Multivariate analysis of predictors of cerebral vasospasm occurrence after aneurysmal subarachnoid hemorrhage.

BACKGROUND AND PURPOSE: The role of type of treatment on cerebral vasospasm occurrence after aneurysmal subarachnoid hemorrhage (SAH) has not been studied. Through multivariate analysis we determined the independent prognostic factors of the occurrence of symptomatic vasospasm following aneurysmal SAH in a study cohort of 244 patients undergoing either surgical or endovascular treatment. The prognostic factors of sequelae after aneurysmal SAH were studied as well. METHODS: Symptomatic vasospasm was defined as the association of deterioration in a patient's neurological condition between 3 and 14 days after SAH with no other explanation and an increase in mean transcranial Doppler velocities of >120 cm/s. The prognostic factors were registered on admission and during the intensive care stay. RESULTS: Symptomatic vasospasm occurred in 22.2% surgical patients compared with 17.2% endovascular treatment patients (P=0.37). Multivariate analysis revealed that the probability of occurrence of symptomatic vasospasm decreased with age >50 years (relative risk [RR], 0.47 [0.25 to 0.88]) and severe World Federation of Neurological Surgeons (WFNS) grade measured on admission (RR, 0.43 [0.20 to 0.90]) and increased with hyperglycemia occurring during the intensive care stay (RR, 1.94 [1.04 to 3.63]). No difference in risk of symptomatic vasospasm could be identified between surgical and endovascular treatment. Symptomatic vasospasm (OR, 4.73 [CI, 1. 77 to 12.6]) as well as WFNS grade of >2 (OR, 8.95 [3.46 to 23.2]), treatment complications (OR, 8.39 [3.16 to 22.3]), and secondary brain insults were associated with an increased risk of 6-month sequelae. CONCLUSIONS: Age <50 years, good neurological grade, and hyperglycemia were all associated with an increased risk of cerebral vasospasm whereas treatment was not. This provides a basis for future clinical prospective randomized trials comparing both treatments.     

Does treatment modality of intracranial ruptured aneurysms influence the incidence of cerebral vasospasm and clinical outcome?

BACKGROUND: Cerebral vasospasm is the most common cause of morbidity and mortality after aneurysmal subarachnoid hemorrhage (SAH). This study is designed to determine whether the incidence of symptomatic vasospasm and the overall clinical outcome differ between patients treated with surgical clipping compared with endovascular obliteration of aneurysms. METHODS: In this prospective study, 98 patients with aneurysmal SAH were treated. Seventy-two patients underwent surgery and clipping and 26 had coil embolization. The incidence of symptomatic vasospasm, permanent neurologic deficit due to vasospasm and clinical outcome were analyzed. Patients with better clinical and radiological grades (World Federation of Neurological Surgeons grades I-III and Fisher grades I-III) were analyzed separately. RESULTS: Symptomatic vasospasm occurred in 22% of the patients; 25% in the surgical group and 15% in the endovascular group. Nine percent of the patients in the surgical group and 7% in the endovascular group suffered ischemic infarction with permanent neurological deficit. These differences did not reach statistical significance (p = 0.42). For patients with better clinical and radiological grades, no significant difference was found for the rate of symptomatic vasospasm; 23% in the surgical and 12% in the endovascular group (p = 0.49). The overall clinical outcome was comparable in both groups, with no difference in the likelihood of a Glasgow Outcome Scale score of 3 or less (15% in the surgical and 16% in the endovascular group; p = 0.87). The same results for outcome were obtained for the subgroup of patients with better clinical grades on admission. CONCLUSION: Symptomatic vasospasm and ischemic infarction rate seem comparable in both groups, even for patients with better clinical and radiological admission grades. There is no significant difference in the overall clinical outcome at the long-term follow-up between both groups.     

Intraarterial Nimodipine Infusion to Treat Symptomatic Cerebral Vasospasm after Aneurysmal Subarachnoid Hemorrhage

Objective

Cerebral vasospasm leading to cerebral ischemic infarction is a major cause of morbidity and mortality in the patients who suffer with aneurysmal subarachnoid hemorrhage. Despite adequate treatment, some patients deteriorate and they develop symptomatic vasospasm. The objective of the present study was to investigate the efficacy and clinical outcome of intraarterial nimodipine infusion on symptomatic vasospasm that is refractory to hemodynamic therapy.

