BACKGROUND:Carotid artery web is a rare and underrecognized cause of ischemic stroke. Current literature emphasizes their underdiagnosis and association with high recurrence rates despite medical management. We report a single-center experience of carotid revascularization in patients with ischemic stroke and ipsilateral carotid webs. METHODS:This retrospective case series includes 20 patients who presented with acute strokes attributed to ipsilateral carotid webs and subsequently underwent carotid revascularization at a Comprehensive Stroke Center between January 2015 and December 2025. Data on demographics, clinical presentation, and imaging findings were collected via chart review. Descriptive statistics summarize patient characteristics and outcomes. RESULTS:Twenty patients with ischemic stroke and ipsilateral carotid artery web underwent carotid revascularization. The median age was 54 years (IQR: 45-62), and 70% were female. Median NIHSS was 9 (IQR: 5-15). Fifteen (75%) underwent mechanical thrombectomy and 8 (40%) received IV thrombolysis. Sixteen (80%) had carotid web on the right side. Revascularization was performed for stroke recurrence (30%), superimposed thrombus (25%), or secondary prevention (60%), with overlapping indications. TCAR was the most common approach (65%), followed by CAS (20%) and CEA (15%). Over a median follow-up of 9 months (IQR: 6-21), no patients experienced recurrent ischemic stroke in the treated vascular territory, suggesting potential effectiveness of revascularization in preventing recurrence in selected patients with carotid webs. CONCLUSION:Our study highlights the significance of early detection and intervention. All forms of carotid revascularization, including TCAR, have shown effectiveness and safety. However, larger studies are essential to validate these findings.
Background It remains uncertain whether remote ischemic conditioning (RIC) with transient cycles of limb ischemia and reperfusion is an effective supplement to standard-of-care management of intracerebral hemorrhage (ICH). Methods This is a predefined sub-study to a randomized clinical trial conducted at four stroke centers in Denmark. RIC was induced by using an inflatable cuff on the upper extremity with a cuff pressure of at least 200 mm Hg and sham cuff pressure of 20 mm Hg. Each treatment application consisted of 5 cycles with 5 minutes of inflation followed by 5 minutes of deflation. Hematoma and edema volumes were manually segmented by blinded assessors. The primary end point was the risk of hematoma expansion (growth exceeding 6 mL or a relative growth of more than 33%). Results Among 1500 prehospital randomized patients, 165 patients had an ICH. Of them, 87 patients were randomly assigned to RIC and 78 to sham treatment. The median age was 71 (IQR: 60, 77), 73 (44%) were females, and the median onset to randomization was 40 minutes (IQR: 30, 69). The median National Institute of Health Stroke Scale score was 12, and 19 patients (12%) had either hematoma evacuation or an external ventricular drain. The study did not provide evidence for a difference in the adjusted risk of 24-hour hematoma expansion in patients treated with RIC compared to sham with a risk difference of -0.052 (95% CI: -0.20;0.10, p=0.504) nor for a difference in the adjusted 7-day hematoma reabsorption rate with a mean difference of 5.47 mL (95% CI: -4.57;15.52, p=0.280). There was no significant difference in edema size at baseline, 24 hours or 7 days. Conclusions and Relevance RIC initiated in the prehospital setting and continued in the hospital did not reduce hematoma expansion or peri-hematoma edema in patients with ICH. Trial registration linicalTrials.gov:NCT03481777
BACKGROUND:The triglyceride-glucose (TyG) index and non-traditional lipid parameters have been linked to cardiovascular and cerebrovascular risk, but longitudinal evidence on their combined utility for predicting incident stroke remains limited. We aimed to evaluate the associations between composite indices integrating the TyG index with seven non-traditional lipid parameters and incident stroke risk, and to determine whether these indices provide incremental predictive value beyond individual parameters. METHODS:We analyzed data from the China Health and Retirement Longitudinal Study (2011-2018), including 7,578 stroke-free participants aged ≥45 years. Seven composite indices were calculated as the product of the TyG index and each non-traditional lipid parameter. Cox proportional hazards models, restricted cubic splines, ROC curves, NRI, IDI, and mediation analyses were employed. RESULTS:During a median 7-year follow-up, 481 incident strokes occurred. After full adjustment, higher quartiles of most composite indices were associated with increased stroke risk, with TyG-LCI showing the strongest association (hazard ratio, 1.84; 95% CI, 1.37-2.47). Restricted cubic splines revealed non-linear exposure-response relationships. Composite indices yielded higher AUC values than conventional lipid parameters, and TyG-AIP, TyG-CRI-I, and TyG-LCI significantly improved risk reclassification and discrimination. The TyG index partially mediated the associations of CRI-II, AC, Non-HDL-C, and CRI-I with stroke (mediation proportions: 41.7%, 62.4%, 63.5%, 62.4%). CONCLUSIONS:Composite indices combining the TyG index with non-traditional lipid parameters were consistently associated with incident stroke in middle-aged and older Chinese adults. Derivable from routine glucose and lipid tests, these measures may serve as adjuncts for primary stroke risk assessment by reflecting the combined burden of insulin resistance and atherogenic dyslipidemia.
