The coexistence of an intracranial aneurysm (IA) and meningioma (MNG) is a rare clinical entity (0.13-1.17%). However, the prevalence of clinically occult MNGs may be underestimated, as routine vascular imaging often misses small lesions. We present two female patients with a history of multiple or recurrent IAs and prior endovascular treatment. During surgical clipping via a pterional approach, suspicious dural lesions-hypervascularization and thickening around the anterior clinoid process-were incidentally identified, despite being invisible on preoperative imaging. Intraoperative biopsies confirmed these lesions as MNGs. While the exact pathogenesis or underlying association remains speculative, these cases highlight the critical importance of unexpected intraoperative findings. Neurosurgeons must maintain high vigilance and strongly consider active biopsy of abnormal dura mater encountered during IA clipping, particularly in patients with multiple IAs or previous endovascular treatments.

Metastatic Meningioma with Systemic Involvement: Discussion of Molecular, Genomic, and Radiological Features.

Canine meningioma is the most common intradural extramedullary and primary spinal cord tumor. Previous studies suggest that postoperative radiation therapy can be effective for spinal meningiomas. Information on radiation-induced complications and prognosis remains limited. This case series evaluated treatment outcomes of surgical and radiation therapy in dogs with spinal meningiomas. Ten dogs were included. All underwent surgery, and histopathological examination confirmed meningioma. Among the four cases where surgical margins were assessed, three had incomplete resections. Postoperative radiation therapy was administered as an adjuvant treatment in nine dogs. One dog that did not receive postoperative radiation underwent radiation upon recurrence, observed at 99 days postsurgery. The radiation protocol consisted of fractionated irradiation (32-55 Gy/12-21 fractions) delivered five times per week. During the observation period, nine of 10 dogs died, with a median survival time of 568 days (range: 165-1823 days). Local recurrence occurred in six dogs at 95, 99, 153, 367, 433, and 1086 days postoperatively, confirmed by magnetic resonance imaging. Among 10 dogs receiving radiation, one experienced worsening limb paralysis on day 1679, suspected as a radiation-induced complication. No clinically evident acute or late radiation-induced side effects were noted in the medical records of the remaining cases.

AB-347. A 29 years old women with spinal meningioma

Fractal analysis and magnetic resonance imaging (MRI) semantic features to identify intracranial solitary fibrous tumours and atypical meningiomas.

An intramedullary spinal cord clear cell meningioma (CCM) is an exceptionally rare diagnosis; there are only 2 similar cases reported in the literature. The authors present a case of an intramedullary spinal cord CCM that was successfully resected with the assistance of sodium fluorescein to guide resection. A 68-year-old male presented with gait instability, decreased sensation, and loss of proprioception in the lower extremities, concerning for thoracic myelopathy. MRI of the thoracic spine revealed an intradural, intramedullary contrast-enhancing mass most concerning for a spinal ependymoma or astrocytoma. Given his progressive neurological decline, need for tissue diagnosis, and tumor cytoreduction, fluorescence-guided resection of the mass was performed. Postoperative pathological analysis demonstrated the presence of polygonal tumor cells with clear cytoplasm that harbored a known pathogenic SMARCE1 frameshift mutation that supported the diagnosis of an intramedullary CCM. The authors present the first reported case of a fluorescence-guided resection of an intramedullary CCM. https://thejns.org/doi/10.3171/CASE251031.

