Non-traumatic stroke (NTS) is associated with high mortality, and dynamic glucose patterns may provide prognostic information beyond static glucose measurements. This study aimed to identify glucose trajectory phenotypes in ICU patients with NTS and evaluate their association with in-hospital mortality. This multicenter retrospective cohort study included ICU patients with NTS from MIMIC-IV, eICU, and NSICU. Glucose trajectories during the first 168 h after ICU admission were identified using latent class growth modeling. Associations with in-hospital mortality were assessed using Cox regression, Kaplan-Meier analysis, competing-risk analysis, and subgroup analyses. Incremental predictive value was evaluated using AUC, integrated discrimination improvement (IDI), net reclassification improvement (NRI), and median improvement in predicted risk. Among 11,177 patients, four glucose trajectory phenotypes were identified: normoglycemia (NG, n = 5,515), stable mild hyperglycemia (SMH, n = 3,425), persistent hyperglycemia (PH, n = 2,080), and highly variable hyperglycemia (HVH, n = 157). Compared with NG, SMH, PH, and HVH were progressively associated with higher in-hospital mortality in the fully adjusted model, with HRs of 1.668 (95% CI: 1.469-1.894), 2.406 (95% CI: 2.083-2.779), and 5.766 (95% CI: 4.319-7.699), respectively. HVH remained associated with increased mortality in both diabetic and non-diabetic patients. Adding glucose trajectories to baseline prediction models modestly improved AUC, IDI, NRI, and predicted risk classification across LASSO, Boruta, and BSS-BIC models. In ICU patients with NTS, glucose trajectory phenotypes were associated with different risks of in-hospital mortality, with HVH showing the strongest association. Glucose trajectories may provide additional prognostic information for risk stratification beyond static glucose measurements.

Abstract Background Microglial lipid handling and mitochondrial failure contribute to brain injury after subarachnoid hemorrhage (SAH), but the lipid signals coupling these processes remain unclear. We investigated whether linoleic acid (LA) restores microglial homeostasis through lysophosphatidylglycerol 16:0 (LPG[16:0]) and peroxisome proliferator-activated receptor-δ (PPARδ). Methods Case-control CSF metabolomics included 30 patients with aneurysmal SAH and 10 controls. Mechanisms were examined in a blood-injection mouse model and hemoglobin-exposed primary mouse microglia using targeted lipidomics, RNA sequencing, mitochondrial and phagocytosis assays, pharmacological perturbation, fractionation, coimmunoprecipitation, thermal shift analysis, and structural modeling. Behavioral outcomes were evaluated by open- field, Y-maze, and Morris water-maze testing. Results CSF LA concentrations were higher in patients with SAH than in controls and discriminated the groups within this cohort (area under the curve, 0.9967 [95% CI, 0.9859–1.000]; P<0.001). LA attenuated inflammatory activation and restored phagocytosis, mitochondrial membrane potential, respiration, and ATP production in hemoglobin-exposed microglia. LA restored PLA2G15-associated LPG(16:0) levels, which phenocopied these effects. Transcriptomic and inhibitor analyses identified PPARδ as a downstream effector. LPG(16:0) increased PPARδ stability, and fractionation and protease protection identified a PPARδ pool on the cytosolic face of the outer mitochondrial membrane. PPARδ associated with PLIN2 and CPT1A, promoted lipid droplet–mitochondria apposition, and supported fatty acid oxidation. In mice, LA reduced neuroinflammatory injury and partially improved anxiety- related behavior and spatial memory. Conclusions The LA–LPG(16:0)–PPARδ axis links glycerophospholipid remodeling to organelle coupling and mitochondrial recovery in microglia after SAH. The preventive dosing paradigm requires validation in clinically relevant treatment settings.

