Neurological Research最新文献

{"title":"Effectiveness of sesame oil and melatonin on P53 level in spinal cord injury of rat menopausal model.","authors":"Maryam Soleimani, Mohammad Mashhadi Ebrahim Tehrani, Seyed Behnamedin Jameie, Mona Farhadi, Sajad Hassanzadeh","doi":"10.1080/01616412.2025.2571947","DOIUrl":"10.1080/01616412.2025.2571947","url":null,"abstract":"<p><strong>Objective: </strong>Identifying mechanisms that prevent neuronal inflammation and apoptosis can offer promising approaches to prevent and treat neuronal degeneration in spinal cord injury (SCI). The latest research confirms the antioxidant action of melatonin (Mel), the hormone that regulates biological rhythms in all mammals. Additionally, sesame oil is traditionally used to treat inflammation. According to recent findings, the nervous system and gonadal hormones also interact reciprocally. One of the most famous regulators of cell death and apoptosis is p53. This study investigated the effects of exogenous Mel, sesame oil, and gonadal steroid deprivation on p53 and GPx-1 expression, as one of the most important antioxidant enzymes, following SCI.</p><p><strong>Methods: </strong>Forty-two female Wistar rats were divided into seven groups. Three weeks after OVX, SCI was created using an aneurysm clip at the T9-T10 level, followed by intraperitoneal (IP) sesame oil and Mel subcutaneously (SC) for 3 weeks. The p53 level was studied by western blotting and real-time PCR. Moreover, the remyelination process was studied using luxol fast blue staining.</p><p><strong>Results: </strong>The animals receiving sesame oil and Mel showed significantly less demyelination and higher GPx-1 levels than the OVX-SCI groups (<i>p</i> < 0.01 and <i>p</i> < 0.05). Additionally, the level of p53 in treated animals was significantly lower than in non-treated animals.</p><p><strong>Conclusion: </strong>It is hypothesized that the combination of sesame oil and Mel might suppress apoptosis, enhance myelination and neuronal survival, and restore functional recovery in animals. Whether this ability is clinically valuable in human subjects needs clarification and more clinical research on SCI.</p>","PeriodicalId":19131,"journal":{"name":"Neurological Research","volume":" ","pages":"1484-1500"},"PeriodicalIF":1.9,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145293159","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Silencing IncRNA BACE1-AS alleviates neuronal injury and neurological deficits after ischemic stroke via targeting miR-103a-3p.","authors":"Kaijie Yu, Fang Liu, Tianrui Yu, Yanping Ding, Juyao Liu, Lianlian Lv","doi":"10.1080/01616412.2025.2568025","DOIUrl":"10.1080/01616412.2025.2568025","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the role of lncRNA BACE1-AS in neuronal injury and neurological deficits after ischemic stroke and explore its underlying molecular mechanism.</p><p><strong>Methods: </strong>MCAO rat model and OGD/R cell model were established. BACE1-AS expression was detected by RT-qPCR. Neurological function was evaluated by mNSS and MWM test. Inflammatory factors (TNF-α, IL-6, IL-10), neuronal injury markers (NSE, GFAP), and apoptosis-related markers (Bcl-2, Bax, Caspase-3) were detected by ELISA and RT-qPCR. Bioinformatics analysis, dual-luciferase reporter assay, and RIP assay were used to validate the targeting relationship between BACE1-AS and miR-103a-3p.</p><p><strong>Results: </strong>BACE1-AS was significantly upregulated in both MCAO rats and OGD/R-treated SH-SY5Y cells. Silencing BACE1-AS alleviated neurological deficits, reduced pro-inflammatory cytokine levels, and inhibited neuronal apoptosis. Mechanistically, BACE1-AS targeted miR-103a-3p, and inhibiting miR-103a-3p reversed the neuroprotective effects of BACE1-AS silencing in vivo and in vitro.</p><p><strong>Conclusion: </strong>Silencing BACE1-AS mitigates neuronal injury and neurological deficits after ischemic stroke by targeting miR-103a-3p, providing a novel therapeutic target for ischemic stroke.</p>","PeriodicalId":19131,"journal":{"name":"Neurological Research","volume":" ","pages":"1375-1385"},"PeriodicalIF":1.9,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145409165","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of sodium imbalance and seizure on hippocampal damage in rats.","authors":"Seren Gülşen Gürgen, Beril Dilber, Özgül Balcı, Ali Cansu","doi":"10.1080/01616412.2025.2566229","DOIUrl":"10.1080/01616412.2025.2566229","url":null,"abstract":"<p><strong>Objectives: </strong>Hyponatremia is a frequent electrolyte disturbance that increases seizure susceptibility and may aggravate neuronal injury. Brain-derived neurotrophic factor (BDNF) is a neurotrophin critical for hippocampal function, yet the relationship between hyponatremia, seizures, and hippocampal BDNF expression remains unclear. This study aimed to investigate the effects of acute and chronic hyponatremia, with and without seizures, on hippocampal integrity in rats using immunohistochemistry and electron microscopy.