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        <title>Frontiers in Neurology | Stroke section | New and Recent Articles</title>
        <link>https://www.frontiersin.org/journals/neurology/sections/stroke</link>
        <description>RSS Feed for Stroke section in the Frontiers in Neurology journal | New and Recent Articles</description>
        <language>en-us</language>
        <generator>Frontiers Feed Generator,version:1</generator>
        <pubDate>2026-08-13T05:20:27.826+00:00</pubDate>
        <ttl>60</ttl>
        <item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneur.2026.1824344</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneur.2026.1824344</link>
        <title><![CDATA[The impact of stroke on intramuscular connective tissue in mice]]></title>
        <pubdate>2026-08-13T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Xiaoxiao Zhao</author><author>Giulio Morri</author><author>Matteo D’Urso</author><author>Caterina Fede</author><author>Lucia Petrelli</author><author>Livia Vignozzi</author><author>Yunfeng Sun</author><author>Claudia Clair</author><author>Gabriele Deidda</author><author>Preeti Raghavan</author><author>Manuela Allegra</author><author>Carla Stecco</author>
        <description><![CDATA[BackgroundPrevious studies about post-stroke peripheral structural remodeling have been focused on muscle fiber alterations, while extracellular matrix (ECM) remodeling in musculoskeletal tissues remains unclear. This study examines changes in extracellular matrix (ECM), specifically hyaluronan (HA) and collagen, in forelimb muscles following distal middle cerebral artery occlusion (dMCAO) in mice.MethodsTwenty-two 8-week-old C57BL/6 mice (10 male, 12 female) were randomly assigned to the control group (n = 10; 4 male, 6 female) or the experimental group (n = 12; 6 male, 6 female). 4 weeks post-stroke, forelimb muscle samples were collected and analyzed for HA and collagen distribution and concentrations.ResultsHA concentrations were significantly elevated in both the left (stroke affected) forelimb muscles (63.74 ± 11.80 μg/g), and right (unaffected) forelimb muscles (64.16 ± 13.52 μg/g) of stroke mice compared to the controls (left: 50.07 ± 8.84 μg/g, p = 0.022; and right: 49.36 ± 12.22 μg/g, p = 0.015). No significant difference in HA levels was observed between the affected and unaffected sides of stroke mice (p = 0.905). Collagen concentrations did not differ significantly among groups (control left: 8.62 ± 2.91 μg/g; control right: 8.77 ± 1.35 μg/g; stroke-affected: 8.24 ± 2.11 μg/g; stroke-unaffected: 8.28 ± 2.45 μg/g).ConclusionThe results revealed a systemic increase in HA concentration in the stroke group, while collagen levels remained unchanged. These findings provide biochemical evidence of early alterations in extracellular matrix composition after stroke.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneur.2026.1824565</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneur.2026.1824565</link>
        <title><![CDATA[Do conventional intracerebral hemorrhage functional scores apply to mild-to-moderate hemorrhage?]]></title>
        <pubdate>2026-08-12T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Ao Chen</author><author>Jiaying Peng</author><author>Liang Guo</author><author>Renhui Zhou</author>
        <description><![CDATA[BackgroundConventional intracerebral hemorrhage (ICH) functional scores are typically developed based on clinical factors for assessing mortality risk, and their applicability in evaluating functional outcomes in patients with the specific hemorrhagic subtype of mild to moderate ICH(MTM-ICH) remains unclear. Therefore, we aimed to construct a nomogram model to predict early functional dependence in this patient population and to validate three previous general ICH functional scores.MethodsWe conducted a retrospective analysis of data from 575 patients with MTM-ICH (GCS score ≥ 9) treated at our hospital between January 2018 and July 2025. The baseline demographic information, clinical characteristics, and clinical outcomes were collected. Early functional dependence was defined as a modified Rankin Scale (MRS) score ≥ 3 at discharge or 30 days after ICH. Least absolute shrinkage and selection operator (LASSO) and stepwise logistic regression analyses were used to screen for risk factors for early functional dependence and construct a predictive model. The model was visualized using a nomogram, and its predictive performance was compared with three existing ICH functional scores (FUNC, ICH-GS and ICH-FOS). Internal validation of the nomogram was performed using a 10-fold cross-validation combined with bootstrap resampling.ResultsAmong 575 patients with MTM-ICH, 198 (34.4%) developed early functional dependence. LASSO and stepwise logistic regression analyses identified six independent predictors: age, admission GCS score, hematoma volume, thalamic hemorrhage, basal ganglia hemorrhage, and mechanical ventilation. The nomogram based on these factors demonstrated good calibration and superior predictive performance compared to three existing ICH functional scores (AUC = 0.856 for our nomogram, 0.579 for FUNC, 0.601 for ICH-GS, and 0.714 for ICH-FOS, respectively). The decision curve analysis further demonstrated that the model had greater net benefit than the three previous general ICH functional scores. Internal validation confirmed the model’s stability and generalizability (10-fold cross-validation mean: 0.846; bootstrap-corrected C-index: 0.844).ConclusionAmong patients with MTM-ICH, advanced age, lower admission GCS score, larger hematoma volume, thalamic or basal ganglia hemorrhage, and mechanical ventilation were associated with a higher risk of early functional dependence. The nomogram developed based on these factors demonstrated high predictive performance. In contrast, conventional ICH functional scores demonstrate certain limitations when assessing this specific hemorrhage subtype.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneur.2026.1847958</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneur.2026.1847958</link>
        <title><![CDATA[β-Hydroxybutyrate induces microglial M2 polarization by inhibiting the NF-κB/NLRP3 pathway to ameliorate cerebral ischemia–reperfusion injury]]></title>
        <pubdate>2026-08-12T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Qiong Chen</author><author>Shui Cheng</author><author>Chang Huang</author><author>Ruping Xiang</author>