AIM:To describe outcomes among treated patients with thrombolysis and compare associations across three therapeutic-window periods in acute ischemic stroke. METHODS:We conducted a subanalysis of the FAICAM registry, a retrospective multicenter cohort from 2022, including patients ≥18 years with acute ischemic stroke treated with intravenous alteplase within or beyond the standard therapeutic window. Patients with baseline Modified Rankin Scale (mRS) of >2 or those who underwent thrombectomy were excluded. Bivariate and multivariate analyses were performed for therapeutic windows of ≤3, 3-4.5, and >4.5 hours RESULTS: We analyzed 355 patients; 283 of whom had 3-month mRS data. Functional independence was 82.0% in group treated within first 3 hours, 68.9% (between 3 and 4.5 hours), and 58.6% (after 4.5 hours) at 3 months. In the multivariate analysis, patients treated between 3 and 4.5 (aRR: 0.83; 95% CI: 0.72-0.96; p = 0.011) and >4.5 hours (aRR: 0.71; 95% CI: 0.56-0.90; p = 0.005) were associated with a lower probability of functional independence versus ≤3 hours.at 3 months CONCLUSIONS: In this real-world cohort of patients treated with intravenous alteplase in Latin American hospitals, treatment closer to symptom onset was associated with a higher probability of functional independence at 3 months; because this study did not include an untreated comparison group, it cannot establish the efficacy of thrombolysis itself. These findings underscore the importance of standardizing selection criteria and hospital protocols to improve safety monitoring for patients treated within the extended window.
BACKGROUND:Secondary brain injury following intracerebral hemorrhage (ICH) is largely driven by regulated cell death and neuroinflammation. Necroptosis, a form of programmed necrotic cell death mediated by the RIP1/RIP3/MLKL pathway, has emerged as a key contributor to tissue injury after ICH; however, effective strategies for its modulation remain limited. OBJECTIVE:This study aimed to determine whether RIP1/RIP3/MLKL-dependent necroptosis is functionally activated after ICH and to investigate whether scalp acupuncture (SA) modulates this pathway, using the necroptosis inhibitor necrostatin-1 (Nec-1) as a mechanistic comparator. METHODS:A total of 168 adult male Sprague-Dawley rats were randomly assigned to sham, ICH, SA + ICH, and Nec-1 + ICH groups. Neurological function, necroptotic cell death, ultrastructural alterations, necroptosis-related signaling molecules, inflammatory mediators, and brain edema were systematically evaluated using behavioral assessments, propidium iodide staining, immunofluorescence, transmission electron microscopy, Western blotting, RT-qPCR, ELISA, and wet/dry weight analysis. RESULTS:Following ICH, multiple independent assays consistently demonstrated marked activation of necroptosis in perihematomal brain tissue, including increased PI-positive cells, RIP1/RIP3 colocalization, mitochondrial structural disruption, and upregulation of RIP1, RIP3, MLKL, PGAM5, DRP1, and HMGB1. Both SA and Nec-1 significantly attenuated necroptosis-related signaling and were associated with improved neurological outcomes. Notably, compared with Nec-1, SA exerted stronger inhibitory effects on proinflammatory cytokine release and brain edema. CONCLUSION:These findings support a prominent role for RIP1/RIP3/MLKL-mediated necroptosis in secondary injury after ICH in male rats. SA effectively attenuates necroptosis-related signaling and associated neuroinflammation, highlighting its potential as a multimodal biological intervention. Given that only male animals were included, further studies incorporating female subjects are warranted to determine whether sex-specific differences influence necroptotic signaling or therapeutic responsiveness.