</p><p><strong>Methods: </strong>Forty-two male Wistar Albino rats were randomly assigned to six groups (<i>n</i> = 7/group): acute hyponatremia, acute hyponatremia + seizures, chronic hyponatremia, chronic hyponatremia + seizures, normonatremic controls, and normonatremic controls + seizures. Hyponatremia was induced by vasopressin and glucose water administration, and seizures were triggered with kainic acid. Plasma sodium levels, seizure onset/duration, BDNF expression, and ultrastructural damage were evaluated.</p><p><strong>Results: </strong>Plasma sodium concentrations were significantly reduced in hyponatremic groups compared with controls (acute: 126.1 ± 3.8; chronic: 121.8 ± 4.3; normonatremic: 135.5 ± 2.3 mEq/L; <i>p</i> < 0.001). Seizures were longer and more severe in chronic hyponatremia + seizure rats compared with acute hyponatremia + seizure rats (<i>p</i> < 0.001). BDNF expression was significantly decreased in both acute and chronic hyponatremia groups relative to controls, with the lowest values in chronic hyponatremia + seizure rats (<i>p</i> < 0.05). Electron microscopy revealed marked ultrastructural injury, including myelin detachment, mitochondrial swelling, and vacuolization, most pronounced in chronic hyponatremia + seizure animals.</p><p><strong>Conclusions: </strong>Hyponatremia, particularly in its chronic form, exacerbates seizure-induced hippocampal injury, reflected by reduced BDNF expression and severe ultrastructural damage. These findings provide novel preclinical evidence linking sodium imbalance to hippocampal vulnerability and highlight the need for further mechanistic and translational studies.</p>","PeriodicalId":19131,"journal":{"name":"Neurological Research","volume":" ","pages":"1352-1360"},"PeriodicalIF":1.9,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145186562","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Real-world outcomes of myasthenia gravis management: a cross-sectional study at a Korean tertiary center.","authors":"Ye Joon Jung, Ha Young Shin, Hyung Jun Park, Seung Woo Kim","doi":"10.1080/01616412.2025.2568028","DOIUrl":"10.1080/01616412.2025.2568028","url":null,"abstract":"<p><strong>Introduction: </strong>The clinical course and treatment response of myasthenia gravis (MG) vary widely, requiring a comprehensive understanding of treatment outcomes. However, real-world data on Korean MG patients remain limited. This study aimed to evaluate treatment outcomes in Korean MG patients at a specific cross-sectional time point.</p><p><strong>Methods: </strong>This retrospective analysis included MG patients who had outpatient visits between October 2023 and September 2024. We assessed treatment outcomes at the index date, including the proportion achieving MM-5-defined as minimal manifestations or better with corticosteroid use ≤5 mg/day - and the proportion meeting criteria for refractory MG.</p><p><strong>Results: </strong>A total of 668 patients were included. At the index date, 16.3% were in pharmacologic remission, 45.1% in minimal manifestation, and 4.9% showed worsening disease. Overall, 48.1% achieved MM-5. The MM-5 rate was 51.9% among those treated with one immunosuppressant but declined to 17.1% in those who had been treated with three. MM-5 was achieved in 41.7% of patients with a history of myasthenic crisis and 49.0% of those without. The median MG-ADL score was 2.0; 33.7% scored 0, while 13.9% scored ≥6. The median prednisolone dose was 5.0 mg/day; 67.2% received ≤5 mg, and 9.0% received ≥15 mg. Depending on the definition used, 1.0% to 22.8% were classified as refractory.</p><p><strong>Conclusion: </strong>This study provides real-world insights into treatment outcomes in Korean MG patients. While about half achieved stable disease with conventional therapies, a substantial proportion remained inadequately controlled, underscoring ongoing treatment challenges.