Intracranial aneurysms often remain asymptomatic until rupture, causing aneurysmal subarachnoid hemorrhage (aSAH). aSAH frequently leads to cerebral vasospasm (CVS) and delayed cerebral ischemia (DCI), significantly increasing the risk of severe neurological deficits and mortality. Identifying reliable biomarkers, such as lipid peroxidation metabolites (LPMs), is crucial for early prediction and timely intervention. This study summarizes current knowledge on LPMs as potential biomarkers for CVS and DCI after aSAH. A systematic review was conducted following PRISMA guidelines. Two independent authors searched PubMed, Web of Science, and Scopus for articles studying the association between non-enzymatic and enzymatic lipid metabolites and CVS or DCI after aSAH. Quality and risk of bias were evaluated using the Newcastle-Ottawa Scale. Extracted data included metabolite concentrations, biological sample types, timing of collection, patient demographics, clinical severity of aSAH, Fisher’s grade, DCI definition, and relationship to DCI. Of 519 records screened, 17 studies were included. Lipid metabolites were measured in blood (5 studies), cerebrospinal fluid (11 studies), and urine (2 studies). F2-isoprostanes (F2-IsoPs), studied in 7 articles, were linked to increased DCI risk, with elevated levels observed within three days post-aSAH. Isofurans (IsoFs) predicted DCI risk between days 5 and 8 post-aSAH, while elevated cholesteryl ester hydroperoxide (CEOOH) levels on day 2 linked to symptomatic vasospasm. Enzymatic arachidonic acid (AA) metabolites, including 6-keto-prostaglandin F1-α, prostaglandin D2, and leukotriene C4, were also associated with early DCI risk. To the best of our knowledge, this review is the first to comprehensively assess all LPMs in relation to CVS and DCI. Elevated concentrations of F2-IsoPs and enzymatic AA derivatives may serve as biomarkers for DCI prediction in aSAH. These findings highlight the need to explore the potential of LPMs, paving the way for risk stratification and timely interventions to improve patient outcomes and aid researchers in developing predictive scoring systems for DCI. Clinical trial number Not applicable.

Functional magnetic resonance imaging (fMRI) is a valuable tool for presurgical brain mapping, traditionally implemented with task-based paradigms (tb-fMRI) that measure blood oxygenation level-dependent (BOLD) signal changes during controlled motor or cognitive tasks. Tb-fMRI is a well-established tool for non-invasive localization of cortical eloquent areas, yet its dependence on patient cooperation and intact cognition limits use in individuals with aphasia, cognitive impairment, or in pediatric and other vulnerable populations. Resting-state fMRI (rs-fMRI) provides a task-free alternative by leveraging spontaneous low-frequency BOLD fluctuations to delineate intrinsic functional networks, including motor and language systems that show good spatial concordance with tb-fMRI and with direct cortical stimulation. This narrative review outlines the methodological foundations of tb-fMRI and rs-fMRI, comparing acquisition protocols, preprocessing and denoising pipelines, analytic approaches, and validation strategies relevant to presurgical planning. Particular emphasis is given to the technical and physiological foundations of BOLD imaging, statistical modeling, and the influence of motion, noise, and standardization on data reliability. Emerging evidence indicates that rs-fMRI can reliably expand mapping to patients with limited task compliance and may serve as a robust complementary modality in complex clinical contexts, though its methodological heterogeneity and absence of unified practice guidelines currently constrain widespread adoption. Future advances in harmonized preprocessing, multicenter validation, and integration with connectomics and machine learning frameworks are likely to be critical for translating rs-fMRI into routine, reliable presurgical workflows.

Cerebral vasospasm (CVS) is a severe complication associated with significant morbidity and in-hospital mortality. While well characterized in aSAH, its occurrence following AVM-related hemorrhage remains less understood. To address this gap, a meta-analysis adhering to PRISMA guidelines was conducted, with two independent authors searching PubMed, Scopus, and Web of Science from inception to July 2024, seeking studies on CVS risk factors following AVM-related hemorrhage. Study quality was assessed using the Newcastle-Ottawa Scale (NOS). Dichotomous variables were pooled into an overriding odds ratio (OR) with a 95% confidence interval (CI), while continuous variables were analyzed using the mean difference (MD) with a 95% CI, both using a random-effects model. Out of 2360 screened articles, 4 studies met the inclusion criteria, totaling 7483 AVM-related hemorrhage patients, 958 of whom developed CVS. All studies were rated high quality, according to NOS. A total of 10 extractable demographic, behavioral, clinical, and radiographic variables reported in the literature were assessed. The following CVS risk factors were statistically significant: younger age (MD = -4.99; 95% CI [-9.40 to -0.57]; p = 0.03), female sex (OR = 1.72; 95% CI [1.50–1.98]; p < 0.00001), and intraventricular hemorrhage (OR = 1.24; 95% CI [1.04–1.48]; p = 0.02). Subarachnoid hemorrhage was close to significance (OR = 1.17; 95% CI [1.00–1.36]; p = 0.05). This is the first systematic review and meta-analysis to identify risk factors for CVS in the context of AVM-related hemorrhage. The presented findings may aid clinicians in recognizing high-risk individuals. Further research is warranted to develop a reliable risk scoring system that can predict AVM-associated CVS in clinical settings and to further explore the differences between CVS following aSAH and AVM-related hemorrhage.

Delayed cerebral ischemia (DCI) is a major complication of aneurysmal subarachnoid hemorrhage (aSAH), strongly associated with neurological deterioration and poor outcomes. Its pathophysiology remains incompletely understood and involves multiple interacting processes. Increasing evidence highlights the role of redox imbalance triggered by hemoglobin breakdown and the subsequent generation of reactive species, leading to vascular dysfunction, impaired nitric oxide signaling, and inflammatory activation This review aims to summarize current knowledge on redox-related mechanisms involved in DCI and to explore the potential role of the peroxiredoxin (PRDX) family in this setting. A narrative review of experimental and preclinical studies was performed, focusing on molecular pathways associated with vascular regulation, cellular injury, and antioxidant defense. Particular attention was given to the distribution and biological functions of PRDX isoforms within the central nervous system. This work addresses a topic not previously systematically discussed, the potential involvement of PRDX proteins in aSAH-related complications. By integrating available data, it provides a conceptual framework linking PRDX to mechanisms relevant for DCI. The manuscript serves as a starting point for future research, particularly translational and clinical studies in humans, which are necessary to verify the relevance of these findings and to better understand their potential clinical implications.