        <description><![CDATA[ObjectiveTo investigate the neuroprotective effects of β-hydroxybutyrate (BHB) on cerebral ischemia–reperfusion injury (CIRI) and its underlying molecular mechanisms; to clarify the association between ketone bodies and the severity of CIRI under obese conditions.MethodsCIRI rat model was established using modified middle cerebral artery occlusion/reperfusion (MCAO/R), while obesity was induced using high fat diet. BHB was administered via subcutaneous osmotic pumps. Lipopolysaccharide (LPS) was intraperitoneally injected to forcibly activate the nuclear factor-κB (NF-κB)/NOD-like receptor protein 3 (NLRP3) pathway. Neurological deficits were evaluated using the Zea–Longa 5-point scoring system. Serum BHB levels were measured by colorimetric assay. Immunofluorescence was performed to detect CD86 (M1 phenotype) and CD206 (M2 phenotype) levels. Inflammatory cytokines in brain tissues were measured. Levels of phosphorylated p65 (p-p65), cleaved caspase-1, and ionized calcium-binding adapter molecule 1 (Iba1) were analyzed by Western blotting.ResultsCIRI rats with obesity exhibited increased serum BHB levels, reduced neurological deficit scores, and markedly decreased infarct volumes. Moreover, levels of p-p65, cleaved caspase-1, Iba1, and pro-inflammatory cytokines, were decreased, while Iba1+CD206+ co-localization was increased. BHB treatment for CIRI rats with normal weight reduced neurological deficit scores, increased serum BHB, and decreased infarct volume. Following further LPS administration, neurological deficit scores and infarct volume were enhanced, with no difference in serum BHB levels.ConclusionElevated endogenous BHB under obese conditions exerts neuroprotective effects against CIRI, and exogenous BHB can mimic this effect. Mechanistically, BHB inhibits activation of the NF-κB/NLRP3 pathway and promotes microglial polarization toward the anti-inflammatory M2 phenotype, thereby alleviating CIRI.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneur.2026.1899933</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneur.2026.1899933</link>
        <title><![CDATA[Adjuvant neuroprotective therapies for acute ischemic stroke in the reperfusion era: a comparative narrative review of clinical evidence for edaravone, edaravone-dexborneol, and butylphthalide]]></title>
        <pubdate>2026-08-12T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Weiqing Wang</author><author>Junsen Ye</author>
        <description><![CDATA[Reperfusion therapies, including intravenous thrombolysis and endovascular treatment (EVT), are central to acute ischemic stroke (AIS) management; however, ischemia–reperfusion injury may limit recovery despite successful recanalization. This structured narrative review compares the clinical evidence, safety signals, and mechanistic literature for edaravone, butylphthalide (NBP), and the fixed-dose combination edaravone-dexborneol (EDB) as adjunctive neuroprotective approaches. The evidence base is heterogeneous with respect to population, background reperfusion treatment, outcome timing, and geographical setting. In TASTE-2, EDB administered before EVT was associated with a modest increase in 90-day functional independence versus placebo (55.0% vs. 49.6%, p = 0.05), without an apparent safety signal; bridging alteplase was permitted in a subset of participants. In the BAST trial, NBP improved the prespecified 90-day functional outcome versus placebo among patients receiving intravenous thrombolysis and/or EVT (56.7% vs. 44.0%). Observational studies and meta-analyses provide supportive but non-confirmatory evidence for edaravone. Network meta-analyses generate relative rankings at individual endpoints, but indirect comparisons and differing outcome networks preclude definitive between-agent selection. Mechanistic studies indicate overlapping antioxidant, anti-inflammatory, mitochondrial, and neurovascular effects rather than exclusive pathway regulation. Biomarker and imaging approaches, including exploratory GFAP and UCH-L1 measurements, are promising research tools but are not yet validated for treatment selection in AIS. Accordingly, these agents should be regarded as candidates for further evidence-informed adjunctive use; future trials are needed to define reproducible patient-selection and treatment-timing strategies.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneur.2026.1861639</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneur.2026.1861639</link>
        <title><![CDATA[Impact of non-amyloid cerebral small vessel disease on the efficacy and safety of argatroban in acute ischemic stroke: a retrospective cohort study]]></title>
        <pubdate>2026-08-11T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Fen Liu</author><author>Qiang Wu</author><author>Yan Lin</author><author>Jie Chen</author>
        <description><![CDATA[ObjectiveTo investigate whether imaging features of non-cerebral amyloid angiopathy cerebral small vessel disease (non-amyloid CSVD) influence the efficacy of argatroban in acute ischaemic stroke (AIS) and to test for effect modification.MethodsPatients with AIS admitted to Songxi County Hospital from January 2022 to December 2023 were enrolled and divided into an argatroban group and a control group. CSVD imaging markers (multiple lacunar infarcts, multiple subcortical white matter lesions, white matter hyperintensities, and brain atrophy) were assessed. Multivariable logistic regression was used to analyse favourable outcome at 90 days (modified Rankin Scale score 0–2), and interaction terms were introduced to test for effect modification.ResultsA total of 139 patients were included (66 in the argatroban group, 73 in the control group). Argatroban reduced early neurological deterioration (adjusted OR 0.045, p = 0.004), but no significant difference was observed in the rate of favourable outcome at 90 days between the two groups (80.3% vs. 79.5%, p = 0.208). Severe white matter hyperintensities modified the efficacy of argatroban (p for interaction < 0.10), with greater benefit seen in patients without severe white matter hyperintensities. Only one intracranial haemorrhage occurred, and it was in the control group.ConclusionIn patients with AIS after exclusion of cerebral amyloid angiopathy, argatroban improves early neurological function but does not improve functional outcome at 90 days. Severe white matter hyperintensities may be potential effect modifiers, generating hypotheses for imaging-based treatment stratification that warrant prospective validation.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneur.2026.1819400</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneur.2026.1819400</link>
