasospasm that were refractory to medical and endovascular therapy. METHODS: Eight of 146 patients with aneurysmal SAH were included in the prospective study, which had been approved by the local ethics committee. Treatment was instituted by intraventricular nimodipine bolus (0.4mg), followed by a continuous lumbar intrathecal infusion (0.4mg/h). Effectiveness was monitored angiographically, with transcranial Doppler (TCD), perfusion CT (pCT), and by neurological examination during treatment course and follow-up. RESULTS: The neurological condition improved directly in three patients and remained unchanged in four patients. Seventeen (70.8%) CT perfusion analyses revealed improved perfusion. A reduction of vasospasm was seen angiographically by digital subtraction angiography (DSA) in seven (66.6%) investigations. Additional ischaemic infarction after onset of the intrathecal therapy was documented in two (25%) patients. There were no serious adverse effects observed. CONCLUSION: The present study has for the first time demonstrated the feasibility and safety of intrathecal nimodipine lavage in patients with severe vasospasm resistant to the established medical and endovascular treatment strategies. The results of the study are therefore encouraging, and further experimental and clinical trials should be carried out so as to investigate the efficacy of intrathecal nimodipine lavage in vasospasm therapy.     

尼莫地平和丹参联合用药治疗外伤性脑血管痉挛的临床研究

目的:通过对60例外伤性脑血管痉挛的病人随机分为两组进行前瞻性对照研究,实验组为尼莫地平和丹参联合用药组,对照组为尼莫地平单独用药组,评价两种治疗方法的疗效。方法：实验组,30例病人发病后第三天始口服国产尼莫地平片剂40mg,每日3次,连续用药14～21天,从第三天开始同时静滴国产丹参注射液16mL,每日1次,连续用药14～21天。对照组：30例病人单独使用尼莫地干片剂,剂量、用药途径及用药时间与实验组相同。结果：脑功能恢复率,实验组为93．33％,对照组为73．33％,P＜0．05。结论：尼莫地平和丹参联合用药的疗效要优于单独用尼莫地平。     

Reversible cerebral angiopathy

Reversible cerebral angiopathy (RCA) is responsible for disabling headache and potential stroke complications. Most patients respond poorly to analgesics. We describe four patients with typical RCA whose headache rapidly disappeared after IV nimodipine treatment was initiated. Received in revised form: 10 April 2006     

辛伐他汀治疗蛛网膜下腔出血的疗效观察

目的探讨辛伐他汀对蛛网膜下腔出血治疗作用。方法将连平县人民医院2003年3月～2005年3月128例蛛网膜下腔出血的住院患者随机分为2组（所有病例均给以常规治疗并静脉注射尼膜地平）：治疗组（口服辛伐他汀组）64例，给予口服或者鼻饲辛伐他汀20mg，每日2次；对照组（常规治疗组）64例，给予安慰剂口服，每日2次。14d后对患者进行神经功能缺损评分并行头颅CT等检查。结果14d的治疗后治疗组较对照组神经功能缺损评分明显降低，二者比较差异有显著性意义（P〈0.05）。脑血管痉挛的发生率：治疗组为4例，对照组11例，二者比较有显著性意义（P〈0，01）。结论口服辛伐他汀能明显改善蛛网膜下腔出血后神经功能缺损评分。     

Posttraumatic vasospasm and its treatment with nimodipine

The aim of our study was to compare the incidence and the time course of vasospasm as well as outcome of patients with tSAH. In group I there were 15 patients treated with nimodipine. Group II consisted of 20 patients in whom nimodipine was not used. All patients suffered from severe head injury, scored 8 points or less according to Glasgow Coma Scale. The initial CT scan revealed tSAH in all of them. Outcome was evaluated according to Glasgow Outcome Scale (GOS) three months after injury. Results were better (but not significantly) in patients in whom nimodipine was used, time course of vasospasm was less severe and follow-up CT scans did not reveal ischaemic infarcts connected with vasospasm.     

Nimodipine Dose Reductions in the Treatment of Patients with Aneurysmal Subarachnoid Hemorrhage

Background

The incidence of cerebral infarction and poor outcome in patients with aneurysmal subarachnoid hemorrhage (aSAH) is reduced by oral nimodipine but acute effects of the drug may include a significant decrease in mean arterial blood pressure (MAP). A dose reduction or discontinuation of the drug is recommended if recurrent MAP drops occur. The aim of our study was to evaluate the frequency and clinical significance of nimodipine dose modifications in patients suffering from aSAH.

