The SNHG12/microRNA-15b-5p/MYLK axis regulates vascular smooth muscle cell phenotype to affect intracranial aneurysm formation.

OBJECTIVE: This research was dedicated to investigating the impact of the SNHG12/microRNA (miR)-15b-5p/MYLK axis on the modulation of vascular smooth muscle cell (VSMC) phenotype and the formation of intracranial aneurysm (IA). METHODS: SNHG12, miR-15b-5p and MYLK expression in IA tissue samples from IA patients were tested by RT-qPCR and western blot. Human aortic vascular smooth muscle cells (VSMCs) were cultivated with H2O2 to mimic IA-like conditions in vitro, and the cell proliferation and apoptosis were measured by MTT assay and Annexin V/PI staining. IA mouse models were established by induction with systemic hypertension combined with elastase injection. The blood pressure in the tail artery of mice in each group was assessed and the pathological changes in arterial tissues were observed by HE staining and TUNEL staining. The expression of TNF-α and IL-1ß, MCP-1, iNOS, caspase-3, and caspase-9 in the arterial tissues were tested by RT-qPCR and ELISA. The relationship among SNHG12, miR-15b-5p and MYLK was verified by bioinformatics, RIP, RNA pull-down, and luciferase reporter assays. RESULTS: The expression levels of MYLK and SNHG12 were down-regulated and that of miR-15b-5p was up-regulated in IA tissues and H2O2-treated human aortic VSMCs. Overexpressed MYLK or SNHG12 mitigated the decrease in proliferation and increase in apoptosis of VSMCs caused by H2O2 induction, and overexpression of miR-15b-5p exacerbated the decrease in proliferation and increase in apoptosis of VSMCs caused by H2O2 induction. Overexpression of miR-15b-5p reversed the H2O2-treated VSMC phenotypic changes caused by SNHG12 up-regulation, and overexpression of MYLK reversed the H2O2-treated VSMC phenotypic changes caused by up-regulation of miR-15b-5p. Overexpression of SNHG12 reduced blood pressure and ameliorated arterial histopathological damage and VSMC apoptosis in IA mice. The mechanical analysis uncovered that SNHG12 acted as an endogenous RNA that competed with miR-15b-5p, thus modulating the suppression of its endogenous target, MYLK. CONCLUSION: Decreased expression of SNHG12 in IA may contribute to the increasing VSMC apoptosis via increasing miR-15b-5p expression and subsequently decreasing MYLK expression. These findings provide potential new strategies for the clinical treatment of IA.

Decreased PDLIM1 expression in endothelial cells contributes to the development of intracranial aneurysm.

INTRODUCTION: Intracranial aneurysm (IA) is a common vascular enlargement that occurs in the wall of cerebral vessels and frequently leads to fatal subarachnoid hemorrhage. PDZ and LIM domain protein 1 (PDLIM1) is a cytoskeletal protein that functions as a platform for multiple protein complex formation. However, whether PDLIM is involved in the pathogenesis of IA remains poorly understood. METHODS: Loss-of-function and gain-of-function strategies were employed to determine the in vitro roles of PDLIM1 in vascular endothelial cells (VECs). A rat model of IA was generated to study the role of PDLIM1 in vivo. Gene expression profiling, Western blotting, and dual luciferase reporter assays were performed to uncover the underlying cellular mechanism. Clinical IA samples were used to determine the expression of PDLIM1 and its downstream signaling molecules. RESULTS: PDLIM1 expression was reduced in the endothelial cells of IA and was regulated by Yes-associated protein 1 (YAP1). Genetic silencing of PDLIM1 inhibited the viability, migratory ability, and tube formation ability of VECs. Opposite results were obtained by ectopic expression of PDLIM1. Additionally, PDLIM1 overexpression mitigated IA in vivo. Mechanistic investigations revealed that PDLIM1 promoted the transcriptional activity of ß-catenin and induced the expression of v-myc myelocytomatosis viral oncogene homolog (MYC) and cyclin D1 (CCND1). In clinical settings, reduced expression of PDLIM1 and ß-catenin downstream target genes was observed in human IA samples. CONCLUSION: Our study indicates that YAP1-dependent expression of PDLIM1 can inhibit IA development by modulating the activity of the Wnt/ß-catenin signaling pathway and that PDLIM1 deficiency in VECs may represent a potential marker of aggressive disease.