Methods

We retrospectively reviewed the procedure reports, the clinical charts and the transcranial doppler, computed tomography and digital subtraction angiography results for the patients who underwent endovascular treatment for symptomatic cerebral vasospasm due to aneurysmal SAH. During the 36 months between Jan. 2005 and Dec. 2007, 19 patients were identified who had undergone a total of 53 procedures. We assessed the difference in the arterial vessel diameter, the blood flow velocity and the clinical outcome before and after these procedures.

Results

Vascular dilatation was observed in 42 of 53 procedures. The velocities of the affected vessels before and after procedures were available in 33 of 53 procedures. Twenty-nine procedures exhibited a mean decrease of 84.1 cm/s. We observed clinical improvement and an improved level of consciousness with an improved GCS score after 23 procedures.

Conclusion

Based on our results, the use of intraarterial nimodipine is effective and safe in selected cases of vasospasm following aneurysmal SAH. Prospective, randomized studies are needed to confirm these results.     

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.     

Serum magnesium levels as related to symptomatic vasospasm and outcome following aneurysmal subarachnoid hemorrhage

Introduction: Recent evidence suggests that magnesium may be neuroprotective in the setting of cerebral ischemia, and therapeutic magnesium infusion has been proposed for prophylaxis and treatment of delayed ischemic neurological deficit (DIND) resulting from vasospasm in patients with aneurysmal subarachnoid hemorrhage (SAH). We studied the association between serum magnesium levels, the development of DIND, and the outcomes of patients with SAH. Methods: We studied 128 consecutive patients with aneurysmal SAH treated at our institution between 1990 and 1997 who had a serum magnesium level measured at least once during the acute phase of their hospitalization. Delayed ischemic neurological deficit was defined as severe (major focal deficit or coma), moderate (incomplete focal deficit or decreased sensorium without coma), or none.     

Intra-arterial papaverine in the management of cerebral vasospasm following subarachnoid haemorrhage

Between July 1992 and January 1993 a prospective pilot study of the efficacy of intra-arterial papaverine in the management of clinically significant angiographically confirmed cerebral vasospasm arising as a consequence of aneurysmal subarachnoid haemorrhage was conducted. During this period 40 patients were managed with aneurysmal subarachnoid haemorrhage. All patients were treated with nimodipine from day of admission and carefully monitored in the neurosurgical intensive care unit. 11 of the 40 patients subsequently developed clinically significant angiographically confirmed cerebral vasospasm and underwent angiography with selective internal carotid or vertebral artery injection of papaverine in 12 to 40 mg boluses to a maximum of 450 mg. A good angiographic response was seen in all cases. Two patients underwent repeat procedures, in one case twice. Overall clinical outcome was good in 7 cases, moderate disability in 2 cases, severe disability in 1 case and death in 1 case. In patients who underwent the procedure in less than 4 hours from the onset of their deficits (n=8) a good outcome was seen to occur in 7 patients with one patient sustaining a moderate deficit. Complications from the procedure were seizures in 3 patients and a momentary locked-in-syndrome in one case. All complications were seen with a fast bolus of the higher volume papaverine and have not occurred with a slow infusion of the lower dose boluses. None of the patients developing these complications had them recur outside the angiogram suite. Our conclusion is that this form of treatment supplements the therapeutic regimens now available in the management of cerebral vasospasm.     

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.     

