AIMS:This study aimed to investigate the specific mechanism by which angiopoietin-2 (ANGPT2)/Tie2 signaling in macrophages promotes endothelial cell (EC) proliferation in the chronically ischaemic brain (CIB). METHODS:We first analyzed the polarization status of primary Tie2-expressing macrophages (TEMs) and Tie2-overexpressing THP-1-derived macrophages (Tie2-TDMs) following ANGPT2 treatment and detected the expression of representative proangiogenic factors. Subsequently, lysine lactylation (Kla) levels were measured, and chromatin immunoprecipitation (ChIP) assays were performed to explore the downstream activity of ANGPT2/Tie2 signaling. Additionally, in vitro functional assays using human umbilical vein endothelial cells (HUVECs) and in vivo experiments in a rat model of chronic cerebral ischaemia were conducted to confirm the effect of ANGPT2/Tie2-regulated macrophages on angiogenesis. RESULTS:In response to ANGPT2 treatment, the expression of M2 polarization markers and proangiogenic factors increased in TEMs and Tie2-TDMs. Concurrently, LDHA and H3K18la were elevated, and ChIP assays confirmed the regulatory role of ANGPT2/Tie2 signaling in H3K18la-mediated transcriptional regulation. The viability of HUVECs cocultured with Tie2-TDMs was increased. Finally, ANGPT2 overexpression increased M2-polarized TEM infiltration in the CIB; additionally, rats injected with ANGPT2-pretreated TEMs exhibited more prominent EC proliferation. CONCLUSION:ANGPT2/Tie2 induces the H3K18la-mediated M2 polarization of macrophages to facilitate EC proliferation and angiogenesis in the CIB.

Cerebral cavernous malformation (CCM) and ischemic stroke (IS) are disabling cerebrovascular disorders with distinct clinical courses yet convergent mechanisms involving endothelial dysfunction and immune-vascular dysregulation. However, shared pathogenic networks and dual-target therapeutic opportunities remain poorly defined. Here, we integrated transcriptomic datasets for CCM (GSE130174, GSE123968) and IS (GSE22255, GSE58294, GSE16561) from the Gene Expression Omnibus and applied differential expression analysis with weighted gene co-expression network analysis (WGCNA) to delineate shared molecular architecture. Functional enrichment, protein-protein interaction (PPI) analysis, and immune deconvolution were used to map key pathways and immune features. To translate network findings into candidate therapeutics, we implemented a structure-guided pipeline comprising pharmacophore modeling, virtual screening, ADMET filtering, molecular docking, and 150-ns molecular dynamics (MD) simulations with MM/PBSA binding free-energy estimation. Integration of 69 shared WGCNA modules with 72 differentially expressed genes yielded 139 convergent genes, enriched for immune regulation, signal transduction, and proliferation-associated programs. PPI topology identified FOSB and KCNJ2 as central hubs with robust diagnostic performance across datasets (AUC >0.75). Immune profiling revealed disease-specific shifts in neutrophils, monocytes, and T-cell subsets, indicating both shared immune involvement and divergent inflammatory contexts in CCM versus IS. Pharmacophore-based screening with ADMET prioritization nominated two blood-brain barrier-permeable compounds (E588-0461 and K284-4583) with favorable docking and sustained binding during MD. MM/PBSA indicated the most favorable complexes for E588-0461-KCNJ2 (-18.67 kcal/mol) and K284-4583-FOSB (-10.81 kcal/mol). Collectively, these results nominate FOSB and KCNJ2 as shared regulatory hubs linking CCM and IS and provide dual-target ligands supporting precision multi-target therapy development in cerebrovascular disease.