</p>","PeriodicalId":19131,"journal":{"name":"Neurological Research","volume":" ","pages":"1394-1404"},"PeriodicalIF":1.9,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145213293","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Postoperative pneumocephalus in unilateral chronic subdural hematoma and its correlation with recurrence: a retrospective single-center study.","authors":"Adrian Liebert, Thomas Eibl, Leonard Ritter, Karl-Michael Schebesch","doi":"10.1080/01616412.2026.2739281","DOIUrl":"https://doi.org/10.1080/01616412.2026.2739281","url":null,"abstract":"<p><strong>Objectives: </strong>Pneumocephalus emerged as a risk factor for recurrence of chronic subdural hematoma (CSDH). However, data on volumetric assessment of subdural air (SA), its risk factors, and correlation with recurrence remain limited.</p><p><strong>Materials and methods: </strong>We retrospectively included patients with unilateral CSDH who underwent surgery. Three analyses were performed: (1) comparison of absolute versus relative SA to preoperative hematoma volume (HV) for predicting recurrence; (2) evaluation of the relationship between SA and recurrence using regression and stratification into four SA-volume subgroups; (3) identification of risk factors for pneumocephalus.Recurrence was defined as symptomatic re-accumulation of CSDH requiring re-surgery within the first three months of surgery.</p><p><strong>Results: </strong>142 patients were included. Absolute SA demonstrated a stronger correlation with recurrence, with a cut-off value of 6.95 ml. Each additional 1 ml of SA was associated with a 4.3% increase in the odds of recurrence, and rates ranged from 12.4% in patients (<7 ml) to 45% (>21 ml) (<i>p</i> < 0.001). Patients with ≥7 ml of SA were older (<i>p</i> = 0.04), more frequently had hemispheric hematomas (<i>p</i> = 0.02), and exhibited greater mass effect, reflected by width, HV, and midline shift (all <i>p</i> < 0.001). Multivariate analysis and ROC-analysis revealed preoperative HV ≥ 105.5 ml as a relevant parameter of increased SA (<i>p</i> < 0.001).</p><p><strong>Conclusion: </strong>Preoperative HV demonstrated strongest relation to elevated postoperative SA. Absolute postoperative SA correlates better with recurrence. Patients with ≤6.95 ml of SA have a lower recurrence risk, whereas higher volumes are associated with progressively increased recurrence.</p>","PeriodicalId":19131,"journal":{"name":"Neurological Research","volume":" ","pages":"1-15"},"PeriodicalIF":1.9,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149112651","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inflammatory-immune crosstalk in aneurysmal subarachnoid hemorrhage: bidirectional Mendelian randomization and causal mediation evidence.","authors":"Xinyang Yan, Liangchao Jiang, Jiachen Wang, Zheng Zhang, Yunfei Zhou, Longxiao Zhang, Zhongbo Yang, Yi Shen, Jiaxi Li, Jinning Song","doi":"10.1080/01616412.2025.2568031","DOIUrl":"10.1080/01616412.2025.2568031","url":null,"abstract":"<p><strong>Background: </strong>The causal interplay between inflammatory mediators and immune cell phenotypes in aneurysmal subarachnoid hemorrhage (aSAH) remains undefined. We investigated whether immune surface antigens influence rupture risk through inflammatory protein mediation.</p><p><strong>Methods: </strong>Using European genetic consortium data, we implemented an integrated Mendelian randomization (MR) framework. First, univariable MR assessed effects of 731 immune cell traits and 91 inflammatory proteins on rupture risk. Second, two-step MR quantified mediation effects where exposures influenced both mediator and outcome. Third, multivariable MR determined direct effects after mediator adjustment. Sensitivity analyses controlled for smoking, systolic blood pressure, and lipid levels.</p><p><strong>Results: </strong>Elevated CD4 abundance on plasma CD28+ CD4+ T cells reduced rupture risk [OR (odds ratio) = 0.901; <i>p</i> = 0.004]. Serum CX3CL1 mediated 12% of this protection (OR _mediation = 0.987; two-step MR <i>p</i> < 0.05). The direct protective effect persisted after CX3CL1 adjustment (OR _direct = 0.913; multivariable MR <i>p</i> = 0.013).Separately, interleukin-7 demonstrated strong independent risk effects (OR = 2.027; <i>p</i> = 1.29×10^{- 4}, Bonferroni-corrected). Our comprehensive screen additionally identified multiple immuno-inflammatory factors significantly associated with aSAH risk (univariable MR <i>p</i><0.05), further evidencing the complex immunoinflammatory network in rupture pathogenesis. No pathway showed significant confounding by cardiometabolic factors.</p><p><strong>Conclusions: </strong>We establish a novel immune-inflammatory axis wherein CD4+ T cell surface signatures confer protection against intracranial aneurysm rupture partially through CX3CL1 downregulation, while interleukin-7 independently promotes rupture. These findings reveal actionable targets for risk stratification and immunomodulatory interventions.