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Ischemic Stroke and COVID-19 Infection: an Analysis of Treatment Outcomes in Patients who Underwent Endovascular Thrombectomy 缺血性中风与 COVID-19 感染:血管内血栓切除术患者治疗效果分析
Q3 Multidisciplinary Pub Date : 2024-04-05 DOI: 10.54101/acen.2024.1.6
Alexander I. Yakovlev, I. A. Voznyuk, Tatiana V. Kharitonova, A. Savello, Mariia V. Prokhorova, S. V. Kolomentsev, Nadezhda А. Tsurikova
Aim. This study aimed to compare and evaluate treatment outcomes in groups of ischemic stroke patients with or without COVID-19 infection who underwent endovascular thrombectomy (EVT). Materials and methods. We conducted a retrospective analysis of 817 case records of IS patients aged 25 to 99 years with confirmed thrombotic occlusion of cerebral arteries and subsequent EVT who were treated in regional vascular centers in St. Petersburg from January 1, 2021 to December 31, 2021. Results. Patients without COVID-19 had favorable outcome more often than patients with confirmed COVID-19 (35.0% vs. 7.3%, p 0.001); mortality rate was 30% vs. 52%, respectively (p 0.001). Conclusions. Intercurrent COVID-19 significantly worsened prognosis and increased risk of death in ischemic stroke patients who underwent EVT.
研究目的本研究旨在比较和评估感染或未感染 COVID-19 并接受血管内血栓切除术(EVT)的缺血性脑卒中患者的治疗效果。材料和方法。我们对 2021 年 1 月 1 日至 2021 年 12 月 31 日期间在圣彼得堡地区血管中心接受治疗的 817 例年龄在 25 至 99 岁之间、确诊脑动脉血栓性闭塞并随后接受 EVT 的 IS 患者病历进行了回顾性分析。结果没有COVID-19的患者比确诊COVID-19的患者更容易获得良好的预后(35.0%对7.3%,P 0.001);死亡率分别为30%对52%(P 0.001)。结论接受EVT治疗的缺血性卒中患者并发COVID-19会明显恶化预后并增加死亡风险。
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引用次数: 0
Mood Disorders After COVID-19 COVID-19 后的情绪失调
Q3 Multidisciplinary Pub Date : 2024-01-05 DOI: 10.54101/acen.2023.4.2
A. Mikheeva, M. Topuzova, Valeriya A. Malko, Ekaterina S. Zhilina, A. A. Mikhailova, D. Lagutina, T. L. Karonova, T. M. Alekseeva
Introduction. The COVID-19 pandemic has led to a high prevalence of post-COVID-19 syndrome (PCS), with mood disorders being the most common manifestations. Objective: To study the prevalence of PCS-associated mood disorders and their features. Materials and methods. We examined patients after COVID-19 (n = 91; age: 24-84 years; median time to recovery: 7 months) using the following tools: the BDI and HADS (screening for anxiety and depression); the Starkstein Apathy Scale; FIS and FSS (fatigue assessment); the MoCA, MMSE, and FAB (cognitive assessment); the FIRST, ESS, PSQI, and ISI (sleep disorders evaluation); the EQ5D (quality of life measurement). We designed a special questionnaire to collect data related to a history of COVID-19 and patients' condition after discharge. In addition, we analyzed electronic medical records and discharge summaries and performed neurological examination. Results. Of all the examined patients, 65 (71.4%) participants had signs and symptoms of PCS. Mood disorders were observed in 33 (50.8%) cases, with apathy (78.7%), anxiety (66.7%), and fatigue (60.6%) being the most common. Depressive disorders were found in 12 (36.3%) patients. Cognitive functions were impaired in 7 (21.2%) patients; sleep disorders were observed in 16 (48.5%) cases. We found a positive correlation between depressive disorders and fatigue based on the BDI, FIS, and FSS scores (rS = 0.711; rS = 0.453), depressive disorders and anxiety (rS = 0.366), fatigue and apathy (rS = 0.350). Anxiety increased the risk of sleep disorders (rS = 0.683). Quality of life has been shown to decrease in patients with mood disorders due to the negative effect of long-term fatigue and depressive disorders. Conclusions. There is a close connection between different types of mood disorders that develop after COVID-19 and exacerbate symptoms of each other. Early diagnosis and treatment of these disorders can improve patients' quality of life and preserve their ability to work.
