Frontiers in Neurology最新文献

Background and objectives: Internal jugular vein (IJV) stenosis, often caused by extrinsic compression from the atlas transverse process, may impair cerebral venous drainage and contribute to cognitive dysfunction, though direct clinical evidence is limited. This study aimed to investigate the correlation between atlas-induced IJV stenosis and cognitive impairment, and to evaluate the effect of surgical decompression on cognitive outcomes.

Methods: From January to June 2025, 47 patients with radiologically confirmed IJV stenosis due to atlas transverse process compression were prospectively enrolled. Cognitive function was assessed using the Montreal Cognitive Assessment (MoCA). Patients were stratified into higher (n = 24) and lower (n = 23) stenosis groups based on the mean of IJV stenosis degree (IJVS degree) for exploratory comparison. Of these, 16 patients completed the strict postoperative outpatient follow-up, including MoCA assessment.

Results: The mean MoCA score for the cohort was 23.21 ± 3.41, indicating cognitive impairment. The higher stenosis group had significantly lower MoCA total scores than the lower group (20.79 ± 0.56 vs. 25.74 ± 0.38, p < 0.001), with pronounced deficits in visuospatial/executive function and delayed recall. Partial correlation analysis, controlling for age and education level, revealed a significant negative correlation between IJVS degree and MoCA score (r = -0.66, p < 0.001). Postoperatively, the mean MoCA score improved from 22.56 ± 0.82 to 24.68 ± 0.64 (p < 0.001), with significant gains in visuospatial/executive function, attention, and delayed recall.

Conclusion: This study indicates that internal jugular vein stenosis caused by atlas transverse process compression is a potentially treatable contributor to cognitive dysfunction. Surgical decompression improved cognitive function, providing direct evidence for the role of the cerebral venous system in cognitive health. Evaluation of patients with cognitive complaints should consider assessment of the head and neck venous system.

Introduction: Acute ischemic stroke (AIS) is a leading cause of global mortality and disability worldwide. Machine learning (ML) models enhance prognostic accuracy by analysing complex, multidimensional clinical data. The aim of this systematic review and meta-analysis is to identify the gaps in the current ML models, along with methodological and performance outcomes in AIS. Further, the study objective was to identify the most frequently used algorithms and compare their relative effectiveness, thereby supporting future research to develop novel ML-based predictive models for stroke care management.

Methods: The systematic review followed PRISMA guidelines with PROSPERO registration. A comprehensive search was performed in PubMed, Scopus, and Web of Science using MeSH keywords. Data extraction captured study characteristics, ML algorithms, and outcome metrics. We used the PROBAST and TRIPOD-AI to assess the qualities and bias of included studies. Meta-analysis of AUC values across ML models were conducted to synthesize model performance used a random-effects model to summarize and analyse the data and assessed heterogeneity (I ²) statistic using SPSS-29 and R-Studio-4.2.0.

Results: A total of 14 studies were included in the systematic review, with 12 eligible for meta-analysis. The pooled AUC of ML models was 0.87 (95% CI, 0.83-0.91), demonstrating strong predictive performance despite substantial heterogeneity (I ² = 99%). Random forest (RF) (AUC = 0.85) and SVM (AUC = 0.82) outperformed logistic regression (LR) (AUC = 0.75), while XGBoost showed stable performance (AUC = 0.82); heterogeneity was mainly driven by study design, publication year, and algorithm type (p < 0.001).

Conclusion: ML-based models show potential for improving prognostic assessment in AIS; however, substantial heterogeneity and methodological limitations across studies limit the generalizability of pooled performance estimates.

Systematic review registration: https://www.crd.york.ac.uk/PROSPERO/view/CRD420251033217, (Registration number: CRD420251033217).

Bacterial infections of the central nervous system (CNS) are characterized by rapid and devastating neuroinflammation. While inflammation plays an important physiological role in defense against bacteria, such responses within the confines of the cranium can be lethal. Glial cells, including microglia and astrocytes, can perceive bacteria or their products and then respond in a manner that can promote inflammation, changes to blood-brain barrier integrity, and recruit leukocytes into the CNS. In this review, we have summarized their ability to produce chemotactic factors in response to bacterial components and clinically relevant bacterial pathogens of the CNS. Importantly, we have highlighted the fact that the chemotactic factors produced by bacterially challenged glia tend to preferentially recruit neutrophils, and we have described how such cells could then respond to the presence of bacteria to further promote glial activation and their own recruitment. This then, could form a vicious cycle that precipitates the rapid inflammatory CNS damage associated with bacterial infection. However, it is also becoming apparent that glia, and perhaps neutrophils, can adjust their responses to bacteria temporally in such a way as to break this positive feedback loop, and we have described the available evidence for the delayed production for anti-inflammatory mediators by these cells following challenge. Finally, we have discussed the present limitations in our understanding of these cell-cell interactions and their study that must be overcome before we can manipulate such a glia-neutrophil axis for therapeutic purposes.

