Neurology International

Background: Early residual or recurrent aneurysm filling remains an important limitation after endovascular treatment of intracranial aneurysms, particularly in large and complex lesions. This study descriptively evaluated 6-month early residual or recurrent filling after coil embolization, stent-assisted coiling, flow-diverting stents, and the Woven EndoBridge (WEB) device in a single-center cohort. Methods: We retrospectively analyzed 151 patients with 161 intracranial aneurysms treated between January 2019 and July 2023. Follow-up imaging at approximately 6 months was performed using computed tomography angiography or magnetic resonance angiography, with digital subtraction angiography when residual filling was suspected. Aneurysm occlusion was evaluated using the Raymond–Roy Occlusion Classification. Clinical, morphological, anatomical, and treatment-related variables associated with early residual or recurrent aneurysm filling were analyzed. Results: Complete occlusion was achieved in 149 aneurysms (92.5%), whereas early residual or recurrent filling occurred in 12 aneurysms (7.5%). Residual or recurrent filling was observed in 4/35 aneurysms treated with coil embolization (11.4%), 1/58 treated with flow-diverting stents (1.7%), 7/60 treated with the WEB device (11.7%), and none of the 8 aneurysms treated with stent-assisted coiling; overall rates did not differ significantly among treatment modalities (p = 0.104). Aneurysm height > 10 mm was significantly associated with early residual or recurrent filling (p = 0.005), and mean aneurysm height was greater in aneurysms with residual or recurrent filling than in completely occluded aneurysms (p = 0.048). In the ICA subgroup, residual or recurrent filling was more frequent after WEB treatment than after other endovascular modalities (p = 0.019). This subgroup signal was based on sparse observations. Conclusions: Aneurysm height > 10 mm was significantly associated with early residual or recurrent aneurysm filling. No statistically significant difference in early residual or recurrent filling was detected among treatment groups. Given the retrospective design, non-random treatment allocation, heterogeneous aneurysm phenotypes, and non-uniform imaging follow-up, these data should be interpreted as a descriptive institutional experience rather than evidence of comparative superiority or equivalence. The ICA subgroup finding is preliminary and hypothesis-generating.

Background/Objectives: Vertebral artery hypoplasia is a common congenital anatomical variant of the vertebral arteries, traditionally considered a benign finding. However, accumulating evidence suggests that VAH may influence vertebrobasilar hemodynamics and contribute to susceptibility to posterior circulation disorders. This systematic review aimed to synthesize current evidence regarding the epidemiology, hemodynamic significance, neurological manifestations, and cerebrovascular outcomes associated with VAH. Methods: This systematic review was conducted according to the PRISMA 2020 guidelines and registered in PROSPERO (CRD420261442242). A systematic search of PubMed/MEDLINE was performed from database inception to 8 June 2026, supplemented by manual reference screening and targeted searches. Studies evaluating VAH diagnosed using vascular imaging or anatomical assessment, including CTA, MRA, Doppler ultrasonography, and DSA, were eligible. Methodological quality was assessed using Joanna Briggs Institute critical appraisal tools, and the level of evidence was classified according to the Oxford Centre for Evidence-Based Medicine framework. Results: Forty-six studies were included in the qualitative synthesis. VAH prevalence varied substantially according to imaging modality, diagnostic criteria, and study population, ranging from approximately 3% to nearly 50%. Across clinical cohorts, VAH was frequently associated with posterior circulation ischemic stroke, transient ischemic attack, and vertebrobasilar insufficiency. Hemodynamic studies demonstrated reduced vertebral artery flow, increased vascular resistance, impaired cerebrovascular reactivity, and altered collateral flow redistribution. VAH was also associated with vestibular disorders, non-stroke neurological syndromes, vertebral artery dissection, and other cerebrovascular anatomical variations. Unlike previous reviews focusing primarily on prevalence or stroke associations, this review integrates epidemiological, anatomical, hemodynamic, computational, and neurological evidence within a unified clinically oriented framework and proposes an evidence-informed conceptual model of VAH as a context-dependent low-flow vascular susceptibility phenotype. Conclusions: Current evidence indicates that VAH represents a clinically relevant vascular susceptibility phenotype rather than merely an incidental anatomical variant. Its clinical significance appears to depend on the interaction between reduced vertebral artery flows, collateral capacity, vascular remodeling, and acquired cerebrovascular risk factors. Standardized diagnostic criteria and prospective multimodal studies are required to define its role in future cerebrovascular risk assessment.

Background: Systemic inflammation contributes to the pathobiology of multiple sclerosis (MS), yet serum biomarker data from Middle Eastern populations remain limited. This study evaluated serum levels of IL-6, IL-16, IL-18, and IL-36 in Saudi adults with MS compared with matched healthy controls and examined associations with disease duration, phenotype, treatment, and disability. Methods: This single-center, cross-sectional, matched case–control study enrolled 26 MS patients and 26 age- and sex-matched controls. Serum cytokines were measured by ELISA. Disability was assessed using EDSS and the Timed 25-Foot Walk (T25FW). Matched comparisons used Wilcoxon signed-rank tests; subgroup comparisons used Wilcoxon rank-sum or Kruskal–Wallis tests; associations used Spearman’s correlation. Results: No correction for multiple comparisons was applied given the exploratory design. All four interleukins were higher in MS patients than in controls (p < 0.001). Age correlated with EDSS (r = 0.573, p = 0.002) and T25FW (r = 0.464, p = 0.014). Only IL-6 showed a notable correlation with disability, with T25FW (r = 0.53, p = 0.008) and, weaker, EDSS (r = 0.38, p = 0.052); IL-18 showed a weak, non-significant correlation with T25FW (r = 0.35, p = 0.126); IL-16 and IL-36 showed no relevant associations. IL-16 was higher in newly diagnosed than in long-standing cases (p = 0.012); no differences by phenotype or treatment were observed for any marker. Conclusions: Serum IL-6, IL-16, IL-18, and IL-36 were elevated in Saudi MS patients versus controls. IL-6 alone showed a modest, unadjusted association with disability, supporting its evaluation as a candidate biomarker in larger, longitudinal, covariate-adjusted cohorts. These findings are hypothesis-generating and should not be interpreted as evidence of independent or clinically actionable biomarker utility.