BackgroundVertebrobasilar dolichoectasia (VBD) carries high risks of stroke and hemorrhage, yet current treatments remain suboptimal and often compromise critical pontine perforators (PPs). We used computational fluid dynamics (CFD) to evaluate a novel hemodynamically-guided, perforator-sparing reconstruction strategy.MethodsPatient-specific CFD models from 24 VBD patients were compared with 24 age-sex-matched controls and virtual post-intervention models simulating idealized partial anterior basilar artery (BA) lumen reduction to establish hemodynamic optimization targets while preserving posterior wall PPs. Transient simulations quantified pressure, velocity, time-averaged wall shear stress (TAWSS), oscillatory shear index (OSI), and relative residence time (RRT) within the BA and nine modeled PPs per case.ResultsUntreated VBD exhibited pathological hemodynamics: elevated aneurysmal pressure (101.73 ± 0.28 vs. 100.59 ± 0.87 mmHg, p < 0.001), flow stasis (velocity: 5.53 ± 3.52 vs. 12.41 ± 3.44 cm/s, p < 0.001), reduced TAWSS (0.007 ± 0.004 vs. 0.03 ± 0.01 Pa, p < 0.001), and increased OSI (0.07 ± 0.04 vs. 0.01 ± 0.00) and RRT (12.73 ± 13.81 vs. 0.33 ± 0.11 /Pa, all p < 0.001). Perforator hemodynamics remained comparable to controls. Virtual reconstruction of BA normalized all aneurysmal parameters toward physiological levels (Post vs. Pre: all p < 0.001) without adversely affecting hemodynamics in the modeled PPs under the assumptions of the CFD framework. Strong correlations existed between BA volume and adverse hemodynamics, with therapeutic benefits approaching saturation at about 250 mm3.ConclusionThis in silico study demonstrates that perforator-sparing partial reconstruction can normalize VBD’s pathological hemodynamics without adversely affecting hemodynamics in the modeled PPs, and establishes a quantitative framework for future endovascular device development, though clinical translation requires validation through experimental models and prospective trials.

Subarachnoid hemorrhage (SAH) is a type of stroke mainly caused by the bursting of brain aneurysms, releasing iron ions into the subarachnoid space and subsequently inducing ferroptosis. Despite the utilization of various ferroptosis-inhibiting pharmacological agents to enhance neurological outcomes post-SAH, challenges such as inadequate targeting and suboptimal drug utilization persist. In response to these limitations, we have developed a novel spatiotemporal cascade reaction liposome that recombinant proteins incorporating neuron-targeting peptides and the functional structural domain of ferroptosis suppressor protein 1 (FSP1) were immobilized on the external surface of liposomes, which were internally loaded with coenzyme Q10 (CoQ10) to construct FSP1-Lipo-CoQ10.The purpose of this study is to investigate the neuroprotective effects of FSP1-Lipo-CoQ10 following SAH. As a result, FSP1-loaded liposomes enable targeted delivery to neurons in the lesion area and increase FSP1 levels on the cell membrane. Among the three liposomal formulations, FSP1-Lipo-CoQ10 demonstrated the most potent anti-ferroptosis effects and the greatest improvement in neurological function. FSP1-Lipo-CoQ10 provides a new approach for the therapeutic management of ferroptosis post-SAH and ameliorates associated pathological conditions.

BackgroundAcute brain injury (ABI) requires early, interpretable risk stratification to support ICU risk assessment. We evaluated whether longitudinal albumin-to–red cell distribution width ratio (ARR) trajectories provide time-dependent prognostic information and support prediction with multicenter validation.MethodsIn this multicenter, retrospective cohort study (NSICU, MIMIC-IV, eICU), latent class growth modeling identified ARR trajectories. Nonproportional hazards were addressed with time-stratified Cox models (0–7, 7–14, >14 days) and restricted mean survival time (RMST) at 7, 14, and 28 days. Multiple machine-learning classifiers were benchmarked to develop an interpretable prediction model with internal and external validation. Performance assessment included discrimination, calibration, decision-curve analysis, and SHAP-based interpretability.ResultsAmong 8,270 ICU patients (NSICU n = 5,093; MIMIC-IV n = 744; eICU n = 2,433), four ARR trajectories were identified. Relative to Gradual Decline, recovery-type trajectories were associated with lower early mortality risk (0–7 days: HRs 0.29 and 0.14; 7–14 days: HRs 0.43 and 0.50), whereas the Sustained High-Risk trajectory showed excess hazard primarily beyond 14 days (HR 1.42). These time-dependent patterns were broadly supported by RMST and sensitivity analyses. The final ExtraTrees model achieved AUROC 0.869 and Brier score 0.066 on the internal hold-out set; external validation yielded AUROC 0.731, PR AUC 0.429, and Brier score 0.161, indicating attenuated but informative external performance with modest decision-curve benefit. A web-based research calculator provides individualized risk estimates and SHAP explanations.ConclusionStandardized ARR trajectories provide dynamic, phase-specific prognostic information in ABI and complement static assessments. When integrated into an interpretable machine-learning model, these trajectories may support adjunctive risk estimation as patient status evolves. Prospective evaluation and site-level recalibration are warranted.