</p>","PeriodicalId":19131,"journal":{"name":"Neurological Research","volume":" ","pages":"1416-1430"},"PeriodicalIF":1.9,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145213325","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LncRNA SNHG14 knockdown mitigates sevoflurane-induced neuronal injury by upregulating miR-22-3p.","authors":"Lei Yang, Yuanzhi Li, Shuai Wang, Yanyan Jiang, Dalong Wang, Quan Lin, Ke Liu, Shuai Zhang, Ying Cheng, Jiaqi Gu","doi":"10.1080/01616412.2025.2568030","DOIUrl":"10.1080/01616412.2025.2568030","url":null,"abstract":"<p><strong>Objective: </strong>Prolonged use of sevoflurane (Sev) anesthesia leads to abnormal neuronal cell apoptosis and damage and cognitive impairment. LncRNA SNHG14 is aberrantly expressed in many neurodegenerative diseases. The aim of this paper is to investigate the role of SNHG14 in apoptosis and injury caused by Sev.</p><p><strong>Methods: </strong>Mouse and HT22 cell injury models induced by sevoflurane were established by treating mice and HT22 cells with the anesthetic. SNHG14 and miR-22-3p as well as Bax, Caspase-3, and Bcl-2 mRNA expression were detected by RT-qPCR. Cell proliferation was detected by CCK-8 kit. Apoptosis was assessed by flow cytometry. The levels of inflammatory factors TNF-α, IL-6, and IL-1β in the cells were assessed by ELISA. DLR verified the binding relationship between SNHG14 and miR-22-3p.</p><p><strong>Results: </strong>Sev treatment resulted in abnormal apoptosis and cell damage, the SNHG14 level was notably elevated and the miR-22-3p level was decreased. Knockdown of SNHG14 resulted in increased levels of miR-22-3p, up-regulation of cell proliferation ability, decreased apoptosis rate, and decreased levels of inflammatory factors in cells and tissues. And all these changes were reversed after inhibiting the expression of miR-22-3p.</p><p><strong>Conclusion: </strong>Sev treatment leads to increased SNHG14 expression levels and decreased miR-22-3p levels. Knockdown of SNHG14 could alleviate Sev-induced inflammation and damage in nerve cells by increasing the level of miR-22-3p. This could be a potential target for the treatment of Sev-induced neuroinflammation.</p>","PeriodicalId":19131,"journal":{"name":"Neurological Research","volume":" ","pages":"1405-1415"},"PeriodicalIF":1.9,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145346336","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Intraprocedural cangrelor during mechanical thrombectomy for acute ischemic stroke: a systematic review and single-arm meta-analysis.","authors":"João Vitor Andrade Fernandes, João Victor de Oliveira Ramos, Maurus Marques de Almeida Holanda","doi":"10.1080/01616412.2025.2568032","DOIUrl":"10.1080/01616412.2025.2568032","url":null,"abstract":"<p><strong>Objective: </strong>To evaluate the safety and efficacy of intravenous cangrelor administered during mechanical thrombectomy in patients with acute ischemic stroke.</p><p><strong>Methods: </strong>We conducted a systematic review and one-arm meta-analysis of prospective or retrospective studies reporting clinical or procedural outcomes after intraprocedural cangrelor use in adults undergoing thrombectomy for acute ischemic stroke. Pooled event rates and 95% confidence intervals (CIs) were calculated using a random-effects model. Leave-one-out sensitivity analyses were performed for all outcomes.</p><p><strong>Results: </strong>Five studies including 131 patients were analyzed. The pooled rate of favorable functional outcome at 90 days (mRS 0-2) was 0.525 (95% CI: 0.286-0.753; I² = 68.9%); sensitivity analysis showed stable estimates (range: 0.448-0.578). Successful reperfusion was achieved in 96.8% (95% CI: 0.894-0.991; I² = 0%), with robust findings across all scenarios (range: 0.962-0.980). Hemorrhagic transformation occurred in 26.6% (95% CI: 0.168-0.395), and symptomatic intracranial hemorrhage in 9.4% (95% CI: 0.049-0.173), both with low-to-null heterogeneity. In-stent thrombosis and thromboembolic events were rare, with pooled rates of 2.0% (95% CI: 0.006-0.067) and 3.8% (95% CI: 0.014-0.098), respectively. Gastrointestinal bleeding and retroperitoneal hematoma were not observed, though the pooled rate for each remained at 2.0%. Ninety-day mortality was 30.9% (95% CI: 0.179-0.480), with consistent estimates across leave-one-out analyses (range: 0.234-0.362).</p><p><strong>Conclusion: </strong>Cangrelor appears to be a safe and effective intraprocedural antiplatelet agent during mechanical thrombectomy for acute ischemic stroke.