Intracranial sarcomas can arise secondarily from primary brain tumors, including gliomas and meningiomas, either spontaneously or following radiotherapy. The current WHO classification recognizes sarcomatous transformation in several tumor entities; however, sarcomas arising from meningiomas remain poorly characterized and are regarded as a possible histological manifestation within the spectrum of anaplastic meningiomas. We analyzed nine matched meningioma-sarcoma pairs using integrated histopathological assessment and molecular profiling, including DNA methylation analysis, next-generation sequencing, copy number profiling, and proteomics. Although recurrent sarcomatous tumors were clonally related to their meningioma precursors-sharing identical NF2 alterations and overlapping chromosomal aberrations-they demonstrated pronounced divergence at the histological, immunophenotypic, and epigenetic levels. Importantly, sarcomatous transformation occurred in four cases without prior radiotherapy. Sarcomatous recurrences exhibited loss of meningothelial markers and acquired expression of cytokeratin and myogenic markers. DNA methylation profiling revealed a shift away from canonical meningioma signatures toward profiles resembling non-meningothelial mesenchymal tumors. Proteomic analysis showed consistent upregulation of SOX2 in sarcomatous tumors compared with their primary counterparts, suggesting acquisition of stem-like features during lineage divergence. Clinically, these tumors were associated with aggressive growth, early recurrence, and extracranial metastases, resembling malignant sarcomas more closely than anaplastic meningiomas. In addition, analysis of an institutional cohort of NF2-mutant intracranial tumors (n = 316) suggests that sarcomas with inactivating NF2 mutations may originate from meningiomas even in the absence of a clinically recognized precursor. Together, these findings suggest that sarcomatous transformation represents a rare evolutionary endpoint in NF2-mutant meningiomas, marked by clonal continuity but pronounced biological divergence. These results highlight limitations of morphology-based classification and emphasize the value of integrated molecular diagnostics in distinguishing these tumors from conventional high-grade meningiomas. Given their sarcoma-like behavior despite a meningioma ancestry, these tumors may not be adequately captured by current meningioma grading schemes.

Meningiomas (MG) are the most common form of benign intracranial tumors. Neuropsychological deficits are often noticed preoperatively. After surgical removal, both improvements and persistent neuropsychological deficits have been reported. Here we present the neuropsychological characteristics of a larger patient group following acute treatment for meningioma. This retrospective study is part of an overall project investigating the postoperative characteristics and rehabilitation outcomes of 151 patients following surgical removal of MG. Patients were recruited at the neurological department of m&i-Fachklinik Enzensberg between 2019 and 2024. In addition to demographic data and tumor characteristics, the neuropsychological reports were evaluated by two experienced (neuro)psychologists. 69 patients underwent standardized testing in the neuropsychology department and were thus included in the analysis. Upon admission, 52.2% of these patients exhibited attention deficits, 48% showed executive deficits, and 44% had memory impairments. No correlation was found between the extent of resection or the occurrence of complications during surgery and cognitive deficits. However, there was a trend showing that higher-grade tumors were more likely to cause cognitive impairment. The location of the tumor did not correlate with the impaired cognitive domains. At discharge, fewer patients exhibited attention deficits, and those that did had less severe symptoms. Meningiomas are considered to be easily treatable. However, our data show that neuropsychological impairments frequently occur after acute treatment, which may not be given sufficient attention in practice. Even mild cognitive impairments can lead to problems in everyday life or at work. We therefore recommend detailed neuropsychological diagnosis and, if necessary, therapy for all patients after acute treatment.

Glioblastoma (GBM) is one of the most aggressive primary brain tumors in adults. Despite various strategies, including differential single-cell gene expression analyses between GBM and healthy tissues, none of the resulting findings could benefit the development of promising therapies, yet. Various macrophage populations coevolve in the tumor microenvironment of GBMs and not only support tumor immune evasion but also tumor spreading throughout the surrounding tissue. To distillate unique immune cell features of GBMs, we compared their immune cell composition with other central nervous system (CNS) tumor entities, in particular meningiomas (MNGs), non-GBM gliomas, and metastases (MTS). We could identify a macrophage population characterized by the coexpression of CX3CR1 and Siglec10, representing a potential indicator population of GBMs. This GBM-specific macrophage subset might be supported by a glioma-characteristic lipid mediator (LM) milieu of enriched docosahexaenoic acid (DHA) and its lipoxygenase (LOX)-derived metabolites. Moreover, the GBM tumor microenvironment (TME) is enriched in arachidonic acid (AA)-derived cyclooxygenase (COX) products prostaglandins (PG) E2 and F2α in combination with enhanced CD24 expression. By our comparative approach, the data hint toward a pro-tumorigenic Siglec10+CX3CR1+ macrophage population depending on the characteristic tumor microenvironment (TME) of highly malignant GBMs.

Metastases from meningioma are very rare and occur predominantly in WHO grade II and III tumors, with the lungs being the most common site. The increasing use of 68Ga-DOTA-peptides PET/CT has improved the detection of primary and secondary tumor sites. This imaging modality, evaluating the tumor expression of somatostatin receptors (SSTR), not only refines the diagnostic accuracy but also can guide a subsequent peptide receptor radionuclide therapy (PRRT). We report a case of meningioma brain tumor becoming refractory after initial neurosurgery and stereotactic radiotherapy. Meningioma has progressed to lung metastases displaying high expression of SSTR, and hence suitable for PRRT.

