A modified double injection model of cisterna magna for the study of delayed cerebral vasospasm following subarachnoid hemorrhage in rats

Background: Majority of aneurysmal subarachnoid hemorrhage (SAH) survivors develop cognitive dysfunction. To better understand the underlying mechanisms and develop treatments, predictive animal models are required. We carried out a detailed physiological and cognitive characterization of pre-chiasmatic cistern (PC) and cisterna magna (CM) SAH models in mice. Methods: SAH was induced by arterial blood injection into the PC (40 μl) or CM (60 μl) in C57BL6/J mice (male, 25g). Controls received normal saline. Cerebral blood flow (CBF) was imaged using laser speckle flowmetry during and for 60 min after SAH. Intracranial pressure (ICP) and blood pressure (BP) were monitored to calculate cerebral perfusion pressure (CPP). Neurological and cognitive function was assessed 3 weeks after the injection, using pole, novel object recognition, Y maze and Morris water maze tests. Results: Mortality was 10% after PC and 4% after CM SAH. In both groups, CPP decreased from about 65 mmHg to less than 10 mmHg immediately after the injection, and recovered to 40 mmHg within 10 min after PC (n=8) and 7 min after CM (n=8) SAH (Fig A). In both groups, CBF was severely reduced to ~20% of baseline in both hemispheres immediately after SAH. CBF recovered to >40% within 5 min after PC and 2 min after CM SAH (Fig A). In saline controls (n=5 in PC and CM each), CPP and CBF changes were much milder and shorter-lasting. Compared with controls (n=12), PC SAH mice (n=12) performed significantly worse in a subset of sensorimotor and cognitive tests for up to 3 weeks (Fig B). CM SAH did not significantly impact neurological function. Conclusions: Pre-chiasmatic cistern but not cisterna magna SAH model reproduces cognitive dysfunction observed in patients with low mortality and high reproducibility in mice.

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

Journal of NeuroInterventional Surgery ◽

10.1136/neurintsurg-2016-012546 ◽

2016 ◽

Vol 9 (1) ◽

pp. 52-59 ◽

Cited By ~ 20

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.

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

Journal of Neurosurgery ◽

10.3171/jns.2002.97.6.1302 ◽

2002 ◽

Vol 97 (6) ◽

pp. 1302-1305 ◽

Cited By ~ 34

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.

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