Neurological Research最新文献

Introduction: We aimed to investigate the effects of central kisspeptin-10 and p234 administration on basal brain activity and epilepsy-like conditions induced by 4-aminopyridine (4-AP), as well as their roles in the electrocorticogram (ECoG) power spectrum and EEG waves.

Methods: Thirty-five male Wistar rats were divided into five groups: sham,4-AP (2.5 mg/kg i.p.), kisspeptin-10 post-treatment (200 pmoli.c.v.), p234 post-treatment (1 nmol i.c.v.), and p234 pre-treatment (1 nmol i.c.v.). We performed 70 minutes of recordings (10 min baseline) for all groups under ketamine/xylazine (90/10 mg/kg) anesthesia. In the post-treatment groups, kisspeptin-10 or p234 injections were administered 20 minutes after epilepsy induction. In the pre-treatment group, p234 was injected after baseline recordings. Following a 20-minute pre-treatment period, 4-AP was administered.

Results: 4-AP alone induced epileptiform activity in all animals, reaching apeak after 30 minutes. Neither kisspeptin-10 nor p234 post-treatment affected 4-AP-induced epileptiform activity (p > 0.05). However, p234 pre-treatment reduced epileptiform activity (p < 0.05). Additionally, kisspeptin-10 did not alter the spectral analysis of the EEG bands or the power of the ECoG (p > 0.05). In contrast, p234 reduced the power of the ECoG and the slow bands (delta and theta) (p < 0.05).

Conclusion: We conclude that p234 pre-treatment has an inhibitory effect on neuronal excitability and epileptiform activity in the neocortex.

Sinking Skin Flap Syndrome(SSFS) is a rare and specific complication following decompressive craniectomy(DC). Another condition, known as syndrome of the trephined(ST), shares many similarities in clinical symptoms and signs with this condition, yet they are fundamentally different. Therefore, they should be considered as two distinct diseases, and their respective concepts should not be used interchangeably as synonyms. Due to a lack of understanding of ST and SSFS, many existing clinical studies often conflate their concepts. Our study further explores and understands the clinical symptoms and radiological features of this condition through typical cases, thereby aiding in the diagnosis and treatment of such diseases.

Objective: This study aimed to evaluate the efficacy of intraoperative intravenous lidocaine administration in the management of sepsis-associated encephalopathy (SAE).

Methods: This retrospective cohort analysis included 165 patients diagnosed with SAE, who were categorized into two groups: the lidocaine group (n = 55) and the control group (n = 110). The lidocaine group received an intravenous injection of lidocaine at 1.5 mg/kg following anesthesia induction, and then received a continuous infusion at 1.5 mg/kg/h until the completion of surgery. The control group did not receive lidocaine during surgery. Data collected included patient demographics, medical history, infection site, Acute Physiology and Chronic Health Evaluation (APACHE) II score, Sequential Organ Failure Assessment (SOFA) score, Glasgow Coma Scale (GCS) score, laboratory results, anesthetic agents used, surgery duration, and length of stay in the intensive care unit (ICU). The primary outcome was the in-hospital prognosis of SAE.

Results: Patients in the lidocaine group had a significantly shorter ICU stay and a significantly higher rate of favorable prognosis compared with the control group (p < 0.05). Multivariate logistic regression analysis identified age and surgery duration as risk factors for SAE prognosis, whereas intraoperative intravenous lidocaine, GCS score, and intravenous dexmedetomidine emerged as protective factors.

Conclusion: Intraoperative intravenous administration of lidocaine significantly enhanced the prognosis of SAE patients.

Objectives: The aim of this study was to investigate the effect of eight weeks of aerobic training (AT) and vitamin C supplementation (VC) on apoptotic markers in hippocampus tissue of AD rats treated with trimethyltin (TMT).

Materials and methods: In this experimental study, 32 Sprague- Dawley rats (mean age: 14-18 months and mean weight 270-320 g) were treated with (10 mg/kg) TMT and divided into 4 groups including: 1) ADcontrol, 2) VC, 3) AT and 4) AT+VC groups. In order to investigate the effects of AD induction on research variables, 8 healthy rats selected as healthy control group (HC). Groups 3 and 4 trained for eight weeks, three sessions per week and each session lasted 15-48 minutes with an intensity of 10-24 m/min. Groups 2 and 4 received 4 mg/kg VC orally. One-way ANOVA with Tukey's post- hoc tests were used for statistical analysis of data (p ≤ 0.05).