Introduction The pathological mechanism of post-intracerebral hemorrhage (ICH) brain injury remains incompletely clarified. This study aims to clarify the role and molecular mechanism of miR-642b-3p in ICH, thereby providing a potential candidate target for clinical treatment. Material and methods We enrolled 66 ICH patients and 70 matched healthy controls with strict inclusion/exclusion criteria, and used multivariable linear regression to analyze independent correlates of miR-642b-3p and SERPINE1. Collagenase-induced rat ICH models with pre-calculated sample size, random grouping and blinded tests were established, followed by intracerebroventricular injection of 5 nmol/rat miR-642b-3p agomir. Neurological function, brain edema and inflammatory cytokines were detected via mNSS, mLPT and ELISA. LPS-stimulated BV-2 microglia, dual-luciferase assay and SERPINE1 overexpression rescue experiments were adopted to validate the miRNA-target regulatory cascade. NLRP3 inflammasome components and microglial polarization markers were further assessed by qPCR. Results miR-642b-3p decreased while SERPINE1 increased in patient serum and rat brain tissue; hematoma volume and GCS score independently predicted their expression. miR-642b-3p overexpression suppressed SERPINE1, relieved edema, improved neurofunction and lowered proinflammatory cytokines in vivo. In LPS-treated BV-2 cells, miR-mimic reversed abnormal SERPINE1 elevation and inflammation, whereas SERPINE1 overexpression abolished such protective effects. Dual-luciferase assay verified direct binding between miR-642b-3p and SERPINE1 3’UTR. Moreover, miR-642b-3p inhibited NLRP3 inflammasome activation and promoted microglial M2 polarization by targeting SERPINE1. Conclusion Our findings support that restoration of miR-642b-3p alleviates post-ICH cerebral edema and neurological deficits via targeted inhibition of SERPINE1-mediated inflammation, involving suppression of NLRP3 inflammasome and promotion of M2 polarization. The miR-642b-3p/SERPINE1 axis may serve as a promising therapeutic target for ICH.
INTRODUCTION:Carotid artery stenting (CAS) is an alternative revascularization method for patients with internal carotid stenosis in whom an endovascular approach is selected instead of carotid endarterectomy. In recent years, dual-layer stents have increasingly been employed due to their better plaque coverage compared to closed-cell stents. The aim of this study was to report the outcomes of these two stent types in a real-world clinical setting. METHODS:Patients with internal carotid artery stenosis who underwent CAS between 2004 and 2023 at two high-volume centers were retrospectively analyzed. Plaques were classified as: type 1(lipid-rich), type 2(fibro lipid) and type 3(calcified). Primary endpoints included technical success (defined as residual stenosis <30% on completion angiography), and the incidence of stroke/death and TIA/stroke within 30 days comparing period of procedures and clinical manifestation (symptomatic and asymptomatic) comparing type of stent and type of plaque. RESULTS:A total of 944 CAS procedures were performed. Most of patients were male (68%) and younger than 80 years (72%). Symptomatic stenosis was present in 236(25%) patients, while 708(75%) were asymptomatic, with calcified plaques being most common (60%). Technical success was achieved in 94% procedures. In 6%, CAS procedure was abandoned due to excessive arch/carotid tortuosity. Before and after 2014 technical success rates were 9.7% and 3.6% (p < 0.001). The overall 30-day TIA/stroke and stroke/death rates were 6.4% and 2.4%, 10% and 4% in symptomatic and 5% and 2% in asymptomatic. Closed-cell stents (Wallstent, Boston Scientific Corporation, Massachusetts, USA) and dual-layer stents (Roadsaver, Terumo Corporation, Tokyo, Japan) were used in 64% and 36% of cases. Stroke/death and TIA/stroke occurred in 2.8%vs.0.8% (p = 0.20) in asymptomatic, and in 14.2%vs.5.4%(p = 0.05) in symptomatic. The 30-day stroke/death rate was 0.7%vs.0.8% (p = 0.80) in asymptomatic, while the 30-day TIA/stroke rate was higher, but not statistically significant, in the Wallstent group (5.9% vs.4.2%p = 0.30) in symptomatic. Patients with type 0-2 plaques treated with dual-layer stents had a significantly lower 30-day TIA/stroke rate (10% vs.3.7%, p = 0.02). Asymptomatic status (OR:0.4,95%CI:0.2-0.8, p = 0.008) and use of dual-layer stents (OR:0.5,95%CI:0.3-1, p = 0.05) are independent protective factors for 30-day TIA/stroke. CONCLUSION:Dual layer devices are associated with a significantly lower 30-day TIA/stroke rate in patients with vulnerable plaque types (1-2). Symptomatic status and stent design both influenced periprocedural outcomes, underscoring the value of tailoring device choice to plaque morphology.