Effects of regulatory B cells on intracranial aneurysms by mediating IL-1ß/IL-1R pathways.

The purpose of this study was to explore the effects of regulatory B-cells (Breg) on intracranial aneurysms by mediating IL-1ß/IL-1R pathways.  The study involved 60 patients undergoing angiography in a hospital from January to June 2022, divided into two groups: 30 with intracranial aneurysms (observation group) and 30 without (control group). Researchers extracted peripheral blood mononuclear cells (PBMC) to analyze the proportion of CD19+CD24hiCD38hiB cells using flow cytometry. These cells, along with T-cells and regulatory T-cells (Treg), were isolated through magnetic bead cell sorting. Following co-culture, the proliferation of T-cells and their related secretory factors were assessed. Additionally, Breg cells, treated with an IL-1R receptor blocker or IL-1R expression adenovirus, were studied to evaluate the levels of IL-10 and TGF-ß. In the study, the observation group showed lower levels of CD19+CD24hiCD38hiB cells, IL-10, and TGF-ß in PBMC than the control group (P<0.05). T-cell proportions were similar in both groups pre and post co-culture (P>0.05). Post co-culture, IFN-γ decreased while IL-4 increased in both groups. The observation group had higher IFN-γ and lower IL-4 than the control group (P<0.05). TNF-α in CD8+T cells, and granzyme B and perforin mRNA levels decreased post co-culture but were higher in the observation group (P<0.05). IL-10 and TGF-ß in Treg cells increased in both groups post co-culture but were lower in the observation group (P<0.05). The observation group also had fewer CD19+IL-1R+IL-10+B cells (P<0.05). After IL-1R blocker addition, IL-10 and TGF-ß in the supernatant decreased in the observation group (P<0.05). Following transfection, IL-1 and TGF-ß levels increased compared to the blank group (P<0.05). The function of peripheral blood CD19+CD24hiCD38hiB cells is impaired in patients with intracranial aneurysms, which may be related to IL-1ß/IL-1R pathways disorder.

Balloon neck-plasty to create a wide-necked aneurysm in the elastase-induced rabbit model.

PURPOSE: The elastase-induced aneurysm (EIA) model in rabbits has been proposed for translational research; however, the adjustment of aneurysm neck size remains challenging. In this study, the technical feasibility and safety of balloon neck-plasty to create a wide-necked aneurysm in rabbit EIA model were investigated. METHODS: Male New Zealand White rabbits (N = 15) were randomly assigned to three groups: group A, EIA creation without neck-plasty; group B, neck-plasty immediately after EIA creation; group C, neck-plasty 4 weeks after EIA creation. The diameter of balloon used for neck-plasty was determined 1 mm larger than origin carotid artery diameter. All rabbits were euthanized 4 weeks after their final surgery. Aneurysm neck, height, dome-to-neck (D/N) ratio, and histologic parameters were compared among the groups. RESULTS: Aneurysm creation was technically successful in 14 out of 15 rabbits (93.3%), with one rabbit experiencing mortality due to an adverse anesthetic event during the surgery. Saccular and wide-necked aneurysms were successfully created in all rabbits. Aneurysm neck was significantly greater in groups B and C compared to group A (all P < .05). D/N ratio was significantly lower in groups B and C compared to group A (all P < .05). Additionally, tunica media thickness, vessel area, and luminal area were significantly greater in groups B and C compared to group A (all P < .05). These variables were found to be significantly greater in group B compared to group C (all P < .05). CONCLUSION: The creation of a wide-necked aneurysm using balloon neck-plasty after elastase induction in rabbits has been determined to be technically feasible and safe.

Elucidating key immunological biomarkers and immune microenvironment dynamics in aging-related intracranial aneurysm through integrated multi-omics analysis.

