Objective: Transcranial magnetic stimulation (TMS), as a non-invasive means of neuromodulation, plays a crucial role in rehabilitation. Recent studies highlight that modeling the TMS-induced electric field (E-field) is essential to maximize the personalized treatment efficacy. Despite advancements in various E-field calculation methods, classic numerical calculation pipelines remain time-consuming and rely on whole head segmentation, and deep learning-based pipelines suffer from limited interpretability and stability. Methods: We develop a comprehensive pipeline that supports both numerical methods and deep learning methods for TMS targeting and optimization based on local E-field, called PLED. This pipeline mainly consists of local image patch extraction, tissue segmentation, local E-field estimation, and coil placement optimization. Notably, prior information about tissue conductivity and primary E-field from the coil is embedded into the deep learning model. Results: We have conducted extensive experiments on four datasets involving millions of local image patches in total. It is examined that our pipeline runs over 40 times faster on CPU and 100 times faster with GPU acceleration than classic numerical calculation pipelines for coil placement optimization. Meanwhile, compared to other deep learning-based pipelines, our pipeline achieves higher accuracy at most potential stimulation sites across the entire brain. Conclusion: Our proposed pipeline enables rapid, accurate, and robust local E-field estimation and coil placement optimization. Significance: Our pipeline would enhance stimulation efficacy and reduce data processing time in the precise personalized TMS treatment and rehabilitation.

Neuroimmune dysregulation, characterized by microglial overactivation and imbalances in mitochondrial dynamics within the central nervous system represents a core pathological mechanism in postoperative cognitive dysfunction (POCD). This study investigated the neuroinflammation-mitochondrial interaction through the establishment of in vivo and in vitro models using lipopolysaccharide (LPS). Findings indicated that LPS-induced microglial overactivation was associated with marked upregulation of mitochondrial fission proteins, including phosphorylated Drp1 at Ser616, mitochondrial Drp1, and Fis1, along with downregulation of mitofusin-2. These alterations promoted mitochondrial fragmentation in hippocampal neurons, which subsequently led to mitochondrial membrane potential depolarization, adenosine triphosphate depletion, and excessive production of reactive oxygen species. This cascade further activated the intrinsic apoptotic pathway via Bax/Bcl-2 imbalance and caspase-9/3 activation. Conversely, administration of the Drp1 inhibitor Mdivi-1 reduced microglial activation, attenuated inflammatory cytokine levels, restored mitochondrial network integrity and function, inhibited neuronal apoptosis, and ameliorated LPS-induced spatial memory impairment in behavioral assays. These findings indicate that microglial activation-induced mitochondrial fission plays a pivotal role in inflammation-related cognitive impairment. Moreover, they highlight mitochondrial fission as a promising therapeutic target for intervention in POCD.

Background Acute ischaemic stroke often leads to significant disability and mortality. Secondary brain injury caused by post-stroke immune and inflammatory responses worsens outcomes.Aim To assess the efficacy and safety of low-frequency deep transcranial magnetic stimulation (LF-dTMS), delivered with an H4 coil to target the insular and prefrontal cortex, and its potential effects on neuroimmune activity and recovery.Design This randomised, multicentre, open-label, parallel-group trial with blinded outcome assessment evaluates early LF-dTMS at 1 Hz using the H4 coil in adults with anterior-circulation acute ischaemic stroke treated within 48 hours of onset. Participants are randomly assigned in a 1:1 ratio to receive either standard care plus LF-dTMS or standard care alone. Active LF-dTMS is delivered as two sessions per day, 1200 pulses per session, for three consecutive days.Study outcomes The primary efficacy outcome is the growth in infarct volume from baseline to day 3, measured by diffusion-weighted MRI. The primary safety outcome is symptomatic intracranial haemorrhage within 3 days of treatment. Secondary outcomes include the modified Rankin Scale and serious adverse events at 90 days. Exploratory analyses in a predefined subgroup will involve dynamic plasma proteomics and single-cell RNA sequencing of peripheral mononuclear cells to understand immune responses (days 0, 3, 7), as well as resting-state functional MRI to evaluate the effects of neuromodulation on brain network connectivity.Summary This study will evaluate the feasibility, safety and preliminary efficacy of early LF-dTMS in acute stroke. It will provide proof-of-concept data on whether modulating post-stroke inflammation and neuroplasticity can improve outcomes. The findings will inform the design of a large definitive trial.Trial registration number NCT06064734.