Background and Purpose Ischemic stroke (IS) remains a leading global cause of mortality and disability. Although current reperfusion strategies have advanced, the complex pathological mechanisms underlying IS continue to significantly limit clinical prognosis. Recently, the pivotal role of the microbiota-gut-brain axis (MGBA) in the pathological evolution of IS has garnered widespread attention. This review systematically delineates the multidimensional regulatory roles of the gut microbiota and its metabolites in IS pathogenesis, with a specific focus on immuno-metabolic crosstalk, cellular senescence, and programmed cell death. Observations Emerging evidence indicates that IS-induced central stress is accompanied by intestinal mucosal barrier dysfunction and gut microbial dysbiosis. Increased intestinal permeability may facilitate the systemic translocation of microbial products and inflammatory mediators, thereby promoting peripheral immune activation and the recruitment of immune cells to the ischemic brain. Aging-associated microbial disturbances and chronic inflammation may further modify these responses and contribute to heterogeneous stroke outcomes. Microbiota-derived metabolites, particularly short-chain fatty acids, participate in immune and metabolic regulation through receptor-mediated and epigenetic mechanisms. However, direct evidence demonstrating the migration of gut-derived immune cells into the human ischemic brain or microbiota-mediated regulation of neuronal ferroptosis remains limited. Conclusions Current evidence supports an association between MGBA dysfunction and the immunometabolic responses involved in IS. Further longitudinal human studies and mechanistically informed clinical trials are required to determine whether microbiota-targeted strategies can improve prevention, prognostic assessment, or treatment.
Background and Purpose Mechanical thrombectomy (MT) is a cost-effective treatment for large-vessel occlusion stroke. However, existing economic evaluations rely on restrictive assumptions regarding care pathways and resource use, limiting their applicability to real-world implementation. We evaluated the cost and cost-effectiveness implications of implementing MT across alternative, empirically observed clinical pathways in England to address this source of decision uncertainty. Methods A state-transition Markov model was populated with detailed United Kingdom clinical, outcome, and micro-costing data from five thrombectomy centres in England to compare MT with standard care. Alternative implementation scenarios reflected real-world variation in treatment pathways, including intervention-centre type, anaesthesia use, intensive care unit setting, and models of care. Scenarios were characterised using detailed pathway and cost data. Costs and quality-adjusted life-years were evaluated over a 5-year time horizon from National Health Service and societal perspectives. Results Mean procedural costs for MT were £6,135 (95% CI, £5,961-£6,318) per patient in the primary analysis, compared with £7,283 in the earlier protocol-based model. Over 5 years, MT was a dominant intervention, associated with both lower costs and improved health outcomes compared with standard care. Mean cost savings were £2,297 per patient, corresponding to an estimated annual saving of £52.6 million if all 22,908 potentially eligible patients were treated. Across all five centres and implementation scenarios, incremental cost-effectiveness ratios consistently remained below currently accepted willingness-to-pay thresholds per quality-adjusted life-year gained. Conclusions Across a range of real-world clinical pathways, MT is highly likely to be a cost-saving alternative to current practice and cost-effective at current health opportunity-cost thresholds. These findings suggest that cost-effectiveness is robust to local variation in service delivery and support broader implementation of MT within the English stroke-care system.
