Christopher C. Young

Objective: Recurrent skull-base malignancies that circumferentially encase the internal carotid artery (ICA) in irradiated fields carry a major risk of vascular injury during repeat surgery. When balloon test occlusion (BTO) shows inadequate collateral supply, high-flow extracranial–intracranial bypass is often required to enable resection. We evaluated staged, segment-specific endoluminal ICA reinforcement with covered and open-cell stents to permit carotid-preserving re-resection. Methods: We conducted a prospective single-center study of patients with recurrent skull-base tumors previously treated with surgery and high-dose radiotherapy, scheduled for repeat resection. Patients with 360° ICA encasement and BTO failure, defined by neurological change and/or delayed venous drainage during hypotensive challenge, underwent preoperative stent reinforcement. High-resolution MRI fused with 3D-rotational angiography characterized the tumor–ICA interface and guided segment-specific deployment. Balloon-expandable covered stents reconstructed encased petrous, lacerum, and cavernous segments; open-cell or flow-diverting devices were used selectively in the clinoidal ICA. Dual antiplatelet therapy continued for 3 months before re-resection under aspirin monotherapy. Results: Gross-total, near-total, and subtotal resection was achieved in two, one, and one patient, respectively; in the subtotal case, all ICA-adjacent disease was removed, with staged management planned for residual extracranial extension. One patient (25%) developed delayed postoperative carotid occlusion from in-stent stenosis after an obligatory interruption of antiplatelet therapy, complicated by an iatrogenic arterial injury during thrombectomy; both were managed endovascularly with recanalization. No intraoperative carotid rupture or permanent stent-related neurological deficit occurred. Conclusion: In carefully selected patients with BTO failure, recurrent irradiated skull-base tumors, and circumferential ICA encasement, segment-specific endoluminal ICA reinforcement is feasible and may serve as an adjunct when carotid preservation is required and bypass carries significant anticipated morbidity. Larger series are warranted.

Background: Endovascular embolization of intracranial meningiomas has traditionally served as a preoperative adjunct but has been sporadically described as a standalone treatment. We present the largest multicenter cohort evaluating standalone embolization for intracranial meningiomas. Methods: We retrospectively analyzed 41 meningiomas in 40 patients treated with standalone embolization across four centers. Radiographic response was assessed using serial volumetric MRI over 12 months. Enhancing tumor volume (ETV) and total tumor volume (TTV) were analyzed longitudinally using mixed-effects models. An early devascularization index (EDI), derived from 24–72-hour postprocedural ETV, was tested as a predictor of subsequent tumor response. The primary clinical endpoint was the modified Rankin Scale (mRS). Results: Mean age was 62.2±13.7 years (82.5% female). Median TTV reduction was 28.6% at 1 month, 57.1% at 6 months, and 81.7% at 12 months (all p≤0.002), with a significant overall time effect (p<0.001). ETV decreased a median of 83.1% within 24–72 hours (p=0.002), consistent with early devascularization, and EDI was positively associated with greater subsequent shrinkage (pooled p=0.002). Neither baseline edema nor tumor location modified the response. mRS was stable or improved in 39 of 40 patients. Complications occurred in 4 of 41 lesions (9.8%), with only one resulting in clinical decrement in mRS from 0 to 1. No patient required subsequent surgery or radiotherapy. Conclusions: Standalone embolization was successfully used as a standalone treatment, inducing significant progressive tumor regression as early as 1 month and sustained at 12 months. Prospective studies are warranted.

Background: To systematically review published reports of standalone bland embolization for intracranial meningioma and summarize clinical, radiographic, and safety outcomes. Methods: A systematic PubMed search was performed from inception through December 2025 in accordance with PRISMA guidelines. Eligible studies included intracranial meningiomas treated with embolization as the primary therapy without planned immediate surgery or radiation. Data on patient characteristics, tumor features, embolic materials, complications, and longitudinal outcomes were extracted and synthesized descriptively. Results: Twelve studies comprising 30 patients met inclusion criteria. Patients were typically older or high-risk surgical candidates, and tumors were most commonly convexity or parasagittal with predominant external carotid artery supply. The middle meningeal artery was embolized in 27/30 cases. Particles (polyvinyl alcohol or tris-acryl gelatin microspheres) were the most commonly used embolic agents, with multiple studies also reporting liquid embolics. Quantitative volumetric follow-up was available in 18 patients and demonstrated a mean tumor volume reduction of 37% over a mean follow-up of 13 months. Durable symptomatic improvement was reported in all cases with available clinical follow-up. Treatment-related complications included two patients with transient edema, one requiring steroids. Two patients underwent delayed additional tumor-directed therapy. Conclusions: This review is limited by low-quality evidence of the existing literature. Nevertheless, the evidence suggests that standalone bland embolization appears technically feasible and may provide symptom improvement and moderate tumor control in selected intracranial meningiomas, without precluding subsequent surgery or radiation. These findings provibaseline outcome data, establish a precedent for possible pragmatic trials, and may inform the design and interpretation of future endovascular therapy studies for meningioma.