Intraventricular sodium nitroprusside therapy: a future promise for refractory subarachnoid hemorrhage-induced vasospasm

A prospective study was carried out to evaluate the efficacy of intraventricular sodium nitroprousside (SNP) in the reversal of refractory vasospasm secondary to aneurysmal subarachnoid hemorrhage (SAH). Ten patients of aneurysmal SAH with symptomatic vasospasm, corroborated on Transcranial Doppler (TCD) and/or angiography, were included in the study. The mean age distribution of the patients was 50.8 years (range 33-65 years) with an equal number of males and females. Once vasospasm was refractory even after 12 hours of SAH therapy, intraventricular SNP was instilled in an escalating dose and the reversal of vasospasm was monitored on TCD and/or angiography. All patients showed improvement in TCD velocity on day 0 through day 3. Partial to complete reversal of vasospasm was demonstrated on angiography in all the patients, though not in all the vessels. Two patients who had weakness of limbs due to vasospasm improved following intraventricular SNP therapy. Vomiting was the commonest adverse effect (7/10). Three patients had mild fluctuation in blood pressure. The overall outcome was good in 6 out of 10 patients. The study suggests that intraventricular SNP therapy is effective in reversing the changes even in established cases of SAH-induced vasospasm.     

Current advances in the diagnosis of vasospasm

Symptomatic vasospasm leading to delayed ischemia and neurological deficits is one of the most serious complications after aneurysmal subarachnoid hemorrhage (SAH). Reliable and early detection of symptomatic vasospasm is one of the major goals in the management of patients with SAH. In awake patients, the close clinical neurological examination still remains the most important diagnostic measure. In comatous or sedated patients, cerebral angiography remains the mainstay of the diagnostic workup for vasospasm. However, angiography does not allow assessing the hemodynamic relevance of vasospasm and is not suited for early identification of cerebral hypoperfusion and ischemia. Therefore, a large panel of new monitoring techniques for the assessment of regional cerebral perfusion has been recently introduced into the clinical management of SAH patients. This article briefly reviews the most relevant methods for monitoring cerebral perfusion and discusses their clinical predictive value for the diagnosis of vasospasm. On the basis of the currently available monitoring technologies, an algorithm for the diagnosis of vasospasm is presented.     

Safety of intrathecal sodium nitroprusside for the treatment and prevention of refractory cerebral vasospasm and ischemia in humans.

BACKGROUND AND PURPOSE: The delayed type of cerebral vasoconstriction known as cerebral vasospasm (DCV) remains an important cause of permanent neurological injury and death following aneurysmal subarachnoid hemorrhage despite best current medical therapy. The mechanism of DCV remains unknown. A new treatment for refractory DCV using intrathecally delivered sodium nitroprusside and results in 21 patients is reported. METHODS: Candidates for treatment were patients with secured cerebral aneurysms presenting with clinical or radiographic SAH of grade 3 or higher. Patients with and without established DCV were treated. In 57% (12/21 patients) the diagnosis of severe DCV refractory to conventional treatment (HHH therapy and nimodipine) was established before treatment. Ten patients received ITSNP prophylactically. All patients with established DCV were in grave neurological condition before treatment. Procedures for vasospasm reversal were performed under simultaneous angiographic control with extensive hemodynamic and neurophysiologic monitoring. ITSNP was delivered by intraventricular or subdural catheter or by direct intraoperative suffusion. End points of intervention for established DCV were (1) durable angiographic reversal of vasoconstriction, (2) failure to effect reversal within 30 minutes, and (3) adverse effect. End points for DCV prevention were (1) post-SAH day 10 without evidence of vasoconstriction and (2) adverse effect. Cerebral angioplasty was used concomitantly in 9 treatments. The total number of treatments recorded was 171. RESULTS: The overall neurological outcome was good or excellent in 76% of patients (16/21) overall and in 88.9% of patients (16/18) having at least a 1-month follow-up. Of the 5 patients with less-than-good outcome, 4 had presented initially with severe neurological injury (clinical SAH grade 4). Angiography demonstrated reversal or amelioration of vasoconstriction in 83% (5/6 cases) of established DCV treated by ITSNP alone. Among patients treated prophylactically, none developed clinical DCV. CONCLUSIONS: These results suggest that ITSNP is a safe and potentially effective treatment for established DCV and cerebral ischemia refractory to conventional treatment. The preliminary results of prophylactic treatment are also favorable with regard to safety.     