BACKGROUND: The exact cause of intracranial aneurysms (IA) is still unclear. However, pro-inflammatory factors are known to contribute to IA progression. The specific changes in the immune microenvironment of IAs remain largely unexplored. METHODS: This study analyzed single-cell sequencing data from a male mouse model of brain aneurysm, focusing on samples before and after elastase-induced Willis aneurysms. The data helped identify eight distinct cell subpopulations: fibroblasts, macrophages, NK cells, endothelial cells, B cells, granulocytes, and monocytes. The study also involved bulk RNA sequencing of 97 IA samples, utilizing ssGSEA and CIBERSORT algorithms for analysis. Intercellular communication among these cells was inferred to understand the immune dynamics in IA. RESULTS: The study found that fibroblasts and macrophages are predominant in various disease states of IA. Notably, the onset of IA was marked by a significant increase in fibroblasts and a decrease in macrophages. There was a marked increase in cellular interactions, especially involving macrophages, at the onset of the disease. Through enrichment analysis, 12 potential immunogenic biomarkers were identified. Of these, Rgs1 emerged as a critical molecule in IA formation, confirmed through secondary validation in a single-cell sequencing dataset. CONCLUSION: This comprehensive analysis of immune cell composition and intercellular communication in IA tissues highlights the significant roles of macrophages and the molecule Rgs1. These findings shed light on the physiological and pathological conditions of IA, offering new insights into its immune microenvironment.

A Systematic Review and Meta-Analysis of the Pathology Underlying Aneurysm Enhancement on Vessel Wall Imaging.

Intracranial aneurysms are common, but only a minority rupture and cause subarachnoid haemorrhage, presenting a dilemma regarding which to treat. Vessel wall imaging (VWI) is a contrast-enhanced magnetic resonance imaging (MRI) technique used to identify unstable aneurysms. The pathological basis of MR enhancement of aneurysms is the subject of debate. This review synthesises the literature to determine the pathological basis of VWI enhancement. PubMed and Embase searches were performed for studies reporting VWI of intracranial aneurysms and their correlated histological analysis. The risk of bias was assessed. Calculations of interdependence, univariate and multivariate analysis were performed. Of 228 publications identified, 7 met the eligibility criteria. Individual aneurysm data were extracted for 72 out of a total of 81 aneurysms. Univariate analysis showed macrophage markers (CD68 and MPO, p = 0.001 and p = 0.002), endothelial cell markers (CD34 and CD31, p = 0.007 and p = 0.003), glycans (Alcian blue, p = 0.003) and wall thickness (p = 0.030) were positively associated with enhancement. Aneurysm enhancement therefore appears to be associated with inflammatory infiltrate and neovascularisation. However, all these markers are correlated with each other, and the literature is limited in terms of the numbers of aneurysms analysed and the parameters considered. The data are therefore insufficient to determine if these associations are independent of each other or of aneurysm size, wall thickness and rupture status. Thus, the cause of aneurysm-wall enhancement currently remains unknown.

[Analysis of intracranial saccular aneurysm wall: neuroimaging and histopathological correlates]. / Issledovanie stenki intrakranial'nykh meshotchatykh anevrizm: neirovizualizatsionnye i gistopatologicheskie korrelyaty.

BACKGROUND: Contrast enhancement of intracranial aneurysm wall during MRI with targeted visualization of vascular wall correlates with previous aneurysm rupture and, according to some data, may be a predictor of further rupture of unruptured aneurysms. OBJECTIVE: To analyze possible causes of aneurysm contrast enhancement considering morphological data of aneurysm walls. MATERIAL AND METHODS: The study included 44 patients with intracranial aneurysms who underwent preoperative MRI between November 2020 and September 2022. Each aneurysm was assessed regarding contrast enhancement pattern. Microsurgical treatment of aneurysm was accompanied by resection of its wall for subsequent histological and immunohistochemical analysis regarding thrombosis, inflammation and neovascularization. Specimens were subjected to histological and immunochemical analysis. Immunohistochemical analysis was valuable to estimate inflammatory markers CD68 and CD3, as well as neurovascularization marker SD31. RESULTS: Aneurysms with contrast-enhanced walls were characterized by higher number of CD3+, CD68+, CD31+ cells and parietal clots. Intensity of contrast enhancement correlated with aneurysm wall abnormalities. CONCLUSION: Contrast enhancement of aneurysm wall can characterize various morphological abnormalities.