        <title><![CDATA[AngioPLUS-derived carotid intraplaque neovascularization predicts recurrent anterior circulation stroke: a prospective cohort study]]></title>
        <pubdate>2026-08-11T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Hao Zhang</author><author>Jun He</author><author>Jimei Xu</author><author>Rongfeng Wang</author><author>Shugang Cao</author><author>Mingwu Xia</author>
        <description><![CDATA[Background and purposeThe predictive value of carotid intraplaque neovascularization (IPN), assessed by the novel AngioPLUS technique, for recurrent anterior circulation ischemic stroke (ACIS) remains unclear. This study aimed to evaluate the prognostic value of IPN for stroke recurrence in patients with ACIS and to develop a parsimonious prediction model by screening core predictors using Lasso regression, with subsequent assessment of its discrimination, calibration, and clinical utility.MethodsConsecutive patients admitted for ACIS who underwent IPN assessment using AngioPLUS ultrasound between August 2020 and February 2025 were prospectively enrolled. Independent predictors of recurrent ischemic stroke were identified using Cox proportional hazards regression models. Least absolute shrinkage and selection operator (Lasso) regression was employed to screen core predictors for constructing a parsimonious Cox model. Model discrimination was evaluated using time-dependent receiver operating characteristic (ROC) curves, and internal validation was performed with Bootstrap resampling B=1000 to calculate the concordance index (C-index). Model calibration was assessed using calibration plots. Risk stratification was conducted based on the optimal cut-off value of the total nomogram score, and differences in survival between groups were compared using the Kaplan–Meier method and the log-rank test.ResultsA total of 143 patients (93 males, 65.0%; mean age 67.6 ± 11.7 years) with a median follow-up of 21 months (range 6–56 months) were enrolled, during which 26 patients experienced recurrent ischemic stroke. The recurrence rate was significantly higher in the high IPN group compared to the low IPN group (35.0% vs. 6.0%, p < 0.001). Lasso regression identified two core predictors: IPN Grades 2 (HR = 5.30, 95% CI 1.99–14.08, p < 0.001) and LDL-C (HR = 2.23, 95% CI 1.41–3.52, p < 0.001). The parsimonious model yielded a concordance index (C-index) of 0.786 (95% CI 0.707–0.866), with time-dependent AUC values of 0.716, 0.809, and 0.815 at 12, 24, and 36 months, respectively. Calibration plots closely approximated the ideal diagonal line. Nomogram-based risk stratification demonstrated that patients in the high-risk group had significantly lower recurrence-free survival rates at 12, 24, and 36 months (80.46, 36.40, and 28.31%, respectively) compared to those in the low-risk group (97.73, 90.80, and 88.21%, respectively). The median survival time was 23.0 months in the high-risk group and was not reached in the low-risk group (log-rank p < 0.001).ConclusionCarotid IPN is an independent predictor of ACIS recurrence. A parsimonious Cox model incorporating IPN Grades 2 and LDL-C demonstrated favorable discrimination and calibration. The nomogram based on this model effectively identifies individuals at high risk of recurrence, offering a simple and practical tool for guiding individualized secondary prevention strategies in clinical practice.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneur.2026.1791832</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneur.2026.1791832</link>
        <title><![CDATA[Association between the Fibrosis-4 index and stroke and related outcomes: a meta-analysis]]></title>
        <pubdate>2026-08-10T00:00:00Z</pubdate>
        <category>Systematic Review</category>
        <author>Wei Lai</author><author>Haojie Yu</author><author>Hongming Wang</author>
        <description><![CDATA[ObjectiveThis meta-analysis evaluated the associations between the Fibrosis-4 index (FIB-4) and overall stroke, ischemic stroke, hemorrhagic outcomes, poor functional outcome, and all-cause mortality.MethodsPubMed, Embase, and the Cochrane Library were searched from inception to November 4, 2025. Cohort and cross-sectional studies evaluating categorical or continuous FIB-4 were eligible. Quantitative syntheses were stratified by outcome, FIB-4 modeling approach, and effect measure, with odds ratios (ORs) and hazard ratios (HRs) analyzed separately. Prediction intervals were calculated for random-effects analyses containing at least three independent estimates.ResultsTwenty-two studies, including 20 cohort studies and two cross-sectional studies, were included, of which 20 contributed to at least one quantitative synthesis. Elevated categorical FIB-4 was associated with greater odds of overall stroke (OR = 1.86, 95% CI: 1.63–2.14), ischemic stroke (OR = 2.03, 95% CI: 1.72–2.40), symptomatic intracranial hemorrhage (OR = 2.52, 95% CI: 1.79–3.53), poor functional outcome (OR = 2.88, 95% CI: 2.47–3.35), and all-cause mortality (OR = 2.98, 95% CI: 2.51–3.53). Continuous FIB-4 was also associated with overall stroke (HR = 1.08, 95% CI: 1.02–1.14), symptomatic intracranial hemorrhage (OR = 1.33, 95% CI: 1.20–1.48), poor functional outcome (OR = 1.26, 95% CI: 1.11–1.43), and all-cause mortality (HR = 1.08, 95% CI: 1.03–1.12). However, prediction intervals crossed the null for the continuous analyses of poor functional outcome and all-cause mortality, and the categorical overall-stroke analysis was exploratory.ConclusionHigher FIB-4 was associated with stroke and adverse stroke-related outcomes across several observational analyses. FIB-4 may provide adjunctive risk information, but prospective validation and formal assessment of its incremental clinical value are required before routine implementation.Systematic review registrationhttps://www.crd.york.ac.uk/prospero/search, identifier: CRD420251207801.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneur.2026.1849476</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneur.2026.1849476</link>
