Search Results (346)

Background: Arterial ischemic stroke (AIS) is not common in pediatric patients; however, it causes significant morbidity and mortality. Reperfusion therapies, including intravenous thrombolysis (IVT) and endovascular mechanical thrombectomy (EVT) are established standards of care in selected adults with acute ischemic stroke; however, their safety and functional outcomes in the pediatric population remain poorly defined. Objective: To assess the safety and functional outcomes of reperfusion therapies in children with AIS. Methods: A systematic search was conducted across major databases including PubMed, Medline, Scopus, Embase, Web of Science, and Cochrane Library. Studies reporting on pediatric patients aged 18 years or less treated with IVT, EVT, or both for acute AIS were included. The primary safety outcome was the risk of developing symptomatic intracerebral hemorrhage (sICH). Primary functional outcomes were 90-day functional independence, measured via the Pediatric Modified Rankin Scale (Ped-mRS ≤ 2) or Pediatric Stroke Outcome Measure (PSOM ≤ 1). Secondary outcomes measured included successful recanalization (Modified Thrombolysis in Cerebral Ischemia [mTICI] grade 2b/3), and death due to any cause at 90 days. Results: Successful angiographic recanalization evaluated across thrombectomy and bridging arm cohorts revealed high success rate with the pooled proportion of 87.4% (95% CI: 79.1–93.9%). Reperfusion therapies are associated with significant early neurological recovery and favorable 90-day functional outcomes (Ped-mRS 0–2 achieved in a substantial majority of treated cohorts), when compared to the best medical treatment (BMT) controls. The overall rate of sICH remains low (<2%), demonstrating a much better safety profile comparable to adult benchmarks. Conclusions: Acute reperfusion therapies in pediatric AIS are associated with high rates of recanalization and favorable functional outcomes and had low observed rates of symptomatic intracranial hemorrhage in selected pediatric observational cohorts. However, given the absence of randomized controlled trials, these findings reflect observational associations and must be interpreted with appropriate clinical caution. Therefore, there is need for further prospective international studies capable of generating higher-quality evidence to guide future pediatric stroke management. Full article

Endovascular thrombectomy [EVT] has revolutionized acute ischemic stroke care by restoring macrovascular reperfusion in large vessel occlusion; however, a persistent “reperfusion–outcome gap” remains, leaving nearly half of successfully recanalized patients without functional independence. This review aims to bridge this translational gap by establishing a mechanistic and procedural framework for adjunctive pharmacotherapy designed to target the microvascular, thromboinflammatory, and reperfusion-related injuries left unaddressed by purely mechanical models. Synthesis of recent literature reveals that futile recanalization is driven by three distinct anatomical and biological bottlenecks: distal microembolization, microcirculatory no-reflow, and ischemia–reperfusion injury. Furthermore, the inconsistency of clinical trial results reflects a critical precision deficit, including dilution of treatment effects across heterogeneous reperfusion grades, inadequate stroke etiology stratification, delayed pharmacologic intervention relative to evolving microvascular injury, and reliance on functional endpoints that inadequately capture tissue-level reperfusion. To address these limitations, this review outlines a tri-axial clinical decision framework integrating reperfusion status, stroke etiology and hemorrhagic risk, which maps specific patient phenotypes, such as incomplete macrovascular reperfusion or underlying intracranial atherosclerotic disease, to targeted pharmacologic strategies including microcatheter-directed intra-arterial thrombolytics and glycoprotein IIb/IIIa inhibitors. The review further argues that future progress will require imaging-guided identification of residual hypoperfusion, mechanistically enriched patient enrolment, and incorporation of biological and tissue-level reperfusion endpoints alongside conventional functional outcomes. Ultimately, closing the reperfusion–outcome gap will require moving beyond empirical, universal drug administration toward a precision, pharmacologically augmented EVT paradigm that aligns adjunctive therapy with mechanism-specific procedural phenotypes and prioritizes true tissue-level recovery over angiographic success alone. Full article

