BACKGROUND AND OBJECTIVES: Cerebral aneurysms are the major cause of spontaneous subarachnoid hemorrhage, and a common treatment is endovascular embolization. Aneurysmal recurrence after embolization is frequent, and clinical follow-up to monitor for this is critical to prevent subarachnoid hemorrhage. Herein, we assess demographic and socioeconomic factors associated with poor clinical follow-up to determine which patients are at high risk of loss to follow-up. METHODS: A retrospective analysis was performed of 937 patients who underwent endovascular treatment of cerebral aneurysms at a single center from 2006 to 2017. Attendance at follow-up visits for 5 years after treatment was correlated with various demographic and socioeconomic factors. Follow-up for patients who initially presented with unruptured vs ruptured aneurysms was also compared. RESULTS: The most significant factors associated with poor follow-up were lack of insurance and non–English-speaking status. Noninsured patients had significantly less follow-up in both mean number of follow-up visits (2.5 ± 1.7 visits for insured patients and 1.0 ± 1.2 visits for noninsured, P < .0001), and in time until lost to follow-up (2.9 ± 1.9 years for insured and 1.1 ± 1.4 years for non-insured, P < .0001). Non–English-speaking patients had less follow-up visits (2.3 ± 1.7 visits for English-speaking and 0.74 ± 1.0 visits for non–English-speaking, P < .0001) and were more quickly lost to follow-up (2.6 ± 1.9 years for English-speaking and 0.82 ± 1.2 years for non–English-speaking, P < .0001). CONCLUSION: Demographics and socioeconomic factors, particularly lack of insurance and non–English-speaking status, are correlated with poor clinical follow-up after endovascular treatment of cerebral aneurysms. Patients at high risk of loss to follow-up should be counseled before treatment about risk of aneurysm recurrence.

The Middle Meningeal Artery (MMA) occupies a pivotal role in the pathophysiology of migraine, functioning as a vascular and neuroimmune interface that precipitates the characteristic pulsatile pain. The inhibition of this pathophysiological cascade has been investigated as a therapeutic strategy. However, fewer than a dozen centers globally have disseminated procedural or mechanistic data. Given the nascency of this field and the imperative for standardization, the present review synthesizes mechanistic and clinical evidence underpinning intra-arterial pharmacological modulation of the MMA for migraine management. Methods: A focused narrative review was undertaken, drawing upon select but influential studies from pioneering research groups investigating intra-arterial interventions targeting the MMA. The extant literature was thematically categorized and organized according to the loci of cascade interruption and their corresponding clinical outcomes. Results: Since 2009, intra-arterial therapies for severe headache syndromes have evolved, initially utilizing nimodipine for vasospasm-related headaches, progressing to verapamil for reversible cerebral vasoconstriction, and more recently, lidocaine for refractory or status migrainosus, occasionally in conjunction with MMA embolization. Contemporary research uses language that conceptualizes migraine as an immunologically mediated neurovascular disorder, as opposed to a purely vascular or neuronal entity. Recent investigations have identified interleukins such as Interleukin-1β, Tumor Necrosis Factor-α, and Interleukin-6 as critical amplifiers of trigeminovascular activation. Purinergic signaling through the P2X3 receptor and the P2Y13 receptor, in conjunction with pituitary adenylate cyclase-activating polypeptide and vasoactive intestinal peptide pathways, has been implicated in the modulation of MMA excitability and neuropeptide release. The development of novel calcitonin gene-related peptide receptor antagonists, such as zavegepant, further substantiates the artery’s significance as a pharmacological target. Conclusions: These findings support a shift toward immune-modulating intra-arterial therapeutic strategies, with migraine interventions targeting cytokine and neuroimmune signaling within the MMA, rather than relying exclusively on vasodilatory mechanisms.