        <title><![CDATA[Prognostic value of the CALLY index for functional outcomes in acute ischemic stroke: a systematic review and exploratory quantitative synthesis]]></title>
        <pubdate>2026-08-07T00:00:00Z</pubdate>
        <category>Systematic Review</category>
        <author>Zongyu Cai</author><author>Shihuan Zhong</author><author>Yifan Liang</author>
        <description><![CDATA[BackgroundThe C-reactive protein-albumin-lymphocyte (CALLY) index is a novel composite biomarker reflecting systemic inflammation, nutritional status, and immune function. Emerging evidence suggests its potential prognostic value in acute ischemic stroke (AIS). However, no systematic analysis has been conducted to evaluate its association with functional outcomes in AIS patients. This systematic review with exploratory quantitative synthesis aimed to assess the prognostic value of the CALLY index for functional outcomes in AIS.MethodsWe systematically searched the Cochrane Library, EMBASE, PubMed, and Web of Science databases from inception to March 2026. The search was initially conducted in February 2025 and updated in March 2026 prior to submission. Observational studies evaluating the association between the CALLY index and functional outcomes in AIS patients were included. The primary outcome was poor functional outcome defined by the modified Rankin Scale (mRS), with poor outcome defined as mRS ≥ 2, mRS > 2, or mRS ≥ 3 at 3 months. Pooled odds ratios (ORs) with 95% confidence intervals (CIs) were calculated using a random-effects model. Study quality was assessed using the Newcastle-Ottawa Scale (NOS). Heterogeneity was evaluated using Cochran’s Q test and I2 statistic.ResultsThree studies involving 1,161 AIS patients were included. The exploratory quantitative synthesis revealed that a higher CALLY index was significantly associated with a lower risk of poor functional outcome (pooled OR = 0.766, 95% CI: 0.695–0.845, p < 0.001), with no significant heterogeneity across studies (I2 = 0.0%, Q = 1.33, p = 0.516). All included studies were of high quality (NOS scores 8-9). Publication bias could not be reliably assessed due to the limited number of included studies.ConclusionThis systematic review with exploratory quantitative synthesis provides preliminary pooled evidence suggesting that the CALLY index may be a potential predictor of functional outcome in AIS patients. A higher CALLY index was associated with a lower risk of poor functional outcomes. However, given the limited number of included studies (only three retrospective studies from China), these findings should be considered hypothesis-generating rather than confirmatory and require validation in large-scale, multicenter, prospective studies across diverse populations before clinical application.Systematic review registrationThe review was registered in PROSPERO: CRD420261350196 https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD420261350196.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneur.2026.1945724</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneur.2026.1945724</link>
        <title><![CDATA[Correction: High-altitude exposure and ischemic stroke: pathophysiological mechanisms and current perspectives]]></title>
        <pubdate>2026-08-06T00:00:00Z</pubdate>
        <category>Correction</category>
        <author>Yuhuan Qiao</author><author>Yuding Luo</author><author>Yu Hu</author><author>Chuanxi Duan</author><author>Junhao Li</author><author>Xiaojing Luo</author><author>Jian Wang</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneur.2026.1882830</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneur.2026.1882830</link>
        <title><![CDATA[Single vs. dual antiplatelet therapy before DOAC initiation in acute ischemic stroke with atrial fibrillation: a retrospective cohort study]]></title>
        <pubdate>2026-08-06T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Guan-xin Hou</author><author>Adili Tuersun</author><author>Zuo-jun Wang</author><author>Han Chen</author><author>Da-sheng Dang</author><author>Qing-chun Zhao</author><author>Yan Wang</author><author>Tian-shu Ren</author>
        <description><![CDATA[BackgroundThe optimal antiplatelet bridging strategy before initiating direct oral anticoagulants (DOACs) in patients with acute ischemic stroke (AIS) and non-valvular atrial fibrillation (NVAF) remains uncertain.MethodsThis single-center retrospective cohort study included 120 patients with AIS and NVAF who received antiplatelet therapy prior to DOAC initiation. Patients were stratified by regimen: single antiplatelet therapy (SAPT, n = 48) or dual antiplatelet therapy (DAPT, n = 72). Primary outcomes included early neurological improvement (≥2-point NIHSS reduction), early neurological deterioration (≥4-point NIHSS increase or death within 48 h), and in-hospital bleeding. Secondary outcomes were 90-day favorable functional outcome (modified Rankin Scale 0–2), 90-day excellent outcome (mRS 0–1), and ordinal mRS shift. Multivariate logistic regression identified independent predictors. Ordinal logistic regression was used for mRS shift analysis.ResultsBaseline characteristics were comparable between groups, with no significant differences in baseline NIHSS score (median 4.00 vs. 2.00, p = 0.136) or mRS score (median 3.00 vs. 3.00, p = 0.435). No significant differences were observed in early neurological improvement (39.6% vs. 37.5%, p = 0.969), early deterioration (4.2% vs. 0%, p = 0.158), or bleeding events (6.2% vs. 1.4%, p = 0.301). In unadjusted analysis, DAPT demonstrated higher 90-day favorable outcome (90.3% vs. 75.0%, p = 0.046). However, after multivariable adjustment, DAPT was not independently associated with mRS 0–2 (adjusted OR 2.40, 95% CI 0.62–10.06, p = 0.211), mRS 0–1 (adjusted OR 1.18, 95% CI 0.43–3.14, p = 0.739), or ordinal mRS shift (adjusted common OR 0.70, 95% CI 0.34–1.44, p = 0.336). Baseline NIHSS score independently predicted all outcomes (p < 0.001 for all).ConclusionIn unadjusted analysis, DAPT prior to DOAC initiation was associated with higher 90-day favorable functional outcome without excess bleeding risk. However, this association was not independent of baseline stroke severity after multivariable adjustment, suggesting that the crude benefit was largely attributable to selection bias rather than a true therapeutic advantage of DAPT. The current data do not support the superiority of DAPT over SAPT. Baseline NIHSS score independently predicted both short-term and long-term outcomes. These hypothesis-generating findings warrant confirmation in adequately powered prospective randomized trials.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneur.2026.1904486</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneur.2026.1904486</link>
