scholarly journals Non-cerebral vasospasm factors and cerebral vasospasm predict delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage

2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Yue Chen ◽  
Guanmin Li ◽  
Xiaoyong Chen ◽  
Dengliang Wang ◽  
Wenhua Fang ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Cerebral Vasospasm ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Delayed Cerebral Ischemia

Cerebrospinal fluid macrophage migration inhibitory factor: a potential predictor of cerebral vasospasm and clinical outcome after aneurysmal subarachnoid hemorrhage

2020 ◽  
Vol 133 (6) ◽  
pp. 1786-1791 ◽  
Author(s):  
Kevin Kwan ◽  
Orseola Arapi ◽  
Katherine E. Wagner ◽  
Julia Schneider ◽  
Heustein L. Sy ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Cerebral Vasospasm ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Delayed Cerebral Ischemia ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Significant Difference

OBJECTIVEIn patients with aneurysmal subarachnoid hemorrhage (aSAH), poor outcomes have been shown to be correlated with subsequent cerebral vasospasm (CV) and delayed cerebral ischemia (DCI). The identification of novel biomarkers may aid in the prediction of which patients are vulnerable to developing vasospasm, cerebral ischemia, and neurological deterioration.METHODSIn this prospective clinical study at North Shore University Hospital, patients with aSAH or normal pressure hydrocephalus (NPH) with external ventricular drains were enrolled. The concentration of macrophage migration inhibitory factor (MIF) in CSF was assessed for correlation with CV or DCI, the primary outcome measures.RESULTSTwenty-five patients were enrolled in the aSAH group and 9 were enrolled in the NPH group. There was a significant increase in aggregate CSF MIF concentration in patients with aSAH versus those with NPH (24.4 ± 19.2 vs 2.3 ± 1.1 ng/ml, p < 0.0002). Incidence of the day of peak MIF concentration significantly correlated with the onset of clinical vasospasm (rho = 0.778, p < 0.0010). MIF concentrations were significantly elevated in patients with versus those without evidence of DCI (18.7 ± 4.93 vs 8.86 ± 1.28 ng/ml, respectively, p < 0.0025). There was a significant difference in MIF concentrations between patients with infection versus those without infection (16.43 ± 4.21 vs 8.5 ± 1.22 ng/ml, respectively, p < 0.0119).CONCLUSIONSPreliminary evidence from this study suggests that CSF concentrations of MIF are correlated with CV and DCI. These results, however, could be confounded in the presence of clinical infection. A study with a larger patient sample size is necessary to corroborate these findings.

scholarly journals Genetic Determinants of Cerebral Vasospasm, Delayed Cerebral Ischemia, and Outcome after Aneurysmal Subarachnoid Hemorrhage

2010 ◽  
Vol 30 (4) ◽  
pp. 676-688 ◽  
Author(s):  
Andrew F Ducruet ◽  
Paul R Gigante ◽  
Zachary L Hickman ◽  
Brad E Zacharia ◽  
Eric J Arias ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Cerebral Vasospasm ◽  
Vascular Reactivity ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Association Studies ◽  
Genetic Research ◽  
Delayed Cerebral Ischemia ◽  
Cerebral Injury ◽  
Genetic Determinants

Despite extensive effort to elucidate the cellular and molecular bases for delayed cerebral injury after aneurysmal subarachnoid hemorrhage (aSAH), the pathophysiology of these events remains poorly understood. Recently, much work has focused on evaluating the genetic underpinnings of various diseases in an effort to delineate the contribution of specific molecular pathways as well as to uncover novel mechanisms. The majority of subarachnoid hemorrhage genetic research has focused on gene expression and linkage studies of these markers as they relate to the development of intracranial aneurysms and their subsequent rupture. Far less work has centered on the genetic determinants of cerebral vasospasm, the predisposition to delayed cerebral injury, and the determinants of ensuing functional outcome after aSAH. The suspected genes are diverse and encompass multiple functional systems including fibrinolysis, inflammation, vascular reactivity, and neuronal repair. To this end, we present a systematic review of 21 studies suggesting a genetic basis for clinical outcome after aSAH, with a special emphasis on the pathogenesis of cerebral vasospasm and delayed cerebral ischemia. In addition, we highlight potential pitfalls in the interpretation of genetic association studies, and call for uniformity of design of larger multicenter studies in the future.

scholarly journals Management of cerebral vasospasm following aneurysmal subarachnoid hemorrhage

2017 ◽  
Vol 5 (20) ◽  
pp. 33
Author(s):  
Mohamed Shehabeldin ◽  
Yazan Alderazi
Keyword(s):  
Critical Care ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Cerebral Vasospasm ◽  
Endovascular Therapy ◽  
Clinical Presentation ◽  
Inflammatory Responses ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Delayed Cerebral Ischemia ◽  
Common Cause

Cerebral vasospasm is a serious complication following aneurysmal subarachnoidhemorrhage (SAH); it causes delayed cerebral ischemia (DCI) or infarction. Arterial vasospasmis considered the most common cause of disability and mortality among survivors of aneurysmalSAH. Monitoring for vasospasm is extremely important starting from the first day following ahemorrhage. The mechanism of vasospasm is not completely understood, but most data andstudies link the incidence of vasospasm to inflammatory responses secondary to extravasationof blood into the subarachnoid space. It is essential for critical care teams and health careproviders caring for patients with aneurysmal SAH to understand the clinical presentation andmanagement of cerebral vasospasm. In our review, we focus on the guidelines for monitoringand basic management of vasospasm and DCI which include monitoring options, hemodynamicand endovascular therapy, triggers for intervention, and triggers for treatment de-escalation.

scholarly journals Therapeutic Implications of Estrogen for Cerebral Vasospasm and Delayed Cerebral Ischemia Induced by Aneurysmal Subarachnoid Hemorrhage

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Dale Ding ◽  
Robert M. Starke ◽  
Aaron S. Dumont ◽  
Gary K. Owens ◽  
David M. Hasan ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Cerebral Vasospasm ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Delayed Cerebral Ischemia ◽  
Therapeutic Implications ◽  
Delayed Neurological Deterioration ◽  
Adenosine A2a ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Cerebral vasospasm (CV) remains the leading cause of delayed morbidity and mortality following aneurysmal subarachnoid hemorrhage (SAH). However, increasing evidence supports etiologies of delayed cerebral ischemia (DCI) other than CV. Estrogen, specifically 17β-estradiol (E2), has potential therapeutic implications for ameliorating the delayed neurological deterioration which follows aneurysmal SAH. We review the causes of CV and DCI and examine the evidence for E2-mediated vasodilation and neuroprotection. E2 potentiates vasodilation by activating endothelial nitric oxide synthase (eNOS), preventing increased inducible NOS (iNOS) activity caused by SAH, and decreasing endothelin-1 production. E2 provides neuroprotection by increasing thioredoxin expression, decreasing c-Jun N-terminal kinase activity, increasing neuroglobin levels, preventing SAH-induced suppression of the Akt signaling pathway, and upregulating the expression of adenosine A2a receptor. The net effect of E2 modulation of these various effectors is the promotion of neuronal survival, inhibition of apoptosis, and decreased oxidative damage and inflammation. E2 is a potentially potent therapeutic tool for improving outcomes related to post-SAH CV and DCI. However, clinical evidence supporting its benefits remains lacking. Given the promising preclinical data available, further studies utilizing E2 for the treatment of patients with ruptured intracranial aneurysms appear warranted.

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