Objective:This study aimed to determine whether activation of the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway within hippocampal microglia contributes to postoperative cognitive dysfunction (POCD) in a diabetic mouse model. Diabetes was induced using a high-fat, high-sugar (HFHS) diet combined with streptozotocin (STZ).Methods:Diabetes was induced in C57BL/6J mice using an HFHS diet followed by STZ. POCD was modeled via tibial fracture surgery under general anesthesia. Cognitive function was assessed using the Open Field Test, Y-maze, and contextual fear conditioning. cGAS-STING pathway activation was evaluated by western blot for cGAS and STING expression. Microglial activation was assessed by co-localization of Iba-1 and CD68 by immunofluorescence, and the co-localization of STING with Iba-1 in the hippocampus was examined by immunofluorescence. Hippocampal neuroinflammation was quantified by enzyme-linked immunosorbent assay (ELISA) for interleukin-1beta (IL-1β) and tumor necrosis factor-alpha (TNF-α). Neuronal injury and apoptosis were evaluated by Nissl staining and western blot for cleaved caspase-3.Results:Compared to non-diabetic controls, diabetic mice exhibited cognitive impairments, which were more pronounced in those that underwent surgery. This was accompanied by significant hippocampal neuronal loss, upregulated cleaved caspase-3 expression, and elevated IL-1β and TNF-α levels. Furthermore, diabetic mice that underwent surgery displayed increased expression of microglial activation markers (Iba-1 and CD68) and evidence of cGAS-STING pathway activation in the hippocampus. Immunofluorescence co-localization experiments further suggested a predominant association of this pathway with the microglial marker Iba-1.Conclusion:These findings suggest that surgery-associated overactivation of the microglial cGAS-STING pathway in the hippocampus may exacerbate neuroinflammation and neuronal injury, thereby contributing to cognitive decline in diabetic mice.

Background This study aimed to investigate the heterogeneity of topographic and connectomic mechanisms underlying diverse functional outcomes in patients with acute ischaemic stroke.Methods and results In 7891 patients from the Third China National Stroke Registry, arterial territory maps, structural disconnection (SDC) maps and functional disconnection (FDC) maps were generated based on their ischaemic lesions. Strategic brain components, associated with functional outcomes, assessed using the modified Rankin Scale scores, were identified using multiperturbation Shapley value analysis. Exploratory subgroup analysis revealed that the strategic components identified in the arterial territory maps and the FDC maps varied by sex and age, but remained consistent in the SDC maps.Conclusion Specific topographic distributions and disconnections associated with adverse functional outcomes were identified, revealing individual heterogeneity related to age and sex. These findings may serve as imaging biomarkers and help generate testable hypotheses for potential neuromodulation targets.

Perioperative neurocognitive disorders (PND) are common and highly heterogeneous neurological complications in older and otherwise vulnerable surgical patients, with clinical manifestations ranging from delayed cognitive recovery to persistent postoperative cognitive decline. Although neuroinflammation is closely associated with the development of PND, an integrative framework is still lacking to explain how perioperative systemic immune activation leads to sustained central immune imbalance and cognitive dysfunction. Here, we propose that the brain immune landscape is a key determinant of susceptibility to PND. This landscape represents a baseline phenotype defined by central immune cell states, inflammatory activation thresholds, and resolution capacity. Within this microglia-centered framework, multiple perioperative factors may jointly drive maladaptive transitions in microglial states. We further discuss mitochondrial stress, glycolytic bias, epigenetic remodeling, non-coding RNA regulation, and trained immunity-like mechanisms, suggesting that these processes may serve as important drivers of sustained neuroimmune imbalance. This perspective supports time- and state-dependent, biomarker-guided intervention strategies aimed at preserving inflammatory resolution and enhancing perioperative cognitive resilience.