Methods

270 patients were included in our retrospective analysis of consecutively collected data of patients suffering from aSAH. The local treatment protocol was in accordance to national and international guidelines. Nimodipine was intended to be applied orally with a dosage of 60 mg every 4 h.

Results

Only 43.6 % of patients eligible for vasospasm prophylaxis with nimodipine received the full daily dose of 60 mg every 4 h. In 28.6 %, the dose had to be reduced by 50 % due to a significant reduction in blood pressure after administration and/or high dose of catecholamines. In 27.7 % of patients, oral administration of the drug was discontinued for the same reason. Dose reduction and discontinuation occurred with a significantly higher frequency in patients in poor clinical condition. Application of the full nimodipine dosage decreased the risk of unfavorable clinical outcome in multivariate analysis (OR 0.895, p = 0.029).

Conclusions

Our results show that dose reduction or discontinuation of nimodipine due to changes in MAP occur frequently in clinical routine and may be associated with unfavorable clinical outcome.

     

A Site-Specific,Sustained-Release Drug Delivery System for Aneurysmal Subarachnoid Hemorrhage

Nimodipine is the only drug approved for use by the Food and Drug Administration for improving outcome after aneurysmal subarachnoid hemorrhage (SAH). It has less than optimal efficacy, causes dose-limiting hypotension in a substantial proportion of patients, and is administered enterally 6 times daily. We describe development of site-specific, sustained-release nimodipine microparticles that can be delivered once directly into the subarachnoid space or cerebral ventricles for potential improvement in outcome of patients with aneurysmal SAH. Eight injectable microparticle formulations of nimodipine in poly(DL-lactide-co-glycolide) (PLGA) polymers of varying composition were tested in vitro, and 1 was advanced into preclinical studies and clinical application. Intracisternal or intraventricular injection of nimodipine–PLGA microparticles in rats and beagles demonstrated dose-dependent, sustained concentrations of nimodipine in plasma and cerebrospinal fluid for up to 29 days with minimal toxicity in the brain or systemic tissues at doses <2 mg in rats and 51 mg in beagles, which would be equivalent of up to 612–1200 mg in humans, based on scaling relative to cerebrospinal fluid volumes. Efficacy was tested in the double-hemorrhage dog model of SAH. Nimodipine–PLGA microparticles significantly attenuated angiographic vasospasm. This therapeutic approach shows promise for improving outcome after SAH and may have broader applicability for similar diseases that are confined to body cavities or spaces, are self-limited, and lack effective treatments.     

尼莫地平不同给药途径治疗蛛网膜下腔出血后脑血管痉挛

脑血管痉挛(CVS)一直被认为是蛛网膜下腔出血(SAH)后严重的并发症.本文回顾了尼莫地平不同给药途径治疗SAH后CVS的研究进展.尼莫地平作为第二代双氢吡啶类钙离子拮抗剂能有效降低SAH后的全脑梗塞和不良预后.尼莫地平局部应用可增加药物浓度,减少全身应用引起的副作用,有效扩张血管管腔,改善术中CVS,减少手术后症状性CVS的发生,改善动脉瘤SAH患者的预后.尼莫地平口服、静脉应用对于治疗SAH后CVS已取得肯定的效果,更加深入研究其局部应用治疗SAH后CVS的作用及其作用机理,可进一步提高尼莫地平的疗效.     

Oral nimodipine reduces prostaglandin and thromboxane production by arteries chronically exposed to a periarterial haematoma and the antifibrinolytic agent tranexamic acid.

The calcium antagonist nimodipine blocks the effects of many vasoconstrictors of cerebrovascular smooth muscle and may reduce the incidence of delayed cerebral ischaemia following subarachnoid haemorrhage though not necessarily by inhibiting the development of angiographic cerebral vasospasm. Post-haemorrhagic CSF contains abnormally large quantities of various eicosanoids that partly reflect enhanced production by cerebral arteries. Does nimodipine affect this process? The extra-arterial and intra-arterial production of PG6 keto-F1 alpha, PGE2, PGF2 alpha and TXB2 were measured in perfused common carotid arteries taken from rabbits in which the arteries had been ensheathed by blood clot in vivo for 7 days. All rabbits were given the antifibrinolytic agent tranexamic acid to retard resolution of the clot, and half were given oral nimodipine (2 mg/kg/day) for 10 days. Nimodipine significantly reduced the extra-arterial production of TXB2 during the third and fourth hours of perfusion and, less consistently, the production of PGF2 alpha, PGE2 and PG6 keto-F1 alpha. Lutrol, the solvent for nimodipine, had no such effect.     