Background: Predictive tools for assessing outcomes after aneurysmal subarachnoid hemorrhage (aSAH) are limited, particularly with respect to long-term functional outcome. Reliable risk stratification in the early course of aSAH is crucial for determining optimal patient management, effective use of clinical resources, and ultimately improving patient outcomes. This study aimed to design a prognostic score based on retrospectively collected clinical variables to predict functional outcome or delayed cerebral ischemia as primary endpoints in patients with aSAH.

Methods: Between January 2014 and March 2022, 386 patients with aSAH were admitted to our hospital. Two hundred thirty of these patients were included in our study. Seventeen clinical, radiological, and demographic variables were analyzed using the chi-squared test and logistic regression to identify significant predictors of an unfavorable outcome (mRS 4-6) after 6 months or DCI development. A nomogram defined the weighting of each factor within a newly developed aSAH-Risk score.

Results: Significant risk factors were identified to predict functional outcome. Of these, five variables were included to create the aSAH-Risk score with a maximum of 13 points: arterial hypertension (p = 0.001, no = 0, yes = 2), intracranial vasosclerosis (p = 0.0002, none = 0, yes = 2), modified Fisher scale (p < 0.001, scale 1 = 0, scale 3 = 2, scale 2 or 4 = 3), intracerebral hemorrhage (no = 1, yes = 2) and World Federation of Neursosurgical Societies grading (p < 0.001, 1 = 0, 2 = 1, 3 or 4 = 3, 5 = 4). Forty percent was the minimal calculated risk of an unfavorable outcome for an aSAH patient, increasing to 80% with an aSAH-Risk score of 13 points. An external cohort is required to validate the proposed score for general applicability.

Conclusion: The aSAH-Risk score is a novel clinical tool to identify patients in need of long-term daily life assistance at admission.

Background: It is generally believed that cerebral hypoperfusion in patients with vasovagal syncope (VVS) is secondary to hypotension; however, current evidence suggests that this is not always the case. Thus, this study aimed to analyze the hemodynamic characteristics of patients with VVS and dynamic cerebral autoregulation (CA) dysfunction (referred to as CA-impaired VVS) to improve the diagnosis and treatment of this VVS subtype.

Methods: This retrospective study included 143 patients with VVS who underwent the head-up tilt test (HUTT) using transcranial Doppler (TCD). Patients were divided into two groups based on pathogenesis: CA-impaired VVS and blood pressure drop-dominant VVS. Hemodynamic parameters, including systolic and diastolic blood pressure, heart rate, and cerebral blood flow velocity (CBFV), were compared between the two groups to further analyze the differences in cardiocerebral hemodynamic indices.

Results: CA-impaired VVS accounted for 58% of the cases. During basic HUTT in the upright tilt position, the minimum systolic blood pressure (SBP), minimum diastolic blood pressure (DBP), and minimum mean arterial pressure (MAP) were significantly higher in the CA-impaired group than in the blood pressure drop-dominant group (p < 0.05). Similarly, during the sublingual nitroglycerin HUTT in the upright tilt position, the minimum SBP, DBP, and MAP were significantly higher in the CA-impaired group than in the blood pressure drop-dominant group (p < 0.05). After returning to the supine position, the mean SBP, DBP, and MAP remained significantly higher in the CA-impaired group than in the blood pressure drop-dominant group (p < 0.05). In addition, the positivity rates for orthostatic tachycardia in the CA-impaired and blood pressure drop-dominant VVS groups were 73.5 and 65.0%, respectively. The incidence of neurogenic orthostatic hypotension was 2.4% in the CA-impaired group, which was significantly lower than the 16.7% in the blood pressure drop-dominant group (p = 0.002).

Conclusion: This study reveals the characteristics and differences in cardiocerebral hemodynamics between CA-impaired and blood pressure drop-dominant subtypes of VVS, deepens the understanding of VVS pathogenesis, facilitates the accurate diagnosis of VVS, and enhances the ability to interpret its results.

Background and aims: We aimed to compare electrophysiological subtypes of Guillain-Barré syndrome (GBS) in a single cohort from northern China using three criteria (Ho's, Hadden's, Rajabally's), to clarify whether GBS subtypes are affected by electrophysiological criteria and nerve conduction studies (NCS) examination timing, to explore the value of sural sparing in subtype classification, and analyze the association between conduction block (CB) and short-term prognosis of Acute Motor Axonal Neuropathy (AMAN).