        <title><![CDATA[Intravenous thrombolysis in acute ischemic stroke after recent direct oral anticoagulant intake: toward evidence-informed care]]></title>
        <pubdate>2026-08-06T00:00:00Z</pubdate>
        <category>Perspective</category>
        <author>Matija Zupan</author><author>Mišo Šabovič</author><author>Pawel Kermer</author><author>Senta Frol</author>
        <description><![CDATA[The use of intravenous thrombolysis (IVT) in acute ischemic stroke (AIS) patients with recent direct oral anticoagulant (DOAC) intake remains one of the most debated issues in contemporary stroke medicine. Current international guidelines generally discourage IVT within 48 h of DOAC ingestion, largely because of concerns regarding symptomatic intracranial hemorrhage (sICH) and the absence of randomized evidence. However, an increasing body of evidence from international registries and multicenter cohorts has not identified a clear increase in sICH among carefully selected patients with recent DOAC exposure who received IVT. Some observational studies have also reported an association with more favorable functional outcomes than those observed in otherwise eligible patients in whom reperfusion therapy was withheld, although these comparisons are susceptible to selection bias and confounding by indication. In this Perspective, we discuss recent advances that have challenged the traditional practice of broadly excluding patients with recent DOAC exposure from IVT. We review observational evidence concerning IVT in selected patients, examine biological hypotheses that could be relevant to the observed clinical findings, and discuss evolving roles of reversal agents and laboratory assessment of anticoagulant activity. We further highlight current implementation barriers and future research priorities, including prospective studies, improved point-of-care anticoagulant testing, and refinement of patient-selection strategies. We argue that contemporary evidence supports reconsideration of rigid time-based exclusion criteria in favor of more individualized, evidence-informed decision-making. Although important uncertainties remain, recent DOAC exposure may not necessarily preclude IVT in appropriately selected patients, particularly when anticoagulant activity can be reliably assessed.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneur.2026.1860647</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneur.2026.1860647</link>
        <title><![CDATA[Quantification of daily upper arm use after stroke using an IMU-based kinematic model]]></title>
        <pubdate>2026-08-06T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Noy Goldhamer</author><author>Yogev Koren</author><author>Tamar Mizrahi</author><author>Adi Lorber-Haddad</author><author>Reut Binyamin-Netser</author><author>Lior Shmuelof</author>
        <description><![CDATA[BackgroundUpper limb (UL) impairment is one of the most common and disabling consequences of stroke, limiting independence and the performance of daily activities. Although rehabilitation aims to reduce impairments and enhance real-world activity performance, clinical motor assessments often fail to capture spontaneous UL use. This discrepancy between motor capacity observed in clinical settings and actual performance of daily activities underscores the need for objective, ecologically valid monitoring tools. Wearable inertial measurement units (IMUs) have emerged as feasible methodology for quantifying real-world UL use; however, the clinical interpretability and validity of kinematic metrics derived from measures of activity in persons with stroke (PwS) remain insufficiently established.ObjectiveTo evaluate the utility of three IMU-derived kinematic measures of UL use in persons with stroke (PwS) during routine daily activity and to examine their associations with clinical assessments of motor impairment.MethodsNineteen individuals in the subacute stage after stroke wore five IMU sensors during routine daytime activities in a rehabilitation hospital. Three kinematic measures - wrist path length, cumulative elbow angular displacement, and movement space volume - were extracted for each arm and combined to asymmetry indices. Clinical assessments included the Fugl-Meyer Assessment for the upper extremity (FMA-UE), Action Research Arm Test (ARAT), and grip strength. Asymmetry indices and their correlations with clinical measures were analyzed.ResultsAll IMU-derived measures were significantly reduced in the paretic arm compared with the non-paretic arm (p < 0.001). Asymmetry indices showed significant correlations with clinical impairment measures, with cumulative elbow angular displacement demonstrating the strongest association, particularly with ARAT scores.ConclusionIMU-based kinematic measures effectively capture reduced daily UL use in PwS and demonstrate associations with clinical impairment. These findings support the potential of wearable sensors to quantify daily arm use as an ecologically valid indicator of activity performance and recovery.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneur.2026.1878428</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneur.2026.1878428</link>
        <title><![CDATA[Advanced radiomics techniques applied on carotid duplex ultrasound data predict adverse outcomes in acute ischemic stroke]]></title>
        <pubdate>2026-08-05T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Lianlian Zhang</author><author>Haiyan Cao</author><author>Lizhu Miao</author><author>Xinyuan Zhang</author><author>Guofu Shi</author>