Background/Objective: The management of acute ischemic stroke (AIS) has evolved from rigid time-based treatment paradigms toward tissue-based selection guided by advanced neuroimaging, thereby expanding eligibility for reperfusion therapies. To provide an updated narrative review of acute ischemic stroke (AIS) classification and management, with emphasis on extended therapeutic windows for intravenous thrombolysis (IVT) and endovascular therapy (EVT), bridging strategies, posterior circulation stroke, and implementation challenges in Latin America and other resource-constrained settings. Methods: A structured narrative review was conducted using the PubMed/MEDLINE, Embase, Scopus, and LILACS databases, covering the period from 2013 to 2025. Results: Sixty-three studies were selected from 412 records and categorized into etiologic classification, extended-window thrombolysis, EVT and bridging therapy, and posterior circulation stroke. Current evidence supports imaging-guided IVT beyond 4.5 h and EVT up to 24 h in selected patients with salvageable brain tissue, including some individuals with large infarct cores. Recent trials also support EVT for basilar artery occlusion. Tenecteplase offers practical workflow advantages in many centers, particularly where transfer delays and limited access to advanced imaging constrain timely reperfusion decisions. Conclusions: Contemporary AIS management is increasingly guided by pathophysiology and imaging rather than strict time thresholds. However, improving outcomes in middle- and low-income settings requires the implementation of adapted clinical algorithms, strengthening of stroke care networks, and optimization of referral pathways. Full article

Background: Flow diverters (FDs) are widely used to treat intracranial aneurysms. Although effective, FD-related thrombosis or progressive stenosis may lead to acute or delayed cerebral hypoperfusion with significant neurological morbidity. Management options are limited when medical or endovascular rescue strategies fail. This study aims to evaluate the role of extracranial–intracranial bypass (EC-IC bypass) as a rescue strategy across the spectrum of FD-related cerebral hypoperfusion. Methods: We retrospectively reviewed all patients who underwent EC-IC bypass for FD-related cerebral hypoperfusion over a 10-year period in our institution. Both acute and chronic presentations were included. Clinical status was assessed using the modified Rankin Scale (mRS). Imaging evaluation included digital subtraction angiography (DSA), computed tomography angiography (CTA), magnetic resonance angiography (MRA) and quantitative magnetic resonance imaging for bypass flow assessment. Surgical technique, antiplatelet therapy, timing of intervention and clinical outcomes were analysed. Results: Five patients with FD-related cerebral hypoperfusion who underwent superficial temporal artery–middle cerebral artery bypass (STA-MCA bypass) were identified. Two distinct patterns emerged. Three patients developed early hypoperfusion within the first month of FD placement, presenting with acute neurological deficits and treated by emergent or urgent bypass under dual antiplatelet therapy. Two patients developed late hypoperfusion years after the procedure, presenting with progressive haemodynamic symptoms and treated by elective flow-augmentation bypass under aspirin monotherapy. At discharge, only one patient had an mRS ≥ 3. At one-year follow-up, a favourable outcome (mRS ≤ 2) was observed in all patients with available data. Follow-up data were missing for one patient. Conclusions: EC-IC bypass represents a feasible rescue strategy for FD-related cerebral hypoperfusion when medical or endovascular treatments fail. In our experience, though limited, STA-MCA bypass can provide sufficient cerebral reperfusion, even in urgent settings and under dual antiplatelet therapy, leading to favourable neurological outcomes. Full article