Background Middle meningeal artery embolization (MMAE) has emerged as a promising adjunctive treatment for chronic subdural hematoma (cSDH); however, the efficacy and safety of adjunctive MMAE compared with surgery alone remains uncertain. Methods We systematically searched PubMed, Embase, and the Cochrane Central Register of Controlled Trials from inception through June 2026. Randomized controlled trials comparing adjunctive MMAE plus surgical evacuation with surgical evacuation alone in patients with cSDH were included. The primary outcome was hematoma recurrence. Pooled odds ratios (ORs) with 95% CIs were calculated using a random-effects model. Results A total of eight randomized controlled trials were included. The mean age of participants ranged from 64 to 77 years, and most participants were male. Adjunctive MMAE was associated with significantly lower odds of recurrence compared with surgery alone (OR, 0.31 [95% CI, 0.16–0.59]). No significant differences were observed in all-cause mortality (OR, 0.91 [95% CI, 0.24–3.42]), good functional outcome (OR, 1.23 [95% CI, 0.23–6.42]), or overall adverse events (OR, 1.02 [95% CI, 0.35–2.91]) between the groups. Conclusions In this updated meta-analysis of randomized controlled trials, adjunctive MMAE significantly reduced recurrence without increasing complication rates. Although no significant improvements were observed in functional outcomes or mortality, these findings support adjunctive MMAE as an effective and safe strategy for improving disease control in patients undergoing surgical treatment for cSDH.
BACKGROUND AND AIMS:Lipoprotein(a) [Lp(a)] is associated with atherosclerotic cardiovascular disease and ischemic stroke, but its relationship with hemorrhagic stroke remains uncertain. We performed a systematic review and meta-analysis evaluating circulating Lp(a) levels and hemorrhagic stroke risk. METHODS:MEDLINE and Scopus were searched from inception to May 10, 2026, for observational studies reporting circulating Lp(a) in adults with hemorrhagic stroke. Continuous Lp(a) outcomes were pooled as standardized mean differences (SMDs); odds ratios (ORs) from case-control studies and hazard ratios (HRs) from prospective cohort studies were analyzed separately using inverse-variance random-effects models. A combined log-ratio model was included as exploratory analysis. RESULTS:Eight studies (526,909 participants; 2,895 hemorrhagic stroke cases) were included in the systematic review; individual analyses drew on subsets. Three studies showed higher Lp(a) levels in hemorrhagic stroke than in healthy controls (SMD, 0.32; 95% CI, 0.18-0.47; I²=0%). Two case-control studies showed greater odds of hemorrhagic stroke (pooled OR, 1.72; 95% CI, 1.31-2.27), whereas four prospective cohort studies showed no association (pooled HR, 0.88; 95% CI, 0.67-1.14; I²=71.8%); the subgroup difference was significant (p = 0.0005). An exploratory model combining OR- and HR-based estimates showed no statistically significant association (1.06; 95% CI, 0.80-1.40). Lp(a) did not differ significantly between hemorrhagic and ischemic stroke (SMD, -0.13; 95% CI, -0.40 to 0.15). CONCLUSIONS:Post-event studies reported higher circulating Lp(a) levels in hemorrhagic stroke, but this evidence was at serious risk of bias and should be regarded as hypothesis-generating. Prospective cohort studies showed no significant association with incident hemorrhagic stroke.
BACKGROUND AND PURPOSE:Despite high rates of macrovascular recanalization, approximately half of patients with large vessel occlusion stroke fail to achieve functional independence after endovascular thrombectomy (EVT). Residual tissue-level perfusion abnormalities - detectable on post-procedural CT perfusion (CTP) - have been proposed as a biomarker of futile recanalization. We aimed to establish post-EVT perfusion imaging (by CT or MR perfusion) as a surrogate marker predictive of functional independence on the modified Rankin Scale - by synthesizing evidence-based perfusion thresholds and defining the optimal acquisition timing. Analysis was restricted to studies performing perfusion imaging exclusively after EVT, so that thresholds reflect post-procedural reperfusion status rather than pre-treatment ischemic burden. METHODS:We systematically searched MEDLINE, EMBASE, and the Cochrane Library from January 2018 through April 2026 for cohort studies performing perfusion imaging after EVT, reporting at least one quantitative CT- or MR-perfusion parameter alongside functional outcome (modified Rankin Scale [mRS] at any post-procedural time point) or neurological outcome (National Institutes of Health Stroke Scale [NIHSS]), and enrolling ≥10 patients. Both anterior and posterior circulation occlusions were eligible. The review was conducted in accordance with PRISMA 2020 (checklist provided as supplementary material). Risk of bias was assessed using the ROBINS-I tool. Pooled odds ratios (ORs) were estimated using the DerSimonian-Laird random-effects estimator. A pre-specified sensitivity analysis excluded our proof-of-concept cohort (which received adjunctive cerebrolysin) to isolate