Objective:To evaluate the efficacy and safety of flow diverter (FD) devices in the treatment of basilar artery aneurysms, and to assess their clinical outcomes and associated complications. Methods:A retrospective analysis was conducted on 30 patients with basilar artery aneurysms treated with FD devices at our institution between 2020 and 2024. Patient demographics, aneurysm characteristics, intraoperative and postoperative imaging, and clinical follow-up data were collected. Statistical analysis was performed to assess treatment efficacy and complication rates. Results:Among the 30 patients, 20 were male (66.7%) and 10 were female (33.3%), with a median age group of 65-69 years. The majority of aneurysms were located in the basilar artery trunk (70%), while 30% were basilar apex aneurysms. All procedures were technically successful (success rate: 100%). The mean aneurysm diameter was 10.6 ± 4.9 mm. The mean follow-up period was 12.9 months. Imaging follow-up demonstrated a complete or near-complete aneurysm occlusion rate of 86.7%; occlusion rates for the Tubridge and Pipeline Flex devices were 83.3 and 88.9%, respectively, with no statistically significant difference between the two devices (p > 0.05). Treatment-related complications occurred in 4 cases (13.3%), all presenting as transient ischemic symptoms, with no cases of permanent severe neurological deficits. 93.3% of patients (28/30) achieved an excellent functional outcome (mRS score of 0-1), and all patients (100%) had a functional outcome of mRS 0-2. Conclusion:In this retrospective cohort, FD treatment for basilar artery aneurysms was associated with a high rate of complete or near-complete occlusion (86.7%) and a favorable safety profile, as evidenced by the low rate of complications (13.3%, all transient). The clinical outcomes were excellent, with 93.3% of patients achieving an mRS of 0-1. The Tubridge and Pipeline devices demonstrated comparable efficacy and safety outcomes in this study, although the small sample size and non-randomized design preclude definitive conclusions regarding superiority or equivalence. Our findings indicate that rigorous preoperative antiplatelet management and meticulous operative technique are critical for these results. This study supports the consideration of FDs for BAAs in carefully selected patients, but further large-scale, prospective studies are warranted to confirm long-term durability and optimize patient selection.

Approximately half of patients with chronic ischemic cerebrovascular disease (CICD) exhibit poor revascularization. Metallothionein 2 A (MT2A) has a high affinity for metal ions and is potentially capable of chelating toxic copper ions to alleviate the impairment of angiogenesis. Therefore, we hypothesized that MT2A could promote angiogenesis in chronically ischemic brains by neutralizing excessive copper ions during copper overload (CPO). We first collected dura matter (DM) samples from CICD patients and examined the expression of cuproptosis-related genes (DLAT, FDX1, and SDHB) to confirm the inhibitory effect of CPO on angiogenesis. Then, we treated human umbilical vein endothelial cells (HUVECs) with different concentrations of elesclomol and CuCl2 to determine the optimal concentration for inducing CPO. HUVEC activity and mitochondrial structure and function were detected to explore the ability of MT2A to alleviate CPO-induced damage. Finally, a rat model of 2-vessel occlusion plus encephalo-myo-synangiosis (2VO + EMS) with CPO was established to test the proangiogenic effect of MT2A through the copper–mitochondria regulatory mechanism in chronically ischemic brains. Compared with those from Matsushima grade A patients, DM samples from Matsushima grade C patients presented significantly greater DLAT and FDX1 expression and significantly lower SDHB expression. The optimal drug concentration for inducing CPO was subsequently determined, and in vitro experiments revealed that HUVEC activity was significantly decreased in the CPO group under hypoxic culture, accompanied by increased DLAT oligomerization, decreased SDHB expression, increased HSP70 expression. Moreover, significantly more common mitochondrial aberrations and significantly lower mitochondrial activity were detected in the CPO group compare with the control group. Additionally, MT2A overexpression alleviated CPO-induced mitochondrial dysfunction and cytotoxicity, improving HUVEC viability. In vivo, a CPO rat model was established, and CPO inhibited cerebral angiogenesis in 2VO + EMS model rats. Moreover, significantly greater CD31 expression, less DLAT accumulation, more mitochondria, and fewer mitochondrial abnormalities were observed in the CPOMT2A+ group than in the CPO group, accompanied by significantly improved cerebral blood perfusion and cognitive function. MT2A can promote angiogenesis in chronically ischemic brains by neutralizing excessive copper ions and rescuing CPO-induced mitochondrial dysfunction.

BACKGROUND:The optimal management of symptomatic vertebral artery in-stent restenosis or occlusion (SVISRO) after stent-assisted angioplasty (SAA) at the vertebral artery origin remains unclear. This study aimed to investigate the efficacy of vertebral artery reconstruction surgery (VRS) surgery among SVISRO patients. METHODS:A retrospective study was conducted to analyze the clinical data for SVISRO patients admitted to the Third Affiliated Hospital of Sun Yat-sen University between May 2011 and November 2021. The stroke recurrence and stroke-free rates during the follow-up (FU) period and the patients' neurological statuses at the last FU were compared between a VRS group and an intensive medical therapy (IMT) group. RESULTS:Sixty-two SVISRO patients with an average age of 60.1 ± 8.3 years and an average FU duration of 67.6 ± 32.5 months were studied. The VRS group had significantly fewer stroke recurrences than the IMT group did (5.7% vs. 25.9%, p = 0.034). A 154-month stroke-free rate of 73.8% (95% CI, 24.5% to 93.7%) was observed in the VRS group, whereas the IMT group had a stroke-free rate of 33.9% (95% CI, 17.3% to 75.0%). The hazard ratio (log-rank) between the two groups was 0.234 (95% CI, 0.063-0.871; p = 0.048). The modified Rankin scale score for the VRS group was significantly better than that for the IMT group at the final FU (p = 0.032). CONCLUSIONS:In patients with SVISRO secondary to SAA, VRS targeting the extracranial vertebral artery (V1-V2) appears to reduce stroke recurrence, increase the stroke-free rate and improve neurological status.