Pregnancy-related acute kidney injury (PR-AKI) increases the risk of chronic kidney disease (CKD) in the postpartum period, yet mechanisms driving this transition remain unclear. Uremic toxins, including indoxyl sulfate (IS), are implicated in AKI-to-CKD progression. Using a rat model of PR-AKI induced by ischemia–reperfusion on gestational day (GD) 18, we assessed IS contributions to renal injury in the postpartum. A subset of rats received the oral adsorbent AST-120 in the postpartum period to reduce IS. Additional groups received IS during pregnancy with or without AST-120 treatment in the postpartum period. Renal function, blood pressure, circulating and urinary IS concentrations, and renal histopathology were evaluated. PR-AKI resulted in sustained postpartum elevations in circulating (p = 0.03) and urinary (p < 0.03) IS, reduced urine output (p = 0.03), increased proteinuria (p < 0.0001), increased serum albumin, and increased renal fibrosis (p = 0.008) compared to normal pregnant control rats. Absorption of indole, a precursor for IS, significantly reduced urinary IS (p = 0.03), reduced serum creatinine (p = 0.006), and attenuated renal fibrosis (p = 0.002) in treated PR-AKI rats. While not significant, indole absorption improved urine output (p = 0.06) and reduced proteinuria (p = 0.07) in treated PR-AKI rats. IS administration during pregnancy recapitulated key features of postpartum CKD. Elevated IS contributes to persistent renal injury following PR-AKI. Postpartum reduction in IS with AST-120 dampens the progression of renal injury. These findings highlight uremic toxins as mechanistic drivers and potential therapeutic targets in post partum CKD following PR-AKI. Full article

Management of acute coronary syndromes (ACS) in the cardiac intensive care unit (CICU) requires rapid diagnosis, timely reperfusion or invasive assessment, appropriate antithrombotic therapy, and early recognition of haemodynamic, electrical, and mechanical complications. This narrative review examines contemporary evidence across ST-segment elevation and non-ST-segment elevation presentations, with emphasis on decisions during hospitalisation and early secondary prevention. High-sensitivity cardiac troponin algorithms support accelerated assessment of suspected non-ST-segment elevation ACS, whereas next-generation assays require further implementation validation. Twelve-month dual antiplatelet therapy remains the default after ACS in patients without high bleeding risk; abbreviated regimens, de-escalation, cangrelor, and combined antiplatelet–anticoagulant treatment are selective strategies. Contemporary care also includes risk-based invasive timing, complete revascularisation in suitable haemodynamically stable patients, culprit-lesion-only initial PCI in cardiogenic shock, and individualised management of frailty and renal impairment. High-intensity statin therapy, with early ezetimibe when needed, is guideline-supported. Early PCSK9 inhibition and low-dose colchicine are selective strategies, whereas SGLT2 inhibitors and GLP-1RAs are established for specific comorbid indications. hs-cTnT Gen 6 and AI-assisted tools remain evidence-evolving, while multiomics and targeted anti-inflammatory therapies remain investigational. Clear separation of guideline-supported, selective, evidence-evolving, and investigational approaches is essential for clinically appropriate ACS care. Full article

Background/Objectives: Myocardial ischemia/reperfusion (I/R) injury remains a critical challenge in cardiovascular disease management. Although Chinese yam polysaccharides (CYPs), the primary bioactive macromolecules isolated from Dioscorea opposita Thunb, exhibit well-documented antioxidant and anti-inflammatory properties, their cardioprotective efficacy against acute I/R injury and the underlying multiscale mechanisms remain unexplored. This study investigated the protective effects of CYPs using an in vivo mouse model of myocardial I/R injury. Methods: An in vivo mouse model of myocardial I/R injury was used to evaluate the effects of 7-day prophylactic CYPs treatment (400 mg/kg). Echocardiographic and histological analyses were performed, and serum myocardial injury biomarkers, oxidative stress indicators, pro-inflammatory cytokines, mitochondrial ultrastructure, ATP bioenergetics, mitochondrial respiratory chain gene expression, and gut microbiota composition were assessed. Results: Echocardiographic and histological analyses revealed that CYPs pretreatment significantly ameliorated cardiac dysfunction, as indicated by increased LVEF from 28.98% to 57.68% and reduced myocardial infarct size by 36.73% compared with the I/R group and decreased serum myocardial injury biomarkers, including CK-MB, LDH, and LDH-1. Mechanistically, CYPs exerted robust cardioprotection by mitigating oxidative damage, with MDA levels reduced by 28.83% and SOD activity increased to 1.76-fold that of the I/R group, and suppressing the release of pro-inflammatory cytokines, including Tnf-α, Il-6, and Il-1β. Crucially, CYPs intervention preserved mitochondrial ultrastructure and ATP bioenergetics, and levels increased to 1.51-fold that of the I/R group and upregulated the expression of essential mitochondrial respiratory chain genes, including mt-Nd1, mt-Nd4l, mt-Cyb, mt-CoII, and mt-Atp6. Furthermore, 16S rRNA sequencing showed that CYPs treatment reshaped gut microbiota and elevated the relative abundance of anti-inflammatory and antioxidant beneficial genus Akkermansia. Conclusions: Collectively, these findings provide novel evidence that CYPs confer profound protection against myocardial I/R injury through a multitargeted network involving the restoration of mitochondrial homeostasis, attenuation of oxidative inflammation, and modulation of the gut microbiome, highlighting CYPs as a promising functional food-derived candidate for adjunctive therapy in ischemic heart disease. Full article