        <description><![CDATA[BackgroundAcute ischemic stroke (AIS) is a leading cause of mortality and morbidity worldwide. This study explores the potential of using carotid duplex ultrasound (CDU) radiomics to predict outcomes in AIS patients, enhancing prognostic assessments through advanced imaging technologies.MethodsWe enrolled 105 AIS patients at the Stroke Center of the First Affiliated Hospital of Soochow University. CDU images were obtained and processed using artificial intelligence to extract 1,477 radiomic features. Key features were identified and used to develop a predictive model for patient outcomes 3 months post-stroke.ResultsThe developed predictive model demonstrated high accuracy and clinical utility, confirmed by decision curve analysis. Inter-observer reliability was excellent, with a Cohen’s kappa coefficient of 0.93, indicating consistent assessments of plaque vulnerability across different observers.ConclusionCarotid duplex ultrasound radiomics significantly enhances the ability to predict adverse outcomes in AIS, offering a precision-based approach that supports personalized management strategies. It could improve clinical outcomes by allowing targeted interventions based on specific radiomic profiles.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneur.2026.1778289</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneur.2026.1778289</link>
        <title><![CDATA[The dual role of APOE ε4 allele in cerebral small vessel disease: independent genetic effects and effect modification of traditional risk factors]]></title>
        <pubdate>2026-08-05T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Feng Liu</author><author>Yulan Gou</author>
        <description><![CDATA[BackgroundThe association between apolipoprotein E (APOE) ε4 and cerebral small vessel disease (CSVD) remains incompletely understood, with inconsistent evidence across imaging phenotypes and limited investigation into gene–environment interactions.MethodThis cross-sectional study included 728 patients with chronic lacunar infarcts who underwent 3 T brain MRI. CSVD burden was quantified using a study-specific composite score (range 0–6), integrating white matter hyperintensities (WMH), cerebral microbleeds (CMBs), and enlarged perivascular spaces (EPVS). APOE ε4 carriers (n = 139) were compared with non-carriers (n = 589). Ordinal logistic regression and Firth‘s penalized logistic regression (for EPVS) were used to assess the independent effect of APOE ε4 on CSVD markers. Multiplicative interaction terms (APOE ε4 × smoking, APOE ε4 × alcohol use) were added to the fully adjusted models, with p values adjusted using the Holm-Bonferroni method. Sensitivity analyses excluded APOE ε2 carriers.ResultsAPOE ε4 was independently associated only with periventricular WMH burden (β = 0.411, 95% CI: 0.046–0.776, p = 0.027), with no significant associations for global CSVD burden, total WMH, deep WMH, CMBs, or EPVS. Significant interactions were observed for APOE ε4 × smoking on global CSVD burden, CMBs, total WMH, and PWMH (adjusted p < 0.05), and for APOE ε4 × alcohol use on global CSVD burden and CMBs (adjusted p < 0.05). These findings remained robust after excluding APOE ε2 carriers.ConclusionAPOE ε4 exhibits both an independent genetic effect—selectively associated with periventricular white matter injury—and a modifying effect on the associations of smoking and alcohol use with specific CSVD phenotypes. These findings highlight the phenotypic specificity of APOE ε4’s dual role in CSVD and support the integration of genetic background with modifiable risk factors for precision risk stratification.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneur.2026.1840105</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneur.2026.1840105</link>
        <title><![CDATA[Lacunar stroke with and without chronic imaging biomarkers of small vessel disease: clinical profiles and stroke etiology]]></title>
        <pubdate>2026-08-05T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Jan Vynckier</author><author>Léonore Jaques</author><author>Basel Maamari</author><author>Martina Goeldlin</author><author>Lorenz Grunder</author><author>Michail Giannakakis</author><author>Elias Auer</author><author>Greta Sökeland</author><author>Janis Rauch</author><author>Bernhard Siepen</author><author>Philipp Bücke</author><author>Johannes Kaesmacher</author><author>Morin Beyeler</author><author>Arsany Hakim</author><author>Marcel Arnold</author><author>Bogdan Draganski</author><author>Jan Gralla</author><author>David J Seiffge</author><author>Urs Fischer</author><author>Thomas Raphael Meinel</author>
        <description><![CDATA[IntroductionChronic cerebral small vessel disease (CSVD) may help distinguish different etiological mechanisms in acute lacunar stroke; this study aimed to compare vascular risk factors and stroke etiology in patients with and without CSVD.MethodsIn this observational study, consecutive patients with magnetic resonance imaging (MRI)–confirmed acute lacunar stroke were included from a prospective stroke database covering the years 2015–2019. CSVD was defined as a summary small vessel disease (SVD) score ≥2 based on established MRI markers, including white matter hyperintensities, lacunes, cerebral microbleeds, and enlarged perivascular spaces. Associations between CSVD, vascular risk factors, and stroke etiology were examined using descriptive statistics and multivariable regression analysis.ResultsAmong 486 patients with acute lacunar stroke, 175 (36%) had CSVD. Median age was 72 years, 40.5% were female, and the median National Institutes of Health Stroke Scale (NIHSS) score on admission was 3. Patients with CSVD had a higher burden of vascular risk factors, including hypertension, previous stroke, diabetes, and atrial fibrillation, and presented with higher NIHSS scores and blood pressure on admission. A patent foramen ovale (PFO)–related stroke mechanism was less frequent in patients with CSVD (1.1% vs. 10.0%), although this association was not statistically significant in multivariable analysis (odds ratio 0.30, 95% CI 0.06–1.38).DiscussionA high SVD burden is consistent with hypertensive arteriopathy as the predominant underlying etiology, whereas minimal SVD may indicate alternative mechanisms such as PFO-related stroke. Recognition of these differences may support more tailored diagnostic evaluation and secondary prevention strategies.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneur.2026.1849475</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneur.2026.1849475</link>
        <title><![CDATA[Neuroimaging characteristics associated with early neurological deterioration in single subcortical infarction patients]]></title>