Accessing the ventral thoracic spinal canal poses a significant challenge due to complex anatomy. Ideal approaches for ventrally located intradural lesions must ensure sufficient exposure while minimizing spinal cord manipulation. Traditional techniques often require resection of stabilizing structures, increasing the risk of spinal instability. With advances in minimally invasive surgery, there is growing interest in anatomical preservation without compromising surgical outcomes. Here, we present a minimally invasive posterolateral approach using foraminal enlargement to access and remove ventrally located intradural lesions. Three patients underwent this approach: two for ventral thoracic meningiomas (Th1-2, Th6) and one for a hemorrhagic cavernoma (Th9-10). In the prone position, a paramedian incision was made 6-10 cm from the midline. After blunt muscle dissection and, if necessary, partial rib resection the intervertebral foramen was exposed. Foraminal enlargement was accomplished by meticulously drilling the articular processes and part of the adjacent pedicles, providing direct access to the ventral spinal canal. Mean operative time was 211 minutes, with minimal blood loss and no complications. Complete resection was confirmed postoperatively. Patients that underwent surgery for spinal meningioma showed early neurological improvement. Patients were discharged by days 3-6 without bracing. At 17-month follow-up, no recurrences or instability were noted. The Minimally Invasive Transforaminal Approach (MI-FLT), achieved through a selective foraminal enlargement, provided a safe lateral access to ventral intradural lesions while preserving spinal stability. The approach minimizes tissue disruption but requires high-level surgical expertise in minimally invasive techniques.

Abstract Central nervous system (CNS) tumors originate from neuroectodermal cells, display biological behaviors ranging from indolent lesions to highly aggressive malignancies. To understand how CNS tumors gain a survival benefits, we performed pathway-level analyses with primary omics datasets and found ISR as a most frequently activated program. ISR is a conserved, stress-adaptation pathway suppresses global protein synthesis while selectively promoting ATF4 translation in tumor cells, makes ISR a potentially targetable vulnerability. However, its relevance in CNS tumors remain understudied. Here, we interrogate multi-omics datasets in CNS tumors to define regulatory programs linked to ISR activation. We evaluated ISR activation using primary single-cell transcriptomes (scRNA-seq) and single-cell chromatin accessibility (scATAC-seq) data from multiple patient-derived pituitary adenomas (PA), schwannomas (SCH), and hemangioblastomas (HB). We used curated ATF4 target genes signature (∼200) to computed ISR activity, parallelly with differential expression analysis and single-cell transcription factor activity inference (SCENIC). Our analysis was expended utilizing publicly available scRNA-seq datasets spanning multiple CNS tumor types, including medulloblastomas (MB), meningiomas (MG), and ependymomas (EPN), alongside normal human spinal cord datasets. Chromatin accessibility of ISR related gene was evaluated using scATAC-seq, and DNA methylation profiling of ISR downstream genes was performed in PA and MG samples to explore epigenetic modulation. Across PA, EPN, MG, SCH, and HB, tumor cells showed significantly (p < 0.05) higher ISR activity compared to normal counterparts . Differential expression and functional enrichment analysis revealed upregulation of genes in tumor-cells related to protein translation, protein folding, ER stress, and proteostasis. ISR associated transcriptional program were activated, including ATF4 and related TFs such as DDIT3, ATF3, ATF5, ATF6, XBP1 and CEBPB. However, elements of the ATF4-DDIT axis linked apoptotic signaling were induced in selected tumor types (MG), tumor cells preferentially engaged with chronic ISR programs that survival, reflected by upregulation of ER stress-resolution and chaperone genes together with HSPA5, HERPUD1, PDIA3, PDIA6, DNAJB9, DNAJC3, SEC61A, CANX, and CALR. scATAC-seq analysis pinpoints increased promoter accessibility across multiple ISR-linked genes and DNA methylation analysis showd heterogeneous promoter methylation patterns, with both hypo and hypermethylation of ISR downstream genes in PA and MG, strongly supporting epigenetic reprogramming of ISR pathways. Overall, our findings demonstrate that ISR activation in CNS tumors (PA, EPN, MG, SCH, HB) contributes to tumor adaptation by enhancing protein homeostasis and stress resilience. Our study highlights adaptive ISR signaling as a key tumor adaptation mechanism and identifying the ISR axis as a potential therapeutic vulnerability in these CNS tumor entities. Only for language editing and grammatical correction AI tools were used. Citation Format: Santosh Kumar, Debjani Mandal, Kory R Johnson, Prashant Chittiboina. Integrated Stress Response (ISR) activation coupled to epigenetic reprogramming enables CNS tumor survival [abstract]. In: Proceedings of the AACR Special Conference in Cancer Research: Brain Cancer; 2026 Mar 23-25; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2026;86(6_Suppl):Abstract nr B018.