Background/Objectives: Acute coronary syndrome (ACS) remains one of the leading causes of cardiovascular mortality worldwide. Rapid diagnosis and timely initiation of reperfusion therapy are crucial for improving patient outcomes. The aim of this narrative review was to summarize current evidence on prehospital 12-lead ECG teletransmission in the diagnosis and management of ACS and to evaluate its impact on systems of care and clinical outcomes. Methods: A narrative literature review was conducted using the PubMed database. The literature search was completed on 15 May 2026 and included publications from 1998 onwards. The review included studies evaluating prehospital ECG teletransmission, ST elevation myocardial infarction (STEMI) networks, interpretation models, treatment delays, and organizational and logistics aspects of ECG teletransmission systems. Current guidelines from the European Society of Cardiology and the 2025 ACC/AHA/ACEP/NAEMSP/SCAI guidelines were also included. Results: Available evidence indicates that prehospital ECG teletransmission enables earlier STEMI diagnosis, direct referral to primary coronary intervention (PCI)-capable centers, and earlier activation of catheterization laboratories. Multiple observational studies and meta-analyses have demonstrated reductions in first medical contact-to-device and door-to-device times associated with teletransmission systems. Limitations include interpretation variability, false-positive catheterization laboratory activations, and infrastructure-related barriers. Conclusions: ECG teletransmission is an essential component of contemporary regional STEMI care systems and contributes to improved organization of care and shorter reperfusion delays. Further development and prospective validation of artificial intelligence-assisted ECG interpretation and integrated telemedicine systems may enhance diagnostic accuracy and the effectiveness of prehospital cardiac care. Full article

