scholarly journals Toll-like Receptor 4 (TLR4) is Associated with Cerebral Vasospasm and Delayed Cerebral Ischemia in Aneurysmal Subarachnoid Hemorrhage

2015 ◽  
Vol 55 (12) ◽  
pp. 878-884 ◽  
Author(s):  
Chunxiao MA ◽  
Wei ZHOU ◽  
Zhaoyue YAN ◽  
Mingqi QU ◽  
Xingyao BU
2020 ◽  
Vol 133 (6) ◽  
pp. 1786-1791 ◽  
Author(s):  
Kevin Kwan ◽  
Orseola Arapi ◽  
Katherine E. Wagner ◽  
Julia Schneider ◽  
Heustein L. Sy ◽  
...  

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.


2010 ◽  
Vol 30 (4) ◽  
pp. 676-688 ◽  
Author(s):  
Andrew F Ducruet ◽  
Paul R Gigante ◽  
Zachary L Hickman ◽  
Brad E Zacharia ◽  
Eric J Arias ◽  
...  

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.


2017 ◽  
Vol 5 (20) ◽  
pp. 33
Author(s):  
Mohamed Shehabeldin ◽  
Yazan Alderazi

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.


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