Background: The middle meningeal artery (MMA) plays a central role in migraine pathophysiology as a vascular and neuroimmune interface driving the throbbing pain. Inhibition of this cascade has been explored as a therapeutic approach, yet fewer than a dozen centers worldwide have published procedural or mechanistic data. Given the nascency of this field and the need for standardization, this review synthesizes the mechanistic and clinical evidence supporting intra-arterial pharmacologic modulation of the MMA for migraine treatment. Methods: A focused narrative review was conducted using limited but high-impact studies from pioneering groups exploring intra-arterial approaches to the MMA. Literature was arranged thematically and organized by the sites of cascade interruption and associated outcomes. Results: Since 2009, the use of intra-arterial therapies for severe headache syndromes has evolved from nimodipine for vasospasm-related headaches to verapamil for reversible cerebral vasoconstriction and, more recently, lidocaine for refractory or status migrainosus cases, sometimes with MMA embolization. Current research reframes migraines as an immunologically mediated neurovascular process, rather than purely a vascular or neuronal phenomenon. Recent studies have identified interleukins such as IL-1β, TNF-α, and IL-6 as key amplifiers of trigeminovascular activation, while emerging evidence implicates purinergic (P2X3, P2Y13) and PACAP/VIP pathways in modulating MMA excitability and neuropeptide release. Novel CGRP receptor antagonists, including zavegepant further reinforce the artery’s role as a therapeutic target. Conclusion: Our findings highlight a transition toward immune-modulating intra-arterial strategies, suggesting that future migraine therapies may increasingly focus on cytokine and neuroimmune signaling within the MMA rather than traditional vasodilatory control.

2. Background: The AXS Vecta 46 intermediate catheter (Stryker) provides a large enough inner diameter to achieve effective aspiration with a small enough outer diameter and soft distal-tip flexibility to track safely through more tortuous and smaller arterial segments to non-traumatically target medium vessel occlusions. The efficacy of the Vecta 46 in the spectrum of large and medium vessel occlusions has not been well elucidated in the literature. Methods: This retrospective cohort study included patients who underwent MT for acute ischemic stroke at the University of Florida between July 2022 and June 2024. The outcomes of patients treated with the Vecta 46 was compared to that of all other catheters used at the institution. Results: The distribution of aspiration and stent retriever attempts in Vecta 46 procedures versus non-Vecta 46 procedures was significantly different (p = 0.00325). Aspiration was attempted 1.66 ± 0.936 times in the Vecta 46 group and 1.12 ± 0.650 times in the non-Vecta 46 group (p = 0.00135). More mechanical thrombectomies with the Vecta 46 included aspiration of a secondary thrombus (p = 0.0314), despite no difference in distribution of primary or secondary occlusion location. There were no statistically significant differences in recanalization success (p = 0.800), recanalization time (p = 0.245), procedure duration (p = 0.580), discharge modified Rankin Score (p = 0.875), or intracranial hemorrhage rate (p = 0.720) between non-Vecta 46 and Vecta 46 procedures. Conclusions: Vecta 46 has similar safety and functional outcomes compared to other endovascular treatment options despite procedural differences.

Objective: Giant thrombosed intracranial aneurysms (GTIAs) are aneurysmal dilatations containing partial or complete intraluminal thrombus. Representing approximately 2–5% of intracranial aneurysms, GTIAs present diagnostic and therapeutic challenges. Optimal management remains controversial and may involve microsurgical, endovascular, or hybrid strategies. Methods: A systematic review was performed in accordance with PRISMA guidelines using PubMed and Embase to identify relevant studies published between January 2000 and August 2025. Eligible studies reported clinical, anatomical, or treatment-related data for patients with GTIAs. Extracted variables included patient demographics, aneurysm characteristics, treatment modality, and outcomes. Data were standardized and analyzed using Python. Complication and recurrence rates were pooled in subsets of studies reporting explicit event counts; comparisons between treatment modalities were assessed using chi-square analysis. Results: In total, 101 studies including 536 patients met our criteria. Mean patient age was 50.2 years. Most aneurysms arose from the anterior circulation (88.2%) involving the internal carotid artery (46.6%) and middle cerebral artery (39.9%). The unweighted mean aneurysm diameter was 39.0 mm, with a patient-weighted mean of 24.3 mm. Hybrid treatment strategies were most frequently reported (62.7%), followed by endovascular (23.3%) and microsurgical (14.0%) approaches. Among studies reporting explicit counts, the pooled complication rate was 17.0% and the recurrence rate was 21.0%. Complication rates did not differ significantly between treatment modalities (p = 0.48), whereas recurrence differed significantly (p = 0.00013). Conclusions: Management of GTIAs remains heterogeneous, with increasing reliance on multimodal and hybrid treatment strategies. However, inconsistent outcome reporting and the predominance of retrospective studies limit definitive comparisons between treatment modalities.