        <pubdate>2026-08-05T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Yating Wu</author><author>Le Chen</author><author>Zezheng Sun</author><author>Jingtao Pi</author><author>Jian Wu</author>
        <description><![CDATA[Background and purposeSingle subcortical infarctions (SSIs) are frequently complicated by early neurological deterioration (END), which adversely impacts long-term functional outcomes. However, the neuroimaging predictors of END in SSI patients remain insufficiently characterized. This study aimed to comprehensively evaluate the predictive value of multiple neuroimaging biomarkers for END in SSI patients.MethodsWe retrospectively enrolled consecutive patients diagnosed with acute SSIs in the middle cerebral artery (MCA) perforating territory. Neuroimaging assessments included apparent diffusion coefficient (ADC) and relative ADC (rADC) values, axial infarct location, MCA plaque status evaluated by whole-brain vessel wall imaging, and cerebral small vessel disease (CSVD) burden. END was defined as an increase of ≥2 points in the total NIHSS score or ≥1 point in the motor subscore within 72 h of admission.ResultsA total of 129 SSI patients were enrolled, of whom 32 (24.8%) developed END. Lower ADC and rADC values, larger maximum infarct diameter, more proximal axial infarct location, and the presence of MCA plaques were significantly associated with END on univariate analysis. rADC demonstrated superior predictive performance over ADC, with an optimal cut-off of 0.61 (sensitivity 84%, specificity 50%). On multivariable logistic regression, rADC < 0.61 (OR = 4.23, 95% CI: 1.58–11.61, P = 0.004) and MCA plaque presence (OR = 2.80, 95% CI: 1.14–6.89, P = 0.025) emerged as independent predictors of END. Neither CSVD burden nor any individual CSVD imaging marker was significantly associated with END.ConclusionsrADC and MCA plaque are independent neuroimaging predictors of END in SSI patients, while CSVD burden showed no significant association. These findings support early magnetic resonance imaging-based risk stratification and individualized therapeutic decision-making in clinical practice.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneur.2026.1895597</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneur.2026.1895597</link>
        <title><![CDATA[Astrocyte–blood–brain barrier crosstalk in cerebral small vessel disease: linking barrier dysfunction to neurovascular failure]]></title>
        <pubdate>2026-08-05T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Mei Xie</author><author>Shuang Wu</author><author>Ling Yang</author><author>Yuqiang Zhang</author>
        <description><![CDATA[Cerebral small vessel disease (CSVD) is a heterogeneous group of disorders involving the cerebral microvasculature and is a major cause of stroke and vascular cognitive impairment. The role of blood–brain barrier (BBB) dysfunction in CSVD is now recognized as a key pathological process; however, conventional vascular risk factors do not fully explain its initiation, progression, or clinical heterogeneity. Astrocyte–BBB crosstalk has been implicated in endothelial dysfunction, pericyte injury, and vascular remodeling, and the mechanisms by which early barrier instability progresses to neurovascular failure remain poorly understood. This review highlights astrocytes as active regulators of BBB integrity and neurovascular unit homeostasis. Astrocytic endfeet support endothelial junctions, regulate basement membrane structure, and maintain water and ion homeostasis, perivascular exchange, inflammatory regulation, and neurovascular coupling. Astrocytes may shift from a homeostatic to a reactive state following chronic hypoperfusion, inflammatory stress, metabolic injury, or APOE4-related vulnerability, leading to increased inflammatory signaling, loss of AQP4 and Kir4.1 polarization, basement membrane remodeling, and pericyte dysfunction. Barrier instability persists, resulting in impaired glymphatic clearance, disrupted cerebral blood flow regulation, and white matter and cognitive impairment. We hypothesize a key mechanistic link between BBB dysfunction and neurovascular failure in CSVD related to disrupted astrocyte–BBB crosstalk. However, much of the current evidence is derived from animal models and in vitro systems, and direct human data–particularly from longitudinal imaging and biomarker cohorts–remain limited. Future work should integrate imaging, biomarkers, and stratified therapies to improve early detection and restore astrocytic endfoot polarity and BBB homeostasis.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneur.2026.1860091</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneur.2026.1860091</link>
        <title><![CDATA[Associated factors for stroke-related sarcopenia: a scoping review]]></title>
        <pubdate>2026-08-04T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Fanchi Xu</author><author>Yaqin You</author><author>Yijing Ling</author><author>Yehong Wei</author><author>Meng Hu</author>
        <description><![CDATA[ObjectiveTo review and summarize research on stroke-related sarcopenia, identify its associated factors, and provide a theoretical foundation for further research and interventions.MethodsA systematic search was conducted in Chinese National Knowledge Infrastructure (CNKI), Wanfang, VIP, SinoMed, PubMed, Web of Science, CINAHL, Embase, and the Cochrane Library for Chinese and English literature on stroke-related sarcopenia. The search covered publications from the inception of each database through March 4, 2026. The study analyzed and summarized the literature by defining the research topic, screening studies, and conducting methodological evaluations, thereby identifying and summarizing the associated factors associated with stroke-related sarcopenia.ResultsThis study included a total of 32 studies, comprising 28 original studies and 4 meta-analyses. Based on the 28 original studies, a total of 32 associated factors for stroke-related sarcopenia were identified, specifically: low BMI, advanced age, low phase angle, reduced calf circumference, low SMI (skeletal muscle index), waist circumference, nutritional status, smoking, low quality of life, decreased activities of daily living, more than three comorbidities, high stroke severity, stroke duration, dysphagia, diabetes, abnormal biochemical markers, tube feeding, length of ICU stay, osteoporosis, number of strokes, cognitive impairment, weight loss, low food texture level, cardiovascular disease, female gender, physical activity level, high risk of falls, oral health issues, pneumonia, speech disorders, gut microbiota diversity, and frailty.ConclusionThe associated factors for stroke-related sarcopenia are multifaceted. Healthcare professionals need to conduct comprehensive assessments of patients to screen for potential factors associated with stroke-related sarcopenia, thereby providing a basis for clinical intervention.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneur.2026.1819306</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneur.2026.1819306</link>