OBJECTIVE:To evaluate the efficacy of a clinical decision support system (CDSS) on stroke care quality and clinical outcomes among patients with acute ischaemic stroke. DESIGN:Multicentre, cluster randomised clinical trial. SETTING:77 hospitals across China. PARTICIPANTS:77 hospitals (38 randomised to intervention group, 39 to control group) enrolled 21 603 patients with acute ischaemic stroke admitted to hospital within seven days after symptom onset. INTERVENTIONS:Hospitals in the intervention group received stroke CDSS support including artificial intelligence assisted imaging analysis, classification of stroke causes, and evidence based treatment recommendations. Hospitals in the control group provided usual care. MAIN OUTCOMES MEASURES:The primary outcome was a new vascular event (composite of ischaemic stroke, haemorrhagic stroke, myocardial infarction, and vascular death) within three months after initial symptom onset. Secondary outcomes included the composite measure and all-or-none measure of evidence based performance measures for acute ischaemic stroke care quality, a new vascular event at six and 12 months, and disability (modified Rankin Scale score 3-6) and all cause mortality at three, six, and 12 months. Safety outcomes were moderate or severe bleeding events and all bleeding events at three, six, and 12 months. RESULTS:11 054 patients in the intervention group and 10 549 patients in the control group were enrolled from January 2021 to June 2023. New vascular events at three months occurred in 2.9% (320/11 054) in the intervention group compared with 3.9% (416/10 549) in the control group (adjusted hazard ratio 0.74, 95% confidence interval (CI) 0.58 to 0.93, P=0.01). The CDSS intervention effect remained significant in the cluster level analysis (-0.01, -0.02 to -0.004, P=0.003). Patients in the intervention group were more likely to have a higher composite measure (91.4% (77 049/84 276) v 89.8% (70 794/78 834), adjusted odds ratio 1.21, 95% CI 1.17 to 1.26, P<0.001). New vascular events were significantly lower in the intervention group at 12 months (4.0% (440/11 054) v 5.5% (576/10 549), adjusted hazard ratio 0.73, 95% CI 0.56 to 0.95, P=0.02). No significant differences were found in disability and all cause mortality. Moderate or severe bleeding, and all bleeding did not differ significantly between the two groups. CONCLUSIONS:Use of the stroke CDSS in patients with acute ischaemic stroke in China led to a significant decrease in new vascular events at three months. The stroke CDSS intervention was also effective in improving stroke care quality and decreasing long term vascular events. TRIAL REGISTRATION:ClinicalTrials.gov NCT04524624.

Background While endovascular therapy (EVT) remains the primary treatment for acute ischaemic stroke (AIS) management, persistent functional deficits in patients with successful recanalisation underscore the necessity for complementary neuroprotective strategies.Aim To investigate the safety and efficacy of low-frequency repetitive transcranial magnetic stimulation (LF-rTMS) as a potential adjunctive neuroprotective intervention following EVT in AIS patients.Design The Low-Frequency REpetitive TRanscranial Magnetic Stimulation Combined with Endovascular Treatment in ACute Ischaemic StrokE (RETRACE-II) trial is a phase II, multicentre, prospective, randomised, double-blind, sham-controlled pilot study. 60 successfully recanalised AIS patients with anterior circulation occlusion were equally randomised (1:1) to active LF-rTMS or sham intervention. The intervention involved administration of 1200-pulse 1-Hz LF-rTMS sessions (two times per day for 3 consecutive days) targeting the ipsilesional primary motor cortex (M1), initiated within 24 hours of symptom onset. Sham procedures maintained equivalent positioning with deactivated magnetic output. Standardised protocol assessments were conducted at 3-day (postintervention), 7-day and 90-day follow-ups.Study outcomes The primary efficacy endpoint was the proportion of early neurological recovery (defined as a reduction of ≥4 points on the National Institutes of Health Stroke Scale (NIHSS) or achieving a score of 0–1) at 3 days. Secondary outcomes included ischaemic penumbral salvage volume ratio, final infarct volume measured by brain MRI at 7 days, and modified Rankin Scale score at 90 days. Safety outcomes encompassed symptomatic intracranial haemorrhage, neurological deterioration (≥4-point increase in NIHSS score) and all-cause mortality through 90-day follow-up.Discussion RETRACE-II establishes methodological rigour for evaluating neuromodulation therapies during the hyperacute stroke phase, with findings expected to inform future trials and advance combination therapy paradigms in cerebrovascular neuroprotection.Trial registration number NCT06064747.

