A rabbit model of aneurysmal subarachnoid hemorrhage by ear central artery-suprasellar cistern shunt

2017 ◽  
Vol 44 ◽  
pp. 300-305 ◽  
Author(s):  
Jing Lu ◽  
Fuxiang Chen ◽  
Bing Cai ◽  
Fan Chen ◽  
Dezhi Kang
2015 ◽  
Vol 8 (4) ◽  
pp. 378-385 ◽  
Author(s):  
Adam N Wallace ◽  
Ross Vyhmeister ◽  
Jeffrey N Dines ◽  
Arindam R Chatterjee ◽  
Akash P Kansagra ◽  
...  

Background and purposePerimesencephalic subarachnoid hemorrhage (PSAH) is not consistently defined in the existing literature. The purpose of this study was to test the inter-observer variability and specificity for non-aneurysmal subarachnoid hemorrhage (SAH) of an anatomic definition of PSAH.MethodsMedical records of all patients who underwent catheter angiography for evaluation of non-traumatic SAH between July 2002 and April 2012 were reviewed. Patients with anterior circulation aneurysms were excluded. Three blinded reviewers assessed whether each admission CT scan met the following anatomic criteria for PSAH: (1) center of bleeding located immediately anterior and in contact with the brainstem in the prepontine, interpeduncular, or posterior suprasellar cistern; (2) blood limited to the prepontine, interpeduncular, suprasellar, crural, ambient, and/or quadrigeminal cisterns and/or cisterna magna; (3) no extension of blood into the Sylvian or interhemispheric fissures; (4) intraventricular blood limited to incomplete filling of the fourth ventricle and occipital horns of the lateral ventricles (ie, consistent with reflux); (5) no intraparenchymal blood.Results56 patients with non-aneurysmal SAH and 50 patients with posterior circulation or posterior communicating artery aneurysms were identified. Seventeen (16%) of the 106 admission CT scans met the anatomic criteria for PSAH. No aneurysm was identified in this subgroup. Inter-observer agreement was excellent with κ scores of 0.89–0.96 and disagreement in 2.8% (3/106) of cases.ConclusionsOur anatomic definition of PSAH correlated with a low risk of brain aneurysm and was applied with excellent inter-observer agreement.


2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Lukas Andereggen ◽  
Volker Neuschmelting ◽  
Michael von Gunten ◽  
Hans Rudolf Widmer ◽  
Javier Fandino ◽  
...  

Background.Microvascular dysfunction and microthrombi formation are believed to contribute to development of early brain injury (EBI) after aneurysmal subarachnoid hemorrhage (SAH).Objective.This study aimed to determine (i) extent of microthrombus formation and neuronal apoptosis in the brain parenchyma using a blood shunt SAH model in rabbits; (ii) correlation of structural changes in microvessels with EBI characteristics.Methods.Acute SAH was induced using a rabbit shunt cisterna magna model. Extent of microthrombosis was detected 24 h post-SAH (n=8) by fibrinogen immunostaining, compared to controls (n=4). We assessed apoptosis by terminal deoxynucleotidyl transferase nick end labeling (TUNEL) in cortex and hippocampus.Results.Our results showed significantly more TUNEL-positive cells (SAH: 115 ± 13; controls: 58 ± 10;P=0.016) and fibrinogen-positive microthromboemboli (SAH: 9 ± 2; controls: 2 ± 1;P=0.03) in the hippocampus after aneurysmal SAH.Conclusions.We found clear evidence of early microclot formation in a rabbit model of acute SAH. The extent of microthrombosis did not correlate with early apoptosis or CPP depletion after SAH; however, the total number of TUNEL positive cells in the cortex and the hippocampus significantly correlated with mean CPP reduction during the phase of maximum depletion after SAH induction. Both microthrombosis and neuronal apoptosis may contribute to EBI and subsequent DCI.


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