Functional outcome after resection of spinal meningiomas (SMs) is mostly considered satisfactory. However, patients with nonresolving neurological symptoms show a reduced quality of life. This study examined factors that determine full neurological recovery after resection of SMs. A single-center retrospective analysis of consecutive patients undergoing surgery on SM between 2007 and 2022 integrated clinical and surgical data with MRI-based automated volumetric tumor analyses. Patients with a favorable outcome (Frankel grade E) were compared to patients with nonresolving neurological symptoms (Frankel grade A-D) at final follow-up. A total of 202 patients with a histologically diagnosed SM were included. The cohort consisted of 159 females (78.7%) and had a median age of 65 (interquartile range [IQR] 55-74) years. Upon admission, clinical examination in 97 patients (48.0%) revealed a Frankel grade of A-D. Gross-total resection was achieved in 193 patients (95.5%) with a surgical complication rate of 8.9% (n = 18). After a median follow-up of 479 (IQR 193-1049) days, 135 patients (66.8%) showed intact neurological function (Frankel grade E). A univariate analysis revealed an overrepresentation of advanced age (OR for age ≤ 60 years = 0.14, p < 0.0001) and higher rates of preoperative neurological deficits (OR 7.39, p < 0.0001) in patients without complete recovery. No significant differences were noted in tumor volume between both groups (mean 2.34 [SD 1.69] vs 2.36 [SD 1.75] cm3, p = 0.962). In a multivariate analysis, age > 60 years, preoperative Frankel grade A-D, and Ki-67/MIB-1 index < 5% were significantly associated with nonresolving deficits at the final follow-up. This volumetry-informed series of patients with SM revealed older age and a low Ki-67 index, along with preoperative neurological deficits, constitute a higher risk of nonresolving neurological symptoms after resection. An early surgical intervention in oligosymptomatic young patients could therefore help preserve excellent long-term neurological function.

Meningiomas (MGMs) are the most common primary intracranial tumors in adults with a substantial subset exhibiting aggressive clinical behavior. Immunotherapy represents a potential alternative treatment option, even though MGMs have traditionally been considered “immunologically cold” tumors. This study explored less characterized immune cell subsets —B cells, natural killer (NK) cells, and granulocytes— and their associations with major immune cell populations as well as their prognostic implications. For this purpose, we performed tissue cytometry analysis in a clinically well-annotated multi-center cohort of 97 newly diagnosed MGMs encompassing all WHO grades (1, 2, 3) and DNA methylation classes (benign, intermediate, malignant). Resulting infiltration data were integrated with previously published data on tumor-associated macrophages (TAMs) and tumor-infiltrating T lymphocytes (TILs) to identify MGM immune ecotypes. Overall, infiltration rates of B cells, NK cells, neutrophils, and eosinophils showed lower frequencies and varied widely across tumors. Notably, we observed significantly lower numbers of B cells in MGM with losses in chromosomal arms 10q and 22q, while lower number of T cells were found in patients with a loss of chromosomal arm 1p. In addition, NK cells and eosinophils were enriched in grade 1 and benign tumors, whereas neutrophils predominated in malignant cases. Despite their relatively low abundance, elevated neutrophil frequencies turned out to be an independent of prognostic factor for poor survival. Importantly, subsequent integration of TAM and TIL data derived from the same patient cohort unraveled five distinct immune ecotypes, each displaying characteristic immune cell infiltration patterns and differential survival outcomes. Altogether, this study provides an expanded overview of various rare immune cell subtypes in MGM and demonstrates their integration into different prognostic immune ecotypes, enabling better stratification in future clinical studies.