BACKGROUND: The predictive value of acute-phase functional connectivity (FC) and neurovascular coupling (NVC) for functional prognosis in stroke patients remains unclear. METHODS: In a prospective cohort of 60 stroke patients, functional near-infrared spectroscopy assessed FC, brain activation pattern, and NVC (indexed by general linear model-derived beta values) within 7 days post-stroke. Functional outcome (modified Rankin Scale [mRS] score at 90 days) was dichotomized as favorable (mRS 0-1) or unfavorable. Least Absolute Shrinkage and Selection Operator regression selected variables for a Firth's logistic regression model predicting unfavorable outcome risk. RESULTS: Patients with a favorable outcome showed stronger global FC and bilateral cortical activation, whereas unfavorable patients exhibited predominantly contralesional compensatory pattern. Task-evoked responses were greater in favorable group in the ipsilesional primary motor cortex (iM1, t = 2.09, q = 0.04) and bilateral somatosensory association cortex (SAC, ipsilesional: t = 3.49, q < 0.001; contralesional: t = 2.34, q = 0.03). A Firth's logistic regression model incorporating four predictors-admission National Institutes of Health Stroke Scale score, the contralesional frontoparietal cortex-ipsilesional supramarginal gyrus FC value, iM1-beta value, and ipsilesional somatosensory association cortex-beta (iSAC-beta) value-achieved an area under the receiver-operating characteristic curve of 0.86, with the iSAC-beta value emerging as the leading neuroimaging contributor. CONCLUSION: Acute-phase FC strength and NVC are predictive of 90-day functional outcome after stroke. Ipsilesional SAC may represent a potential target for acute-phase prognostic stratification and mechanistically informed interventions.

Background In stroke recovery, the heterogeneity of lesions and symptoms makes it challenging to target neuromodulation precisely. Conventional one-size-fits-all neuromodulation approaches yield inconsistent outcomes, highlighting the need for precision strategies, such as lesion network mapping (LNM), to identify patient-specific symptom-related networks.Aim To evaluate the efficacy and safety of LNM-guided continuous theta-burst stimulation (cTBS) in improving motor recovery in patients with acute ischaemic stroke (AIS) treated within 14 days of symptom onset.Design The mapping navigated continuous theta-burst stimulation for motor recovery (MASTRE) trial is a multicentre, randomised, double-blind, sham-controlled Phase 2 study. Eligible participants will be randomly assigned (1:1) to receive either active LNM-guided cTBS or sham stimulation. For each participant, individualised stimulation targets will be determined through LNM, and real-time neuronavigation will be used to ensure precise modulation of the disrupted sensorimotor network. Treatment will consist of one daily session for seven consecutive days. In each session, cTBS will be delivered as bursts of three pulses at 50 Hz, repeated every 200 ms for 40 s.Study outcomes The primary efficacy outcome is the change in Fugl–Meyer Assessment total motor score from baseline to Day 7 post-randomisation. Safety assessments will include symptomatic intracranial haemorrhage and adverse events, which will be monitored through Day 90 post-randomisation.Discussion The MASTRE study introduces an innovative approach to optimise cTBS therapy in AIS patients by employing LNM to identify patient-specific targets within affected sensorimotor networks. Results from this trial may inform a new precision neurorehabilitation framework, promoting personalised therapeutic interventions tailored to individual neural connectivity profiles.Trial registration number NCT06400407.

Acute ischemic cerebrovascular disease (AICVD) exhibits high recurrence rates, necessitating novel biomarkers for refined risk stratification. While MRI-derived brain age correlates with stroke incidence, its prognostic utility for recurrence is unestablished. We developed the Mask-based Brain Age estimation Network (MBA Net), a deep learning framework designed for AICVD patients. MBA Net predicts contextual brain age (CBA) in non-infarcted regions by masking acute infarcts on T2-FLAIR images, thereby mitigating the confounding effects of dynamic infarcts during acute-phase neuroimaging. The model was trained on data from 5353 healthy individuals and then applied to a multicenter cohort of 10,890 AICVD patients. Brain age gap (BAG), defined as the deviation between CBA and chronological age, independently predicted stroke recurrence at both 3 months and 5 years, outperforming chronological age. Incorporating BAG into established prediction models significantly improved discriminative performance. These findings support brain age’s potential utility in AI-driven precision strategies for secondary stroke prevention.