Background Dynamic metabolic changes may influence outcomes after acute brain injury (ABI), but most ICU studies use only a single triglyceride-glucose (TyG) value. We examined whether ICU TyG trajectories and a cumulative TyG burden provide time-sensitive prognostic information and can be embedded in an interpretable mortality model. Methods Adults with ABI from three ICU databases (NSICU, MIMIC-IV, eICU) were retrospectively analyzed. TyG trajectories were derived from serial ICU measurements, cumulative exposure was summarized as prespecified threshold-based mean area under the curve (TBM), and in-hospital mortality was evaluated with 7-day time-stratified Cox models. A machine-learning model including TyG trajectory, TBM, and routinely available clinical variables was trained in NSICU and validated in the pooled external cohort. Results Among 4,760 admissions, three trajectories were identified-low-slightly increasing (LSI), moderate-increasing (MI), and persistently high (PH). Mortality did not differ across trajectories during days 0-7, but after day 7 both MI (HR 1.48, 95% CI 1.18-1.86; P < 0.001) and PH (HR 1.51, 95% CI 1.17-1.93; P = 0.001) showed higher in-hospital mortality than LSI. TBM showed a parallel positive association; TBM8p7 remained significant in fully adjusted models (HR 1.42, 95% CI 1.18-1.70; P < 0.001). ExtraTrees was selected for its consistent internal and external validation performance, and model interpretability analyses placed TyG trajectory and TBM8p7 among the next most important predictors alongside SOFA score and vasopressor use. Conclusion In ICU-treated ABI, TyG is better modeled as a time-aware exposure: trajectory differences become prognostically relevant only after the first week, whereas cumulative TBM8p7 shows a graded, independent association with mortality. Both metrics add risk information beyond conventional severity indicators and can be integrated into an interpretable, externally tested model.

INTRODUCTION:Subarachnoid hemorrhage (SAH) is a common subtype of stroke characterized by bleeding into the subarachnoid space. Increasing evidence suggests that neuronal ferroptosis- an iron-dependent, non-apoptotic form of cell death-contributes significantly to the secondary brain injury and poor prognosis observed in SAH patients. However, there are currently no effective pharmacological interventions specifically targeting ferroptosis in this context. METHODS:In this study, network pharmacology was combined to explore the potential mechanism of baicalin in alleviating neuronal ferroptosis after SAH by Western blot, qPCR, DHE probe, TMRE probe, and transmission electron microscopy in in vivo and in vitro SAH models. RESULTS:The results of network pharmacology showed that baicalin mainly acted on the ferroptosis marker PTGS2, and the results of KEGG analysis suggested that the effect of baicalin in attenuating ferroptosis might be realized by activating the PI3K/AKT pathway. Baicalin partially restored the SAH-induced reduction of GPX4 expression and effectively suppressed the upregulation of NLRP3. These effects were abolished by the PI3K/AKT inhibitor LY294002. Baicalin was found to be effective in improving neurological function in mice in an in vivo SAH model. DISCUSSION:This study demonstrated that baicalin attenuates neuronal ferroptosis after SAH by activating the PI3K/AKT pathway, which in turn upregulates GPX4 and suppresses NLRP3. These findings offer new insights into the pharmacological treatment of neuronal ferroptosis following SAH. CONCLUSION:Baicalin can alleviate ferroptosis after SAH by activating the PI3K/AKT pathway.