Heightened activation of embryonic megakaryocytes causes aneurysms in the developing brain of mice lacking podoplanin.

During early embryonic development in mammals, including humans and mice, megakaryocytes (Mks) first originate from primitive hematopoiesis in the yolk sac. These embryonic Mks (eMks) circulate in the vasculature with unclear function. Herein, we report that podoplanin (PDPN), the ligand of C-type lectin-like receptor (CLEC-2) on Mks/platelets, is temporarily expressed in neural tissue during midgestation in mice. Loss of PDPN or CLEC-2 resulted in aneurysms and spontaneous hemorrhage, specifically in the lower diencephalon during midgestation. Surprisingly, more eMks/platelets had enhanced granule release and localized to the lower diencephalon in mutant mouse embryos than in wild-type littermates before hemorrhage. We found that PDPN counteracted the collagen-1-induced secretion of angiopoietin-1 from fetal Mks, which coincided with enhanced TIE-2 activation in aneurysm-like sprouts of PDPN-deficient embryos. Blocking platelet activation prevented the PDPN-deficient embryo from developing vascular defects. Our data reveal a new role for PDPN in regulating eMk function during midgestation.

Vascular smooth muscle cells in intracranial aneurysms.

Intracranial aneurysm (IA) is a severe cerebrovascular disease characterized by abnormal bulging of cerebral vessels that may rupture and cause a stroke. The expansion of the aneurysm accompanies by the remodeling of vascular matrix. It is well-known that vascular remodeling is a process of synthesis and degradation of extracellular matrix (ECM), which is highly dependent on the phenotype of vascular smooth muscle cells (VSMCs). The phenotypic switching of VSMC is considered to be bidirectional, including the physiological contractile phenotype and alternative synthetic phenotype in response to injury. There is increasing evidence indicating that VSMCs have the ability to switch to various phenotypes, including pro-inflammatory, macrophagic, osteogenic, foamy and mesenchymal phenotypes. Although the mechanisms of VSMC phenotype switching are still being explored, it is becoming clear that phenotype switching of VSMCs plays an essential role in IA formation, progression, and rupture. This review summarized the various phenotypes and functions of VSMCs associated with IA pathology. The possible influencing factors and potential molecular mechanisms of the VSMC phenotype switching were further discussed. Understanding how phenotype switching of VSMC contributed to the pathogenesis of unruptured IAs can bring new preventative and therapeutic strategies for IA.

Automated unruptured cerebral aneurysms detection in TOF MR angiography images using dual-channel SE-3D UNet: a multi-center research.

OBJECTIVES: Time of flight magnetic resonance angiography (TOF-MRA) is the primary non-invasive screening method for cerebral aneurysms. We aimed to develop a computer-aided aneurysm detection method to improve the diagnostic efficiency and accuracy, especially decrease the false positive rate. METHODS: This is a retrospective multicenter study. The dataset contained 1160 TOF-MRA examinations composed of unruptured aneurysms (n = 1096) and normal controls (n = 166) from six hospitals. A total of 1037 examinations acquired from 2013 to 2019 were used as training set; 123 examinations acquired from 2020 to 2021 were used as external test set. We proposed an equalized augmentation strategy based on aneurysm location and constructed a detection model based on dual channel SE-3D UNet. The model was trained with a 5-fold cross-validation in the training set, then tested on the external test set. RESULTS: The proposed method achieved 82.46% sensitivity on patient-level, 73.85% sensitivity on lesion-level, and 0.88 false positives per case in the external test set. The performance did not show significant differences in subgroups according to the aneurysm site (except ACA), aneurysm size (except smaller than 3 mm), or MRI scanners. The performance preceded the basic SE-3D UNet by increasing 15.79% patient-level sensitivity and decreasing 4.19 FPs/case. CONCLUSIONS: The proposed automated aneurysm detection method achieved acceptable sensitivity while controlling fairly low false positives per case. It might provide a useful auxiliary tool of cerebral aneurysms MRA screening. KEY POINTS: • The need for automated cerebral aneurysms detecting is growing. • The strategy of equalized augmentation based on aneurysm location and dual-channel input could improve the model performance. • The retrospective multi-center study showed that the proposed automated cerebral aneurysms detection using dual-channel SE-3D UNet could achieve acceptable sensitivity while controlling a low false positive rate.