        <title><![CDATA[Admission systemic inflammatory indices and 6-month functional outcome after endovascular thrombectomy for acute ischemic stroke: an exploratory single-center cohort study]]></title>
        <pubdate>2026-08-04T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Xiang Fang</author><author>Wei-fen Chen</author><author>Juan Wu</author><author>Taijian Liao</author><author>Chengmin Tong</author><author>Biyu Xu</author>
        <description><![CDATA[BackgroundMany patients still have poor functional outcomes after endovascular thrombectomy (EVT) for acute ischemic stroke. Systemic inflammatory indices from routine blood tests have been proposed as accessible prognostic biomarkers. We evaluated the association of admission neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), systemic immune-inflammation index (SII), and systemic inflammation response index (SIRI) with 6-month functional outcome after EVT, and tested whether they provide incremental prognostic value beyond the National Institutes of Health Stroke Scale (NIHSS).MethodsWe retrospectively analyzed consecutive patients undergoing EVT for anterior circulation acute ischemic stroke at one center. The primary outcome was poor functional outcome (modified Rankin Scale [mRS] 4–6) at 6 months. Associations were assessed with logistic regression and ROC analysis. Incremental value over NIHSS was assessed with likelihood-ratio tests, AUC comparison (DeLong), reclassification metrics (NRI, IDI), and decision-curve analysis.ResultsOf 90 patients, 82 (91.1%) completed follow-up, of whom 40 (48.8%) had poor outcomes; regression used 75 patients with complete inflammatory-index data (35 events). At the univariable level, poor outcome was associated with higher NIHSS (median 15.5 vs. 8.0, p < 0.001), NLR, SII, and SIRI (all p < 0.05). In multivariable analysis, only age was independently associated with poor outcome (OR 1.09, 95% CI 1.02–1.16, p = 0.008); the inflammatory indices were not, reflecting strong collinearity with NIHSS (rs = 0.88). NIHSS showed the highest discrimination (AUC 0.754, 95% CI 0.636–0.858), followed by SII (0.716, 0.592–0.836) and NLR (0.695, 0.570–0.808). Adding any inflammatory index to NIHSS did not improve discrimination or reclassification (likelihood-ratio p ≥ 0.40; ΔAUC ≤ 0.006; IDI ≈ 0; no meaningful net benefit), and results were unchanged under multiple imputation, though the sample could not exclude a small effect.ConclusionAdmission NLR, SII, and SIRI are associated with 6-month poor outcome after EVT, but this association is largely explained by stroke severity, with no detectable incremental value beyond NIHSS. These exploratory findings are hypothesis-generating and require prospective multicenter validation before clinical use.]]></description>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fneur.2026.1793860</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fneur.2026.1793860</link>
        <title><![CDATA[Gut-brain axis: a revolutionary paradigm in the pathogenesis and treatment of ischemic stroke]]></title>
        <pubdate>2026-08-03T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Yu Gou</author><author>Hong Bai</author><author>Xingshun Zhou</author><author>Cong Huang</author>
        <description><![CDATA[Ischemic stroke is a devastating neurological disorder. Despite advances in acute reperfusion therapy, patients still face high risks of poor functional recovery and stroke recurrence, highlighting the urgent need to explore new pathological mechanisms and therapeutic targets. In recent years, the Gut-Brain Axis—a bidirectional communication network connecting the brain, gut, and gut microbiota—has provided a novel framework for understanding stroke pathophysiology. This review systematically summarizes how gut microbiota correlates with the progression of major stroke risk factors including hypertension and atherosclerosis, and explicitly distinguishes that most human observational data only support correlative associations, while causal evidence is largely limited to preclinical animal models. We further clarify the two-way communication pathway after stroke: cerebral ischemia impairs intestinal barrier function and causes microbial imbalance through autonomic and inflammatory responses; in turn, disturbed gut microbiota and metabolites correlate with aggravated brain damage and hindered repair via immune, metabolic, and neural signaling, mainly by regulating neuroinflammation and controlling key metabolites such as short-chain fatty acids and trimethylamine N-oxide. Based on these mechanisms, we comprehensively assess preclinical and clinical evidence of microbiota-targeted interventions, including dietary modification, probiotics, and fecal microbiota transplantation. We emphasize that existing clinical evidence is mostly derived from small-sample, single-center trials with inconsistent outcomes, and large-scale multicenter sham-controlled randomized controlled trials are mandatory before any routine clinical application can be recommended. We also discuss key challenges such as distinguishing causal relationships from correlative observations, bridging preclinical translational gaps, and addressing inter-individual heterogeneity across patient populations, and propose future translational research directions. Targeting the Gut-Brain Axis represents a promising preclinical systemic strategy for stroke prevention, acute care, and long-term rehabilitation, yet robust human validation is still lacking. This approach marks a fundamental paradigm shift in the field of stroke research, though overoptimistic clinical translation expectations should be avoided given the substantial unresolved translational limitations.]]></description>
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