Brain natriuretic peptide and cerebral vasospasm in subarachnoid hemorrhage. Clinical and TCD correlations

BACKGROUND AND PURPOSE: Hyponatremia has been shown in association with cerebral vasospasm (CVS) following aneurysmal subarachnoid hemorrhage (SAH). In the past few years there has been increasing evidence that brain natriuretic peptide (BNP) is responsible for natriuresis after SAH. The purpose of the present study was to investigate the relationship between BNP plasma concentrations and CVS after aneurysmal SAH. METHODS: BNP plasma concentrations were assessed at 4 different time periods (1 to 3 days, 4 to 6 days, 7 to 9 days, and 10 to 12 days) in 19 patients with spontaneous SAH. BNP plasma levels were investigated with respect to neurological condition, SAH severity on CT, and flow velocities measured by means of transcranial Doppler. RESULTS: Thirteen patients had Doppler evidence of CVS; 7 of these had nonsymptomatic CVS. In 6 patients, CVS was severe and symptomatic, with delayed ischemic lesion on CT in 5 of these. CVS was severe and symptomatic in 6 patients, and delayed ischemic lesions were revealed on CT in 5 of these. BNP levels were found to be significantly elevated in SAH patients compared with control subjects (P=0.024). However, in patients without CVS or with nonsymptomatic CVS, BNP concentrations decreased throughout the 4 time periods, whereas a 6-fold increase was observed in patients with severe symptomatic CVS between the first and the third periods (P=0.0096). A similar trend in BNP plasma levels was found in patients with severe SAH compared with those with nonvisible or moderate SAH (P=0.015). CONCLUSIONS: In conclusion, our results show that BNP plasma levels are elevated shortly after SAH, although they increase markedly during the first week in patients with symptomatic CVS. The present findings suggest that secretion of BNP secretion after spontaneous SAH may exacerbate blood flow reduction due to arterial vasospasm.     

Diffusion- and perfusion-weighted imaging in vasospasm after subarachnoid hemorrhage

BACKGROUND AND PURPOSE: Better measures of cerebral tissue perfusion and earlier detection of ischemic injury are needed to guide therapy in subarachnoid hemorrhage (SAH) patients with vasospasm. We sought to identify tissue ischemia and early ischemic injury with combined diffusion-weighted (DW) and hemodynamically weighted (HW) MRI in patients with vasospasm after SAH. METHODS: Combined DW and HW imaging was used to study 6 patients with clinical and angiographic vasospasm, 1 patient without clinical signs of vasospasm but with severe angiographic vasospasm, and 1 patient without angiographic spasm. Analysis of the passage of an intravenous contrast bolus through brain was used to construct multislice maps of relative cerebral blood volume (rCBV), relative cerebral blood flow (rCBF), and tissue mean transit time (tMTT). We hypothesize that large HW imaging (HWI) abnormalities would be present in treated patients at the time they develop neurological deficit due to vasospasm without matching DW imaging (DWI) abnormalities. RESULTS: Small, sometimes multiple, ischemic lesions on DWI were seen encircled by a large area of decreased rCBF and increased tMTT in all patients with symptomatic vasospasm. Decreases in rCBV were not prominent. MRI hemodynamic abnormalities occurred in regions supplied by vessels with angiographic vasospasm or in their watershed territories. All patients with neurological deficit showed an area of abnormal tMTT much larger than the area of DWI abnormality. MRI images were normal in the asymptomatic patient with angiographic vasospasm and the patient with normal angiogram and no clinical signs of vasospasm. CONCLUSIONS: We conclude that DW/HW MRI in symptomatic vasospasm can detect widespread changes in tissue hemodynamics that encircle early foci of ischemic injury. With additional study, the technique could become a useful tool in the clinical management of patients with SAH.     

The Utility and Benefits of External Lumbar CSF Drainage after Endovascular Coiling on Aneurysmal Subarachnoid Hemorrhage

Objective

Cerebral vasospasm still remains a major cause of the morbidity and mortality, despite the developments in treatment of aneurysmal subarachnoid hemorrhage. The authors measured the utility and benefits of external lumbar cerebrospinal fluid (CSF) drainage to prevent the clinical vasospasm and its sequelae after endovascular coiling on aneurysmal subarachnoid hemorrhage in this randomized study.

