To investigate the patterns of iron deposition using quantitative susceptibility mapping (QSM) and their relationship with epilepsy duration in patients with low-grade glioma-related epilepsy (GRE). This retrospective study enrolled 59 patients with low-grade gliomas, who were subsequently stratified into an epilepsy group and a non-epilepsy group. QSM was employed to quantify iron content in these patients. Regions of interest (ROIs) were defined as the tumor region, cortical regions, and deep gray matter nuclei. The mean magnetic susceptibility values within each ROI were calculated and compared between the two groups. Furthermore, the correlation between these values and epilepsy duration was analyzed in the epilepsy group. Analysis of the 59 patients revealed that, compared to those without epilepsy, patients with epilepsy had significantly higher magnetic susceptibility values in the tumor region (p = 0.018), frontal cortex (p = 0.037), precentral gyrus (p = 0.003), and parietal cortex (p = 0.037). Although a positive correlation was observed in the epilepsy group between putamen susceptibility and epilepsy duration (r² = 0.172, p = 0.023), it did not retain statistical significance after adjustment for age. Iron deposition in the tumor region and certain cortical areas is higher in patients with epilepsy than in non-epilepsy patients. However, iron deposition demonstrates no significant correlation with the duration of epilepsy.

BACKGROUND:CT angiography (CTA) is a key investigation in cerebrovascular disease. However, CTA is not always available and it also requires intravenous injection of iodinated contrast agents. It is increasingly possible to derive additional information from standard imaging sequences using artificial intelligence techniques. We investigated whether CTA maps could be derived from non-contrast CT (NCCT). METHODS:We conducted a retrospective, multicenter study across five Chinese hospitals, enrolling 3709 patients who underwent head NCCT paired with CTA. The dataset encompassed three cerebrovascular conditions: intracranial aneurysms (IA), intracranial atherosclerotic stenosis (IAS), and normal intracranial arteries. We developed the Cerebrovascular CTA Generative Artificial Intelligence Model (CTA-GAI) to synthesize CTA images directly from NCCT head scans. Synthetic outputs were evaluated against five typical models using quantitative metrics and visual assessment by clinicians. We also assessed the potential clinical utility of synthetic CTA for preliminary screening and triage by evaluating its ability to distinguish diseased from normal intracranial arteries and to classify common cerebrovascular subtypes. RESULTS:CTA-GAI demonstrated consistent and robust performance across both the validation and test sets. In internal validation, synthetic CTA images achieved a mean absolute error (MAE) of 0.0416, mean squared error (MSE) of 0.0178, peak signal-to-noise ratio (PSNR) of 25.59 dB, and structural similarity index measure (SSIM) of 85.41%. Clinicians assigned an average visual quality score of 4.45 out of 5. These metrics reflect close approximation to real CTA images. Performance remained consistent across four external validation sets. In a test set of 110 patients, clinicians achieved an overall accuracy, precision, sensitivity, specificity, and F1 score of 92.7%, 97.7%, 86.0%, 98.3%, and 91.5%, in distinguishing diseased intracranial arteries. Differentiation between IA and IAS within diseased arteries reached 90.7% accuracy. CONCLUSION:CTA-GAI can synthesize CTA-like images from NCCT that show promising utility for preliminary assessment in clinical practice. These results support its potential role as a rapid, low-cost, and non-invasive tool for large-scale screening or triage of cerebrovascular diseases.

