Beyond Delayed Cerebral Vasospasm: Infarct Patterns in Patients with Subarachnoid Hemorrhage

2012 ◽  
Vol 23 (2) ◽  
pp. 87-95 ◽  
Author(s):  
M. Wagner ◽  
P. Steinbeis ◽  
E. Güresir ◽  
E. Hattingen ◽  
R. du Mesnil de Rochemont ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Delayed Cerebral Vasospasm

Treatment of cerebral vasospasm with self-expandable retrievable stents: proof of concept

2016 ◽  
Vol 9 (1) ◽  
pp. 52-59 ◽  
Author(s):  
Pervinder Bhogal ◽  
Yince Loh ◽  
Patrick Brouwer ◽  
Tommy Andersson ◽  
Michael Söderman
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
High Volume ◽  
Radial Force ◽  
Proof Of Concept ◽  
Stent Angioplasty ◽  
Delayed Cerebral Vasospasm ◽  
Stent Retrievers ◽  
Cerebral Vasodilation ◽  
Standard Techniques

ObjectiveTo report our preliminary experience with the use of stent retrievers to cause vasodilation in patients with delayed cerebral vasospasm secondary to subarachnoid hemorrhage.MethodsFour patients from two different high volume neurointerventional centers developed cerebral vasospasm following subarachnoid hemorrhage. In addition to standard techniques for the treatment of cerebral vasospasm, we used commercially available stent retrievers (Solitaire and Capture stent retrievers) to treat the vasospastic segment including M2, M1, A2, and A1. We evaluated the safety of this technique, degree of vasodilation, and longevity of the effect.ResultsStent retrievers can be used to safely achieve cerebral vasodilation in the setting of delayed cerebral vasospasm. The effect is long-lasting (>24 hours) and, in our initial experience, carries a low morbidity. We have not experienced any complications using this technique although we have noted that the radial force was not sufficient to cause vasodilation in some instances. The vasospasm did not return in the vessel segments treated with stent angioplasty in any of these cases. In two of our cases stent angioplasty resulted in the reversal of focal neurological symptoms.ConclusionsStent retrievers can provide long-lasting cerebral vasodilation in patients with delayed cerebral vasospasm.

scholarly journals Increased levels of lipid peroxides as predictive of symptomatic vasospasm and poor outcome after aneurysmal subarachnoid hemorrhage

2002 ◽  
Vol 97 (6) ◽  
pp. 1302-1305 ◽  
Author(s):  
Takao Kamezaki ◽  
Kiyoyuki Yanaka ◽  
Sohji Nagase ◽  
Keishi Fujita ◽  
Noriyuki Kato ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Lipid Peroxides ◽  
Medical Complication ◽  
Content Type ◽  
Poor Outcome ◽  
Symptomatic Vasospasm ◽  
Delayed Cerebral Vasospasm ◽  
Fine Print

Object. Cerebral vasospasm remains a devastating medical complication of aneurysmal subarachnoid hemorrhage (SAH). Reactive oxygen species and subsequent lipid peroxidation are reported to participate in the causes of cerebral vasospasm. This clinical study was performed to investigate the relationships between levels of lipid peroxides in cerebrospinal fluid (CSF) and both delayed cerebral vasospasm and clinical outcome after SAH. Methods. Levels of phosphatidylcholine hydroperoxide (PCOOH) and cholesteryl ester hydroperoxide (CEOOH) in the CSF were measured in 20 patients with aneurysmal SAH. The patients' CSF was collected within 48 hours of hemorrhage onset and on Day 6 or 7 post-SAH. On Day 7, angiography was performed to verify the degree and extent of the vasospasm. The relationship between the patients' clinical profiles and the levels of lipid peroxides in the CSF were investigated. Both PCOOH and CEOOH were detectable in CSF, and their levels decreased within 7 days after onset of SAH. The levels of CEOOH within 48 hours after onset of hemorrhage were significantly higher in patients in whom symptomatic vasospasm later developed than in patients in whom symptomatic vasospasm did not develop (p = 0.002). Levels of PCOOH measured within 48 hours after onset of hemorrhage were significantly higher in patients with poor outcomes than in patients with good outcomes (p = 0.043). Conclusions. Increased levels of lipid peroxides measured in the CSF during the acute stage of SAH were predictive of both symptomatic vasospasm and poor outcome. Measurements of lipid peroxides in the CSF may be useful prognostically for patient outcomes as well as for predicting symptomatic vasospasm.

Preliminary Results of an ICP-Controlled Subarachnoid Hemorrhage Rabbit Model for the Study of Delayed Cerebral Vasospasm

2011 ◽  
pp. 163-165
Author(s):  
Serge Marbacher ◽  
Camillo Sherif ◽  
Volker Neuschmelting ◽  
Janine-Ai Schläppi ◽  
Jukka Takala ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Rabbit Model ◽  
Preliminary Results ◽  
Delayed Cerebral Vasospasm

scholarly journals Bilirubin Production and Oxidation in CSF of Patients with Cerebral Vasospasm after Subarachnoid Hemorrhage

2005 ◽  
Vol 25 (8) ◽  
pp. 1070-1077 ◽  
Author(s):  
Gail J Pyne-Geithman ◽  
Chad J Morgan ◽  
Kenneth Wagner ◽  
Elizabeth M Dulaney ◽  
Janice Carrozzella ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Cerebral Spinal Fluid ◽  
Spinal Fluid ◽  
Oxidation Products ◽  
Mortality And Morbidity ◽  
Delayed Cerebral Vasospasm ◽  
And Oxidative Stress

Delayed cerebral vasospasm after subarachnoid hemorrhage (SAH) remains a significant cause of mortality and morbidity; however, the etiology is, as yet, unknown, despite intensive research efforts. Research in this laboratory indicates that bilirubin and oxidative stress may be responsible by leading to formation of bilirubin oxidation products (BOXes), so we investigated changes in bilirubin concentration and oxidative stress in vitro, and in cerebral spinal fluid (CSF) from SAH patients. Non-SAH CSF, a source of heme oxygenase I (HO-1), and blood were incubated, and in vitro bilirubin production measured. Cerebrospinal fluid from SAH patients was collected, categorized using stimulation of vascular smooth muscle metabolism in vitro, and information obtained regarding occurrence of vasospasm in the patients. Cerebral spinal fluid was analyzed for hemoglobin, total protein and bilirubin, BOXes, malonyldialdehyde and peroxidized lipids (indicators of an oxidizing environment), and HO-1 concentration. The formation of bilirubin in vitro requires that CSF is present, as well as whole, non-anti-coagulated blood. Bilirubin, BOXes, HO-1, and peroxidized lipid content were significantly higher in CSF from SAH patients with vasospasm, compared with nonvasospasm SAH CSF, and correlated with occurrence of vasospasm. We conclude that vasospasm may be more likely in patients with elevated BOXes. The conditions necessary for the formation of BOXes are indeed present in CSF from SAH patients with vasospasm, but not CSF from SAH patients without vasospasm.

Hydroperoxide in Internal Jugular Venous Blood Reflects Occurrence of Subarachnoid Hemorrhage-Induced Delayed Cerebral Vasospasm

2014 ◽  
Vol 23 (9) ◽  
pp. 2217-2224 ◽  
Author(s):  
Hiroyuki Uekusa ◽  
Chikao Miyazaki ◽  
Kosuke Kondo ◽  
Naoyuki Harada ◽  
Jun Nomoto ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Venous Blood ◽  
Delayed Cerebral Vasospasm
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