Aneurysm wall enhancement, atherosclerotic proteins, and aneurysm size may be related in unruptured intracranial fusiform aneurysms.

OBJECTIVE: This cross-sectional study aimed to investigate the associations between aneurysm wall enhancement (AWE), atherosclerotic protein levels, and aneurysm size in unruptured intracranial fusiform aneurysms (IFAs). METHODS: Patients with IFAs underwent high-resolution magnetic resonance imaging (HR-MRI) and atherosclerotic protein examinations from May 2015 to December 2021 were collected. A CRstalk (signal intensity [SI] of IFA wall/SI of pituitary stalk) > 0.60 was considered to indicate AWE. Atherosclerotic protein data was obtained from the peripheral blood. Aneurysmal characteristics included the maximal diameter of the cross-section (Dmax), location, type of IFA, presence of mural thrombus, and mural clots. Statistical analyses were performed with univariate analysis, logistic regression analysis, and Spearman's correlation coefficient. RESULTS: Seventy-one IFAs from 71 patients were included in the study. Multivariate analysis revealed statin use (OR = 0.189, p = 0.026) and apolipoprotein B (Apo-B) level (OR = 6.019, p = 0.026) were the independent predictors of AWE in IFAs. In addition, statin use (OR = 0.813, p = 0.036) and Apo-B level (OR = 1.610, p = 0.003) were also the independent predictors of CRstalk. Additionally, we found that CRstalk and AWE were significantly positively associated with Dmax (rs = 0.409 and 0.349, respectively; p < 0.001 and p = 0.003, respectively). CONCLUSIONS: There may be correlations between AWE, atherosclerotic protein levels, and aneurysm size in patients with IFAs. Apo-B and statin use were independent predictors of AWE in IFAs, which have the potential to be new therapeutic targets for IFAs. KEY POINTS: • There may be correlations between aneurysm wall enhancement, atherosclerotic protein levels in the peripheral blood, and aneurysm size in patients with intracranial fusiform aneurysms. • Apolipoprotein B and statin use were independent predictors of aneurysm wall enhancement in intracranial fusiform aneurysms.

Risk factors for perianeurysmal vasogenic oedema (pavo) following embolization therapy: literature review.

Perianeurysmal vasogenic oedema (PAVO) is a rare complication associated post-embolisation of intracranial aneurysms. The prevalence, risk factors predisposing to susceptibility, and pathologic mechanisms underlying this process are not clearly understood. Since this complication may be associated with poor clinical outcomes, the authors designed this study to describe possible risk factors, underlying mechanisms, and management of PAVO through published case reports. Developing a priori protocol according to PRISMA guidelines, we searched MEDLINE/PubMed, Embase and Web of Science to identify case studies and reports of adult patients with intracranial aneurysms who developed perianeurysmal oedema following coil embolization therapy. Data extracted from these studies included patient demographics, aneurysm characteristics, coil type, PAVO characteristics, treatment, and outcomes. Quality was assessed using a standardized tool. 21 eligible studies of acceptable quality were identified, comprising 40 unique cases from 9 countries. The mean patient age was 56.4 years and 25 (62.5%) were female. Aneurysm size ranged from 6 to 30 mm, with a mean size of 15.2 mm; only 6 (15%) of cases were giant intracranial aneurysm (≥ 25 mm). The more frequent locations of intracranial aneurysms associated with PAVO were the ICA (50%) and posterior circulation (32.5%), with 7.5% and 10% of cases occurring in MCA and anterior circulation, respectively. 16 cases (40%) were treated with bare platinum coils, and 14 (35%) with a combination of BPCs and bioactive coils; in 10 cases (25%), the coil type was not mentioned. PAVO presented between 0 days and 8 years of coil embolization, with 23 (57.5% cases) presenting symptomatically in relation to brain region affected. Management strategies for PAVO included conservative, steroids, re-embolization, clipping, stenting, parent artery occlusion either as monotherapy or as combination therapy. Of reported studies, 26 treated cases (65%) resolved, with 8 (20%) remaining stable, and 4 (10%) deteriorating. PAVO can be associated with small or large intracranial aneurysms, bare and bioactive platinum coils, and all regions of the intracranial circulation. The understanding of the risk factors of this complication lies in the underlying mechanisms, which will ultimately guide appropriate patient follow-up and subsequent optimal management.