Gamma Knife radiosurgery (GKS) delivers highly conformal intracranial irradiation, yet clinical decision-making still relies predominantly on physical dose metrics that do not account for fractionation, dose rate, treatment time, or DNA repair. Classical radiobiological models-including the linear-quadratic (LQ) formula and the Jones-Hopewell single-session repair model-do not extend naturally to 3- and 5-fraction GKS. Meanwhile, growing evidence suggests that biologically effective dose (BED) may better capture radiosurgical response in selected pathologies. A unified, biologically grounded, multi-fraction GKS framework has been lacking. We developed AI-BED-Fx, the first multi-fraction extension of the Jones-Hopewell radiobiological model capable of computing fraction-resolved BED for 1-, 3-, and 5-fraction GKS. The framework incorporates α/β ratio, dual-component repair kinetics, isocentre geometry, beam-on-time structure, and lesion-specific biological parameters. Four synthetic pathology-specific cohorts-arteriovenous malformation (AVM), meningioma (MEN), vestibular schwannoma (VS), and brain metastasis (BM)-were generated using distinct radiobiological signatures. Machine-learning models were trained to quantify the predictive value of physical dose versus BED for local control or obliteration. Additional experiments included Bayesian estimation of α/β and a neural-network surrogate for fast BED prediction. An exploratory comparison with a 60-lesion clinical brain-metastasis dataset was performed to assess whether key trends observed in the synthetic BM cohort were consistent with real radiosurgical outcomes. AI-BED-Fx produced realistic pathology-specific BED distributions (AVM 60-210 Gy2.47; MEN 41-85 Gy3.5; VS 46-68 Gy3; BM 37-75 Gy10) and biologically coherent dose-response relationships. Predictive modeling demonstrated strong pathology dependence. In AVM, the three models achieved AUCs of 0.921 (Model A), 0.922 (Model B), and 0.924 (Model C), with corresponding Brier scores of 0.054, 0.051, and 0.051, with BED-based models performing best. In meningioma, BED was the dominant predictor, with AUCs of 0.642 (Model A), 0.660 (Model B), and 0.661 (Model C) and Brier scores of 0.181, 0.177, and 0.179, respectively. In vestibular schwannoma, the narrow BED range resulted in minimal BED contribution, with AUCs of 0.812, 0.827, and 0.830 and Brier scores of 0.165, 0.160, and 0.162, with physical dose and tumor volume determining performance. In brain metastases, outcomes were driven primarily by volume and physical dose, with AUCs of 0.614, 0.630, and 0.629 and Brier scores of 0.254, 0.250, and 0.253, showing negligible improvement from BED. AI-BED-Fx also accurately recovered the true α/β from synthetic outcomes (posterior mean 2.54 vs. true 2.47), and a neural-network surrogate reproduced full radiobiological BED calculations with near-perfect fidelity (R2 = 0.9991). AI-BED-Fx provides the first unified, biologically explicit framework for modeling single- and multi-fraction Gamma Knife radiosurgery. The findings show that the predictive usefulness of BED is pathology-specific rather than universal, and that radiobiological dose provides additional predictive value only when repair kinetics and dose-response biology support it. By integrating mechanistic radiobiology with machine learning, AI-BED-Fx establishes the conceptual and computational foundations for biologically adaptive, AI-guided radiosurgery, and cross-pathology comparison of treatment response. This work uses large radiobiologically grounded synthetic cohorts for methodological validation; limited real-patient data are included only for exploratory consistency checks, and full clinical validation is planned.

Abstract An 8-year-old female central bearded dragon (Pogona vitticeps) was presented for evaluation of 2-week history of seizure activity. On physical examination, the patient was quiet, dehydrated, underconditioned, and had several intracoelomic masses. A neurologic exam revealed quiet mentation but no other abnormal findings. Complete blood count and biochemistry panel results were consistent with non-regenerative anemia and a mild inflammatory leukogram with a left shift. Abdominal ultrasound demonstrated post-ovulatory follicles with scant free fluid. Treatment with subcutaneous fluids, antibiotics, and nutritional support was initiated. During hospitalization, the patient’s seizures were monitored and eventually controlled with midazolam (0.34-0.75 mg/kg IM as needed) and levetiracetam (20 mg/kg every 12 h SQ-40 mg/kg SQ every 24 h). On day 17, due to a worsening clinical state, an ovariosalpingohysterectomy was performed. The patient did not recover from anesthesia and euthanasia was elected. The main necropsy findings included a diffuse meningeal neoplasm surrounding and invading the brain that was most consistent with a poorly-pigmented chromatophoroma based on immunohistochemistry with PNL2 and S100. No other evidence of neoplasia was seen throughout the body and so this was considered a primary tumor. Other findings included oophoritis, salpingitis, and coelomitis, consistent with known reproductive disease. This case details the clinical presentation, associated seizure management, and pathological findings of the first known presumptive primary meningeal chromatophoroma in a reptile.