Endothelial cell glycolysis plays a novel and significant role in Schwann cells and peripheral nerve injury repair, which represents an emerging and important area of research. Glycolysis in endothelial cells is a conserved and tightly regulated biological process that provides essential energy (ATP) and intermediates by ultimately converting glucose into lactate. This metabolic pathway is crucial for maintaining the normal function of endothelial cells. During peripheral nerve injury repair, endothelial cell glycolysis influences the function of Schwann cells and the efficiency of nerve regeneration. Beyond glycolysis, endothelial cells also secrete various factors, including growth factors and extracellular vesicles, which further modulate Schwann cell activity and contribute to the repair process. This review will summarize the role of endothelial cell glycolysis in Schwann cell function and peripheral nerve injury repair, aiming to provide new insights for the development of novel strategies for peripheral nerve injury treatment.

The triglyceride-glucose (TyG) index is related to various cardiovascular diseases, but its relationship with stroke and all-cause mortality (ACM) in individuals with coronary artery disease (CAD) is still not well understood. This research sought to analyze the interaction between the TyG index and the occurrence of stroke and ACM in CAD participants. The dataset was derived from the National Health and Nutrition Examination Survey (NHANES), with 809 CAD patients included from 1999 to 2018. TyG index was determined by ln[fasting triglycerides (mg/dL) × fasting glucose (mg/dL)/2]. Findings showed that heightened TyG index values were markedly associated with a greater risk of stroke; a U-shaped interconnection was detected between the TyG index and stroke risk, with the threshold at 8.14. Individuals with a TyG index exceeding this threshold exhibited a markedly higher rate of stroke occurrence. Additionally, a J-shaped correlation was observed between the TyG index and ACM, with the threshold at 9.25, above which the risk of death increased. These findings indicate that the TyG index could act as a practical indicator for predicting stroke and ACM among CAD patients, particularly when considering threshold values.

This study aimed to develop and validate a nomogram model for predicting cerebral infarction risk after superficial temporal artery–middle cerebral artery (STA-MCA) bypass in patients with intracranial atherosclerotic stenosis (ICAS). Patients with ICAS who received STA-MCA bypass were enrolled in this study. The independent risk factors for post bypass infarction were identified using univariate and multivariate logistic regression analyses. A nomogram model was developed and subsequently evaluated using receiver operating characteristic (ROC) curves, calibration curves, and decision curve analysis (DCA). Eventually, 316 patients with ICAS were included in the study. Diabetes, smoking, and high triglyceride and total cholesterol levels were identified as the independent risk factors, and a nomogram model was developed. The model achieved areas under the curve (AUCs) of 0.88 (95

OBJECTIVE:To investigate the independent predictors of dura-brain neoangiogenesis (DBN) after superficial temporal artery-to-middle cerebral artery bypass combined with dural inversion in patients with symptomatic atherosclerotic cerebral arterial occlusion (SACAO). METHODS:We retrospectively analyzed SACAO patients who underwent superficial temporal artery-to-middle cerebral artery bypass combined with dural inversion at our center between November 2014 and October 2021. DBN was evaluated by superselective digital subtraction angiography and scored by the DBN scoring system. Independent predictors of DBN were identified by a multivariate logistic regression analysis. The differences in clinical outcomes between patients with "good" and "poor" DBN were also analyzed. RESULTS:A total of 179 SACAO patients with an average age of 61.3 ± 7.0 years and an average follow-up of 63.0 ± 22.0 months were studied. Ninety-nine patients (55.3%) had good DBN, and 80 patients (44.7%) had poor DBN. The multivariate analysis revealed that old age (P < 0.001, odds ratio [95% confidence interval] 1.288 [1.184-1.400]) was an independent predictor of poor DBN. Diabetes (P = 0.005, odds ratio [95% confidence interval] 3.358 [1.434-7.867]) also independently predicted poor DBN. The recurrence rate of ischemic events in the good DBN group was significantly lower than that in the poor DBN group (2.0% vs. 10.0%, P = 0.044). The neurological status of patients in the good DBN group was also significantly better. CONCLUSIONS:Old age and diabetes status were independent predictors of poor DBN after combined revascularization in SACAO patients. Good DBN was associated with a lower recurrence rate of stroke and better neurological status.