the pooled estimate from any treatment-related influence. RESULTS:Eight independent post-EVT perfusion imaging studies (670 patients; five CT-perfusion, two MR-perfusion, and one mixed CT/MR cohort) met inclusion criteria. Residual hypoperfusion was present in 21-53% of angiographically successful reperfusions and was consistently associated with reduced odds of functional independence (pooled OR 0.28, 95% CI 0.15-0.51; I²=6%). The pre-specified sensitivity analysis excluding the cerebrolysin-treated cohort yielded a pooled OR of 0.30 (95% CI 0.16-0.54; I²=0%), confirming that the pooled effect is not driven by the adjuvant-treated subgroup. A Tmax >6 s volume <3.5 mL at 30-90 min post-EVT was the most consistently validated CT-perfusion threshold (adjusted OR 3.5, 95% CI 1.6-7.8); for MR perfusion, an rCBV-defined impaired-microvascular-reperfusion volume >5 mL was the corresponding threshold. The optimal perfusion acquisition window is 30-120 min post-EVT. CONCLUSIONS:Post-EVT perfusion imaging (CT or MR) provides tissue-level reperfusion information that complements modified Thrombolysis in Cerebral Infarction (mTICI) grading and identifies biologically distinct patient subgroups. Standardized post-EVT perfusion imaging at 30-120 min, applied with the proposed threshold framework, should be considered as an eligibility criterion and stratification variable in future trials of post-EVT adjuvant therapy across the pharmacological spectrum.
BACKGROUND:The erythrocyte sedimentation rate (ESR) is a non-specific marker of systemic inflammation. White matter lesions (WMLs), appeared as hyperintensities on T2-weighted and FLAIR MRI, reflect chronic microvascular ischemia of cerebral white matter. Inflammation has been implicated in the pathogenesis and progression of WML. We hypothesized that higher ESR levels are associated with greater WML progression. METHODS:We retrospectively screened 2356 patients aged ≥40 years or older who underwent serial MRI brain at least one year apart between 2011 and 2015 at the Mayo Clinic 1,377 patients with an available baseline ESR measurement were included in the analysis. ESR was annual rate of of WMH progression stratified into quartiles; high ESR was defined as values >23 mm/hr (Q4), whereas low ESR was defined as values ranging from 0 to 23 mm/hr (Q1-Q3). . The primary outcome was the annualized change in WML volume (cc/year). Univariate and multivariable linear regression analyses assessed the association between ESR and WML progression. RESULTS:Of the 1377 patients meeting the inclusion criteria, 54.2% were female, and the median age was 69 (IQR 60-76) years. The annual rate of WMH progression was faster in high-ESR group than in the low-ESR group (median 0.93 cc/year vs. 0.76 cc/year, p = 0.010). In univariate regression analysis, high ESR was significantly associated with greater WML progression (β = 0.42, p = 0.013). After multivariable adjustment, including baseline WML volume, upper-quartile ESR remained independently associated with greater annualized WML progression (β = 1.23; 95% CI 0.17-2.28; p = 0.023). CONCLUSION:Elevated ESR independently predicts WML progression, suggesting that systemic inflammation may contribute to the progression of cerebral small vessel disease.
BACKGROUND:Among stroke syndromes, acute basilar artery occlusion (BAO) is associated with the worst outcomes and highest mortality. Existing studies suggest that endovascular thrombectomy (EVT) significantly improves functional outcomes at 90 days. While EVT is generally safe across ages and severities, additional data are needed to identify patients at risk of unfavourable long-term outcomes. METHODS:This prospective, registry-based, single-centre, cohort study spanning 18 years evaluated functional independence in BAO patients at 3 months (primary outcome) and 1 year (secondary outcome) post-intervention (n=149; median age 70 years). Patients from the recent 8-year period were individually analysed at discharge and 3 months (n=126; median age 77 years). Safety outcomes included reperfusion status, major complications, and mortality, with one-year outcomes assessed through standardised telephone interviews. RESULTS:Successful reperfusion was achieved in up to 91.9%. Favourable outcomes occurred in 34.2% of patients at three and 36.9% at 12 months. Overall mortality was 34.2% at 3 months and increased to 45.6% at 12 months, regardless of reperfusion success. Mortality was significantly higher in those aged ≥80, at 41.9% (3 m) and 62.8% (12 m), with only 14% achieving favourable outcomes at 12 months. An initial National Institutes of Health Stroke Scale (NIHSS) score ≥20 further predicted poorer outcomes, with no patient ≥80 with a score ≥20 (n=25) having favourable outcomes at one year, and 68% died. CONCLUSION:While EVT increases the chances of independent living one-year post-event in patients with favourable predictive factors, elderly individuals with significant initial deficits are at a high risk of severe disabilities and mortality. Prognoses based solely on the first three months may lead to overestimations of benefit in this demographic.