OBJECTIVE:The objective was to evaluate the Superior Sagittal Sinus Involvement Grading (SSIG) system as an imaging-based surgical stratification framework for parasagittal meningiomas adjacent to the superior sagittal sinus (SSS) and to assess its relationship with established sinus invasion grading, venous sinus patency, and operative strategy. METHODS:In this single-center retrospective cohort study, the authors included 62 consecutive parasagittal meningioma resections performed by a single surgeon. SSIG grade was assigned primarily on contrast-enhanced coronal MRI, with CT/MR venography used when available to evaluate sinus patency and collateral venous drainage. Operative variables, resection strategy, and clinicopathological factors were compared across SSIG and Sindou grades, and postoperative complications were compared between low- and high-involvement SSIG groups. RESULTS:SSIG correlated significantly with Sindou grade (rs = 0.790, τb = 0.702, both p < 0.001), and among patients with available venous imaging, it also correlated with the venous sinus involvement grade (rs = 0.742, τb = 0.665, both p < 0.001). With increasing SSIG grade, operative time, intraoperative blood loss, and intraoperative fluid administration increased (p = 0.012, p = 0.008, and p = 0.007, respectively). Compared with the low-involvement group (SSIG grades 1, 2, and 4a), the high-involvement group (SSIG grades 3, 4b, and 5) was less likely to achieve Simpson grade I resection and more likely to adopt Simpson grades II-III strategies (66.7% vs 13.6%, p < 0.001; OR 12.667). Surgery-related complication rates did not differ significantly between groups. The mean follow-up was 13.3 ± 7.9 months, with no radiographic recurrence or progression at last follow-up. CONCLUSIONS:SSIG characterizes parasagittal meningiomas by integrating sinus invasion, venous patency, falcine extension, and parasagittal convexity involvement on preoperative imaging. This surgically oriented framework may help anticipate operative exposure, sinus handling, and resection strategy. Its predictive value for complications and long-term oncological outcomes requires validation in larger cohorts with longer follow-up.

Glioblastoma (GBM) is the most aggressive primary brain tumor and remains associated with poor prognosis despite multimodal treatment. Increasing evidence indicates that lipid metabolic reprogramming is a critical hallmark of GBM progression and therapeutic resistance. Beyond supporting membrane biosynthesis and energy production, dysregulated lipid metabolism profoundly influences tumor plasticity, oxidative stress adaptation, immune suppression, stemness maintenance, and ferroptosis sensitivity within the tumor microenvironment. GBM cells dynamically rewire lipid metabolic pathways through enhanced de novo lipogenesis, fatty acid uptake, cholesterol remodeling, lipid droplet accumulation, and fatty acid oxidation to adapt to hypoxia, nutrient deprivation, and therapeutic stress. In parallel, lipid metabolic interactions between tumor cells and immune components, including tumor-associated macrophages and exhausted T cells, further contribute to immunosuppressive microenvironment formation and resistance to chemotherapy, radiotherapy, and immunotherapy. Recent advances in spatial transcriptomics, single-cell metabolomics, and multi-omics integration have substantially improved understanding of lipid metabolic heterogeneity in GBM. These emerging technologies have also facilitated the identification of novel metabolic vulnerabilities and therapeutic targets. In this review, we summarize current insights into lipid metabolic plasticity in GBM and discuss the mechanistic links between lipid metabolism, tumor microenvironment remodeling, ferroptosis regulation, and therapeutic resistance, highlighting potential opportunities for precision metabolic therapy in GBM.

Less-aggressive lower-grade gliomas (LGGs) frequently transform into glioblastoma (GBM). Most previous studies of gliomas have not focused on LGG-original high-risk subpopulations, which may be one of the most critical hallmarks of glioma progression. In this study, LGG samples are collected to perform single-cell sequencing (scRNA-seq) and identify a unique cell subpopulation marked by CDC20, KIF20A and PTTG1, correlating with poor survival in multiple cohorts. Importantly, the CDC20+KIF20A+PTTG1+ cell subpopulation is strongly associated with transforming LGG to GBM according to scRNA-seq and multiplexed immunofluorescence staining assays. In vitro, ex vivo and in vivo investigations further hint that this cell subpopulation is critical to the proliferation and growth of gliomas, and is associated with the hypoxia core activation. Pharmaceutically and therapeutically, the inhibition of this cell subpopulation showed significant anti-tumor effects and effective enhancement of the Temozolomide treatment efficiency. These findings provide insights into the therapeutic strategies of glioma progression, highlighting promising ways to avoid early-stage gliomas developing into advanced gliomas.