BACKGROUND: Over the past 25-years, progress in the treatment of central nervous system (CNS) tumors has been limited and outcomes for malignancies such as glioblastoma and diffuse intrinsic pontine glioma remain dismal. There has been great interest in harnessing endovascular neurointerventional techniques and to use the cerebral vasculature as a route for therapeutic delivery in neuro-oncology. Several selective intra-arterial clinical trials are currently underway targeting a range of CNS tumors with different therapeutic agents. METHODS: The Society of NeuroInterventional Surgery (SNIS) convened the inaugural Neurointerventional Oncology Summit which was held on April 26-27, 2024, at the University of Texas MD Anderson Cancer Center in Houston, Texas. The group consisted of neuro-interventionists, neurosurgeons, neuro-oncologists, neuroradiologists, basic scientists and industry representatives who are current practitioners in this emerging space. We report the current state of practice and our efforts to develop an organizational platform to treat patients suffering from CNS cancers and to advance research in this emerging field. KEY MESSAGE: Endovascular surgical neuro-oncology is an emerging clinical endeavor which aims to provide novel therapeutic options for CNS cancers. Novel therapeutic agents including yttrium-90, oncolytic viruses and cellular immunotherapy are being tested as intraarterial therapy. Technological advances in imaging modalities, selective methods of blood brain barrier opening, and devices and catheters will aid advancement of the field. Multi-disciplinary cooperation and collaboration will be integral to the success of this endeavor. ABBREVIATIONS: BBB = blood brain barrier; CAR = chimeric antigen receptor; DIPG = diffuse intrinsic pontine glioma; ESIA = endovascular selective intra-arterial; ESSIA = endovascular super-selective intra-arterial; FUS = focused ultrasound; GBM = glioblastoma; MSC-D24 = delta 24 oncolytic virus in mesenchymal stem cell; NK = natural killer; Y-90 = yttrium-90

Background The optimal duration for dual antiplatelet therapy (DAPT) after stent-assisted coiling (SAC) of intracranial aneurysms is unclear. Longer-term therapy may reduce thrombotic complications but increase the risk of bleeding complications. Methods A retrospective review of prospectively maintained data at 12 institutions was conducted on patients with unruptured intracranial aneurysms who underwent SAC between January 1, 2016 and December 31, 2020, and were followed ≥6 months postprocedure. The type and duration of DAPT, stent(s) used, outcome, length of follow-up, complication rates, and incidence of significant in-stent stenosis (ISS) were collected. Results Of 556 patients reviewed, 450 met all inclusion criteria. Nine patients treated with DAPT 42 days after SAC did not reduce the risk of thrombotic complications or in-stent stenosis, although the risk of additional hemorrhagic complications remained low. It may be reasonable to discontinue DAPT after 42 days following non-flow diverting SAC of unruptured intracranial aneurysms.

Galectin-3 (Gal-3) is an evolutionarily conserved and multifunctional protein that drives inflammation in disease. Gal-3’s role in the central nervous system has been less studied than in the immune system. However, recent studies show it exacerbates Alzheimer’s disease and is upregulated in a large variety of brain injuries, while loss of Gal-3 function can diminish symptoms of neurodegenerative diseases such as Alzheimer’s. Several novel molecular pathways for Gal-3 were recently uncovered. It is a natural ligand for TREM2 (triggering receptor expressed on myeloid cells), TLR4 (Toll-like receptor 4), and IR (insulin receptor). Gal-3 regulates a number of pathways including stimulation of bone morphogenetic protein (BMP) signaling and modulating Wnt signalling in a context-dependent manner. Gal-3 typically acts in pathology but is now known to affect subventricular zone (SVZ) neurogenesis and gliogenesis in the healthy brain. Despite its myriad interactors, Gal-3 has surprisingly specific and important functions in regulating SVZ neurogenesis in disease. Gal-1, a similar lectin often co-expressed with Gal-3, also has profound effects on brain pathology and adult neurogenesis. Remarkably, Gal-3’s carbohydrate recognition domain bears structural similarity to the SARS-CoV-2 virus spike protein necessary for cell entry. Gal-3 can be targeted pharmacologically and is a valid target for several diseases involving brain inflammation. The wealth of molecular pathways now known further suggest its modulation could be therapeutically useful.