OBJECTIVE:To systematically evaluate the association between lipoprotein-associated phospholipase A2 (Lp-PLA2) levels and the risk of recurrent cerebrovascular events in patients with ischemic stroke. METHODS:PubMed, Web of Science, Embase, the Cochrane Library, and China National Knowledge Infrastructure were systematically searched from inception to May 20, 2026. Observational studies reporting the association between Lp-PLA2 levels and the risk of recurrent cerebrovascular events in patients with ischemic stroke were included. The primary outcome was recurrent cerebrovascular events, mainly including ischemic stroke, acute cerebral infarction, or cerebral infarction recurrence. Because studies comparing high versus low Lp-PLA2 levels reported both hazard ratios (HR) and odds ratios (OR), the pooled results were expressed as pooled relative effect estimates with 95% confidence intervals (CI). For the continuous-variable analysis, effect estimates were rescaled and expressed as ORs per 1 standard deviation (SD) increase in Lp-PLA2. All meta-analyses were performed using random-effects models. RESULTS:Ten studies involving 2,527 patients with ischemic stroke were included in the meta-analysis. Higher Lp-PLA2 levels were associated with an increased risk of recurrent cerebrovascular events (pooled relative effect estimate = 2.99, 95% CI 2.24-3.99; P < 0.001). After excluding the study that did not report the cutoff value for the high and low Lp-PLA2 groups, the association remained stable (pooled relative effect estimate = 2.76, 95% CI 2.20-3.47; P < 0.001). In the continuous-variable analysis, each 1-SD increase in Lp-PLA2 was associated with an increased risk of recurrent cerebrovascular events (pooled OR = 2.62, 95% CI 1.08-6.33; P = 0.033). CONCLUSION:Higher Lp-PLA2 levels are associated with an increased risk of recurrent cerebrovascular events in patients with ischemic stroke. Lp-PLA2 may be a promising prognostic marker for secondary prevention after ischemic stroke.
Background Lower-limb motor dysfunction after stroke severely compromises mobility and quality of life. Brain–computer interface (BCI) technology, which employs a “central–peripheral–central” closed-loop to promote neuroplasticity, offers a promising rehabilitation approach. However, its optimal dosing parameters remain unclear. Objective This study aimed to evaluate the efficacy of BCI-based training on lower-limb motor function, balance, walking capacity, and activities of daily living (ADL) after stroke, and to explore the impact of total training dose, session duration, and stroke phase. Methods We systematically searched major databases for randomized controlled trials (RCTs) published up to April 2026. All included studies were RCTs. Methodological quality was assessed using the PEDro scale. A meta-analysis was conducted using RevMan 5.4 to calculate mean differences (MD) and 95% confidence intervals (CI). Results Ten RCTs involving 366 participants were included. BCI training significantly improved lower-limb motor function (Fugl-Meyer Assessment for Lower Extremity: MD = 2.38, 95% CI 1.72 to 3.04, P < 0.00001). Although this mean difference is below the anchor-based Minimal Clinically Important Difference (MCID) of 6 points reported for chronic stroke populations, it represents a statistically robust and consistent improvement across RCTs, suggesting potential clinical relevance, particularly in subacute patients or specific intervention subgroups. Conclusions BCI-based training effectively improves lower-limb motor recovery after stroke. Subgroup analyses suggested that a moderate total dose (401–800 minutes) combined with 20–40-minute sessions may represent a potentially optimal regimen, although these findings are based on limited RCTs and require confirmation in larger studies.