</p>","PeriodicalId":19131,"journal":{"name":"Neurological Research","volume":" ","pages":"1431-1441"},"PeriodicalIF":1.9,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145200449","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NLRX1 orchestrates neuronal mitophagy in Alzheimer's Disease: a mechanistic exploration.","authors":"Baoying Qiu, Jiajun He, Shu Li, Qiaoling Wang, Wenhua Feng, Xiaotong Yu, Yuanyuan Jia, Shuyu Liu, Dijin Jiao, Ling Xie","doi":"10.1080/01616412.2025.2566230","DOIUrl":"10.1080/01616412.2025.2566230","url":null,"abstract":"<p><strong>Background: </strong>Mitophagy dysfunction in Alzheimer's Disease (AD) accelerates disease progression, highlighting the need for novel therapeutic targets. Although Nucleotide oligomerization domain - like receptor X1 (NLRX1) regulates mitophagy, its role in AD remains unclear. This study aimed to elucidate NLRX1's function in AD - associated mitophagy and its therapeutic potential.</p><p><strong>Methods: </strong>APP/PS1 transgenic mice and N2A - SW cells were used to establish AD models. Behavioral assays evaluated cognitive function in APP/PS1 mice, while transmission electron microscopy examined mitochondrial morphology. ELISA measured β - amyloid (Aβ)1-42 levels, and RT - qPCR and Western blot analyzed NLRX1 and mitophagy - related proteins after manipulating NLRX1 expression.</p><p><strong>Results: </strong>APP/PS1 mice had cognitive impairment, elevated Aβ1-42, and abnormal mitochondrial morphology, with reduced NLRX1 expression. NLRX1 - RNAi worsened mitochondrial function, increased Aβ1-42 and mitochondrial ROS, decreased the LC3B - II/I ratio, and upregulated Cyt - C, HSP60, and TIM23, while NLRX1 overexpression alleviated these effects. Co-immunoprecipitation confirmed NLRX1's interaction with key mitophagy protein.</p><p><strong>Conclusion: </strong>NLRX1 is a key regulator of neuronal mitophagy in AD, and its downregulation impairs mitophagy, suggesting it as a potential therapeutic target.</p>","PeriodicalId":19131,"journal":{"name":"Neurological Research","volume":" ","pages":"1361-1374"},"PeriodicalIF":1.9,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145177016","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Low-dose heparin reduces radial artery injury in transradial cerebral angiography: a 375-case retrospective study.","authors":"Rongxin He, Xiaohan Zhang, Lingwan Yan, Min Tao, Tian Wang, Cai Zhong, Kaimin Xiao, Lu Gan, Man Luo","doi":"10.1080/01616412.2025.2568027","DOIUrl":"10.1080/01616412.2025.2568027","url":null,"abstract":"<p><strong>Background: </strong>Transradial cerebral angiography carries a risk of radial artery injury, which may affect subsequent approaches for angiography or endovascular therapy. The role of heparin in mitigating this risk remains controversial.</p><p><strong>Objective: </strong>To evaluate the efficacy and safety of heparin in preventing radial artery injury with transradial cerebral angiography. Methods: In a single-center retrospective study, we analyzed 375 patients undergoing diagnostic cerebral angiography via the right radial approach between August 2022 and July 2025. Patients were stratified by heparin dose: no heparin (<i>n</i> = 235), low-dose (30 IU/kg, <i>n</i> = 90), or standard-dose (60 IU/kg, <i>n</i> = 50). Primary outcomes included radial artery injury, ecchymosis, pain and ischemic manifestations. Statistical analyses employed Kruskal-Wallis and chi-square tests with Bonferroni correction for multiple comparisons. Results: Radial artery injury was significantly lower with heparin administration (low-dose: 3.3% [3/90]; standard-dose: 2.0% [1/50]) versus no heparin (14.5% [34/235]; both <i>p</i> < 0.0167), with no difference between heparin doses (<i>p</i> = 0.21). No intergroup differences were observed in ecchymosis (2.1% vs. 1.1% vs. 2.0%, <i>p</i> = 0.83) or pain (4.3% vs. 2.2% vs. 2.0%, <i>p</i> = 0.56). Ischemic manifestations (pallor) occurred exclusively in the no-heparin group (3.4%, 8/235; <i>p</i> = 0.088).</p><p><strong>Conclusions: </strong>Low-dose heparin (30IU/kg) significantly reduces radial artery injury rates without increasing risk of ecchymosis. Routine administration of low-dose heparin through the arterial sheath is recommended to protect radial artery.</p>","PeriodicalId":19131,"journal":{"name":"Neurological Research","volume":" ","pages":"1386-1393"},"PeriodicalIF":1.9,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145239316","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}