Please cite this article as: Liu G, Huang Z, Yan G, Luo S, Xia M, Yu Q, Peng D, Chen Q, Ling C, WITHDRAWN: Dual-Target Strategies for Cerebral Cavernous Malformations and Ischemic Stroke, World Neurosurgery (2025), doi: https://doi.org/10.1016/j.wneu.2025.124332. This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. © 2025 Published by Elsevier Inc

OBJECTIVE:In adult patients with moyamoya disease (MMD), insufficient postoperative collateral formation is usually seen after combined bypass surgery. The arachnoid membrane, a critical anatomical barrier between extracranial and intracranial vascular systems, has an unclear role in postoperative angiogenesis. The aim of this study was to investigate whether intraoperative arachnoid membrane opening enhances angiogenesis in adult patients undergoing combined bypass surgery for MMD. METHODS:This multicenter, prospective, randomized controlled trial (Membrane Opening to Promote Angiogenesis in Adult MMD [MOPOAM]) was conducted across 8 institutions in China. Between June 2022 and August 2023, 104 patients diagnosed with MMD through digital subtraction angiography were randomly assigned to two groups: one group underwent arachnoid opening (n = 51), while the other group had arachnoid preservation (n = 53). The primary endpoint was the rate of good angiogenesis (Matsushima grade A and B) assessed 6-12 months postoperatively, and the secondary endpoint was the incidence of surgical complications within 1 month postsurgery. RESULTS:All 104 patients completed the study. The rate of good angiogenesis was 54.9% in the arachnoid opening group and 64.2% in the arachnoid preservation group, with no significant difference between groups (OR 1.470, 95% CI 0.669-3.229; p = 0.337). Postoperative complications were observed in 2 patients (3.9%) in the arachnoid opening group and in 5 patients (9.4%) in the arachnoid preservation group, showing no significant difference (OR 2.552, 95% CI, 0.472-13.796; p = 0.276). No significant association between arachnoid opening procedures and functional recovery (assessed by modified Rankin Scale scores) was found during the 6- to 12-month follow-up period (p = 0.831). CONCLUSIONS:In adults with MMD, arachnoid membrane opening during combined bypass surgery did not significantly improve postoperative angiogenesis rates or increase perioperative complications.

Over half of patients with chronically ischaemic cerebrovascular disease (CICD) exhibit poor revascularization potential. Tie2-expressing monocytes/macrophages (TEMs) have been reported to promote angiogenesis in tumour tissue; however, whether TEMs promote angiogenesis in chronically ischaemic brain tissue (CIBT) and the regulatory mechanism through which TEMs are recruited to CIBT remain unclear. We first analysed the proportion of TEMs in blood from the internal jugular veins (IJVs) of CICD patients and then isolated TEMs for coculture with human umbilical vein endothelial cells (HUVECs) and for intraventricular injection into nude mice to explore the proangiogenic effects of TEMs in CIBT. Then, molecular biology experiments were performed to verify the upstream regulatory mechanism of the ANGPT2-Tie2 axis, and cell transfection experiments were conducted to confirm the regulatory effects of the detected pathway on Tie2 receptors on the endothelial cell surface. Additionally, a 2-vessel occlusion plus encephalomyosynangiosis rat model was established to confirm the recruitment mechanism of TEMs in CIBT and their ability to improve cerebral blood perfusion (CBP) and cognitive function. The proportion of TEMs from the IJV blood of CICD patients significantly increased, especially in patients who exhibited Matsushima Grade-A revascularization. The viability of HUVECs cocultured with TEMs was significantly increased, and CBP and the expression of CD31 in the CIBT of nude mice treated with TEMs were significantly increased. The above increases were positively correlated with the concentration of TEMs used for coculture and intraventricular injection. Moreover, molecular biology experiments indicated that miR-126-5p can directly bind to the 3'UTR of TRPS1 mRNA and that TRPS1 can directly bind to the promoter of Angpt2. HUVECs transfected with miR-126-5p mimics presented significantly decreased TRPS1 expression, a reduced pTie2/Tie2 ratio, increased ANGPT2 expression, and increased cell viability. Finally, significantly increased TEMs infiltration, downregulated TRPS1 expression, and upregulated ANGPT2, CD31, VEGFA, and IGF1 expression were detected in the CIBT of the rats transfected with the miR-126-5p agomir, accompanied by significant improvements in CBP and cognitive function. TEMs promote angiogenesis in CIBT through a paracrine mechanism, and the recruitment of TEMs to CIBT is regulated by the miR-126-5p/TRPS1/ANGPT2 pathway.

