scholarly journals Vasa Vasorum Formation is Associated With Rupture of Intracranial Aneurysms

Neurosurgery ◽  
2019 ◽  
Vol 66 (Supplement_1) ◽  
Author(s):  
Haruka Miyata ◽  
Hirokazu Koseki ◽  
Kampei Shimizu ◽  
Yu Abekura ◽  
Mieko Oka ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Intracranial Aneurysms ◽  
Histopathological Examination ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Vasa Vasorum ◽  
Systemic Hypertension ◽  
External Carotid ◽  
Anterior Communicating Artery ◽  
Sprague Dawley ◽  
The Right

Abstract INTRODUCTION Subarachnoid hemorrhage has a poor outcome despite a modern advancement in medical care. The development of a novel therapeutic strategy to prevent rupture of intracranial aneurysms (IAs) or a novel diagnostic marker to predict rupture-prone lesions is thus mandatory. Therefore, in the present study, we established a rat model in which IAs spontaneously rupture and examined this model to clarify histopathological features associated with rupture of lesions. METHODS In detail, female Sprague-Dawley rats were subjected to the bilateral ovariectomy, the ligation of the left common carotid, the right external carotid, and the right pterygopalatine arteries, the induced systemic hypertension, and the administration of a lysyl oxidase inhibitor. RESULTS Aneurysmal subarachnoid hemorrhage occurred one-thirds of manipulated animals and locations of ruptured IAs were exclusively at a posterior or an anterior communicating artery. Histopathological examination using ruptured IAs, rupture-prone ones induced at a posterior or an anterior communicating artery, ones induced at an anterior cerebral artery-olfactory artery bifurcation that never rupture revealed the formation of vasa vasorum as an event associated with rupture of IAs. CONCLUSION We thus proposed the contribution of a structural change in an adventitia, vasa vasorum formation, to rupture of IAs. Findings from this study provide important insights about the pathogenesis of IAs.

Vasa vasorum formation is associated with rupture of intracranial aneurysms

2020 ◽  
Vol 133 (3) ◽  
pp. 789-799 ◽  
Author(s):  
Haruka Miyata ◽  
Hirohiko Imai ◽  
Hirokazu Koseki ◽  
Kampei Shimizu ◽  
Yu Abekura ◽  
...  
Keyword(s):  
Intracranial Aneurysms ◽  
Lysyl Oxidase ◽  
Histopathological Examination ◽  
Oxidase Inhibitor ◽  
Vasa Vasorum ◽  
Systemic Hypertension ◽  
External Carotid ◽  
Anterior Communicating Artery ◽  
Sprague Dawley ◽  
The Right

OBJECTIVESubarachnoid hemorrhage (SAH) has a poor outcome despite modern advancements in medical care. The development of a novel therapeutic strategy to prevent rupture of intracranial aneurysms (IAs) or a novel diagnostic marker to predict rupture-prone lesions is thus mandatory. Therefore, in the present study, the authors established a rat model in which IAs spontaneously rupture and examined this model to clarify histopathological features associated with rupture of lesions.METHODSFemale Sprague Dawley rats were subjected to bilateral ovariectomy; the ligation of the left common carotid, the right external carotid, and the right pterygopalatine arteries; induced systemic hypertension; and the administration of a lysyl oxidase inhibitor.RESULTSAneurysmal SAH occurred in one-third of manipulated animals and the locations of ruptured IAs were exclusively at a posterior or anterior communicating artery (PCoA/ACoA). Histopathological examination using ruptured IAs, rupture-prone IAs induced at a PCoA or ACoA, and IAs induced at an anterior cerebral artery–olfactory artery bifurcation that never ruptured revealed the formation of vasa vasorum as an event associated with rupture of IAs.CONCLUSIONSThe authors propose the contribution of a structural change in an adventitia, i.e., vasa vasorum formation, to the rupture of IAs. Findings from this study provide important insights about the pathogenesis of IAs.