BackgroundThe prognostic value of body mass index (BMI) in primary WHO grade 4 gliomas is not widely acknowledged. This study aims to assess the survival outcomes of patients with different BMIs.MethodsReal-world data of patients diagnosed with primary WHO grade 4 (2021 version) glioma was assessed. All 127 patients admitted in this study were administered with standard-of-care from September 2018 to September 2021. The outcomes of overall survival and progression-free survival were analyzed.ResultsThe baseline characteristics of clinical features, molecular features, and secondary treatment in BMI subsets showed no significant difference. The survival analyses showed a significantly superior overall survival (OS) in the overweight group compared to the normal weight group. A trend of better OS in the overweight group compared to the obesity group was observed. The univariate Cox regression demonstrated patients of round-BMI 25 and 26 had superior OS outcomes.ConclusionIn this real-world setting, patients with a BMI between 24 and 28 have superior overall survival. Patients in the proper BMI range may acquire survival benefits undergoing standard-of-care of primary WHO grade 4 gliomas. The prospective studies on a larger scale on these subsets of patients are necessary to solve the paradox of BMI in glioma.

BackgroundGlioblastoma is one of the deadliest tumors, and limited improvement in managing glioblastoma has been achieved in the past decades. The unmethylated promoter area of 6-O-Methylguanine-DNA Methyltransferase (MGMT) is a significant biomarker for recognizing a subset of glioblastoma that is resistant to chemotherapy. Here we identified MGMT methylation can also work as a specific biomarker to classify the lipid metabolism patterns between methylated and unmethylated glioblastoma and verify the potential novel therapeutic strategy for unmethylated MGMT glioblastoma.MethodsLiquid Chromatograph Mass Spectrometer has been applied for non-targeted metabolome and targeted lipidomic profiling to explore the metabolism pattern correlated with MGMT promoter methylation. Transcriptome has been performed to explore the biological differences and the potential mechanism of lipid metabolism in glioblastoma samples. In vivo and ex vivo assays were performed to verify the anti-tumor activity of atorvastatin in the administration of glioblastoma.ResultsMulti-omics assay has described a significant difference in lipid metabolism between MGMT methylated and unmethylated glioblastoma. Longer and unsaturated fatty acyls were found enriched in MGMT-UM tumors. Lipid droplets have been revealed remarkably decreased in MGMT unmethylated glioblastoma. In vivo and ex vivo assays revealed that atorvastatin and also together with temozolomide showed significant anti-tumor activity, and atorvastatin alone was able to achieve better survival and living conditions for tumor-hosting mice.ConclusionsMGMT promoter methylation status might be a well-performed biomarker of lipid metabolism in glioblastoma. The current study can be the basis of further mechanism studies and implementation of clinical trials, and the results provide preclinical evidence of atorvastatin administration in glioblastoma, especially for MGMT unmethylated tumors.

Background Glioblastoma (GBM) is a highly aggressive primary brain tumor with a poor prognosis. This study investigates the therapeutic potential of human Vγ9Vδ2 T cells in GBM treatment. The sensitivity of different glioma specimens to Vγ9Vδ2 T cell-mediated cytotoxicity is assessed using a patient-derived tumor cell clusters (PTCs) model. Methods The study evaluates the anti-tumor effect of Vγ9Vδ2 T cells in 26 glioma cases through the PTCs model. Protein expression of BTN2A1 and BTN3A1, along with gene expression related to lipid metabolism and glioma inflammatory response pathways, is analyzed in matched tumor tissue samples. Additionally, the study explores two strategies to re-sensitize tumors in the weak anti-tumor effect (WAT) group: utilizing a BTN3A1 agonistic antibody or employing bisphosphonates to inhibit farnesyl diphosphate synthase (FPPS). Furthermore, the study investigates the efficacy of genetically engineered Vγ9Vδ2 T cells expressing Car-B7H3 in targeting diverse GBM specimens. Results The results demonstrate that Vγ9Vδ2 T cells display a stronger anti-tumor effect (SAT) in six glioma cases, while showing a weaker effect (WAT) in twenty cases. The SAT group exhibits elevated protein expression of BTN2A1 and BTN3A1, accompanied by differential gene expression related to lipid metabolism and glioma inflammatory response pathways. Importantly, the study reveals that the WAT group GBM can enhance Vγ9Vδ2 T cell-mediated killing sensitivity by incorporating either a BTN3A1 agonistic antibody or bisphosphonates. Both approaches support TCR-BTN mediated tumor recognition, which is distinct from the conventional MHC-peptide recognition by αβ T cells. Furthermore, the study explores an alternative strategy by genetically engineering Vγ9Vδ2 T cells with Car-B7H3, and both non-engineered and Car-B7H3 Vγ9Vδ2 T cells demonstrate promising efficacy in vivo, underscoring the versatile potential of Vγ9Vδ2 T cells for GBM treatment. Conclusions Vγ9Vδ2 T cells demonstrate a robust anti-tumor effect in some glioma cases, while weaker in others. Elevated BTN2A1 and BTN3A1 expression correlates with improved response. WAT group tumors can be sensitized using a BTN3A1 agonistic antibody or bisphosphonates. Genetically engineered Vγ9Vδ2 T cells, i.e., Car-B7H3, show promising efficacy. These results together highlight the versatility of Vγ9Vδ2 T cells for GBM treatment.