The roles of cerebellum after ischemic stroke remains unclear. This study aimed to assess the influence of cerebellar regional volumes on health-related quality of life (HRQoL) outcomes in patients with ischemic stroke. Using data from the China National Stroke Registry III (CNSR-III) cohort, patients having supratentorial ischemic stroke (SIS) with complete clinical and neuroimaging data were included. Volumes of 39 cerebellar regions, derived from structural magnetic resonance imaging via anatomical segmentation, were evaluated as exposures. The European Quality of Life five-dimension three-level questionnaire, defined short- and long-term multidimensional HRQoL outcomes at 3 and 12 months post-SIS respectively, further categorized into mobility, self-care, usual activity, and anxiety/depression dimensions. The population proportion of moderate and severe problems in 3-month HRQoL outcomes was higher than that in 12-month outcomes in the CNSR-III. Among 8,210 patients with SIS, the mean age was 62.39 ± 11.12 years, and 67.64

Mitochondria-associated endoplasmic reticulum membranes serve as crucial signaling hubs mediating communication between the endoplasmic reticulum and mitochondria, and play a central role in calcium ion exchange. This dynamic interface regulates key cellular processes including bioenergetic metabolism, apoptosis, autophagy, and stress responses. Dysregulation of calcium transport associated with mitochondria-associated endoplasmic reticulum membranes can disrupt intracellular homeostasis, leading to mitochondrial dysfunction, oxidative stress, and neuronal death, which are hallmarks of aging and neurodegenerative diseases. This review systematically examines the functions of protein complexes within mitochondria-associated endoplasmic reticulum membranes and the pathogenic mechanisms of calcium signaling regulated by these membranes in neurodegenerative disorders. It places particular emphasis on structural alterations in calcium ion transport machinery as a common mechanism underlying various neurodegenerative diseases. In Alzheimer's disease, mitochondria-associated endoplasmic reticulum membranes exhibit a hyperactive state, promoting the generation of amyloid-β and enhancing calcium ion flux from the endoplasmic reticulum to the mitochondria. In contrast, in Parkinson's disease and amyotrophic lateral sclerosis, the activity of mitochondria-associated endoplasmic reticulum membranes is reduced, leading to a decline in mitochondrial calcium ion buffering capacity and exacerbating excitotoxicity. Proteins residing in mitochondria-associated endoplasmic reticulum membranes are disrupted across various neurodegenerative diseases, resulting in abnormal communication between the endoplasmic reticulum and mitochondria. Recent studies indicate that mitochondria-associated endoplasmic reticulum membranes play a bidirectional role in disease progression, and compensatory mechanisms often exacerbate the pathological process. Therapeutic strategies aimed at preserving the integrity of mitochondria-associated endoplasmic reticulum membranes hold promise for alleviating neurodegenerative damage. Therefore, calcium ion exchange mediated by mitochondria-associated endoplasmic reticulum membranes plays a key role in aging and neurodegenerative diseases, making it a highly promising therapeutic target.

Alzheimer’s disease (AD) represents the most widespread neurodegenerative disorder, distinguished by a gradual onset and slow progression, presenting a substantial challenge to global public health. The mitochondrial-associated membrane (MAMs) functions as a crucial center for signal transduction and material transport between mitochondria and the endoplasmic reticulum, playing a pivotal role in various pathological mechanisms of AD. The dysregulation of mitochondrial quality control systems is considered a fundamental factor in the development of AD, leading to mitochondrial dysfunction and subsequent neurodegenerative events. Recent studies have emphasized the role of MAMs in regulating mitochondrial quality control. This review will delve into the molecular mechanisms underlying the imbalance in mitochondrial quality control in AD and provide a comprehensive overview of the role of MAMs in regulating mitochondrial quality control.

Objective This study aimed to explore whether cerebrovascular disease clinical decision support system(CDSS)could improve the key performance indicators of medical care quality. Methods In our study,ischemic stroke patients hospitalized in Ward 2 of Vascular Neurology,Beijing Tiantan Hospital,Capital Medical University before applying cerebrovascular disease CDSS(January to November 2020)were retrospectively included as the control group.Ischemic stroke patients admitted after the application of CDSS assisted diagnosis and treatment(January to November 2021)were included as the intervention group.The baseline characteristics and key performance indicators of medical care quality for ischemic stroke in these two groups were compared to assess the impact of cerebrovascular disease CDSS on medical care quality of stroke. Results A total of 1331 patients were included in this study,including 651 in the control group and 680 in the intervention group.The mean age of the control group was(71.7±11.8)years,with 490 males(75.3％),and the mean age of the intervention group was(72.3±10.2)years,with 498 males(73.2％).Among the key performance indicators of medical care quality of ischemic stroke,the proportion of patients who were unable to walk within 48 h of admission received deep vein thrombosis prevention(86.3％vs.65.0％,P<0.01),the rate of patients who were discharged with antithrombotic therapy(98.1％vs.96.2％,P=0.03),and the rate of patients with atrial fibrillation with anticoagulation therapy(70.1％vs.44.2％,P<0.01)in the intervention group were higher than those in control group. Conclusions Cerebrovascular disease CDSS can improve the key performance indicators of medical care quality in patients with ischemic stroke.