Abstract WMP33: Neutrophils Infiltrating Through Vasa Vasorum Facilitate Rupture of Intracranial Aneurysms

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Tomohiro Aoki ◽  
Mika Kushamae ◽  
Haruka Miyata ◽  
Tohru Mizutani ◽  
Kazuhiko Nozaki
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Rna Sequencing ◽  
Intracranial Aneurysms ◽  
Structural Changes ◽  
Inflammatory Responses ◽  
Vasa Vasorum ◽  
Therapeutic Modality ◽  
Systemic Hypertension ◽  
Sequencing Analysis ◽  
Sprague Dawley

Introduction: Subarachnoid hemorrhage due to rupture of intracranial aneurysms (IAs) has quite a poor outcome once after the onset despite an intensive medical care. An appropriate treatment intervention of IAs to prevent rupture is thus mandatory for social health. To achieve this goal, a novel therapeutic modality should be developed based on accurate understanding of the underlying pathogenesis. Although the crucial contribution of macrophage-mediated chronic inflammatory responses in the initiation and progression of IAs has been clarified, much still remains to be elucidated, e.g. what factor triggers rupture of IAs. Methods: 10-week-old female Sprague-Dawley rats weresubjected to the combined ligation of carotid arteries and systemic hypertension to induce IAs. In this model, two different type of IAs can be induced in a same animal, spontaneously ruptured ones and ones which never rupture. Using this model, we compared ruptured IAs and unruptured ones to clarify histological features related with rupture of the lesions. Gene expression profile data was obtained by RNA-sequencing analyses of induced IAs to identify molecular cascades functioning in the process of rupture. We also examined effect of neutrophils on the rupture, subcutaneous injection of G-CSF was done. Results: We found the significant increase of vasa vasorum at the adventitia of ruptured IA walls compared with that in unruptured ones. Through the RNA-sequencing analysis, we identified cascades related with neutrophils as over-represented ones in ruptured lesions. The increase of neutrophils in number by G-CSF treatment then significantly facilitated rupture of IAs and inflammatory responses in situ. Conclusions: These results combined together propose that rupture of lesions requires structural changes of arterial walls, vasa vasorum formation, and infiltration of neutrophils across there beyond the well-known involvement of macrophage-mediated chronic inflammation in the process of initiation, making rupture being qualitatively different process. The present study also highlights the potential of vasa vasorum formation or neutrophils as a target for drug therapy to prevent subarachnoid hemorrhage.

scholarly journals Characteristics of Unruptured Compared to Ruptured Intracranial Aneurysms: A Multicenter Case–Control Study

Neurosurgery ◽  
2017 ◽  
Vol 83 (1) ◽  
pp. 43-52 ◽  
Author(s):  
Isabel C Hostettler ◽  
Varinder S Alg ◽  
Nichole Shahi ◽  
Fatima Jichi ◽  
Stephen Bonner ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Artery ◽  
Intracranial Aneurysms ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Anterior Communicating Artery ◽  
Imaging Data ◽  
Unruptured Aneurysms ◽  
Ruptured Aneurysms ◽  
Multivariable Analyses ◽  
Different Characteristics

Abstract BACKGROUND Only a minority of intracranial aneurysms rupture to cause subarachnoid hemorrhage. OBJECTIVE To test the hypothesis that unruptured aneurysms have different characteristics and risk factor profiles compared to ruptured aneurysms. METHODS We recruited patients with unruptured aneurysms or aneurysmal subarachnoid hemorrhages at 22 UK hospitals between 2011 and 2014. Demographic, clinical, and imaging data were collected using standardized case report forms. We compared risk factors using multivariable logistic regression. RESULTS A total of 2334 patients (1729 with aneurysmal subarachnoid hemorrhage, 605 with unruptured aneurysms) were included (mean age 54.22 yr). In multivariable analyses, the following variables were independently associated with rupture status: black ethnicity (odds ratio [OR] 2.42; 95% confidence interval [CI] 1.29-4.56, compared to white) and aneurysm location (anterior cerebral artery/anterior communicating artery [OR 3.21; 95% CI 2.34-4.40], posterior communicating artery [OR 3.92; 95% CI 2.67-5.74], or posterior circulation [OR 3.12; 95% CI 2.08-4.70], compared to middle cerebral artery). The following variables were inversely associated with rupture status: antihypertensive medication (OR 0.65; 95% CI 0.49-0.84), hypercholesterolemia (0.64 OR; 95% CI 0.48-0.85), aspirin use (OR 0.28; 95% CI 0.20-0.40), internal carotid artery location (OR 0.53; 95% CI 0.38-0.75), and aneurysm size (per mm increase; OR 0.76; 95% CI 0.69-0.84). CONCLUSION We show substantial differences in patient and aneurysm characteristics between ruptured and unruptured aneurysms. These findings support the hypothesis that different pathological mechanisms are involved in the formation of ruptured aneurysms and incidentally detected unruptured aneurysms. The potential protective effect of aspirin might justify randomized prevention trials in patients with unruptured aneurysms.