Background: Intermediate-risk acute pulmonary embolism (PE) is clinically heterogeneous, and early deterioration may occur despite initial normotension. The Endothelial Activation and Stress Index (EASIX) is a readily available laboratory index reflecting endothelial activation, cellular injury, renal-perfusion stress, and platelet-related thromboinflammatory burden. We investigated whether admission EASIX and echocardiographic right ventricular-pulmonary arterial (RV-PA) coupling assessed by the TAPSE/PASP ratio identify intermediate-risk PE patients at increased risk for an early adverse clinical outcome (EACO). Methods: This retrospective cohort study included 900 consecutive intermediate-risk acute PE patients admitted between 1 January 2020 and 10 June 2025. EASIX was calculated as LDH (U/L) × creatinine (mg/dL)/platelet count (10⁹/L). The primary endpoint was EACO within the first seven days after PE diagnosis during the index hospitalization, including hemodynamic decompensation, vasopressor/inotrope requirement, intensive care unit transfer, rescue reperfusion therapy, ventilatory support, cardiac arrest, or PE-related death. Hierarchical logistic regression, ROC analysis, calibration assessment, bootstrap internal validation, and 10-fold cross-validation were performed. Results: EACO occurred in 110 patients (12.2%). Patients with EACO had higher EASIX (2.28 [1.52–3.27] vs. 1.27 [0.86–2.00], p < 0.001) and lower TAPSE/PASP ratio (0.29 [0.23–0.36] vs. 0.42 [0.33–0.57], p < 0.001). log2-EASIX correlated inversely with TAPSE/PASP (Spearman rho = −0.30, p < 0.001). In the final combined model, log2-EASIX (OR 1.55 per doubling, 95% CI 1.14–2.10, p = 0.005) and TAPSE/PASP per 0.1-unit decrease (OR 1.36, 95% CI 1.10–1.68, p = 0.004) remained independently associated with EACO after adjustment for clinical variables, troponin, lactate, D-dimer, and C-reactive protein-to-albumin ratio. The final model showed higher discrimination than the clinical-laboratory model, although the absolute AUC increment was modest (AUC 0.920 vs. 0.904). Bootstrap optimism-corrected AUC was 0.910 and 10-fold cross-validated AUC was 0.904. Conclusions: Admission EASIX and impaired RV-PA coupling may provide complementary prognostic information for early risk stratification in intermediate-risk acute PE. Because this was a retrospective single-center study without external validation, these findings should be considered hypothesis-generating and should not be used as definitive treatment-escalation triggers before independent external validation. Full article

Background: Intermediate-high and high-risk pulmonary embolism (PE) are associated with substantial mortality despite anticoagulation. While reperfusion therapies may improve outcomes, real-world evidence comparing treatment strategies and identifying predictors of mid-term mortality remains limited. We aimed to evaluate predictors of 90-day mortality and the impact of reperfusion therapy in patients with intermediate-high and high-risk PE managed within a multidisciplinary Pulmonary Embolism Response Team (PERT). Methods: This retrospective cohort study included 114 consecutive patients with intermediate-high or high-risk acute PE admitted to a tertiary referral center between October 2023 and December 2024. Risk stratification was performed according to ESC guidelines, and simplified Pulmonary Embolism Severity Index (sPESI) scores were calculated. Treatment strategies included anticoagulation alone or reperfusion therapy (systemic thrombolysis or catheter-directed therapy). The primary endpoint was all-cause 90-day mortality. Multivariate logistic regression was performed to identify independent predictors of mortality. Results: The mean age was 68 ± 16 years, and 88% had at least one comorbidity. Reperfusion therapy was administered to 27% of patients. Mortality rates were 1% at 24 h, 6% at 7 days, 17% at 30 days, and 25% at 90 days. In multivariate analysis, hemoglobin ≤ 11.7 g/dL (OR 5.06, 95% CI 1.58–16.17, p = 0.006), sPESI > 2 (OR 4.86, 95% CI 1.49–15.84, p = 0.009), prior stroke (OR 11.59, 95% CI 2.08–64.51, p = 0.005), and high 30-day mortality risk classification (OR 14.14, 95% CI 1.19–167.89, p = 0.036) were independent predictors of mortality. Reperfusion therapy was independently associated with a significant reduction in 90-day mortality (OR 0.05, 95% CI 0.003–0.65, p = 0.022). The regression model demonstrated good explanatory power (Nagelkerke R² = 0.487). Conclusions: In this real-world cohort of intermediate-high and high-risk PE, reperfusion therapy was independently associated with lower 90-day mortality and low bleeding risk. In addition to established predictors, sPESI retained strong prognostic value beyond its traditional 30-day timeframe. These findings support risk-adapted reperfusion strategies guided by multidisciplinary teams and reinforce the role of integrated clinical risk assessment in optimizing outcomes. Full article

