Subarachnoid Hemorrhage Associated with Intratumoral Aneurysm Rupture within a Posterior Fossa Hemangioblastoma: The Importance of Continued Surveillance for Cerebral Vasospasm

Abstract CEREBRAL VASOSPASM IS one of the leading causes of morbidity and mortality after aneurysmal subarachnoid hemorrhage. Despite maximal medical therapy, however, up to 15% of patients surviving the ictus of subarachnoid hemorrhage experience stroke or death from vasospasm. For those cases of vasospasm that are refractory to medical treatment, endovascular techniques are frequently used, including balloon angioplasty with or without intra-arterial infusion of vasodilators, combined endovascular modalities, and aortic balloon devices. In this article, we review each of these therapies and their expanding role in the management of this condition. Moving forward, rigorous prospective outcome assessments after endovascular treatment of cerebral vasospasm are necessary to clearly delineate the efficacy and indications for these techniques.

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The role of hemoglobin in the etiology of cerebral vasospasm

Journal of Neurosurgery ◽

10.3171/jns.1983.59.2.0231 ◽

1983 ◽

Vol 59 (2) ◽

pp. 231-236 ◽

Cited By ~ 46

Author(s):

David J. Boullin ◽

Philip Tagari ◽

George du Boulay ◽

Victoria Aitken ◽

J. Trevor Hughes

Keyword(s):

Subarachnoid Hemorrhage ◽

Cerebral Vasospasm ◽

Cerebral Angiography ◽

Aneurysm Rupture ◽

Neurological Deficits ◽

Arterial Spasm ◽

Content Type ◽

Experimental Animals ◽

Fine Print

✓ Oxyhemoglobin was injected intracisternally into three baboons, and methemoglobin into one baboon, in an attempt to mimic the prolonged cerebral arterial spasm sometimes seen after subarachnoid hemorrhage due to aneurysm rupture. Cerebral angiography was performed for up to 7 days after injection of hemoglobin, and the degree of vasospasm was estimated from the angiograms. Oxyhemoglobin caused slight arterial narrowing, which lasted for 3 days. Methemoglobin had no significant effects. Motor neurological deficits and histopathological signs, characteristic of prolonged cerebral vasospasm, were not observed. It was concluded that hemoglobin alone is not capable of causing the cerebral vasospasm syndrome in these experimental animals.

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Reversal of cerebral vasospasm via intravenous sodium nitrite after subarachnoid hemorrhage in primates

Journal of Neurosurgery ◽

10.3171/2011.7.jns11390 ◽

2011 ◽

Vol 115 (6) ◽

pp. 1213-1220 ◽

Cited By ~ 40

Author(s):

Ali Reza Fathi ◽

Ryszard M. Pluta ◽

Kamran D. Bakhtian ◽

Meng Qi ◽

Russell R. Lonser

Keyword(s):

Subarachnoid Hemorrhage ◽

Cerebral Vasospasm ◽

Sodium Nitrite ◽

Whole Blood ◽

Intravenous Infusion ◽

Blood Clot ◽

Vessel Diameter ◽

Aneurysm Rupture ◽

Saline Infusion ◽

Similar Treatment

Object Subarachnoid hemorrhage (SAH)-induced vasospasm is a significant underlying cause of aneurysm rupture-related morbidity and death. While long-term intravenous infusion of sodium nitrite (NaNO2) can prevent cerebral vasospasm after SAH, it is not known if the intravenous administration of this compound can reverse established SAH-induced vasospasm. To determine if the intravenous infusion of NaNO2 can reverse established vasospasm, the authors infused primates with the compound after SAH-induced vasospasm was established. Methods Subarachnoid hemorrhage–induced vasospasm was created in 14 cynomolgus macaques via subarachnoid implantation of a 5-ml blood clot. On Day 7 after clot implantation, animals were randomized to either control (saline infusion, 5 monkeys) or treatment groups (intravenous NaNO2 infusion at 300 μg/kg/hr for 3 hours [7 monkeys] or 8 hours [2 monkeys]). Arteriographic vessel diameter was blindly analyzed to determine the degree of vasospasm before, during, and after treatment. Nitric oxide metabolites (nitrite, nitrate, and S-nitrosothiols) were measured in whole blood and CSF. Results Moderate-to-severe vasospasm was present in all animals before treatment (control, 36.2% ± 8.8% [mean ± SD]; treatment, 45.5% ± 12.5%; p = 0.9). While saline infusion did not reduce vasospasm, NaNO2 infusion significantly reduced the degree of vasospasm (26.9% ± 7.6%; p = 0.008). Reversal of the vasospasm lasted more than 2 hours after cessation of the infusion and could be maintained with a prolonged infusion. Nitrite (peak value, 3.7 ± 2.1 μmol/L), nitrate (18.2 ± 5.3 μmol/L), and S-nitrosothiols (33.4 ± 11.4 nmol/L) increased significantly in whole blood, and nitrite increased significantly in CSF. Conclusions These findings indicate that the intravenous infusion of NaNO2 can reverse SAH-induced vasospasm in primates. Further, these findings indicate that a similar treatment paradigm could be useful in reversing cerebral vasospasm after aneurysmal SAH.