Abstract 3499: Novel Nitric Oxide-Containing Echogenic Liposome for the Treatment of Vasospasm Following Subarachnoid Hemorrhage

Stroke ◽  
2012 ◽  
Vol 43 (suppl_1) ◽  
Author(s):  
George L Britton ◽  
Tao Peng ◽  
Jaroslaw Aronowski ◽  
David D McPherson ◽  
Shao-Ling Huang ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Femoral Vein ◽  
High Morbidity ◽  
Sprague Dawley ◽  
Treatment Groups ◽  
Echogenic Liposomes ◽  
The Right

Background: Cerebral vasospasm following aneurysmal subarachnoid hemorrhage (SAH) is a major cause of high morbidity and mortality. The reduced availability of nitric oxide (NO) in blood and cerebrospinal fluid (CSF) is suggested an important mechanism underlying cerebral vasospasm, a complication of SAH. NO or NO donors are known to have potent effects on cerebral vascular relaxation. We have developed NO-containing echogenic liposomes (NO-ELIP) for NO delivery to assess the role of NO in SAH-induced vasospasm. We hypothesized that NO-ELIP can produce vasodilation and provide an effective therapeutic approach to treat vasospasm following SAH. Methods: NO-ELIP was created by a freeze-under-pressure method. Male Sprague- Dawley rats (n=9) underwent SAH by puncturing the right middle cerebral artery with a sharp tip nylon monofilament. In the treatment groups, NO-ELIP were administered through the right femoral vein at 24 hours after SAH onset. The brain tissue was obtained for H&E staining at 30 min after NO-ELIP administration. Measurement of the posterior communicating artery was performed to evaluate the effects of NO-ELIP treatment on vasospasm following SAH. Results: After SAH, the normalized lumenal and wall thickness areas decreased from 1.02 ± 0.08 to 0.40 ± 0.15 (p<0.001). NO-ELIP inhibited SAH-induced vasospasm by 67% (normalized area decreased to 0.82 ± 0.10 (p=0.004). Conclusion: This study demonstrates that NO-ELIP have the potential to deliver NO for therapeutic treatment of vasospasm. Enhancing the release of NO from circulating NO-ELIP by combining ultrasound exposure over the carotid artery may further provide an improved treatment strategy. This suggests that targeted therapeutic gas can be delivered to the cerebral circulation for the treatment of vasospasm following SAH

Terson sign:

2020 ◽  
Vol 2 (1) ◽  
pp. 38-43
Author(s):  
Luiz Severo Bem Junior ◽  
Gustavo De Souza Andrade ◽  
Joao Ribeiro Memória Júnior ◽  
Hildo Rocha Cirne de Azevedo Filho
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Early Recognition ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Case Reports ◽  
Clinical Status ◽  
Vitreous Hemorrhage ◽  
Anterior Communicating Artery ◽  
Inclusion Criteria ◽  
Relationship Of ◽  
The Relationship

Terson's sign (TS) is classically defined as vitreous hemorrhage associated with subarachnoid hemorrhage of aneurysmal origin, being an important predictor of severity, indicating greater morbidity and mortality when compared to patients without the sign. The objective of this study is to review the relationship of Terson syndrome/Terson sign with the prognosis of aneurysmal subarachnoid hemorrhage. A search for original articles, research and case reports was performed on the PubMed, Scielo, Cochrane and ScienceDirect platform, with the following descriptors: Terson sign and subarachnoid hemorrhage. Retrospective, prospective articles and case reports published in the last 5 years and which were in accordance with the established objective and inclusion criteria were selected. Ten (10) articles were selected, in which the available results show an unfavorable prognostic relationship of TS and subarachnoid hemorrhage, because these patients had a worse clinical status assessed on the Glasgow scales ≤ 8, Hunt & Hess > III, Fisher > 3, in addition to intracranial hypertension and location of the aneurysm in the anterior communicating artery complex. The early recognition of this condition described by Albert Terson in 1900 brought an important contribution to neurosurgery, being recognized until nowadays.

scholarly journals Levosimendan as a therapeutic strategy to prevent neuroinflammation after aneurysmal subarachnoid hemorrhage?