Angiographic Features and Clinical Outcomes of Intra-Arterial Nimodipine Injection in Patients with Subarachnoid Hemorrhage-Induced Vasospasm

Objective

The aim of this study was to determine the role of intra-arterial (IA) nimodipine injections for cerebral vasospasm secondary to ruptured subarachnoid hemorrhage (SAH) and to investigate the factors that influence vasodilation and clinical outcomes.

Methods

We enrolled 29 patients who underwent aneurysm clipping for ruptured cerebral aneurysms between 2009 and 2011, and who received IA nimodipine after subsequently presenting with symptomatic vasospasm. The degree of vasodilation shown in angiography was measured, and the correlation between the degree of vasodilation and both the interval from SAH to cerebral vasospasm and the interval from clipping to cerebral vasospasm was determined. The change in blood flow rate after IA injection was assessed by transcranial Doppler ultrasound. Multiple clinical parameters were completed before and after IA nimodipine injection to evaluate any improvements in clinical symptoms.

Results

For eight patients, Glasgow Coma Scale (GCS) scores increased by two or more points. The regression analysis demonstrated a positive correlation between the change in GCS scores after IA nimodipine injection and the change in blood vessel diameter (p=0.025). A positive correlation was also observed between the interval from SAH to vasospasm and the change in diameter (p=0.040); and the interval from clipping to vasospasm and the change in diameter (p=0.022).

Conclusion

IA nimodipine injection for SAH-induced vasospasm led to significant vasodilation in angiography and improvement in clinical symptoms without significant complications. Our findings suggest that IA nimodipine injection should be utilized when intractable vasospasm develops despite rigorous conservative management.     

Vasogenic Edema of the Basal Ganglia after Intra-Arterial Administration of Nimodipine for Treatment of Vasospasm

The intra-arterial administration of nimodipine (IAN) is commonly used for cerebral vasospasm refractory to medical treatments. We report two cases of vasogenic edema after IAN. Our patients with aneurismal subarachnoid hemorrhage presented with vasospasm, which was treated by IAN. Consequently, vasogenic edema developed in the basal ganglia. Reperfusion following IAN for vasospasm may have the potential for inciting vasogenic edema in the ischemic brain.     

Outcome of aneurysmal subarachnoid haemorrhage following the introduction of papaverine angioplasty

This is a prospective study reporting the impact of angiographic vasospasm on the outcome following aneurysmal subarachnoid haemorrhage utilising a common regimen that includes nimodipine and angioplasty. The first 100 patients suffering an aneurysmal subarachnoid haemorrhage treated by surgery and this angioplasty driven protocol are reviewed. Angiography was performed if the Glasgow Coma Score (GCS) fell by two, a focal neurological deficit developed, hyponatraemia was detected, or routinely on days 5-7 following the subarachnoid haemorrhage. Angioplasty with papaverine was administered intra-arterially in all patients with significant angiographic vasospasm. Neurological deficits on admission were not present in 49% and associated with a GCS less than 14 in 38%. Angiographic vasospasm was detected in 48% of patients (all of whom received papaverine). Overall 3 month outcome was normal in 60%, neurological deficit but independence with regard to activities of daily living in 18%, loss of independence in 17%, and death in 5% of cases. Analysis of admission neurological condition (GCS < vs GCS > 13), presence of angiographic vasospasm, aneurysm size (less than or greater than 1.5 cm), and aneurysm circulation (anterior vs posterior) on outcome (normal vs abnormal) found that only admission neurological condition significantly influenced outcome (P < 0.0001). The results suggest that with the protocol of nimodipine and angioplasty the impact of vasospasm on outcome is far less significant than the clinical severity of the initial haemorrhage. This is in contradistinction to the experience with aneurysmal subarachnoid haemorrhage prior to this regimen (nimodipine and angioplasty) where vasospasm was the most significant determinant of a poor outcome.     