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Endovascular treatment strategies for cerebral vasospasm

Neurosurgical FOCUS ◽

10.3171/foc.2006.21.3.13 ◽

2006 ◽

Vol 21 (3) ◽

pp. 1-7 ◽

Cited By ~ 14

Author(s):

Stefan A. Mindea ◽

Benson P. Yang ◽

Bernard R. Bendok ◽

Jeffrey W. Miller ◽

H. Hunt Batjer

Keyword(s):

Subarachnoid Hemorrhage ◽

Cerebral Vasospasm ◽

Strong Predictor ◽

Treatment Strategies ◽

Aneurysm Rupture ◽

Pathological State ◽

Endovascular Techniques ◽

Poor Clinical Outcome ◽

Pharmacological Agents ◽

Symptomatic Vasospasm

✓Cerebral vasospasm is a significant cause of morbidity and mortality in patients who have sustained a subarachnoid hemorrhage from aneurysm rupture. Symptomatic cerebral vasospasm is also a strong predictor of poor clinical outcome and has thus drawn a great deal of interest from cerebrovascular surgeons. Although medical management is the cornerstone of treatment for this condition, endovascular intervention may be warranted for those in whom this treatment fails and in whom symptomatic vasospasm subsequently develops. The rapid advancements in endovascular techniques and pharmacological agents used to combat this pathological state continue to offer promise in broadening the available treatment armamentarium. In this article the authors discuss the rationale and basis for using the various endovascular options for the treatment of cerebral vasospasm, and they also discuss the limitations, complications, and efficacy of these treatment strategies in regard to neurological condition and outcome.

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Cerebral Vasospasm in Subarachnoid Hemorrhage Through Aneurysm Rupture - Clinical Considerations and Case Report

ARS Medica Tomitana ◽

10.1515/arsm-2016-0040 ◽

2016 ◽

Vol 22 (4) ◽

pp. 232-238

Author(s):

B.M. Caraban ◽

Aurelia Romila ◽

L.T. Hangan ◽

Mihaela Lungu

Keyword(s):

Subarachnoid Hemorrhage ◽

Cerebral Vasospasm ◽

Cerebral Arteries ◽

Aneurysm Rupture ◽

Arterial Aneurysm ◽

Arterial Vasospasm ◽

Life Threatening ◽

Clinical Considerations ◽

The Brain ◽

Calcium Channels Blockers

Abstract Arterial aneurysm ruptures of the circle of Willis determine subarachnoid hemorrhage, which evolving due to the irritating effect of the blood in the subarachnoid space may lead to complications such as large arterial vasospasm in the origin of the large cerebral arteries, from the base of the brain. Cerebral vasospasm causes a downstream cerebral ischemia, that may lead to the establishment of an ischemic stroke which is life threatening. Early treatment against the vasospasm with calcium channels blockers should prevent occurrence of ischemia. However, the effectiveness of this treatment is not fully confirmed, fact that was mentioned even in the presentation of our case.

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A Highly Predictive MicroRNA Panel for Determining Delayed Cerebral Vasospasm Risk Following Aneurysmal Subarachnoid Hemorrhage

Frontiers in Molecular Biosciences ◽

10.3389/fmolb.2021.657258 ◽

2021 ◽

Vol 8 ◽

Author(s):

Wang-Xia Wang ◽

Joe E. Springer ◽

Kevin Xie ◽

David W. Fardo ◽

Kevin W. Hatton

Keyword(s):