Ischemia–reperfusion injury (IRI) of the kidney represents a serious medical issue with complex pathological mechanisms that remain poorly elucidated. The development of ischemic acute kidney injury (AKI) may be mediated by NADPH oxidase and angiotensin II type 2 receptors. The aim of our study was to explore the effects of novokinin (NOV), angiotensin II type 2 receptor (AT2R) agonist and apocynin (APO), an NADPH oxidase inhibitor, on kidney structure and function, as well as the level of oxidative stress in spontaneously hypertensive rats (SHR) with induced IRI. Animals were randomly assigned into five experimental groups: the Sham-operated animals (SHAM) group, the AKI group, and AKI groups receiving APO, NOV, or their combination. Slight improvements in renal function were noted across all treated groups; however, only the combined action of APO + NOV led to a significant decrease in kidney injury molecule-1 (KIM-1) levels and markedly reduced oxidative stress compared with the control AKI group. Our results demonstrate that additively targeting NADPH oxidase and AT2R provides new insights in comparison to individual treatments. These findings suggest a potentially promising new therapeutic strategy for managing IRI and improving outcomes in critically ill patients with AKI. Full article

Background: Evidence regarding optimal reperfusion strategies in older patients with acute ischemic stroke remains inconsistent, particularly in real-world settings where patient selection and comorbidity burden differ from randomized trials. Objective: This study evaluates real-world outcomes of ischemic stroke interventions among older adults in a tertiary medical center. Methods: This single-center retrospective cohort study included patients aged ≥ 65 years with acute ischemic stroke admitted between August 2022 and December 2023. Mortality follow-up continued until September 2024. Patients were categorized according to treatment: intravenous thrombolysis (tPA) alone, endovascular thrombectomy (EVT) alone, or combined (tPA + EVT) therapy. Data included demographics, comorbidities, stroke severity (NIHSS), imaging, treatment timing, and mortality outcomes. Results: Among 200 patients (mean age 77.5 years), 66 received tPA, 86 underwent EVT, and 48 received tPA + EVT therapy. Patients treated with tPA alone presented with milder strokes and had low in-hospital and six-month mortality (1.5% and 6.1%, respectively). In contrast, EVT-only patients had substantially higher in-hospital and six-month mortality (21% and 43%, respectively). Patients receiving tPA + EVT therapy had low mortality rates comparable to the tPA group (2.1% and 6.3%, respectively), despite greater stroke severity at presentation. Conclusions: Despite greater stroke severity, patients receiving tPA + EVT therapy had outcomes comparable to those treated with tPA alone, while EVT-only patients experienced substantially higher mortality. These findings underscore the importance of patient selection and suggest that treatment allocation may strongly influence real-world outcomes in older adults. Full article

Background and Objectives: Angiographic no-reflow (NRF) after percutaneous coronary intervention (PCI) reflects impaired microvascular reperfusion despite successful treatment of the epicardial culprit lesion. Brain-derived neurotrophic factor (BDNF) is a neurotrophin involved in endothelial signaling, platelet biology, inflammation, and angiogenesis. Its relationship with NRF in non-ST-segment elevation myocardial infarction (NSTEMI) remains insufficiently characterized. Materials and Methods: This single-center prospective observational cohort study included 700 consecutive NSTEMI patients undergoing culprit-lesion PCI. Admission serum total BDNF was measured before PCI using a standardized enzyme-linked immunosorbent assay protocol. Angiographic NRF was defined as final thrombolysis in myocardial infarction (TIMI) flow <3 and/or TIMI 3 flow with myocardial blush grade (MBG) 0–1 in the absence of residual stenosis, dissection, severe spasm, or other mechanical obstruction. Four sequential logistic regression models were used to evaluate the stability of the association between BDNF and NRF: Model 1 adjusted for clinical variables; Model 2 further adjusted for laboratory and inflammatory variables; Model 3 further adjusted for cardiac injury and functional variables; and Model 4 further adjusted for angiographic and procedural variables. Discrimination, calibration, reclassification, decision-curve analysis, and internal validation were assessed. Results: NRF occurred in 114 of 700 patients (16.3%). Serum total BDNF was higher in the NRF group than in the reflow group [555 (465–688) vs. 386 (292–496) pg/mL, p < 0.001]. BDNF remained independently associated with NRF across sequential models: Model 1 OR 1.67 per 100 pg/mL (95% CI 1.43–1.96), Model 2 OR 1.49 (95% CI 1.24–1.79), Model 3 OR 1.41 (95% CI 1.16–1.72), and Model 4 OR 1.31 (95% CI 1.07–1.60). The BDNF-only AUC was 0.787, while the final BDNF-enriched Model 4 reached an AUC of 0.866. The optimism-corrected bootstrap AUC was 0.852 and the 10-fold cross-validated AUC was 0.845. Conclusions: Higher admission serum total BDNF was independently associated with angiographic NRF in NSTEMI patients undergoing PCI and improved risk discrimination when added to clinical, biochemical, cardiac, and angiographic predictors. These findings suggest that serum total BDNF may reflect a context-dependent biomarker signal related to acute thrombo-inflammatory, platelet-associated, and microvascular injury pathways; however, the observed incremental value was modest and requires external validation. Full article