Thunderclap headache

Thunderclap headache (TCH) is head pain that begins suddenly and is severe at onset. TCH might be the first sign of subarachnoid haemorrhage, unruptured intracranial aneurysm, cerebral venous sinus thrombosis, cervical artery dissection, acute hypertensive crisis, spontaneous intracranial hypotension, ischaemic stroke, retroclival haematoma, pituitary apoplexy, third ventricle colloid cyst, and intracranial infection. Primary thunderclap headache is diagnosed when no underlying cause is discovered. Patients with TCH who have evidence of reversible, segmental, cerebral vasoconstriction of circle of Willis arteries and normal or near-normal results on cerebrospinal fluid assessment are thought to have reversible cerebral vasoconstriction syndrome. Herein, we discuss the differential diagnosis of TCH, diagnostic criteria for the primary disorder, and proper assessment of patients. We also offer pathophysiological considerations for primary TCH.     

Recommendations for the management of patients with aneurysmal subarachnoid hemorrhage

After SAH, primary and secondary complications are frequent and often require neurosurgical interventions to avoid secondary brain damage. The authors of the present paper have summarized the available data about the treatment modalities often used for patients with SAH. The present recommendations have been developed as a neurosurgical and neuroanestesiological consensus. Evidence from prospective, randomized, double blind, placebo-controlled studies support grade A recommendations (standard) for the prophylaxis and treatment of cerebral vasospasm with oral Nimodipine in good grade patients. For intravenous Nimodipine or for oral nimodipine treatment in poor grade patients, available data only support grade C recommendations (options). Despite the lack of data supporting standards (grade A) or guidelines (grade B), avoidance and rigorous treatment of hypotension and hypovolemia remains the mainstay in the prophylaxis and treatment of a delayed ischemic neurological deficit (DIND). Prophylactic hypervolemia or prophylactic hypertension and hypervolemia was shown to be ineffective in reducing symptomatic vasospasm and improving outcome (grade B). Therapeutic hypertensive hypervolemic hemodilution is recommended as a treatment of symptomatic vasospasm but no prospective studies are available (grade C recommendation). Suggested target values for moderate triple-H-therapy are CPP 80- 120 mmHg (MAP 90-130), CVP > 7 mmHg and Hk 0.25-0.40. Balloon angioplasty should be considered for treatment of DIND cause by focal, proximal cerebral vasospasm. There is no evidence supporting the routine use of antifibrinolyticals, steroids or anticonvulsive prophylaxis. Clinical data indicate that current prophylaxis and treatment of cerebral vasospasm is still insufficient and aggressive triple-H-therapy is associated with an increased incidence of complications.     

Intravenous Magnesium Infusion for the Prevention of Symptomatic Cerebral Vasospasm after Aneurysmal Subarachnoid Hemorrhage

Objective

The study examined the difference in the incidence of symptomatic cerebral vasospasm with magnesium supplementation in aneurysmal subarachnoid hemorrhage (SAH) in a Korean population.

Methods

This retrospective analysis was performed in 157 patients diagnosed with aneurysmal SAH from January 2007 to December 2011 at a single center. Seventy patients (44.6%) received a combination treatment of nimodipine with magnesium and 87 patients (55.4%) received only nimodipine. A matched case-control study using propensity scores was conducted and 41 subjects were selected from each group. A dosage of 64 mmol/day of magnesium was administrated.

Results

The infusion of magnesium did not reduce the incidence of symptomatic cerebral vasospasm (n=7, 17.1%, p=0.29) compared with simple nimodipine injection (n=11, 26.8%). The ratios of good clinical outcome (modified Rankin scale 0-2) at 6 months were similar, being 78% in the combination treatment group and 80.5% in the nimodipine only group (p=0.79). The proportions of delayed cerebral infarction was not significantly lower in patients with combination treatment (n=2, 4.9% vs. n=3, 7.3%; p=0.64). There was no difference in the serum magnesium concentrations between the patients with symptomatic vasospasm and without vasospasm who had magnesium supplementation. No major complications associated with intravenous magnesium infusion were observed.

Conclusion

Magnesium supplementation (64 mmol/day) may not be beneficial for the reduction of the incidence of symptomatic cerebral vasospasm in patients with aneurysmal SAH.