Neurological Research最新文献

Background: Whether concurrent extracranial vertebral artery occlusion influences outcomes after mechanical thrombectomy for basilar artery occlusion remains uncertain.

Methods: Data were analyzed from a prospectively maintained stroke registry (January 2019-April 2025). Patients with angiographically confirmed basilar artery occlusion treated with mechanical thrombectomy were grouped by the presence versus absence of concurrent extracranial vertebral artery occlusion. Baseline features, workflow metrics, angiographic results, and in-hospital outcomes were compared. Multivariable logistic regression adjusted for age, sex, admission National Institutes of Health Stroke Scale (NIHSS), and intravenous thrombolytic use.

Results: Among 56 patients, 26 (46.4%) had extracranial vertebral artery occlusion. The proportion of patients with an NIHSS score <10 at discharge was lower in patients with extracranial vertebral artery occlusion compared with those without extracranial vertebral artery occlusion (11.5% versus 33.3%, p = 0.0540). These patients had significantly longer puncture-to-reperfusion times (48.9 vs 32.2 min, p = 0.0136), and higher in-hospital mortality (38.5% vs 16.7%, p = 0.0662) despite similar recanalization rates (92.3% vs 96.7%, p = 0.4700). On multivariate analysis, extracranial vertebral artery occlusion independently predicted increased mortality (odds ratio 5.37; 95% confidence interval, 1.23-23.42; p = 0.0253).

Conclusions: In basilar artery thrombectomy, concurrent extracranial vertebral artery occlusion is associated with longer procedures and higher in-hospital mortality despite comparable recanalization success. Pre-procedural recognition may improve procedural strategy and risk assessment.

Objective: This study aimed to identify the different development trajectories of post-stroke cognition and the influential factors in stroke patients based on the group-based trajectory model.

Design: A longitudinal study.

Methods: This longitudinal cohort study recruited 1060 stroke patients from three hospitals from September 2021 to February 2023 and completed three follow-up visits at 1 month, 3 months, and 6 months, respectively. Based on the group-based trajectory model, we used the longitudinal changes of the Mini-Mental State Examination to fit the continuous dynamic development trajectory of post-stroke cognition over time in patients.

Results: A total of 655 stroke patients completed the follow-up in this study. The result of the study shows that the cognitive development trajectory after stroke can be divided into four subgroups, namely the "persistent severe post-stroke cognitive impairment (PSCI) group" "persistent mild PSCI group" "PSCI risk group" and "normal cognitive group".

Conclusion: There is heterogeneity in the development trajectory of post-stroke cognition based on the group-based trajectory model. It is necessary to focus on the characteristics of the development trajectory of different subgroups, which helps to more accurately distinguish the populations at risk, to provide more effective monitoring and interventions.

Objective: To evaluate the predictive value of parameters derived from nerve conduction studies (NCS) for respiratory failure in patients with Guillain-Barré syndrome (GBS).

Methods: We conducted a retrospective analysis of 213 patients with GBS admitted between January 2020 and August 2023. Patients were categorized into respiratory failure (n = 92) and non-respiratory failure groups (n = 121). Demographic, clinical, and neuro-electrophysiological parameters were compared. Multivariate logistic regression analysis was performed to identify independent predictors of respiratory failure. The model's predictive performance was assessed using receiver operating characteristic (ROC) curve analysis.

Results: Among 213 GBS patients (92 with respiratory failure, 121 without), multivariate logistic regression analysis identified two independent electrophysiological predictors of respiratory failure: slower peroneal motor conduction velocity (MCV, OR = 0.230, 95% CI: 0.063-0.838, p = .026) and slower tibial MCV (OR = 0.640, 95% CI: 0.539-0.760, p = .032). The predictive model demonstrated excellent discriminative ability with an AUC of 0.947 (95% CI: 0.921-0.973), sensitivity of 81.8%, and specificity of 95.7%. Patients with respiratory failure also had significantly higher Hughes functional scores (p < 0.001).

Conclusion: Motor conduction velocities of the peroneal and tibial nerves provide reliable and objective predictors for respiratory failure in GBS patients. Incorporating these markers into early risk assessment may facilitate prompt intervention and improve clinical outcomes.

Background: Early diagnosis and treatment of carotid artery stenosis (CAS) are crucial for preventing related cerebral ischemic events, making the identification of safe, non-invasive biomarkers highly necessary.

Aim: To explore the expression and diagnostic value of miR-7110-5p and miR-4484 in CAS, and to clarify their mechanism of action.

Methods: The expression levels of miR-7110-5p and miR-4484 were detected by RT-qPCR. The receiver operating characteristic (ROC) curves for diagnosing different degrees of CAS were constructed for miR-7110-5p and miR-4484. The target genes and common target genes of miR-7110-5p and miR-4484 were predicted using TargetScan Human, miRTarbase and miRDB databases and confirmed by dual-luciferase reporter gene assays. The activity and apoptosis rate of human carotid artery endothelial cells (HCAECs) were detected by CCK-8 assay and flow cytometry.