梗阻性脑积水是丘脑出血的常见并发症.青岛市城阳区人民医院神经外科于2020年7月行侧脑室穿刺手术治疗1例丘脑出血患者,术后患者病情好转;术后3周出现迟发梗阻性脑积水并发阵发性交感神经过度兴奋,经第三脑室底造瘘手术治疗,患者脑积水和阵发性交感神经过度兴奋症状改善,预后较好.

-OBJECTIVE: The clinical features and surgical tech- -iques related to patients undergoing resection of extra-cranial large primary intraosseous meningiomas are studied. -METHODS: The clinical characteristics, treatment, and prognosis of 6 patients with primary intraosseous menin-giomas larger than 5 cm in diameter were retrospectively reviewed in the 10th Neurosurgical Department of Beijing Tiantan Hospital, Capital Medical University. -RESULTS: Five males and one female (18-57 years old) suffered from large primary intraosseous meningiomas. The main symptoms were headaches accompanied by head swelling. CT showed irregular thickening of the bone diploe with increased density and uneven surface. MRI showed partial bone destruction of the skull, local thickening of the internal and external plates, shell and palisade changes of the external cranial plate, and enhancement of the adjacent meninges. A horseshoe or coronary incision plus the "Mercedes-Benz" incision were chosen to expose the skull bone, and drilling was performed in the normal skull bone at the transition zone between abnormal and normal skull bone. After drilling, the sub flap dura was dissected, the hyperplastic skull was dissected with a milling cutter, and the residual tu-mor was then resected. A cranioplasty was performed 6 months to 1 year later. -CONCLUSIONS: Surgical treatment and precise periop-erative management can achieve a better prognosis for large intraosseous meningiomas.

BACKGROUND:Surgical site infection (SSI) is a common complication following craniotomy that increases morbidity, mortality, and medical expenses. The objectives of this study were to determine the relevant risk factors associated with SSI after elective craniotomy for brain tumor and analyse the treatments for SSI.METHODS:A retrospective nested case‒control study was conducted using data from patients who underwent craniotomy for brain tumor resection at the Neurosurgical Oncology Department No. 6 of Beijing Tiantan Hospital, Capital Medical University, between January 2019 and December 2021. Risk factors for SSI were determined using multivariate logistic regression analysis. We analyzed microbiological and related treatment data for different SSI types.RESULTS:Among 2061 patients who underwent craniotomy for brain tumor, 31 had SSI (1.50%). In the multivariate logistic regression analysis, body mass index (BMI) and operative duration were identified as independent risk factors for SSI. The most common microorganism isolated from SSIs was Staphylococcus epidermidis (22.9%), and drug sensitivity results showed that gram-positive bacteria were sensitive to linezolid, vancomycin and tigecycline, whereas gram-negative bacteria were sensitive to meropenem, cefepime and ceftazidime. Six of the seven patients who underwent bone flap removal due to osteomyelitis were infected with gram-negative bacteria.CONCLUSIONS:BMI and operative duration were identified as independent risk factors for SSI. Diabetes mellitus, previous ratio therapy, type of incision, recurrence tumor and other risk factors were not found to be associated with the occurrence of SSI in this study.