Results: The gene expression levels of Caspase 3, FasL, Cyt-C and AP-1 in the AT, VC and AT+VC groups were significantly lower than TMT group (p ≤ 0.05); Caspase 3, FasL and Cyt-C levels were significantly lower in the AT+VC group compare to VC and ET groups (p ≤ 0.05). CytC levels in AT group were significantly lower than VC group (p = 0.002). Also, AP-1 levels in AT+VC group were significantly lower than AT group (p = 0.01).

Conclusions: It seems that AT and VC, both alone and interactively, can probably induce their anti-apoptotic effects in the hippocampus tissue of rats with AD via a common signaling pathway.

Background: It has been suggested that smokers have higher recanalization rate, lower risk of cerebral hemorrhage and better prognosis than non-smokers (smoking paradox) after reperfusion therapy in patients with acute ischemic stroke (IS). This study aimed to assess the effects of smoking on recanalization, intracranial hemorrhage, and clinical outcomes in patients with acute IS following reperfusion therapy.

Methods: Patients were categorized into smokers and non-smokers, with data collected on types of reperfusion therapy, demographics, medication use, comorbidities, stroke etiology, mRS and NIHSS scores, TICI and ECASS classifications.

Results: The study involved 662 patients (344 men and 318 women) treated with rtPA and/or thrombectomy. Smoking was more prevalent among men. Smokers were typically younger, had lower hypertension rates, lower systolic blood pressure, and higher triglyceride and HDL levels compared to non-smokers. They exhibited a higher incidence of cardioembolic strokes and strokes with known causes but a lower incidence of small vessel occlusion. Smokers had higher GCS scores and more posterior cerebral circulation strokes upon hospital admission. NIHSS scores were lower at admission and on the third day, and poor outcome rates (mRS) were lower at both hospital admission and three months post-stroke for smokers. However, smokers who developed hemorrhagic complications had a higher frequency of parenchymal hematoma according to ECASS classification.

Conclusions: Our findings did not support claims that smoking increases recanalization rates, reduces cerebral hemorrhage risk, or improves clinical outcomes. Further prospective studies with larger samples are needed to explore smoking's impact on stroke outcomes.

Background: Cerebral venous sinus thrombosis (CVST) is an uncommon form of cerebrovascular disease. Although our understanding of CVST has improved significantly over the past decades, there has been no bibliometric analysis of CVST until now. We aimed to examine and visualize the hotspots and trends of the research related to CVST using a bibliometric analysis based on Citespace and provide new insights for scholars in their future researches in this area.

Methods: The literature on CVST was collected from the Web of Science Core Collection database. Bibliometric analysis was performed using CiteSpace (6.2.R3) Advanced software.

Results: A total of 2396 articles were included in the analysis. Publications regarding CVST have increased over time. U.S.A. contributed the most articles. Ferro JM had the highest number of published papers. Stroke was the journal with the most publications and the most commonly cited journal. Nine out of the top 10 cited journals belong to Q1. The risk factors for CVST, emerging and current treatment of CVST, and CVST related to COVID-19 and COVID-19 vaccines are the major potential research hot spots and trends.

Conclusions: CVST is a rapidly expanding research area and has received increasing attention by the researchers. Our study can provide researchers valuable information on the current status and trends in this area and guide for future studies.

Objectives: Exposure to aluminum (Al) has been shown to be strongly associated with the pathogenesis of Alzheimer's disease (AD). Recent evidence indicates that the toxicity of Al nanoparticle (Al-NP) is far greater than Al itself due to its particle size. Epidemiological studies suggest that curcumin lower the prevalence of AD. MAPKs (ERK, p38 and JNK) were suggested to be involved in AD pathology and memory impairment. The present study aimed to evaluate if curcumin has the ability to protect against behavioral deficits induced by subcutaneously administered Al-NP in mice. Furthermore, the levels of phosphorylated and total hippocampal MAPKs were assessed using western blottechnique.

Methods: Al-NP (10 mg/kg/s.c.) was administered to adult male NMRI mice for 10 days with or without curcumin in doses of 2.5 or 25 mg/kg/oral gavage). Memory was assessed using passive avoidance apparatus and anxiety-like behavior was evaluated using elevated plus maze. Following the behavioral tasks, western blot analysis was performed on the hippocampal tissues to detect the levels of phosphorylated and total MAPKs.

Results: The results revealed that Al-NP deteriorated memory with no significant effect on anxiety-like behaviors. Additionally, it activated hippocampal p38 signaling pathway with no effect on ERK and JNK. Curcumin treatment at the dose of 25 mg/kg restored memory and p38 activation.

Discussion: This study suggests that subcutaneous Al-NP administration impairs memory and hippocampal p38 signaling with no effect on ERK and JNK. Co-administration of curcumin restored Al-NP induced memory impairment and hippocampal p38 phosphorylation.