Methods

Between January 2004 and March 2006, 280 patients with aneurysmal subarachnoid hemorrhage were treated at our institution. Among them, 107 patients met our study criteria. The treatment group consisted of 47 patients who underwent lumbar CSF drainage during vasospasm risk period (about for 14 days after SAH), whereas the control group consisted of 60 patients who received the management according to conventional protocol without lumbar CSF drainage. We created our new modified Fisher grade on the basis of initial brain computed tomography (CT) scan at admission. The authors established five outcome criteria as follows : 1) clinical vasospasm; 2) GOS score at 1-month to 6-month follow-up; 3) shunt procedures for hydrocephalus; 4) the duration of stay in the ICU and total hospital stay; 5) mortality rate.

Results

The incidence of clinical vasospasm in the lumbar drain group showed 23.4% compared with 63.3% of individuals in the control group. Moreover, the risk of death in the lumbar drain group showed 2.1% compared with 15% of individuals in the control group. Within individual modified Fisher grade, there were similar favorable results. Also, lumbar drain group had twice more patients than the control group in good GOS score of 5. However, there were no statistical significances in mean hospital stay and shunt procedures between the two groups. IVH was an important factor for delayed hydrocephalus regardless of lumbar drain.

Conclusion

Lumbar CSF drainage remains to play a prominent role to prevent clinical vasospasm and its sequelae after endovascular coiling on aneurysmal subarachnoid hemorrhage. Also, this technique shows favorable effects on numerous neurological outcomes and prognosis. The results of this study warrant clinical trials after endovascular treatment in patients with aneurysmal SAH.     

Angiographic vasospasm in a contemporary series of patients with aneurysmal subarachnoid haemorrhage

Over the last decade there have been significant changes in the management of patients with aneurysmal subarachnoid haemorrhage (SAH). Many of these changes, such as haemodilutional, hypervolaemic, hypertensive therapy and the use of calcium channel blockers, have been directed at the prevention and treatment of vasospasm. The angiograms of a contemporary series of 56 consecutive surgically treated patients with aneurysmal SAH were examined to compare angiographic vasospasm with that seen in historical studies. The time course of angiographic vasospasm was found to be broadly similar to that reported in previous studies, with onset after day 3 following SAH, maximal narrowing during the second week, and resolution after day 16. The times of peak narrowing and resolution were slightly earlier in previous studies. 30% of patients had clinical vasospasm (delayed neurological deficit for which other causes had been excluded), and these patients had a trend to more severe angiographic narrowing than those without clinical vasospasm, particularly in the second week following SAH. 44 angiograms were performed between days 1-3 post SAH and repeated between days 4-16. 95% of these showed arterial narrowing at the second angiogram. Patients not achieving an independent outcome tended to have had both more clinical vasospasm and more severe angiographic spasm than those achieving independence. It is concluded that angiographic vasospasm remains a common occurrence in the modern era, and continues to be associated with clinical events and a poor outcome.     

颅内动脉瘤性蛛网膜下腔出血血管痉挛治疗的临床探讨

目的探讨颅内动脉瘤性蛛网膜下腔出血脑血管痉挛的治疗方法。方法回顾性分析颅内动脉瘤性蛛网膜下腔出血合并脑血管痉挛患者临床资料67例。结果 23例并发脑血管痉挛,6例发生一侧肢体功能障碍,3例发生脑血栓形成。经治疗后61例C-反应蛋白恢复正常,6例明显下降,4例肢体功能恢复正常,1例恢复到4级,1例死亡。结论炎症因子在脑血管痉挛中明显升高;钙离子拮抗剂尼莫地平加抗氧化剂依达拉奉中药川芎嗪联合治疗动脉瘤性蛛网膜下腔出血所致的脑血管痉挛有较好疗效。     

The effect of ecdysterone on cerebral vasospasm following experimental subarachnoid hemorrhage in vitro and in vivo