Peroxisome proliferator-activated receptor-γ (PPARγ) plays a protective role against brain injury after stroke in mice. However, the relationship between PPARγ gene polymorphisms and the functional outcome of acute ischemic stroke (AIS) remains unknown. 8822 patients from The Third China National Stroke Registry (CNSR-III) after whole-genome sequencing, two functional single nucleotide polymorphisms(SNPs) in PPARγ, rs1801282 C > G and rs3856806 C > T, were further analysed. The primary outcome was neurological functional disability at three months. Of the 8822 patients, 968 (11.0%) and 3497 (39.6%) were carriers of rs1801282 and rs3856806, respectively. Carriers of rs3856806 showed reduced risks for three-month neurological functional disability (OR, 0.84; 95% CI, 0.73-0.98; p = 0.02) and reduced risks for higher infarct volume (OR 0.90, 95% CI, 0.81-0.99, p = 0.04). They also had a reduced risk of neurological functional disability only in case of lower baseline IL-6 levels (OR 0.64, 95% CI 0.48-0.84, Pinteraction = 0.01). Carriers of rs1801282 had a reduced risk for three-month neurological functional disability (OR 0.77, 95% CI, 0.61-0.99, p = 0.04). Our study suggested that PPARγ polymorphisms are associated with a reduced risk for neurological functional disability and higher infarct volume in AIS. Therefore, PPARγ can be a potential therapeutic target in AIS.

BACKGROUND: Hemodynamic impairment of blood pressure may play a crucial role in determining the mechanisms of stroke in symptomatic intracranial atherosclerotic stenosis). We aimed to elucidate this issue and assess the impacts of modifications to blood pressure on hemodynamic impairment. METHODS: From the Third China National Stroke Registry III, computed fluid dynamics modeling was performed using the Newton-Krylov-Schwarz method in 339 patients with symptomatic intracranial atherosclerotic stenosis during 2015 to 2018. The major exposures were translesional systolic blood pressure (SBP) drop and poststenotic mean arterial pressure (MAP), and the major study outcomes were cortex-involved infarcts and borderzone-involved infarcts, respectively. Multivariate logistic regression models and the bootstrap resampling method were utilized, adjusting for demographics and medical histories. RESULTS: In all, 184 (54.3%) cortex-involved infarcts and 70 (20.6%) borderzone-involved infarcts were identified. In multivariate logistic model, the upper quartile of SBP drop correlated with increased cortex-involved infarcts (odds ratio, 1.92 [95% CI, 1.03-3.57]; bootstrap analysis odds ratio, 2.07 [95% CI, 1.09-3.93]), and the lower quartile of poststenotic MAP may correlate with increased borderzone-involved infarcts (odds ratio, 2.07 [95% CI, 0.95-4.51]; bootstrap analysis odds ratio, 2.38 [95% CI, 1.04-5.45]). Restricted cubic spline analysis revealed a consistent upward trajectory of the relationship between translesional SBP drop and cortex-involved infarcts, while a downward trajectory between poststenotic MAP and borderzone-involved infarcts. SBP drop correlated with poststenotic MAP negatively (rs=-0.765; P<0.001). In generating hemodynamic impairment, simulating blood pressure modifications suggested that ensuring adequate blood pressure to maintain sufficient poststenotic MAP appears preferable to the reverse approach, due to the prolonged plateau period in the association between the translesional SBP drop and cortex-involved infarcts and the relatively short plateau period characterizing the correlation between poststenotic MAP and borderzone-involved infarcts. CONCLUSIONS: This research elucidates the role of hemodynamic impairment of blood pressure in symptomatic intracranial atherosclerotic stenosis-related stroke mechanisms, underscoring the necessity to conduct hemodynamic assessments when managing blood pressure in symptomatic intracranial atherosclerotic stenosis.