Objectives: Intracranial aneurysms (IA), often remain asymptomatic until they get ruptured, invariably leads to subarachnoid hemorrhage (SAH), and is influenced by both genetic and environmental factors. Recent studies indicated inflammation as a key player in IA development. This study delves into genetic variations within inflammatory pathways, focusing on TLR4-mediated cytokine release as potential IA biomarkers.

Methods: Eighty IA patients and eighty healthy controls from North India participated, and demographic and clinical data were analyzed, including gender-stratified comparisons of TLR4 Asp299Gly genotype and TLR4 expression. Histological and molecular analyses of blood and brain tissue were done using SEM imaging, qPCR, and western blot.

Results: Our result revealed elevated TLR4 expression in IA patients, with SEM imaging indicating intracerebral damage. TLR4 Asp299Gly heterozygote genotype was less prevalent in IA patients, suggesting a protective effect against IA development. Moreover, TNF-α levels were significantly higher in IA patients, indicating an inflammatory response. Further, TNF-α expression was downregulated in heterozygous patients, suggesting TLR4 Asp299Gly gene polymorphism affects the activation of TNF-α expression. Gender-based analysis between control and aneurysm cases showed a decrease in TLR4 Asp299Gly heterozygote genotype with heightened TLR4 expression and neurological deficits in IA female patients compared to males.

Conclusions: This study highlights the association between TLR4 Asp299Gly genotype and IA susceptibility in North Indian populations, linking increased TLR4 expression to IA pathogenesis. Gender-specific disparities in TLR4 genotype and expression underscore the need for personalized treatment strategies, with TLR4 signaling modulation emerging as a promising therapeutic avenue warranting further investigation.

Objectives: Since neurogenic inflammation and hemoconcentration have a prominent role in the pathophysiology of migraine, evaluation of hemogram parameters and indices showing inflammation can yield important information. In this study, we have investigated blood cell counts and ratios, systemic inflammation index (SII), systemic inflammation response index (SIRI) and red cell index (RCI) in the painless periods between pain attacks in patients with episodic migraine without aura.

Methods: Hemogram data of both 309 patients diagnosed with migraine without aura related to pain-free periods and 199 healthy individuals were retrospectively retrieved from hospital records. Data related to erythrocyte, leukocyte, lymphocyte, platelet, monocyte, eosinophil counts; hemoglobin, hematocrit, mean corpuscular volume, red blood cell distribution width (RDW), mean platelet volume (MPV), neutrophil/lymphocyte ratio, platelet/lymphocyte ratio, monocyte/lymphocyte ratio (MLR), and neutrophil/monocyte ratio, SII, SIRI and RCI values were scanned to reveal intergroup differences in terms of these parameters.

Results: A comparison of laboratory parameters revealed that certain indices differed significantly between the migraine and control groups. MLR (p = 0.005) and RDW (p < 0.001) values were significantly lower, while platelet (p = 0.016), MPV (p < 0.001) and hematocrit (p = 0.014) were significantly higher in the migraine patient group compared to the control group. There was no significant difference between the two groups regarding other parameters.

Discussion: Higher hematocrit, platelet, mean platelet volume and lower monocyte/lymphocyte ratio values in this study support that hemoconcentration and chronic inflammation persist even in the absence of pain attacks in migraine patients without aura.

Objectives: Due to the complex and unclear pathogenesis of neuropathic pain, there is a lack of effective therapeutic strategy. miR-363-5p was considered of great potential in mediating the development of neuropathic pain, which has not been confirmed with direct evidence. This study evaluated the role of miR-363-5p in neuropathic pain with animal and cell models, aiming to reveal the potential of miR-363-5p in target therapy of neuropathic pain.

Methods: Chronic constriction injury (CCI) rat models were established as the neuropathic pain model. The expression of miR-363-5p and its target was evaluated by PCR. The painology behaviors were evaluated to assess the function of miR-363-5p. Schwann cells were induced with LPS mimicking cell injury during neuropathic pain. Inflammation and cell growth were estimated by ELISA and CCK8 assays.

Results: Significant downregulation of miR-363-5p and upregulation of SERPING1 were observed in CCI rats. miR-363-5p negatively regulated SERPING1 in CCI rats and LPS-induced Schwann cells. Overexpressing miR-363-5p could improve pain threshold and alleviate inflammation in CCI rats. It also a ttenuated LPS-induced inflammation and reduced proliferation in Schwann cells. The overexpression of SERPING1 could reverse the protective effect of miR-363-5p on CCI rats and LPS-induced Schwann cell injury.

Conclusion: miR-363-5p protected from neuropathic pain via alleviating Schwann cell injury by negatively modulating SERPING1.