Increased macrophage M2/M1 ratio is associated with intracranial aneurysm rupture.

PURPOSE: Intracranial aneurysm (IA) rupture results in one of the most severe forms of stroke, with severe neurological sequelae. Inflammation appears to drive aneurysm formation and progression with macrophages playing a key role in this process. However, less is known about their involvement in aneurysm rupture. This study is aimed at demonstrating how relationship between the M1 (pro-inflammatory) and M2 (reparative) macrophage subtypes affect an aneurysm's structure resulting in its rupture. METHODS: Forty-one saccular aneurysm wall samples were collected during surgery including 13 ruptured and 28 unruptured aneurysm sacs. Structural changes were evaluated using histological staining. Macrophages in the aneurysm wall were quantified and defined as M1 and M2 using HLA-DR and CD163 antibodies. Aneurysm samples were divided into four groups according to the structural changes and the M2/1 ratio. Data were analyzed using the Mann-Whitney U test. RESULTS: This study has demonstrated an association between the severity of structural changes of an aneurysm with inflammatory cell infiltration within its wall and subsequent aneurysm rupture. More severe morphological changes and a significantly higher number of inflammatory cells were observed in ruptured IAs (p < 0.001). There was a prevalence of M2 macrophage subtypes within the wall of ruptured aneurysms (p < 0.001). A subgroup of unruptured IAs with morphological and inflammatory changes similar to ruptured IAs was observed. The common feature of this subgroup was the presence of an intraluminal thrombus. CONCLUSIONS: The degree of inflammatory cell infiltration associated with a shift in macrophage phenotype towards M2 macrophages could play an important role in structural changes of the aneurysm wall leading to its rupture.

Wall enhancement as a biomarker of intracranial aneurysm instability: a histo-radiological study.

BACKGROUND: The aim of this is to explore the histological basis of vessel wall enhancement (WE) on magnetic resonance imaging (MRI), which is a strong radiological biomarker of aneurysmal prone to rupture compared to other classical risk predictors (e.g., PHASES score, size, morphology). METHODS: A prospective observational study was performed including all consecutive patients presenting with a saccular intracranial aneurysm at Vall d'Hebron University Hospital between October 2017 and May 2019. The patients underwent high-resolution 3 T MRI, and their aneurysms were classified into asymptomatic, symptomatic, and ruptured. A histological and immunohistochemical study was performed in a subgroup of patients (n = 20, of which 15 presented with WE). Multiple regression analyses were performed to identify predictors of rupture and aneurysm symptoms. RESULTS: A total of 132 patients were enrolled in the study. WE was present in 36.5% of aneurysms: 22.9% asymptomatic, 76.9% symptomatic, and 100% ruptured. Immunohistochemical markers associated with WE were CD3 T cell receptor (p = 0.05) and CD45 leukocyte common antigen (p = 0.05). Moreover, WE is an independent predictor of symptomatic and ruptured aneurysms (p < 0.001). CONCLUSIONS: Aneurysms with WE present multiple histopathological changes that may contribute to wall disruption and represent the pathophysiological basis of radiological WE. Moreover, WE is an independent diagnostic predictor of aneurysm symptoms and rupture.