Acute ischemic stroke is one of the leading causes of mortality and disability globally, characterized by a complex and temporally structured cascade of cellular and molecular events. Although reperfusion therapies have improved outcomes, their narrow therapeutic window and limited availability leave many patients without effective treatment, highlighting the need for effective neuroprotective strategies capable of targeting multiple interconnected pathways. Melatonin has been proposed as a potential adjunctive neuroprotective agent based on its pleiotropic properties, modulating cellular signaling networks including antioxidant, anti-inflammatory, mitochondrial stabilizing, and BBB-preserving effects. Melatonin regulates key signaling pathways, thereby coordinating cellular responses to injury in multiple stages of ischemic pathophysiology, positioning it as a potential adjunctive therapy. Preclinical studies consistently demonstrate reductions in infarct volume, preservation of neuronal architecture, and improvements in neurological outcomes. However, clinical evidence remains limited to a small number of clinical trials, which suggest safety and possible early neurological benefit but are underpowered to determine long-term efficacy. Importantly, translational gaps persist regarding optimal dosing, duration of administration, and alignment with the temporal dynamics of post-ischemic injury. This review integrates current knowledge on the cellular and molecular mechanisms underlying the potential neuroprotective actions and its role as a pleiotropic modulator of ischemic injury. Full article

Background: Acute focal neurological deficits require rapid differentiation between ischemic stroke and stroke mimics to avoid treatment delays and inappropriate therapy. Seizures, including ictal deficits, status epilepticus, and post-ictal/Todd’s phenomena, are among the most challenging mimics. This review summarizes the role of multimodal neuroimaging in distinguishing acute ischemic stroke from seizure-related deficits. Methods: We performed a focused narrative review of neuroimaging findings in acute stroke mimics, emphasizing non-contrast computed tomography (CT), CT angiography, CT perfusion, magnetic resonance imaging (MRI), including diffusion weighted imaging (DWI), apparent diffusion coefficient (ADC), fluid attenuated inversion recovery (FLAIR), and arterial spin labeling (ASL) sequences. Imaging patterns, diagnostic pitfalls, and practical clues for hyperacute stroke pathways were synthesized. Results: Acute ischemic stroke is typically suggested by vascular-territorial abnormalities, including arterial occlusion or stenosis, territorial hypoperfusion, and congruent DWI/ADC restriction. Seizure-related deficits more often show non-territorial cortical perfusion changes, ictal or status-related hyperperfusion, reversible MRI abnormalities, and absence of arterial occlusion. However, post-ictal hypoperfusion, peri-ictal diffusion restriction, and reperfusion-related hyperperfusion may overlap with ischemic patterns. Conclusions: A multimodal approach integrating vascular imaging, perfusion distribution, DWI/ADC, ASL, clinical timing, and EEG findings can improve diagnostic accuracy in the stroke–seizure differential without delaying treatment in true acute ischemic stroke. Full article