Subarachnoid Hemorrhage ◽

Differential Expression ◽

Cerebral Vasospasm ◽

Aneurysmal Subarachnoid Hemorrhage ◽

Early Time ◽

Aneurysm Rupture ◽

Delayed Cerebral Vasospasm ◽

Differential Expression Pattern ◽

Neurologic Disability ◽

Risk Predictors

Approximately one-third of aneurysmal subarachnoid hemorrhage (aSAH) patients develop delayed cerebral vasospasm (DCV) 3–10 days after aneurysm rupture resulting in additional, permanent neurologic disability. Currently, no validated biomarker is available to determine the risk of DCV in aSAH patients. MicroRNAs (miRNAs) have been implicated in virtually all human diseases, including aSAH, and are found in extracellular biofluids including plasma and cerebrospinal fluid (CSF). We used a custom designed TaqMan Low Density Array miRNA panel to examine the levels of 47 selected brain and vasculature injury related miRNAs in CSF and plasma specimens collected from 31 patients with or without DCV at 3 and 7 days after aSAH, as well as from eight healthy controls. The analysis of the first 18-patient cohort revealed a striking differential expression pattern of the selected miRNAs in CSF and plasma of aSAH patients with DCV from those without DCV. Importantly, this differential expression was observed at the early time point (3 days after aSAH), before DCV event occurs. Seven miRNAs were identified as reliable DCV risk predictors along with a prediction model constructed based on an array of additional 19 miRNAs on the panel. These chosen miRNAs were then used to predict the risk of DCV in a separate, testing cohort of 15 patients. The accuracy of DCV risk prediction in the testing cohort reached 87%. The study demonstrates that our novel designed miRNA panel is an effective predictor of DCV risk and has strong applications in clinical management of aSAH patients.

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Preventive Effect of Clazosentan against Cerebral Vasospasm after Clipping Surgery for Aneurysmal Subarachnoid Hemorrhage in Japanese and Korean Patients

Cerebrovascular Diseases ◽

10.1159/000475824 ◽

2017 ◽

Vol 44 (1-2) ◽

pp. 59-67 ◽

Cited By ~ 12

Author(s):

Miki Fujimura ◽

Jin-Yang Joo ◽

Jong-Soo Kim ◽

Motonori Hatta ◽

Yoshinari Yokoyama ◽

...

Keyword(s):

Placebo Group ◽

Subarachnoid Hemorrhage ◽

Cerebral Infarction ◽

Cerebral Vasospasm ◽

Aneurysmal Subarachnoid Hemorrhage ◽

Study Drug ◽

Aneurysm Rupture ◽

Dose Finding ◽

Double Blind ◽

Korean Patients

Background: Clazosentan has been explored worldwide for the prophylaxis of cerebral vasospasm after aneurysmal subarachnoid hemorrhage (aSAH). In a dose-finding trial (CONSCIOUS-1) conducted in Israel, Europe, and North America, clazosentan (1, 5, and 15 mg/h) significantly reduced the incidence of cerebral vasospasm, but its efficacy in Japanese and Korean patients was unknown. We conducted a double-blind comparative study to evaluate the occurrence of cerebral vasospasm in Japanese and Korean patients with aSAH. Methods: The aim of this multicenter, double-blind, randomized, placebo-controlled, dose-finding phase 2 clinical trial, was to evaluate the efficacy, pharmacokinetics, and safety of clazosentan (5 and 10 mg/h) against cerebral vasospasm after clipping surgery in Japanese and Korean patients with aSAH. Patients aged between 20 and 75 years were administered the study drug within 56 h after the aneurysm rupture and up to day 14 post-aSAH. The incidence of vasospasm, defined as an inner artery diameter reduction of major intracranial arteries ≥34% based on catheter angiography, was compared between each treatment group. Cerebral infarction due to vasospasm at 6 weeks and patients' outcome at 3 months was also compared. Results: Among 181 enrolled patients, 158 completed the study and were analyzed. The incidence of vasospasm up to day 14 after aSAH onset was 80.0% in the placebo group (95% CI 67.0-89.6), 38.5% in the 5 mg/h clazosentan group (95% CI 25.3-53.0), and 35.3% in the 10 mg/h clazosentan group (95% CI 22.4-49.9), indicating that the incidence of vasospasm was significantly reduced by clazosentan treatment (placebo vs. 5 mg/h clazosentan, p < 0.0001; placebo vs. 10 mg/h clazosentan, p < 0.0001). The occurrence of cerebral infarction due to vasospasm was 20.8% in the placebo group (95% CI 10.8-34.1), 3.8% in the 5 mg/h clazosentan group (95% CI 0.5-13.2), and 4.2% in the 10 mg/h clazosentan group (95% CI 0.5-14.3), indicating that clazosentan significantly reduced the occurrence of cerebral infarctions caused by vasospasm (placebo vs. 5 mg/h clazosentan, p = 0.0151; placebo vs. 10 mg/h clazosentan, p = 0.0165). The overall incidence of all-cause death and/or vasospasm-related morbidity/mortality was significantly reduced in the 10 mg/h clazosentan group compared with the placebo group (p = 0.0003). Conclusion: These results suggest that clazosentan prevents cerebral vasospasm and subsequent cerebral infarction, and could thereby improve outcomes after performing a clipping surgery for aSAH in Japanese and Korean patients.

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