OBJECTIVES: Cerebral vasospasm has been the dreaded complication of ruptured intracranial aneurysms. Worldwide effort has led to many promising experimental treatments but none was confirmed to be effective in clinical trials. Ecdysterone is an insect steroid hormone. Our previous study showed that ecdysterone might prevent cerebral vasospasm in vitro. Even after all these works, rare attempts have been made to test the effect of ecdysterone on vascular adventitial fibroblast (VAF) proliferation, a process known to play an important role in various pathogenic vascular conditions. Thus, we tested the hypothesis that ecdysterone could affect VAF characteristics and have an effect on SAH induced cerebral vasospasm. METHODS: OxyHb of 100 microM was used in the in vitro study to mimic the clinical situation. The effect of OxyHb on the cell proliferation and migration of cultured aortic smooth muscle cells was investigated. In the in vivo study, 20 rabbits were equally divided into four groups: control group, SAH group, SAH/nimodipine group and SAH/ecdysterone group. Changes in neurological function and cerebral angiograms were observed after SAH. RESULTS: OxyHb increased the proliferation of vascular adventitial fibroblasts at 24 hours. Ecdysterone co-treatment was apparently similar to the suppression of proliferation. Cell cycle analysis indicated that ecdysterone inhibited the progression of vascular adventitial fibroblasts from G1 to S. The results of the migration assay showed that 100 microM OxyHb obviously prompted vascular adventitial fibroblast migration and that ecdysterone would attenuate this effect. In the SAH/nimodipine and SAH/ecdysterone groups, neurological deficit, cerebral vasospasm and structural changes in basilar artery were alleviated with nimodipine or ecdysterone treatment. CONCLUSION: Ecdysterone could affect vascular adventitial fibroblast characteristics and attenuate vasospasm after SAH.     

Early cerebral hemodynamic alternations in patients operated on the first, second and third day after aneurysmal subarachnoid hemorrhage

Surgery timing after aneurysmal subarachnoid hemorrhage (SAH) may influence the risk of vasospasm after early surgical procedure and is correlated with SAH extensiveness. A group consisting of 127 patients with aneurysmal SAH was studied. The changes of mean flow velocity (MFV) were measured in middle cerebral artery (MCA) and in anterior cerebral artery (ACA) by transcranial Doppler sonography (TCD) in three groups of patients divided according to the surgery timing (on the first, second and third day after SAH). Changes of MFV values in MCA and in ACA were similar in all groups. MFV values in the group of patients operated on the third day were the lowest and the pathologic values lasted for the shortest time. In patients with massive SAH (Fisher IV group) and mild SAH (Fisher II group), the lowest MFV values were observed, if patients were operated within 24 hours after SAH. In patients without SAH (Fisher I group), the MFV values were the lowest, if they were operated on the third day after SAH. In patients with severe SAH (Fisher III group), the lowest risk of vasospasm was observed, if they were operated on the second day after SAH; however, the highest risk was found in patients operated on the first day after SAH. Our study suggests: (1) in patients with severe SAH operated on the second day, the lowest risk of vasospasm was observed, and the highest risk of vasospasm was observed if those were operated on the first day; (2) the highest risk of vasospasm was observed in patients operated within 24 hours with mild and massive SAH and in patients without SAH operated on the third day after SAH.     

硫酸镁对颅内动脉瘤性蛛网膜下腔出血后脑血管痉挛的治疗作用

目的观察硫酸镁对动脉瘤性蛛网膜下腔出血后症状性脑血管痉挛和神经功能预后的治疗作用。方法39例动脉瘤性蛛网膜下腔出血患者在发病48 h内,随机分到生理盐水组(A组)、硫酸镁治疗1组(B组)、硫酸镁治疗2组(C组),B组首次静脉推注25％硫酸镁10 mL后,继以每日25％硫酸镁40 mL静脉滴注,C组首次静脉推注25％硫酸镁20 mL后,继以每日25％硫酸镁80 mL静脉滴注,A组输入等量生理盐水,均连续输入14 d并每日检测血清Mg2+浓度、血压及TCD检测大脑中动脉平均血流速度。6个月后随访并记录患者Glasgow Outcome Scall-Extended、Modified Rankin Scall用以评价患者神经功能预后情况。结果17例患者发生症状性脑血管痉挛,A组7例,B组5例、C组5例;17例症状性脑血管痉挛患者的6个月GOSE评分,A组1／7例,B组3／5例、C组3／5例患者神经功能恢复良好;39例患者中硫酸镁治疗组患者6个月后GOSE、Modified Rankin Scale评分与生理盐水组比较,神经功能预后有改善倾向。然而,这些疗效评分差异均没有达到统计学意义(P>0．05)。结论硫酸镁治疗安全且血清Mg2+水平较容易维持,硫酸镁有减少症状性脑血管痉挛发生和改善患者神经功能预后的趋势,但由于样本例数较少,其治疗作用仍有待于进一步研究证实。     