Aneurysmoraphy or bypass? Surgical strategy for large M1 bifurcation aneurysm involving two branches based on vessel wall high-resolution MRI and intraoperative angiography.

BACKGROUND: Middle cerebral artery (MCA) M1 bifurcation aneurysms are common because of hemodynamic. For regular-shaped and small aneurysms, direct clipping is optimal. Aneurysmoraphy or bypass blood flow reconstruction are most commonly used in large aneurysm clipping. Based on preoperative vessel wall high-resolution magnetic resonance imaging (VW-HRMRI) and intraoperative angiography, an appropriate surgery strategy could be decided. METHOD: We report a case of large MCA M1 bifurcation aneurysm aneurysmoraphy according to preoperative VW-HRMRI. Intraoperative digital subtraction angiography (DSA) showed an aneurysm neck remnant, and we adjusted clips according to intraoperative DSA. This patient recovered well with a modified Rankin scale of 0 at discharge. CONCLUSION: This case demonstrates that preoperative VWHRMRI could supply more aneurysm characteristics for direct aneurysmoraphy. Intraoperative DSA effectively reduces the possibility of aneurysm remnant.

Technical note: the use of frameless stereotactic guidance in the treatment of peripheral intracranial aneurysms.

Frameless stereotactic guidance (FSG) has previously been reported to have advantages over intraoperative computed tomography (CT) and frame-based imaging guidance methods in the targeting of intracranial lesions. We report our experience using FSG to minimize brain dissection during microsurgical repair of peripheral aneurysms. We used FSG as a surgical adjunct in the management of 91 peripheral aneurysms. It was used to localise and avoid larger bridging veins, enabling us to minimise unnecessary brain dissection by coming directly down on the aneurysm dome in unruptured lesions or targeting the parent artery just proximal to the aneurysm in ruptured cases. We treated 72 aneurysms located on the distal ACA (79%), 7 on the PCA (7.7%), 6 on the MCA distal to the MCA bifurcation (6.6%), and 6 on the SCA (6.6%). There were no complications related to FSG use. However, we noted a tendency to create an overly limited corridor to the aneurysm, which did not allow sufficient proximal or distal control of the parent artery. In these cases, we had to widen our exposure by further opening the interhemispheric fissure to obtain more proximal control once the aneurysm was reached. Subsequently, we learned to avoid this problem by creating a slightly wider corridor during the initial exposure. Using FSG as a surgical adjunct for peripheral intracranial aneurysms allowed us to safely limit craniotomy size and brain dissection while more confidently exposing these unusually situated lesions, facilitating aneurysm clipping in our series.

Clinical features and management of traumatic ophthalmic artery aneurysm: a case report and literature review.

We report a 52-year-old man with progressive disturbance of visual acuity following a head injury. Magnetic resonance imaging (MRI) showed an aneurysm of the internal carotid artery. Digital subtraction angiography (DSA) 57 days after onset found that the aneurysm originated in the proximal ophthalmic artery. We treated the patient with an intravascular coil embolization, partially filling the aneurysm. Follow-up DSA indicated that the aneurysm did not recur.

Dense, deep learning-based intracranial aneurysm detection on TOF MRI using two-stage regularized U-Net.

BACKGROUND AND PURPOSE: The prevalence of unruptured intracranial aneurysms in the general population is high and aneurysms are usually asymptomatic. Their diagnosis is often fortuitous on MRI and might be difficult and time consuming for the radiologist. The purpose of this study was to develop a deep learning neural network tool for automated segmentation of intracranial arteries and automated detection of intracranial aneurysms from 3D time-of-flight magnetic resonance angiography (TOF-MRA). MATERIALS AND METHODS: 3D TOF-MRA with aneurysms were retrospectively extracted. All were confirmed with angiography. The data were divided into two sets: a training set of 24 examinations and a test set of 25 examinations. Manual annotations of intracranial blood vessels and aneurysms were performed by neuroradiologists. A double convolutional neuronal network based on the U-Net architecture with regularization was used to increase performance despite a small amount of training data. The performance was evaluated for the test set. Subgroup analyses according to size and location of aneurysms were performed. RESULTS: The average processing time was 15 min. Overall, the sensitivity and the positive predictive value of the proposed algorithm were 78% (21 of 27; 95% CI: 62-94) and 62% (21 of 34; 95%CI: 46-78) respectively, with 0.5 FP/case. Despite gradual improvement in sensitivity regarding aneurysm size, there was no significant difference of sensitivity detection between subgroups of size and location. CONCLUSIONS: This developed tool based on a double CNN with regularization trained with small dataset, enables accurate intracranial arteries segmentation as well as effective aneurysm detection on 3D TOF MRA.