Subarachnoid hemorrhage (SAH) results in the accumulation of blood in the subarachnoid space, which can trigger inflammatory responses and oxidative damage, thereby exacerbating secondary brain injury. Microglia play a critical role in clearing hematomas and cellular debris during pathological recovery. This study aimed to investigate the regulatory role of SIRT2 in phagocytic function and its potential mechanisms. The SAH model of endovascular perforation in Sprague-Dawley (SD) rats and in vitro model of primary microglia culture with Oxygenated hemoglobin (OxyHb) stimulation were used. Flow cytometry, Western blot, immunofluorescence, ELISA were used to detect the microglial phagocytic ability, expressions of SRIT2 and LC3-associated phagocytosis (LAP)-related proteins. Molecular docking, and immunoprecipitation were used to explore the underlying mechanism of the SIRT2/NRF2/CD36 signaling pathway. Behavioral experiments were conducted to evaluate changes in neurological function. Within 24 h after SAH, the expression of SIRT2 in brain and microglia was significantly increased, while the phagocytic ability and the expression of LAP-related proteins Rubicon, NOX2 were decreased. After inhibiting SIRT2, microglial LAP function was enhanced and the phagocytic index was increased. Mechanistically, SIRT2 inhibited NRF2 nuclear translocation by deacetylation, thereby downregulating CD36 expression and suppressing microglia LAP. ML385 reversed the enhancement of LAP and the improvement in neurological function induced by SIRT2 inhibition. SIRT2 suppresses microglial LAP by deacetylating NRF2, thereby impairing its nuclear translocation and reducing transcriptional expression of CD36 subsequently. Inhibiting SIRT2 may effectively enhance microglial LAP function via activating NRF2/CD36 pathway, promoting blood clearance and improving neurological prognosis after SAH.

To summarize the clinical and radiological outcomes of a novel cerebral revascularization technique based on the superficial temporal artery patency concept (STAPC) in patients with moyamoya disease (MMD). A retrospective review was conducted of adult patients with MMD treated at Beijing Hospital and Nanjing Drum Tower Hospital between January 2019 and December 2021. The cohort comprised 170 patients who underwent superficial temporal artery–middle cerebral artery bypass with encephalo-duro-arterio-synangiosis (EDAS) (STA-MCA/EDAS), and 133 who underwent EDAS alone. Radiological follow-up included computed tomography (CT) angiography (CTA) to assess bypass patency and CT perfusion (CTP) for hemodynamic staging at 3 and 12 months post-revascularization. Clinical follow-up recorded perioperative complications and recurrent stroke events that occurred > 12 months postoperativerly. Of the 303 patients, 37 cases (12.21

OBJECTIVE:The pathophysiological distinctions and modifiable risk factors underlying ischemic versus hemorrhagic conversion in moyamoya disease (MMD) remain incompletely characterized, hindering subtype-specific management. This study aimed to delineate subtype-specific risk patterns and validate biomarkers for asymptomatic progression. METHODS:The authors analyzed the medical records of 774 adult MMD patients from Nanjing Jinling Hospital (2010-2020) and Nanjing Drum Tower Hospital (2013-2020). MMD was stratified as asymptomatic (n = 139), ischemic (n = 450), or hemorrhagic (n = 185). Multivariable logistic regression and Cox proportional hazards models were used to evaluate metabolic profiles, angiographic features (posterior cerebral artery [PCA] involvement and choroidal and lenticulostriate anastomoses), and longitudinal outcomes. RESULTS:Symptomatic patients demonstrated higher PCA involvement prevalence versus asymptomatic patients (p < 0.001). Ischemic MMD was independently associated with male sex (OR 2.00, 95% CI 1.30-3.07; p = 0.002), hypertension (OR 2.30, 95% CI 1.49-3.54; p < 0.001), hypertriglyceridemia (OR 1.36, 95% CI 1.01-1.83; p = 0.04), hyperglycemia (OR 1.22, 95% CI 1.03-1.45; p = 0.02), and PCA involvement (OR 2.43, 95% CI 1.40-4.20; p = 0.001). Hemorrhagic MMD correlated with BMI (OR 0.88 per kg/m2, 95% CI 0.81-0.97; p = 0.007), hypercholesterolemia (OR 1.53, 95% CI 1.14-2.07; p = 0.005), choroidal anastomosis formation (OR 2.38, 95% CI 1.21-4.70; p = 0.01), and PCA involvement (OR 3.41, 95% CI 1.76-6.61; p < 0.001). During the median 44-month follow-up, asymptomatic patients with PCA involvement (adjusted hazard ratio [HR] 4.86, 95% CI 1.07-22.14; p = 0.04) or choroidal anastomosis (adjusted HR 5.92, 95% CI 1.27-27.62; p = 0.02) exhibited an elevated risk of symptomatic conversion. CONCLUSIONS:Ischemic MMD was independently associated with male predominance, hypertension, and dyslipidemia, while hemorrhagic transformation correlated with lower BMI, hypercholesterolemia, and choroidal anastomosis. PCA involvement and choroidal anastomosis emerged as critical biomarkers for asymptomatic risk stratification.