Objective:To analyze and compare the efficacy of neuroendoscopic surgery and microscopic craniotomy in the treatment of early basal ganglia hypertensive intracerebral hemorrhage (HICH).Methods:The clinical data of 188 patients with early basal ganglia HICH treated in Neurosurgery Department of Zhangjiakou First Hospital from March 2016 to March 2021 were analyzed retrospectively. According to surgical methods, 95 cases were enrolled into neuroendoscopic group and 93 cases were in microscopic group. The intraoperative blood loss, operation duration, the hematoma clearance rate, the incidence of complications (intracranial infection) and the score of modified Rankin scale (mRs) at 6 months after operation were compared and analyzed between the two groups.Results:The neuroendoscopy group was compared with the microscope group, the operation duration was significantly shortened [(96.6±10.7) min vs (171.3±26.4) min], the amount of intraoperative bleeding was significantly reduced [(32.8±6.2) mL vs (112.8.0±17.0) mL], and the hematoma clearance rate was increased (95.9%±4.2% vs 87.4%±6.5%), the differences were statistically significant (all P<0.05). There was no significant difference in complications between two groups (P>0.05). According to the mRs score at 6 months after operation, the good prognosis rate of neuroendoscopy group (26.3%, 25/95) was higher than that of microscope group (15.1%, 14/93) (P<0.05).Conclusion:For the patients with early basal ganglia HICH, less time was needed in neuroendoscopic surgery than that in microscopic surgery. Additionally, there was more clear visual field and better prognosis under neuroendoscopic surgery, indicating that neuroendoscopic surgery is a safer surgery method.

Objective:To discuss the treatment and prognosis of poor healing of scalp incision after craniotomy.Methods:A retrospective analysis was conducted on the clinical data of 22 patients with poor healing of scalp incision after elective surgery in the Sixth Ward of Neuro-Oncology, Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University from January 2014 to November 2020. Those patients accounted for 0.6%(22/3 667) of patients undergoing elective surgery in the same period. According to the scope of poor healing of the incision and the presence or absence of skin defects, the patients were divided into groups: poor healing of scalp incision without scalp defection (Group A1); poor healing of chronic wounds with cerebrospinal fluid leakage rather than defection of scalp (Group A2); poor scalp healing with skin defects (Group B); complex healing defect with osteomyelitis (Group C); complex healing defect, osteomyelitis and epidural abscess or brain abscess (Group D). Group A1 and A2 were given suture after exploring the scalp wound; Group B was given an incision dressing, and then underwent a second stage of suture; Group C and Group D were given debridement, bone flap removal and incision suture. Regular telephone or outpatient follow-up was performed to evaluate the patients′ incision healing.Results:Among the 22 patients, 7 were in group A1, 7 were in group A2, 4 were in group B, 1 was in group C, and 3 were in group D. Among 22 patients, 1 patient with recurrent craniopharyngioma in group D died of secondary subcutaneous empyema and brain abscess, and the remaining 21 patients completed the clinical follow-up of 3 to 60 months. One patient in group A2 after suboccipital far-lateral craniotomy had cerebrospinal fluid leakage lasting for 2 months and underwent ventriculoperitoneal shunt at another hospital due to hydrocephalus. By the last follow-up, the incisions of 21 patients were all healed, and the median healing time was 14 days (range: 7-42 d).Conclusion:Patients with poor incision healing after craniotomy have a generally good prognosis after individualized treatment according to the scope of the incision and the presence or absence of skin defects.