Results: Both miR-7110-5p and miR-4484 were found to be downregulated in the serum of CAS patients and in ox-LDL-induced HCAECs. The combined diagnostic performance of miR-7110-5p and miR-4484 was superior to that of either alone. IL16 was identified as a common target gene of miR-7110-5p and miR-4484. The miR-7110-5p and miR-4484 mimics significantly reduced the luciferase activity of HCAECs transfected with the wild-type IL16 vector. Both miR-7110-5p and miR-4484 mimics increased the cell viability and decreased the apoptosis rate of ox-LDL-induced HCAECs, while overexpressing IL16 reversed these effects.

Conclusion: miR-7110-5p and miR-4484 have good diagnostic value in CAS and they mediate ox-LDL-induced HCAECs injury by negatively regulating IL16.

Background: Middle cerebral artery (MCA) territory infarction commonly induces a variety of motor function deficits because it involves multiple descending motor pathways, including the corticospinal tract (CST) and corticofugal tract (CFT). Despite the importance of the MCA territory for motor function, there is currently insufficient evidence regarding an injury of the CFT from the secondary motor area in MCA territory infarctions.

Objective: We investigated injury of the CFT from the secondary motor area and CST in patients with MCA using diffusion tensor tractography (DTT).

Methods: Thirty-five patients with MCA territory infarctions and 30 controls were recruited. DTT parameters, including fractional anisotropy (FA) and tract volume (TV), of the CST and CFTs from the dorsal premotor cortex (dPMC) and supplementary motor area (SMA), were analyzed.

Results: In the affected hemisphere, the FA values of the CFTs from the secondary motor areas and CST were significantly lower than those in the unaffected hemisphere and control groups. Additionally, the TV of the CFTs from the dPMC and SMA were significantly lower than those from the unaffected hemisphere.

Conclusion: We observed concurrent injury to the CFTs from the secondary motor area and CST after MCA territory infarction. Our findings contribute to the anatomical understanding of MCA infarction disruption of multiple descending motor pathways.

Background: Ventriculostomy is a common intervention to treat acute hydrocephalus in patients with primary intracerebral (PICH) and primary intraventricular hemorrhage (PIVH). A variety of risk-factors for external ventricular drain (EVD)-associated infections (EVDAI) have been identified, however, it remains unclear how blood extent in PICH and PIVH impacts EVDAI-rates.

Methods: Retrospective single-center cohort study of PICH and PIVH patients undergoing EVD-placement between 01/2009 and 02/2023. Uni- and multivariable logistic regression analysis was used to assess potential predictors of EVDAI.

Results: We included a total of 165 patients with PICH and PIVH who underwent ventriculostomy. EVDAI occurred in 13/165 patients (7.8%) with a median onset time of 8 days (IQR 7;10). Diabetes mellitus (OR 4.91, 95%-CI [1.53-15.71]), postoperative CSF-leakage (OR 4.06, 95%-CI [1.11-12.79]) and CSF-sampling frequency (OR 1.11, 95%-CI [1.00-1.24]) were positively associated with EVDAI. A higher IVH score (OR 1.27, 95%-CI [0.95-1.70]) and intracerebral blood volume (OR 0.76, 95%-CI [0.21-2.80]) showed no significant correlation with higher EVDAI-rates.

Conclusion: In the subpopulation of PICH and PIHV patients, the risk of EVDAI was not associated with a larger radiological blood clot extent. These findings contribute to narrowing down risk factors and targeting further research.

Objective: To evaluate the clinical outcomes and safety of venous sinus stenting in idiopathic intracranial hypertension (IIH) patients across multiple centers in the Middle East and North Africa (MENA) region through the Venous stEnt for idiopathic intraCranial hypertEnsion (VEHICLE) Registry.

Methods: We conducted a retrospective analysis of prospectively collected data from the VEHICLE Registry (NCT06692790) between August 2023 and August 2024. From an initial pool of 187 cases, 100 patients met all inclusion criteria: IIH diagnosis based on modified Dandy criteria, neuroimaging-confirmed venous sinus stenosis, refractory or intolerant to medical therapy, underwent venous pressure manometry, and had complete follow-up data. All patients underwent venous sinus stenting at nine collaborating centers.

Results: Of 100 patients, 73% were female. All presented with headaches, while 87% reported visual disturbances. Venous stenoses predominantly affected the right transverse sinus (56%). At six months, 83% achieved marked symptom resolution, 80% had normalized optic nerve heads, and stent patency was confirmed in 90%. Papilledema grades improved significantly from median Grade III at baseline to Grade I at 6 months (p < 0.001), correlating with increased QOL scores (p < 0.001). Sixteen percent required revision procedures. Complication rates were low, with no procedure-related mortality.

Discussion: Significant improvements in headache, papilledema, and quality of life were observed with a favorable safety profile with venous sinus stenting for medically refractory IIH. However, the retrospective design and lack of a control group limit definitive conclusions about efficacy.

