High-grade gliomas—particularly glioblastoma (GBM)—remain refractory to standard-of-care surgery followed by chemoradiation, with a median overall survival of ~15 months. Oncolytic viruses (OVs), which selectively infect and lyse tumor cells while engaging antitumor immunity, offer a mechanistically distinct therapeutic modality. This review synthesizes clinical progress of OVs in GBM, with emphasis on oncolytic herpes simplex virus (oHSV) and coverage of other vectors (adenovirus, reovirus, Newcastle disease virus, vaccinia virus) across phase I–III trials, focusing on efficacy and safety. Key observations include the encouraging clinical trajectory of oHSV exemplars—T-VEC (approved for melanoma) and G47Δ (approved in Japan for recurrent GBM)—the multi-center exploration of the adenovirus DNX-2401 combined with programmed death-1 (PD-1) blockade, and the early-stage status of reovirus (pelareorep) and Newcastle disease virus programs. Emerging evidence indicates that oHSV therapy augments immune infiltration within the tumor microenvironment and alleviates immunosuppression, with synergy when combined with chemotherapy or immune checkpoint inhibitors. Persistent challenges include GBM’s inherently immunosuppressive milieu, limitations imposed by the blood–brain barrier, intrapatient viral delivery and biodistribution, and concerns about viral shedding. Future directions encompass programmable vector design, optimization of systemic delivery, biomarker-guided patient selection, and rational combination immunotherapy. Collectively, OVs represent a promising immunotherapeutic strategy in GBM; further gains will hinge on vector engineering and precision combinations to translate mechanistic promise into durable clinical benefit.

Background: Although chronic subdural hematoma (CSDH) has been known for over several hundred years, the etiology and pathogenesis of it are still not completely understood. Neurosurgical procedures resulting in CSDH are a rare clinical complication, and there was no report about how subdural effusion (SDE) evolves into CSDH after deep brain stimulation (DBS) surgery. The formation mechanism of CSDH after surgery, especially in DBS surgery, and the effect of recovery, need to be explored. Methods: We present two cases, complicated with SDE after DBS surgery, serious dysfunction complications such as hemiplegia and aphasia occurred on the postoperative day 36 and 49 individually, and images showed CSDH. Fusion image showed the bilateral electrodes were significantly shifted. Then, they were performed to drill craniotomy with a closed system drainage. Result: The symptoms of hemiplegia and aphasia caused by CSDH were completely recovered, and the follow-up images showed CSDH was disappeared. However, DBS stimulation is poorly effective, it cannot reach the preoperative level, especially in the ipsilateral side of CSDH. Conclusions: The iatrogenic SDE that evolved into CSDH in the present two cases shows that SDE is one of the causes of CSDH. Patients develop SDE after DBS, which increases the risk of developing CSDH. CSDH after DBS can be successfully treated. however, the postoperative efficacy of DBS will decline.

Development of a circulating extracellular vesicle-based IDH mutant protein detection technology for diagnosis of IDH mutation status in glioma, enabling personalized resection strategies, precision medication, and disease dynamics monitoring in IDH-mutant glioma. We developed a tumor-classification strategy that discriminates tumor types by detecting the IDH1.R132H mutant protein in plasma extracellular vesicles using a bead-assisted, flow-cytometry–based assay. We assessed the differential expression’s capacity to distinguish tumor grades, analyzed pre-operative and post-operative expression variations, and verified consistency with histopathological immunohistochemistry. The method demonstrated a diagnostic sensitivity of 76.2% (95%CI: 54.9%–89.4%) and a specificity of 86.7% (95%CI: 62.1%–96.3%) for IDH-mutant glioma. Further analysis revealed that the expression level of the IDH mutant protein in plasma EVs was significantly associated with tumor grade in IDH-mutant glioma (P < 0.0001). Moreover, the expression level of the IDH mutant protein in plasma EVs significantly decreased in post-operative patients (P < 0.01) and showed a high degree of consistency with the pathological immunohistochemical results at different tumor grades. We propose a novel plasma extracellular-vesicle liquid biopsy with potential preoperative application in detecting IDH-mutant glioma, affording noninvasive, rapid, efficient, and low-cost assessment of IDH mutation status. The online version contains supplementary material available at 10.1186/s12885-026-15810-z.