Background and objective:Postoperative cerebral hyperperfusion syndrome (CHS) remains a common and serious complication after extracranial-intracranial (EC-IC) bypass for moyamoya disease (MMD). This study aimed to identify preoperative hemodynamic predictors of CHS using quantitative whole-brain CT perfusion (WB-CTP) analysis. Methods:The author retrospectively analyzed 103 hemispheres from 89 MMD patients who underwent direct bypass from January 2024 to December 2024. Preoperative WB-CTP scans based on the Alberta Stroke Program Early CT score (ASPECTS) topography were processed to quantify cerebral blood flow (CBF) and time to peak (Tmax) across various brain regions, with the cerebellum serving as the reference. CHS was diagnosed based on clinical and radiological criteria. Univariable and multivariable logistic regression analyses were performed to identify independent predictors, and receiver operating characteristic (ROC) analysis was used to evaluate predictive performance. Results:Postoperative CHS occurred in 11.7% (12/103) of the included cases. Univariable analysis revealed Suzuki stage, moyamoya vessel density, and Tmax values in the thalamus (THAL) and posterior cerebral artery (PCA) regions as significant factors. Multivariable analysis confirmed advanced Suzuki stage (OR (95% CI), 8.87(1.44-54.45), p = 0.018), and lower PCA Tmax (OR (95% CI), 0.03 (0.00-0.69), p = 0.029) as independent predictors. ROC analysis demonstrated that combining Suzuki stage and PCA Tmax achieved an AUC of 0.83 (cut-off value = 0.060), indicating good discriminative performance for predicting postoperative CHS. Conclusion:Advanced Suzuki stage and reduced PCA Tmax are independent risk factors for postoperative CHS after direct bypass in MMD patients. Preoperative ASPECTS-based quantitative CTP analysis can effectively stratify CHS risk and support individualized surgical planning and perioperative management.

BACKGROUND:Acute brain injury (ABI) often elevates intracranial pressure (ICP), yet static measurements miss dynamic risk. We evaluated the prognostic value of early ICP trajectories. METHODS:We formed a multicenter ICU cohort from MIMIC-IV (2008-2022), eICU (2014-2015), and NSICU (2024-2025). Latent class growth modeling identified ICP trajectories over the first 120 h. Associations with in-hospital mortality were tested with Cox models, and incremental value beyond baseline clinical variables was quantified by AUC, integrated discrimination improvement (IDI), and net reclassification improvement (NRI). Sensitivity analyses were performed across datasets and age groups. RESULTS:Among 1700 patients with ABI, four trajectories emerged-Severe Progressive, Stabilized Elevated, Mildly Elevated Stable, and Normal. Versus Normal, mortality risk was highest for Severe Progressive (HR 13.54; 95% CI 9.35-19.59), followed by Stabilized Elevated (HR 2.53; 1.83-3.49) and Mildly Elevated Stable (HR 1.48; 1.16-1.91). In patients aged ≥ 55 years, risk with Stabilized Elevated was amplified (HR 2.87; 1.97-4.20). Adding trajectories improved risk stratification (IDI +0.065; NRI +0.201) with modest AUC gains. CONCLUSIONS:Early ICP trajectories define reproducible phenotypes with distinct mortality risk. Incorporating trajectories-particularly the stabilized-elevated pattern in older adults-adds prognostic value beyond clinical variables and supports prospective validation.