Background and Objectives Brain arteriovenous malformation (bAVM) is a congenital disorder and a leading cause of hemorrhagic stroke. Germline genetic variants play an essential role in the pathogenesis of bAVM. However, the biological relevance of disease-associated genes identified in previous studies is elusive. In this study, we aim to systematically investigate the contribution of germline variants to bAVM and explore the critical molecular pathways underlying the pathogenesis of bAVM. Methods Probands with sporadic bAVM were consecutively recruited into this study from November 2015 to November 2018 and underwent exome sequencing. The controls were aggregated from individuals who were not known to have vascular malformation and underwent exome sequencing for clinical or research purposes. The retained control dataset included 4,609 individuals, including 251 individuals with parental samples sequenced. We first analyzed de novo variants in cases and controls and performed a pathway enrichment analysis. A gene-based rare variant association analysis was then performed to identify genes whose variants were significantly enriched in cases. Results We collected an exome-sequenced bAVM cohort consisting of 152 trios and 40 singletons. By first focusing on de novo variants, we observed a significant mutational burden of likely gene-disrupting variants in cases vs controls. By performing a pathway enrichment analysis of all nonsynonymous de novo variants identified in cases, we found the angiopoietin-like protein 8 (ANGPTL8) regulatory pathway to be significantly enriched in patients with bAVM. Through an exome-wide rare variant association analysis utilizing 4,394 in-house exome data as controls, we identified SLC19A3 as a disease-associated gene for bAVM. In addition, we found that the SLC19A3 variants in cases are preferably located at the N ' side of the SLC19A3 protein. These findings implicate a phenotypic expansion of SLC19A3-related disorders with a domain-specific effect. Discussion This study provides insights into the biological basis of bAVM by identifying novel molecular pathways and candidate genes.

Circular RNA (circRNA) is considered to be non-coding RNA due to the deletion of the 5' cap structure and lacks the function of encoding proteins or polypeptides. With the development of high-throughput transcriptome sequencing, ribosome sequencing and other technologies, researchers have discovered that there were short open reading frames (sORF) and internal ribosome entry sites (IRES) in the sequence of some circRNAs which can encode polypeptides or protein and play important roles in the proliferation of malignant tumors such as glioma, hepatoma, gastric cancer, breast cancer, and colon cancer. This paper reviews the coding function of circRNA and analyzes the role of its encoded production-polypeptides or protein in the proliferation mechanism of human malignant tumors.

Circular RNA (circRNA) is a widely expressed non-coding RNA element characterized by a covalently closed continuous loop. Emerging evidence suggests important roles of circRNAs in the pathogenesis of human cancers. However, the functions and underlying mechanisms of circRNAs in glioma remain largely unclear. Previously, our studies uncovered a batch of abnormally expressed circRNAs in glioma tissue, among which circPARP4 was significantly upregulated with the top fold change. Here, we focused on the functional investigation toward circPARP4 in glioblastoma progression and looked for insight into its underlying mechanisms. The results confirmed the elevated expression of circPARP4 in glioma and found its association with glioma pathological grade. Gain- and loss-of-function strategies showed that circPARP4 could obviously promote glioma cell proliferation, migration, invasion, and epithelial-mesenchymal transition. Mechanistically, in vivo and in vitro studies demonstrated that circPARP4, as a miRNA sponge, directly interacted with miR-125a-5p, which then regulated FUT4 to exert the oncogenic effect on glioma behavior. Our findings illustrate functions of circPARP4 in modulating glioma progression through miR-125a-5p/FUT4 pathway, which provides a novel and potential target for glioma therapy.

Background::Previous studies have demonstrated that various circular RNAs are involved in the malignant proliferation of cancers, such as liver cancer, lung cancer, breast cancer, and others. The potential role of circular RNAs in glioblastoma, however, is still uncertain. In this study, we aimed to study the potential role of hsa_circ _01844 in glioblastoma.Methods::Using reverse transcription-polymerase chain reaction (RT-PCR) method, hsa_circ_01844 expression was measured in five glioblastoma samples and five normal brain samples. To evaluate the potential function of hsa_circ_01844 in glioblastoma, hsa_circ_01844 was overexpressed in glioblastoma cell lines (U251 and U87 cells). Using these two cell lines, in vitro experiments including the flow cytometry assay, 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide assay, Transwell assay, and cell apoptosis assay were performed to investigate the role of hsa_circ_01844 in glioblastoma. Student t test and one-way analysis of variance were used for statistical analysis. Results::The expression of circular RNA hsa_circ_01844 was lower in glioblastoma tissues when compared with the normal brain tissues by RT-PCR method (0.034 ± 0.036 vs. 1.630 ± 0.891, P < 0.001). Using two glioblastoma cell lines, we found that overexpression of hsa_circ_01844 in glioblastoma cells suppressed their proliferation, colony formation, migration, and increased the apoptotic rate compared with empty vector group and blank control group (all P < 0.05). Conclusion::Hsa_circ_01844 shows decreased expression in glioblastoma and its overexpression induces apoptosis and inhibits proliferation, migration, and invasion of glioblastoma cells.