2021 ◽  
pp. neurintsurg-2021-017504
Author(s):  
Stefan Wanderer ◽  
Lukas Andereggen ◽  
Jan Mrosek ◽  
Sepide Kashefiolasl ◽  
Gerrit Alexander Schubert ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Delayed Cerebral Ischemia ◽  
Severe Heart Failure ◽  
Prostaglandin F2alpha ◽  
Sprague Dawley ◽  
Delayed Cerebral Vasospasm ◽  
Sprague Dawley Rats ◽  
Solvent Control ◽  
Anti Inflammatory

BackgroundPoor patient outcomes after aneurysmal subarachnoid hemorrhage (SAH) occur due to a multifactorial process, mainly involving cerebral inflammation (CI), delayed cerebral vasospasm (DCVS), and delayed cerebral ischemia, followed by neurodegeneration. CI is mainly triggered by enhanced synthesis of serotonin (5-HT), prostaglandin F2alpha (PGF2a), and cytokines such as interleukins. Levosimendan (LV), a calcium-channel sensitizer, has already displayed anti-inflammatory effects in patients with severe heart failure. Therefore, we wanted to elucidate its potential anti-inflammatory role on the cerebral vasculature after SAH.MethodsExperimental SAH was induced by using an experimental double-hemorrhage model. Sprague Dawley rats were harvested on day 3 and day 5 after the ictus. The basilar artery was used for isometric investigations of the muscular media tone. Vessel segments were either preincubated with LV or without, with precontraction performed with 5-HT or PGF2a followed by application of acetylcholine (ACh) or LV.ResultsAfter preincubation with LV 10−4 M and 5-HT precontraction, ACh triggered a strong vasorelaxation in sham segments (LV 10−4 M, Emax 65%; LV 10−5 M, Emax 48%; no LV, Emax 53%). Interestingly, SAH D3 (LV 10−4, Emax 76%) and D5 (LV 10−4, Emax 79%) segments showed greater vasorelaxation compared with sham. An LV series after PGF2a precontraction showed significantly enhanced relaxation in the sham (P=0.004) and SAH groups (P=0.0008) compared with solvent control vessels.ConclusionsLV application after SAH seems to beneficially influence DCVS by antagonizing 5-HT- and PGF2a-triggered vasoconstriction. Considering this spasmolytic effect, LV might have a role in the treatment of SAH, additionally in selected patients suffering takotsubo cardiomyopathy.

scholarly journals Surgical treatment of intracranial aneurysms: six-year experience in Belo Horizonte, MG, Brazil

2004 ◽  
Vol 62 (2a) ◽  
pp. 245-249 ◽  
Author(s):  
Leodante Batista da Costa Jr ◽  
Josaphat Vilela de Morais ◽  
Agustinho de Andrade ◽  
Marcelo Duarte Vilela ◽  
Renato P. Campolina Pontes ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Surgical Treatment ◽  
Intracranial Aneurysms ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
The United States ◽  
Anterior Circulation ◽  
Common Location ◽  
Belo Horizonte ◽  
Spontaneous Subarachnoid Hemorrhage ◽  
Anterior Circulation Aneurysms

Spontaneous subarachnoid hemorrhage accounts for 5 to 10 % of all strokes, with a worldwide incidence of 10.5 / 100000 person/year, varying in individual reports from 1.1 to 96 /100000 person/year. Angiographic and autopsy studies suggest that between 0.5% and 5% of the population have intracranial aneurysms. Approximately 30000 people suffer aneurysmal subarachnoid hemorrhage in the United States each year, and 60% die or are left permanently disabled. We report our experience in the surgical treatment of intracranial aneurysms in a six year period, in Belo Horizonte, Minas Gerais, Brazil. We reviewed the hospital files, surgical and out-patient notes of all patients operated on for the treatment of intracranial aneurysms from January 1997 to January 2003. Four hundred and seventy-seven patients were submitted to 525 craniotomies for treatment of 630 intracranial aneurysms. The majority of patients were female (72.1%) in the fourth or fifth decade of life. Anterior circulation aneurysms were more common (94.4%). The most common location for the aneurysm was the middle cerebral artery bifurcation. The patients were followed by a period from 1 month to 5 years. The outcome was measured by the Glasgow Outcome Scale (GOS). At discharge, 62.1% of the patients were classified as GOS 5, 13.9% as GOS 4, 8.7% as GOS 3, 1.7% as GOS 2 and 14.8% as GOS 1.

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