Background: Subarachnoid hemorrhage (SAH) is a devastating cerebrovascular disease with high incidence and mortality rates, often associated with aneurysm rupture. Neuroinflammation, primarily mediated by microglial activation, is a critical process in the secondary injury following SAH. Despite extensive research, current Western medicine treatments have shown limited efficacy in mitigating neuroinflammation caused by microglia. In contrast, traditional Chinese medicine has garnered increasing attention for its anti-inflammatory properties. Isoorientin, a flavonoid compound, has demonstrated anti-inflammatory and antioxidant effects in various diseases. We hypothesize that isoorientin may inhibit microglia-induced neuroinflammation after SAH through the AKT/GSK3(3 pathway. Purpose: To elucidate whether isoorientin can regulate neuroinflammation following subarachnoid hemorrhage via the AKT/GSK3(3 pathway. Methods: We established in vitro and in vivo SAH models using hemoglobin and blood injection methods, respectively. The regulatory effects of isoorientin on neuroinflammation were investigated using Western blotting (WB), quantitative polymerase chain reaction (qPCR), enzyme-linked immunosorbent assay (ELISA), and immunofluorescence staining (IF). Network pharmacology and molecular docking studies were conducted to explore the potential mechanisms. Additionally, the AKT inhibitor (MK2206) was employed to investigate its effects on the AKT/GSK3(3 pathway and neurological function after SAH. Neuroprotective effects were assessed using neurological function scores, open field tests, and rotarod tests. Results: Isoorientin significantly inhibited the mRNA expression levels of pro-inflammatory cytokines (TNF-alpha, IL-1(3, and IL-6) and promoted the expression levels of anti-inflammatory cytokines (CD206, IL-4, and IL-10). It facilitated the transformation of microglia from the M1 (pro-inflammatory) to the M2 (anti-inflammatory) phenotype. Further experiments revealed that isoorientin increased the expression of p-AKT protein in microglial cells, leading to the inactivation of GSK3(3 and upregulation of p-GSK3(3 protein, thereby suppressing neuroinflammation. However, these effects were reversed upon the addition of the AKT inhibitor (MK2206). In vivo experiments demonstrated that isoorientin improved short-term neurological functions, including motor functions, balance, and coordination abilities. Conclusion: This study provides compelling evidence that isoorientin exerts neuroprotective effects by regulating the AKT/GSK3(3 pathway, which may play a crucial role in mitigating neuroinflammation and neurological dysfunction after SAH. Isoorientin holds promise as a valuable therapeutic candidate for SAH treatment.

This study aimed to investigate the antitumor effects and underlying mechanisms of β-boswellic acid (β-BA) in glioblastoma (GBM). U251 and U87 cells were treated with β-BA, and cell growth, migration/invasion, pyroptosis, and mitochondrial function were evaluated using viability, proliferation, LDH release, immunofluorescence, ultrastructure, and Western blot assays. In vivo efficacy was assessed in a U251 xenograft mouse model. β-BA significantly inhibited GBM cell proliferation, migration, and invasion in a dose-dependent manner. β-BA induced mitochondrial structural disruption, loss of mitochondrial membrane potential, and excessive ROS accumulation, which activated the NLRP3 inflammasome and triggered pyroptosis, as evidenced by elevated cleaved Caspase-1, GSDMD-N, and ASC expression. MCC950 partially reversed these effects, confirming NLRP3 involvement. In vivo, β-BA markedly reduced tumor growth and consistently induced mitochondrial damage, NLRP3 activation, pyroptosis execution, decreased Ki-67/PCNA levels, and suppression of EMT progression. β-BA exerts potent anti-GBM activity by inducing mitochondrial dysfunction and NLRP3-mediated pyroptosis, providing a mechanistic basis for developing β-BA as a promising natural therapeutic candidate for GBM.

Background:Stroke remains the leading cause of long-term disability worldwide. Approximately 60% of individuals with chronic ischemic stroke experience persistent upper limb impairment that limits daily activities. The Repair Study aims to evaluate the safety and efficacy of vagus nerve stimulation (VNS) paired with rehabilitation in patients with chronic ischemic stroke in developing countries, including those with severe upper limb dysfunction, thereby generating evidence to support broader global application. Methods:It is a multicenter, triple-blinded, randomized controlled trial conducted across 13 centers in China. Up to 99 participants with upper limb motor impairment, 9 months to 10 years post-stroke, will be enrolled. All participants will undergo VNS implantation (Model G115R/G115, PINS Medical, Beijing, China) and be randomized 2:1 by a central randomization system to active stimulation (0.8 mA) or sham stimulation (0 mA) paired with standardized upper limb rehabilitation. The blinded phase includes 6 weeks of clinical therapy (three sessions/week, 90-120 min/session, ≥300 stimulation-movement repetitions) followed by 6 weeks of home-based therapy (30 min/day). Post-unblinding, the active VNS group continues home-based therapy, while the sham group receives 6 weeks of clinic-based therapy. Discussion:The primary outcome is the between-group difference in Fugl-Meyer Assessment for Upper Extremity scores at the end of 6 weeks of clinical therapy. Secondary outcomes include additional motor, functional, and quality-of-life measures. Safety will be assessed through adverse event monitoring. The Repair Study is a multicenter randomized controlled trial targeting chronic ischemic stroke populations in developing countries. It supplements the existing clinical evidence by enrolling patients with more servere motor dysfunction and being conducted in a developing country. Trial Registration:ClinicalTrials.gov: NCT06722677.