Intracranial aneurysms (IAs) represent a prevalent cerebrovascular disorder characterized by localized abnormal dilation of cerebral arterial walls. Although the majority of IAs remain clinically asymptomatic, their rupture can lead to subarachnoid hemorrhage, resulting in severe disability or even mortality. With advancements in modern imaging technologies, an increasing number of unruptured aneurysms are being detected, with an estimated prevalence of 2% to 3% in the adult population. The formation of IAs involves a complex interplay of genetic, environmental, and pathophysiological factors. This review comprehensively examines the pathophysiological mechanisms underlying IAs, including vascular wall abnormalities, hemodynamic alterations, and inflammatory responses. Although surgical interventions, such as aneurysm clipping and endovascular coil embolization, remain the primary treatment modalities, their associated complication rates remain significant. Consequently, the development of noninvasive therapeutic strategies, particularly those targeting pharmacological interventions, is of paramount importance. Future research should focus on precision medicine approaches based on individual genetic and hemodynamic profiles to enhance treatment efficacy and patient outcomes.

Peripheral nerve injury (PNI) can result in severe disabilities, profoundly impacting patients' quality of life and potentially endangering their lives. Therefore, understanding the potential molecular mechanisms that facilitate the regeneration of damaged nerves is crucial. Evidence indicates that Schwann cells (SCs) play a pivotal role in repairing peripheral nerve injuries. Previous studies have shown that RNA, particularly non-coding RNA (ncRNA), plays a crucial role in nerve regeneration, including the proliferation and dedifferentiation of SCs. In this review, the individual roles of ncRNA in SCs and PNI are analyzed. This review not only enhances the understanding of ncRNA's role in nerve injury repair but also provides a significant theoretical foundation and inspiration for the development of new therapeutic strategies.

BACKGROUND AND PURPOSE:The triglyceride-glucose (TyG) index, a novel reliable biomarker for IR that incorporates blood glucose and triglyceride, is linked to intracranial atherosclerotic stenosis (ICAS). In this study, we aimed to further investigate the association between the TyG index and the outcomes of ICAS patients following extracranial-to-intracranial (EC-IC) bypass grafting. METHODS:489 ICAS patients who underwent EC-IC bypass between Jan 2009 and Jan 2022 at our hospital were retrospectively collected. The major adverse cardiac and cerebrovascular events (MACCEs), and anastomotic restenosis, both of which are critical factors leading to poor prognosis of ICAS patients after EC-IC bypass, were mainly recorded and analyzed. Kaplan-Meier survival curve and Log-rank tests were sequentially conducted. Cox regression model was used to investigate the association between the TyG index and MACCEs & anastomotic stenosis. C-statistics, continuous net reclassification improvement (NRI), and integrated discrimination improvement (IDI) evaluated the incremental predictive value of the TyG index. RESULTS:A higher incidence of MACCEs and anastomotic stenosis was found in higher-tertile TyG index group. The TyG index was significantly associated with an increased risk of MACCEs and anastomotic stenosis, independent of confounding factors, with a value of HR (1.30, 95%CI 1.10-1.51, p < 0.001) and (1.27, 95%CI 1.16-1.40, p < 0.001) respectively. The area under the curve (AUC) in the model with the TyG index for predicting the occurrence of MACCEs and anastomotic stenosis were 0.708 (95%CI 0.665-0.748) and 0.731 (95%CI 0.689-0.770) respectively. The addition of the TyG index significantly improved the global performance of the baseline model according to the C-statistics, NRI, and IDI (All p < 0.05). CONCLUSIONS:Higher TyG levels were associated with poorer outcomes in ICAS patients after EC-IC bypass. TyG could be a key factor in managing ICAS risk and standardizing the indications for EC-IC bypass.