Objectives: Cerebral ischemia-reperfusion (CI/R) injury is a significant hurdle in ischemic stroke treatment. Substantial evidence indicates that long non-coding RNAs (lncRNAs) are implicated in CI/R injury. Here, we explore the function of lncRNA MCM3AP-AS1 in CI/R injury.

Methods: Employed the middle cerebral artery occlusion/reperfusion (MCAO/R) mice model and oxygen-glucose deprivation/reoxygenation (OGD/R) HT22 cell model to mimic in vivo and in vitro CI/R injury. Morris water maze test assessed mice platform-finding latency and swimming distance. Real-time quantitative reverse transcription PCR were conducted to examine the levels of MCM3AP-AS1 and microRNA (miR)-27b-3p. Modified Neurological Severity Score (mNSS) assessed neurological deficits, and triphenyl tetrazolium chloride staining assessed cerebral infarct volume. Enzyme-linked immunosorbent assay quantified inflammatory factor levels. Cell count kit-8 and flow cytometry detected cell viability and apoptosis, respectively. Dual luciferase reporter and RNA immunoprecipitation assays verified targeting relationships.

Results: MAMC3AP-AS1 expression decreased in the brain tissue of MCAO/R mice and OGD/R-treated cells, while miR-27b-3p levels were rose. Upregulating MCM3AP-AS1 notably suppressed mNSS scores, reduced infarct volume, and alleviated cognitive dysfunction in MCAO/R mice; however, miR-27b-3p attenuated the function of MCM3AP-AS1. Furthermore, OGD/R treatment inhibited cell viability, increased apoptosis, and promoted inflammatory factors secretion, MCM3AP-AS1 reversed these effects, but miR-27b-3p significantly impaired this reversal. Mechanistically, MCM3AP-AS1 targeted miR-27b-3p.

Discussion: MCM3AP-AS1 exerts neuroprotection by attenuating miR-27b-3p levels, thereby mitigating CI/R injury.

Background: Biomarkers for disease activity are lacking in chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). We aimed to investigate whether motor nerve conduction studies (NCSs) and nerve ultrasound and their follow-up changes could predict steroid-dependency and treatment refractoriness.

Methods: Sixty-three CIDP patients were followed up with both nerve ultrasound and NCS. Cross-sectional areas (CSAs) were measured on the bilateral median, ulnar nerves and brachial plexus. NCSs were performed on the median and ulnar nerves.

Results: Patients with normal or mildly slow MCV at the first visit were less likely to be steroid-dependent and had lower INCAT at the last follow-up (median 0 [0,1]), whereas those with dramatically slow MCV were more likely to be steroid-dependent and had higher INCAT at the last follow-up (median 2[2,2]) (p = 0.009 for steroid dependent, p = 0.004 for INCAT). None of the patients whose MCV improved above the lower normal limit were steroid-dependent, whereas nearly half of those whose MCV decreased or remained unchanged were steroid-dependent (p = 0.005). A two-step method had a sensitivity of 85% and specificity of 80% for distinguishing patients with steroid dependency. First, we divided patients into three groups according to the MCV change. Second, we explored the trend of steroid-dependent and treatment-refractory based on the CSA at admission and change in CSA.

Conclusions: For patients whose MCV improved beyond the threshold, the risk of relapse was low, and we suggest more rapid tapering of steroid. For those with decreased MCV, the risk of relapse was greater and slower steroid tapering or immunosuppressant use is suggested.

Objective: This study aims to elucidate the mechanism by which astragaloside IV (AS-IV) mitigates cerebral ischemia-reperfusion injury (CIRI), with a focus on serotonin receptor 2B (HTR2B)-mediated microglial polarization and neuroinflammation.

Methods: In vivo, CIRI was induced in rats via middle cerebral artery occlusion-reperfusion (MCAO/R). Rats received AS-IV or HTR2B overexpression vector. In vitro, highly aggressive proliferating immortalized (HAPI) microglia were polarized to M1 with lipopolysaccharide (LPS), followed by AS-IV treatment and co-culture with neuron-like PC12 cells. Neurological function was scored using the Longa scale. Infarct volume and histopathology were assessed by TTC and HE staining, respectively. Levels of inflammatory cytokines in rat brain tissues and HAPI cells were quantified by enzyme-linked immunosorbent assay (ELISA). The viability of HAPI and PC12 cells was assessed using cell counting kit-8 (CCK-8). PC12 apoptosis was evaluated via terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining.

Results: CIRI rats exhibited significant neurological deficits, enlarged infarct area, and pronounced neuronal damage, which were markedly alleviated by AS-IV treatment. AS-IV also inhibited HTR2B expression and reduced pro-inflammatory cytokine release in both in vivo and in vitro models. In HAPI-PC12 co-culture system, AS-IV reversed LPS-induced microglial activation, restoring PC12 viability and reducing apoptosis. HTR2B overexpression abolished neuroprotective effects of AS-IV, promoting microglial M1 polarization and exacerbating neuroinflammation.

Conclusion: AS-IV protects against CIRI by downregulating HTR2B and inhibiting microglial M1 polarization. These findings identify the HTR2B-microglial axis as a promising therapeutic target for ischemic stroke.