Background: Although Ki-67 is not included among the grading criteria in the current WHO Classification of Tumours of the Central Nervous System (CNS), it provides valuable, albeit limited, prognostic information. Immunohistochemistry for Ki-67 can reveal uneven proliferation patterns and assist in the assessment of mitotic counts. Several studies indicate that meningiomas with a proliferation index > 4% show recurrence rates comparable to CNS WHO grade 2 (atypical) tumors, while tumors with an index > 20% are associated with mortality rates similar to CNS WHO grade 3 (anaplastic) meningiomas. Issues related to Ki-67 assessment include interobserver variability, the use of different cut-off values among pathologists, and the presence of a complex inflammatory tumour microenvironment, which may lead to an overestimation of the proliferative index (PI). Methods: In this study, we describe how Double Staining Immunohistochemistry (dIHC) with EMA/Ki-67 better highlights neoplastic meningothelial cells compared with single-stain evaluation. Furthermore, the application of Digital Pathology provides quantitative digital data that allow a more accurate assessment of proliferation. Results: Ki-67 expression varied by grade, with digital image analysis (dIHC) showing high agreement with manual assessments. dIHC improved accuracy in evaluating diagnostic and proliferative markers within tumor samples. Conclusions: dIHC combined with DP can support and standardize the evaluation of the proliferative index in meningiomas in routine diagnostic practice.

Multiple spinal and intraventricular meningiomas: Report of a rare case

6P Anaplastic meningioma: A single-center retrospective analysis

Recurrent intracranial meningiomas are a significant therapeutic challenge due to their invasive growth and high recurrence risk after surgery and radiotherapy. This study investigates the feasibility of a novel integrated approach combining 5-aminolevulinic acid (5-ALA) fluorescence-guided surgery (FGS) with intraoperative photodynamic therapy (PDT) for recurrent atypical and anaplastic meningiomas. In a single-center, prospective cohort study, 23 patients with recurrent atypical and anaplastic meningiomas received the experimental treatment protocol (FGS+PDT). A retrospective control group (n=35) underwent conventional microsurgery. The intervention included preoperative 5-ALA administration, FGS with visual (Fluorescence Intensity Score, FIS) and quantitative biospectroscopy (Fluorescence Index, FI) guidance, tumor resection, and subsequent PDT (635 nm laser) applied to the resection cavity and tumor matrix. Biospectroscopy guided PDT endpoint (photobleaching and decreasing of FI). Primary outcomes included feasibility, safety, and extent of resection (Simpson Grade), short follow-up period. Histopathological and immunofluorescence analyses of paired pre-/post-PDT biopsies assessed biological effects. The FGS+PDT protocol was successfully completed in all patients with an excellent safety profile; no adverse events were attributed to 5-ALA or PDT. All tumors exhibited visible 5-ALA fluorescence. Gross-total resection (Simpson I-II) was achieved in 95.6% (22/23) of the study group versus 77.1% (27/35) in controls (p<0.05). Biospectroscopy revealed significant PpIX accumulation even in visually low-fluorescence tumors. Over a median follow-up of 16 months, no recurrences were observed in the experimental group. Histopathological analysis demonstrated profound PDT-induced effects, including total ablation of progesterone receptor expression in the tumor matrix and a significant increase in caspase-3-mediated apoptosis in the peritumoral zone (36.3 ± 9.6 vs. 14.8 ± 2.2 cells/mm², p<0.0001). Confocal microscopy confirmed subcellular damage, including mitochondrial dysfunction, nuclear degradation, and Hsp70 overexpression. The integrated FGS and PDT protocol is feasible, safe, and demonstrates compelling preliminary efficacy for recurrent atypical and anaplastic meningiomas. It enhances resection and induces profound cytotoxic and apoptotic effects in the residual tumor bed and peritumoral zone. These results need to be further validated in larger, randomized controlled trials.