MRI of unruptured infectious intracranial aneurysms in infective endocarditis. A case-control study.

PURPOSE: To evaluate the usefulness of T2* and FLAIR sequences in the detection of unruptured infectious intracranial aneurysms (UIIAs) in infective endocarditis (IE) including the relationships between the lesion patterns within subarachnoid spaces and the presence of UIIA. METHODS: Retrospective review of 15 consecutive patients with definite IE undergoing MR imaging (FLAIR, T2*, DWI, CE-MRA, 3D-T1, CE-3DT1 sequences), in whom DSA detected infectious intracranial aneurysms (IIA). Aneurysmal features (diameter, location, morphology on DSA) and signal patterns onT2*, FLAIR and conventional MR sequences at the site of the UIIA, follow-up MRI and IE background, were analyzed. A control-group of 15 IE-patients without IIA at DSA served for comparison. RESULTS: Among 17 UIIAs studied, T2* sequence displayed a susceptibility vessel sign in 15/17 (88.2%), both distal and proximal, which matched with the IIA visualized on DSA. Three patterns of hyposignal areas were identified: (a) signet-ring or target-sign appearance (n = 7), (b) homogeneous, round-, oval- or pear-shaped area (n = 4), and (c) heterogeneous area (n = 4). A FLAIR hyperintensity of the lumen and of the adjacent cortex was present in 6 (35.3%) and 9 (53%) UIIAs, respectively. On T1 (12 UIIAs) a rounded hyposignal (n = 2), within the UIIA lumen matched with the FLAIR hypersignal. Using both T2* and FLAIR had an incremental value with 100% sensitivity and specificity. CONCLUSION: The susceptibility vessel sign is an MR imaging pattern frequently observed at the site of UIIAs in IE-patients. Both T2* and FLAIR may have the potential to depict UIIAs, regardless of their location and shape.

[Magnetic resonance imaging of saccular intracranial aneurysm wall]. / MR-vizualizatsiya sosudistoi stenki meshotchatykh intrakranial'nykh anevrizm.

BACKGROUND: Hemorrhage from intracranial aneurysms is associated with high risk of adverse outcomes. In this regard, surgical treatment of unruptured asymptomatic aneurysms has been actively developed in recent decades. One of the objectives is searching for predictors of aneurysm rupture to clarify the indications for surgery. Non-invasive analysis of vascular wall is actively discussed in last years. OBJECTIVE: To evaluate the possibilities of MRI of ruptured and unruptured intracranial aneurysm walls and determine clinical significance of certain morphological patterns. MATERIAL AND METHODS: The study included 111 patients with 158 ruptured and unruptured saccular aneurysms who underwent MRI according to a special protocol between November 2020 and September 2023. We analyzed each aneurysm regarding features of contrast enhancement and changes in SWAN images. After that, we compared these data with ruptures. RESULTS: Wall of ruptured and unruptured aneurysms can accumulate contrast agent. We found 5 types of contrast enhancement. Thick-layer contrast enhancement was accompanied by 9.6-fold higher risk of aneurysm rupture compared to aneurysms without contrast enhancement. Dark MR signal from intracranial aneurysm wall in SWAN imaging is a significant sign of rupture. CONCLUSION: MRI of the vascular wall is valuable to verify ruptured aneurysms. Unruptured aneurysms can accumulate contrast agent inside the wall, and pattern of accumulation differs from ruptured aneurysms. Morphological analysis is needed to confirm contrast enhancement as a marker of aneurysm rupture.