Objective:To explore the clinical effects and safety of neuroendoscopic aspiration of early hypertensive hematoma in the basal ganglia (EHHBG).Methods:A retrospective analysis was conducted on the clinical data of 90 patients with EHHBG who underwent surgical treatment at Department of Neurosurgery, Zhangjiakou First Hospital from March 2016 to March 2019. Among them, neuroendoscopic surgery was performed in 47 cases and microscopic surgery in 43. Differences were compared between the two groups in operative duration, intraoperative blood loss, clearance rate of hematoma, incidence of complication (intracranial infection) and scores of modified Rankin Scale (mRS) at 6 months post operation.Results:Compared with microscopic surgery group, neuroendoscopic surgery group had shorter operative duration (93.5±10.7 h vs. 193.1±15.4 h, P<0.05) and less intraoperative blood loss in operation (30.9±5.8 ml vs. 119.0±17.9 ml, P<0.05) and elevated clearance rate of hematoma[(96.8±4.5)% vs. (88.3±6.2)%, P<0.05], and there were statistical differences between those two groups (all P<0.05). There was no significant difference in the rate of postoperative intracranial infection between two groups ( P>0.05). In terms of mRS at 6 months post operation, the rate of favorable outcome in neuroendoscopic surgery group was better than that in microscopic surgery group with significant difference[25.5% (12/47) vs. 11.6% (5/43), P<0.05]. Conclusion:Neuroendoscopic removal of EHHBG has the advantages of clear and direct vision, little invasiveness, short operation time and good prognosis, and is a safe and effective surgical method for cerebral hemorrhage in the basal ganglia.

目的 分析无颅外转移的非小细胞肺癌脑转移瘤患者的手术效果及预后.方法 回顾性分析103例无颅外转移的非小细胞肺癌脑转移瘤患者的手术及预后相关资料.结果 103例患者中,男59例,女44例,均接受了脑转移瘤切除术.病理诊断腺癌96例,鳞状细胞癌7例.103例患者的1年和2年生存率分别为81.6％和39.8％.脑转移瘤全切除患者(85例)中位生存期为34个月,长于脑转移瘤部分切除患者(18例)的12个月(P＜0.05).表浅部脑转移瘤患者(75例)中位生存期为34个月,长于深部脑转移瘤患者(28例)的16个月(P＜0.05).单因素和多因素分析均显示,脑转移瘤切除程度和脑转移瘤位置是患者预后的影响因素(P＜0.05).结论 非小细胞肺癌脑转移瘤部分切除和深部脑转移瘤的患者预后较差.

目的 探讨肺癌脑转移瘤(BM)的手术治疗效果及其预后影响因素.方法 回顾性分析北京天坛医院神经外科2013年1月—2018年12月手术治疗的123例肺癌脑转移瘤患者的临床资料.分析患者的生存时间及独立预后影响因素.结果 本组患者术后的中位生存时间为22个月;1年、2年生存率分别为73.2％和35.8％.单因素分析显示,肺癌是否颅外转移、脑转移瘤的深浅部位、肺癌脑转移瘤的病理类型及脑转移瘤切除程度对患者的生存期有明显影响(P<0.05～0.001).多因素Cox回归分析显示,肺癌是否颅外转移、脑转移瘤的深浅部位和转移瘤切除程度是影响患者预后的独立因素.结论 肺癌脑转移瘤手术治疗能明显延长患者的生存期,而有肺癌颅外转移、深部脑转移瘤和转移瘤部分切除的患者预后较差.