Ventriculoperitoneal shunting (VPS) helps reduce intracranial pressure and alleviate clinical symptoms caused by hydrocephalus in hemorrhagic Moyamoya disease (MMD). To date, no literature describes the occurrence of subdural fluid collection (SDFC) in hemorrhagic MMD patients undergoing VPS prior to cerebral revascularization. This report aims to explore the potential pathological mechanisms underlying SDFC following cerebral revascularization after prior VPS, and to provide effective strategies for future prevention. Clinical data of hemorrhagic MMD patients undergoing VPS prior to bypass admitted to our hospital from 2021 January and 2024 December were selected. Medical records were reviewed to analyze patient characteristics and the entire disease course. Among the 7 patients (9 cases), postoperative SDFC occurred in 7 cases (7/9, 77.8

The purpose of this study was to determine whether dynamic Glasgow Coma Scale (GCS) trajectories are associated with mortality risk and provide incremental prognostic information beyond selected baseline clinical variables in intensive care unit (ICU)-admitted patients with non-traumatic stroke (NTS). In this retrospective cohort study of 7876 patients from the MIMIC-IV, eICU, and NSICU databases, latent class growth modeling (LCGM) was used to identify GCS trajectories. The associations of trajectory groups and threshold-based GCS metrics with in-hospital mortality were evaluated using multivariable Cox regression. The incremental value of trajectories was assessed using variable sets selected by Boruta, least absolute shrinkage and selection operator (LASSO), and best subset selection (BSS). Four distinct GCS trajectories were identified: stable high (35.7

Objective:Fixed cerebral perfusion pressure (CPP) targets may not fully capture dynamic changes in acute brain injury (ABI). We aimed to identify CPP trajectory phenotypes, evaluate cumulative CPP metrics, and examine their associations with in-hospital mortality in ICU patients with ABI. Methods:This multicenter retrospective cohort study included 1,466 adults with ABI from three ICU databases (MIMIC-IV, eICU, and NSICU). CPP trajectory phenotypes were identified using latent class growth modeling. Cumulative CPP metrics were derived using threshold-specific methods at 50, 60, and 70 mmHg and a mixed-effects approach. Associations with in-hospital mortality were assessed using multivariable Cox regression and survival analyses. The incremental prognostic value of CPP trajectory was evaluated as a secondary exploratory analysis. Results:Four CPP trajectory phenotypes were identified: Stable Normal, Gradual Recovery, Labile Improvement, and Rapid Decline. Compared with Stable Normal, mortality risk increased progressively in Gradual Recovery (HR 1.720, 95% CI 1.252-2.362), Labile Improvement (HR 2.081, 95% CI 1.508-2.873), and Rapid Decline (HR 5.313, 95% CI 3.547-7.958; all P < 0.001). Higher cumulative CPP metrics derived from threshold-specific and mixed-effects approaches were consistently associated with lower in-hospital mortality (all P < 0.001). Survival analyses showed clear separation across phenotypes, with Stable Normal showing the highest survival probability and Rapid Decline the lowest. Adding CPP trajectory to a baseline model modestly improved discrimination and reclassification (AUC 0.759 to 0.773, P = 0.011; IDI 0.025; continuous NRI 0.157; both P < 0.001). Conclusions:Distinct CPP trajectory phenotypes and cumulative CPP metrics were associated with in-hospital mortality in ICU patients with ABI. CPP trajectory also provided modest incremental prognostic information and warrants prospective validation.