Abstract Background Endothelial cell (EC)-driven intraneural revascularization (INRV) and Schwann cells-derived exosomes (SCs-Exos) both play crucial roles in peripheral nerve injury (PNI). However, the interplay between them remains unclear. We aimed to elucidate the effects and underlying mechanisms of SCs-Exos on INRV following PNI. Results We found that GW4869 inhibited INRV, as well as that normoxic SCs-Exos (N-SCs-Exos) exhibited significant pro-INRV effects in vivo and in vitro that were potentiated by hypoxic SCs-Exos (H-SCs-Exos). Upregulation of glycolysis emerged as a pivotal factor for INRV after PNI, as evidenced by the observation that 3PO administration, a glycolytic inhibitor, inhibited the INRV process in vivo and in vitro. H-SCs-Exos more significantly enhanced extracellular acidification rate/oxygen consumption rate ratio, lactate production, and glycolytic gene expression while simultaneously suppressing acetyl-CoA production and pyruvate dehydrogenase E1 subunit alpha (PDH-E1α) expression than N-SCs-Exos both in vivo and in vitro. Furthermore, we determined that H-SCs-Exos were more enriched with miR-21-5p than N-SCs-Exos. Knockdown of miR-21-5p significantly attenuated the pro-glycolysis and pro-INRV effects of H-SCs-Exos. Mechanistically, miR-21-5p orchestrated EC metabolism in favor of glycolysis by targeting von Hippel-Lindau/hypoxia-inducible factor-1α and PDH-E1α, thereby enhancing hypoxia-inducible factor-1α-mediated glycolysis and inhibiting PDH-E1α-mediated oxidative phosphorylation. Conclusion This study unveiled a novel intrinsic mechanism of pro-INRV after PNI, providing a promising therapeutic target for post-injury peripheral nerve regeneration and repair. Graphical Abstract

BACKGROUND: The ventriculoperitoneal (VP) shunt is widely acknowledged as a treatment option for managing intracranial hypertension resulting from non -human immunodeficiency virus (HIV) cryptococcal meningitis (CM). Nonetheless, there is currently no consensus on the appropriate surgical indications for this procedure. Therefore, it is crucial to conduct a preoperative evaluation of patient characteristics and predict the outcome of the VP shunt to guide clinical treatment effectively. - METHODS: A retrospective analysis was conducted on data from 85 patients with non -HIV CM who underwent VP shunt surgery at our hospital. The analysis involved studying demographic data, preoperative clinical manifestations, cerebrospinal fluid (CSF) characteristics, and surgical outcomes and comparisons between before and after surgery. A nomogram was developed and evaluated. - RESULTS: The therapy outcomes of 71 patients improved, whereas 14 cases had worse outcomes. Age, preoperative cryptococcus count, and preoperative CSF protein levels were found to influence the surgical outcome. The nomogram exhibited exceptional predictive performance (area under the curve [ 0.896, 95% confidence interval: 0.8292 e0.9635). Internal validation confirmed the nomogram 's excellent predictive capabilities. Moreover, decision curve analysis demonstrated the nomogram 's practical clinical utility. - CONCLUSIONS: The surgical outcome of VP shunt procedures patients with non -HIV CM was associated with age, preoperative cryptococcal count, and preoperative CSF protein levels. We developed a nomogram that can be used to predict surgical outcomes in patients with non -HIV CM.

Objective Despite revascularization has been proven to be the optimal choice of moyamoya disease (MMD), many complications may occur in this context.. This study aimed to analyse the risk factors for new or expanded symptomatic infarctions of patients with MMD after revascularization.Methods Patients with MMD who received revascularization in our department were retrospectively enrolled, new or expanded cerebral infarction within a month after revascularization was the main concern. Basic and clinical information, and intraoperative conditions were evaluated. Univariate and multivariate analyses were performed to evaluate the risk factors. Receiver operating characteristic curve analysis was conducted to evaluate the efficiency of the risk factors.Results Eventually, 108 consecutive patients received 174 surgeries were enrolled, experienced new or expanded infarction occured in 13 (7.47%) surgeries, which showed higher Suzuki stage on the non-operative side, more posterior cerebral artery (PCA) involvement, and more intraoperative hypotension compared to those without infarction(p < .05). The Suzuki stage on the non-operative side had the highest area under the curve (AUC) of 0.737, with a sensitivity of 0.692 and specificity of 0.783. Combination of the three factors showed better efficiency, with an AUC of 0.762, a sensitivity of 0.692, and a specificity of 0.907.Conclusions Revascularization was a safe option for patients with MMD, higher Suzuki stage on the non-operative side, PCA involvement, and intraoperative hypotension might be the risk factors for new or expanded infarction after revascularization in patients with MMD.