Background/Objectives Stroke represents one of the main causes of permanent disability, with persistent upper limb motor deficits in 50% of patients; post-stroke spasticity limits functional recovery and quality of life. The aim of the study was to evaluate the effects of robotic device RYMO (Mobi-L) on spasticity management, motor function recovery, and subjective satisfaction in patients with chronic stroke. Methods A descriptive case-series study was conducted on three patients with chronic stroke (>2 years). Each subject performed five sessions of robotic training with RYMO (Mobi-L) in active-assisted mode (45 minutes of effective training per session). Pre- and post-treatment assessments (T0–T1) included the Modified Ashworth Scale, Fugl-Meyer Assessment, Motricity Index, Barthel Index, Client Satisfaction Questionnaire and Patient Global Impression of Change. Conclusions All patients completed the treatment cycle without adverse events, and showed a positive direction of change for MAS score at elbow and wrist districts. Motor improvements were more evident in proximal segments on FMA-UE, with slight increases of Motricity Index. Barthel Index remained unchanged, while satisfaction (CSQ-8) was high (31/32) and perceived change (PGIC) was moderate-positive (2/3). Despite the short duration of the protocol and the small sample size, results suggest a clinically impact on tone modulation and functional perception, with a higher self-perceived efficacy in daily activities.
Background Stressful life events (SLEs) across the life course have been recognized as important psychosocial stressors that may adversely influence cardiometabolic and cerebrovascular health. However, the cumulative and stage-specific impact of SLEs on stroke risk, and the potential mediating role of intrinsic capacity, remain insufficiently understood in aging populations. Methods We analyzed data from 7,605 participants aged ≥45 years in the China Health and Retirement Longitudinal Study (CHARLS). Childhood and adulthood SLEs were retrospectively assessed using the 2011 baseline survey and 2014 Life History Survey, covering six domains in each life stage. Stroke was defined as self-reported physician diagnosis. Logistic regression models estimated the associations between SLEs and stroke, with sequential adjustment for demographic, lifestyle, clinical, and biochemical covariates, including heart disease and depressive symptoms as additional confounders. Subgroup and sensitivity analyses were performed across sex, residence, education, marital status, smoking, drinking, and geographic region. Causal mediation analysis further examined whether intrinsic capacity mediated the relationship between SLEs and stroke. Results Participants with stroke were older, more often male, and had higher prevalence of adulthood and cumulative SLEs, as well as higher rates of heart disease (36.1% vs. 17.6%) and depression (41.6% vs. 30.7%). Our findings demonstrate that adulthood and cumulative life-course SLEs are robustly associated with increased odds of stroke, while childhood SLEs alone show no independent association. Each one-unit increase in the cumulative SLEs score was associated with higher odds of stroke (fully adjusted OR=1.35, 95% CI: 1.12–1.64, p = 0.002). Compared with no exposure, adulthood SLEs (OR=1.55, 95% CI: 1.06–2.26, p = 0.023) and combined childhood and adulthood SLEs (OR=1.82, 95% CI: 1.22–2.70, p = 0.003) were strongly associated with stroke, whereas childhood SLEs alone were not significant (OR=1.35, 95% CI: 0.94–1.92, p = 0.102). These associations remained robust after additional adjustment for heart disease and depressive symptoms. Subgroup analyses indicated consistent associations across most strata, with stronger effects in urban residents, individuals with higher education, and drinkers. Notably, the association was stronger in females (OR=1.80, 95% CI: 1.32–2.46) than males. Mediation analyses reveal that intrinsic capacity partially mediates these relationships, accounting for approximately 4.6–17.3% of the total effect (proportion mediated declining from 17.3% in the unadjusted model to 4.6% after full adjustment), suggesting that maintaining functional reserve may partially mitigate the adverse cerebrovascular consequences of psychosocial stress. Sensitivity analyses excluding participants aged >80 years (OR=1.34, 95% CI: 1.10–1.63, p = 0.003) and >85 years (OR=1.35, 95% CI: 1.11–1.64, p = 0.002) confirmed the robustness of the findings. Conclusions These results provide novel insights into the life-course mechanisms linking stress exposure to cerebrovascular health and highlight potential intervention targets for stroke prevention in aging populations. Life-course stressful life events, particularly those occurring in adulthood and cumulative across childhood and adulthood, are robustly associated with increased stroke risk in Chinese middle-aged and older adults. Intrinsic capacity partially mediates this relationship, suggesting that maintaining functional reserve may buffer the adverse effects of psychosocial stressors. These findings underscore the importance of life-course approaches to stroke prevention and highlight the need for integrated strategies targeting psychosocial stress and intrinsic capacity in aging populations.