A double-blind clinical evaluation of the effect of Nizofenone (Y-9179) on delayed ischemic neurological deficits following aneurysmal rupture

The effect of Nizofenone (Y-9179), a vertebral protective agent, on delayed ischemic neurological deficits following subarachnoid hemorrhage (SAH) due to aneurysmal rupture was investigated by a cooperative double-blind clinical trials. Delayed ischemic neurological deficits following SAH are closely associated with the occurrence of vasospasm, and the effectiveness of any cerebral protective agent depends on sufficient coverage by the drug over the period around the onset of ischemic insult. Therefore, the study was designed so that the effect of Nizofenone could be analyzed in terms of these two factors. In patients admitted within day 9 of SAH, drug administration was immediately initiated and continued for 5 days. When delayed ischemic neurological deficits occurred, angiography was carried out to confirm the presence of vasospasm, and then drug administration was extended for an additional 5 days. Ten of the 100 cases enlisted in the study were excluded prior to code-breaking because of the occurrence of severe complications not related to vasospasm. Out of the 42 cases of the Nizofenone group and 48 of the placebo group, 25 and 29 developed vasospasm, respectively. Thus Nizofenone did not prevent vasospasm. Of the 25 cases of the Nizofenone group with vasospasm, 13 cases received sufficient drug coverage around the onset of vasospasm. The placebo group, the total Nizofenone group, and the Nizofenone group with sufficient drug coverage were stratified according to the occurrence of vasospasm. The disability status index one month after admission and the neurological functions, such as motor and speech functions, of each group were then compared. In patients who developed vasospasm, only the Nizofenone group with sufficient drug coverage had a significantly better outcome than the placebo group (p less than 0.05). No particular side effect of Nizofenone was observed. Thus, the results indicate that Nizofenone may be useful in the therapy of delayed ischemic neurological deficits following SAH, although the effect of the drug may be considerably influenced by the timing of its administration.     

CT and CT-Perfusion Findings of Reversible Leukoencephalopathy During Triple-H Therapy for Symptomatic Subarachnoid Hemorrhage-Related Vasospasm

BACKGROUND: Reversible leukoencephalopathy syndrome (RLS) is an acute neurological syndrome associated with altered mental status and visual disturbances described in patients with sudden elevations in systemic blood pressure and other medical conditions. In this process, neuroimaging studies usually demonstrate diffuse edema involving the subcortical structures of the posterior regions of the brain. Triple H (HHH) therapy is an established treatment for symptomatic vasospasm following subarachnoid hemorrhage (SAH). RLS has not been reported in the scientific literature as a complication of HHH therapy with perfusion computed tomography (CTP) imaging documentation. CASE: A 73-year-old woman developed iatrogenic RLS during HHH therapy for SAH-related vasospasm. The computed tomography (CT) revealed bilateral parieto-occipital hypodensities. The CTP study showed increased cerebral blood volume and blood flow as well as decreased mean transit time in both parietal-occipital regions, which is compatible with vasogenic edema. CONCLUSION: The induction of hypertension as part of HHH therapy for SAH-related cerebral vasospasm may result in RLS. Therefore, it should be considered as a potentially reversible cause in the differential diagnosis of neurological deterioration in SAH patients while on HHH therapy. CTP study can offer an alternative for the assessment of this cerebrovascular syndrome.