Methods: We retrospectively collected GBS patients hospitalized in the Department of Neurology, the Second Hospital of Hebei Medical University (Jan 2017-Jan 2022), who met Brighton diagnostic criteria and had complete NCS data. Patients were classified via three electrophysiological criteria (Ho's, Hadden's, Rajabally's); we analyzed subtype distribution by NCS timing (1, 2, or ≥3 weeks post-onset) and used discharge Hughes Functional Grading Scale (HFGS) to assess short-term prognosis.

Results: A total of 262 patients were enrolled. AMAN was the main subtype (40.1% by Hadden's, 46.6% by Ho's, 59.5% by Rajabally's criteria). Fleiss Kappa showed strong consistency among the three electrophysiological criteria (κ = 0.75, p < 0.001); Subtype composition showed greater consistency at ≥3 weeks post-onset (p > 0.05). Acute Inflammatory Demyelinating Polyneuropathy (AIDP)had higher sural sparing than AMAN (32.4%-50% vs. 0.9%-4%, p < 0.001). AMAN with CB had lower discharge HFGS (p = 0.012). Serial NCS enhanced the accuracy of GBS subtype classification.

Conclusion: GBS electrodiagnosis depends on criteria and NCS timing (≥3 weeks more consistent). AMAN is predominant in our cohort from northern China regardless of criteria used. Sural sparing and serial NCS enhance subtype classification accuracy.

Background: Heparin may mitigate secondary brain injury in subarachnoid hemorrhage (SAH), but its effect on survival in non-traumatic SAH (NSAH) remains uncertain. This study aimed to investigate the association between early prophylactic heparin use (within 72 h of admission) and mortality outcomes in patients with NSAH.

Methods: We performed a retrospective cohort study using the Medical Information Mart for Intensive Care (MIMIC) and the eICU Collaborative Research Database (eICU-CRD). Patients were stratified by early heparin use. Cox models, Kaplan-Meier (KM) curves, subgroup analyses, and comprehensive propensity score-based sensitivity analyses were applied to assess the robustness of the observed associations. The primary outcome was in-hospital mortality; 28-, 90-, 180-, and 365-day mortality were secondary outcomes. Findings were validated using the eICU-CRD cohort.

Results: In the MIMIC-IV cohort, early heparin use was associated with lower in-hospital mortality (HR 0.62, 95% CI 0.39-0.97, p = 0.037), which was confirmed in the eICU-CRD cohort (HR 0.47, 95% CI 0.22-1.00, p = 0.049). Consistent reductions were also observed for 28-day (HR 0.57, p = 0.009), 90-day (HR 0.62, p = 0.010), 180-day (HR 0.63, p = 0.009), and 365-day mortality (HR 0.61, p = 0.004) in the MIMIC-IV cohort. Subgroup analyses and KM curves further supported these findings. Propensity score-based sensitivity analyses further validated the robustness of these findings in both cohorts.

Conclusion: Early prophylactic heparin was associated with lower risk-adjusted short- and long-term mortality in NSAH.

Following Benson's seminal paper published in 1988 visual field loss in Posterior Cortical Atrophy (PCA) has been largely denied or ignored. This is despite an earlier description by Cogan of a similar case of pathologically verified Alzheimer disease featuring homonymous hemianopia (HH). Although HH is now recognised as a core feature of PCA its characteristics and relationship to other PCA features are unexplored. This study aimed to characterise the perimetric abnormalities in PCA patients presenting with HH, focusing on the response to static and kinetic stimuli; progression of the deficit over time; and the relationship to co-existing cognitive deficits. 24 patients were recruited for the cross-sectional study, of whom 19 participated in the longitudinal study. Each assessment consisted of kinetic and static perimetry and a comprehensive neuropsychological evaluation. The latter included tests to all basic cognitive domains plus tests of posterior cortical function. Thirteen patients underwent additional kinetic perimetry using three target velocities. Left HH was predominant and a deficit in object perception universal. Neglect was uncommon and did not correlate with the laterality of the HH. Stato-kinetic dissociation (SKD) was observed in all patients, greater in the more affected hemifield. Longitudinally, static perimetric deficits declined at a greater rate in the initially more affected hemifield. The rate of decline to kinetic testing was lower and varied with target size and velocity. Deterioration to the smallest and lowest velocity target mirrored that of static loss. A longitudinal mixed-model analysis showed that right HH was associated with greater deficits in predominantly left hemisphere cognitive functions and bilateral HH with greater bilateral occipital deficits. However, no association was found between the laterality of the HH and right hemisphere cognitive deficits. The characteristic SKD (also known as the Riddoch phenomenon) does not represent a complete dissociation as kinetic detection deteriorates over time in all cases. The correlation of the HH with lateralised parietal deficits challenges the concept that HH is restricted to an extreme posterior variant of PCA and highlights the need for routine (static and kinetic) perimetry in the diagnosis, characterisation and monitoring of PCA.