导言。COVID-19 大流行导致 COVID-19 后综合征(PCS)的高发病率,其中情绪障碍是最常见的表现形式。研究目的研究 PCS 相关情绪障碍的发病率及其特征。材料与方法我们使用以下工具对 COVID-19 患者(n = 91;年龄:24-84 岁;康复时间中位数:7 个月)进行了检查:BDI 和 HADS(焦虑和抑郁筛查);Starkstein 冷漠量表;FIS 和 FSS(疲劳评估);MoCA、MMSE 和 FAB(认知评估);FIRST、ESS、PSQI 和 ISI(睡眠障碍评估);EQ5D(生活质量测量)。我们设计了一份特殊问卷,收集与 COVID-19 病史和患者出院后情况相关的数据。此外,我们还分析了电子病历和出院摘要,并进行了神经系统检查。结果在所有受检患者中,65 人(71.4%)有 PCS 的体征和症状。33例(50.8%)患者出现情绪障碍,其中最常见的是冷漠(78.7%)、焦虑(66.7%)和疲劳(60.6%)。12例(36.3%)患者出现抑郁障碍。7例(21.2%)患者的认知功能受损;16例(48.5%)患者出现睡眠障碍。根据 BDI、FIS 和 FSS 评分,我们发现抑郁障碍与疲劳(rS = 0.711;rS = 0.453)、抑郁障碍与焦虑(rS = 0.366)、疲劳与冷漠(rS = 0.350)之间存在正相关。焦虑会增加睡眠障碍的风险(rS = 0.683)。由于长期疲劳和抑郁障碍的负面影响,情绪障碍患者的生活质量已被证明会下降。结论在 COVID-19 之后出现的不同类型的情绪障碍之间存在密切联系,并会加重彼此的症状。这些疾病的早期诊断和治疗可提高患者的生活质量,并保护他们的工作能力。
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引用次数: 0
Neurobehavioral Testing as Cognitive Function Evaluation tool in Experimentally Induced Neurodegeneration in Mice 将神经行为测试作为实验诱导小鼠神经变性的认知功能评估工具
Q3 Multidisciplinary Pub Date : 2024-01-05 DOI: 10.54101/acen.2023.4.9
Yulia A. Panina, O. Lopatina, A. I. Mosyagina, Yulia K. Komleva, A. V. Morgun, Yana V. Gorina, Elena D. Hilazheva
Neurodegeneration is a complex and multifactorial process presenting one of the major issues of fundamental science and clinical medicine due to its high prevalence, multiple nosological entities, and variations in pathogenesis. Translational research contributes to the study of neurodegenerative diseases, with modeling of such pathologies being an important part of this research. Behavioral testing in various animal models of neurodegenerative diseases allows to assess the model validity and reliability, as well as to investigate the potential efficacy of pharmacotherapy and other management approaches. In this overview we present test batteries that evaluate behavior, cognitive performance, and emotional states in animals with experimentally induced neurodegeneration.
神经变性是一个复杂的多因素过程,由于其发病率高、病理实体多、发病机制各不相同,因此是基础科学和临床医学的主要问题之一。转化研究有助于神经退行性疾病的研究,而此类病症的建模则是这一研究的重要组成部分。通过对各种神经退行性疾病动物模型进行行为测试,可以评估模型的有效性和可靠性,并研究药物疗法和其他管理方法的潜在疗效。在本综述中,我们将介绍评估实验诱导神经变性动物的行为、认知能力和情绪状态的测试套件。
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引用次数: 0
Copper Ions Reduced Toxicity of Sodium Azide and Lipopolysaccharide on Cultured Cerebellar Granule Neurons 铜离子可降低叠氮化钠和脂多糖对培养小脑颗粒神经元的毒性
Q3 Multidisciplinary Pub Date : 2024-01-05 DOI: 10.54101/acen.2023.4.6
E. Stelmashook, O. P. Alexandrova, E. Genrikhs, Y. Verma, A. B. Salmina, N. Isaev
Introduction. Copper ions (Cu2+) are structural elements of proteins such as cytochrome с oxidase (Complex IV), an enzyme that catalyzes the final step of electron transfer to oxygen during oxidative phosphorylation in the mitochondria. With Cu2+ homeostasis being of utmost importance, its disturbances in the central nervous system are involved in the mechanisms of many neurodegenerative and other brain disorders. This study aimed to assess the effects of non-toxic copper ion levels on death of cerebellar granule neurons associated with lipopolysaccharide (LPS; in vitro inflammation model) or azide sodium (NaN3; cytochrome с oxidase inhibitor). Materials and methods. LPS (10 μg/mL) or NaN3 (250 μM) was added on day 7 to 8 to the culture medium with rat cerebellar cells for 24 hours in vitro. Nitrite concentrations were measured in the culture medium by Griess assay; absorbance was recorded with a spectrophotometer at 540 nm, and morphologically intact cells were counted as survived neurons. Results. Added to the culture medium, LPS or NaN3 reduced neuron survival to 15 ± 2% or 20 ± 3% vs. control, respectively. Cu2+ (0.5 to 5.0 μM) increased neuron survival in a dose-dependent manner to 78 ± 4% with toxic levels of LPS and to 86 ± 6% with NaN3 with 5 μM Cu2+. The concentration of nitrites in the control culture medium was 2.0 ± 0.2 μM. Added to the cell cultures, LPS increased the concentration of nitrites to 8.5 ± 0.5 μM. Cu2+ 5 μM did not show any significant effects on nitrite accumulation in the culture medium. Conclusions. We showed that copper ions can exert protective effects on neurons against LPS-induced or NaN3-induced toxicity. This protection is likely to be associated rather with Cu2+ interaction with Complex IV of the electron transfer chain in the mitochondria than with inhibition of NO production. Effects of Cu2+ on apoptosis pathway proteins also cannot be ruled out.
导言。铜离子(Cu2+)是细胞色素с氧化酶(Complex IV)等蛋白质的结构元素,这种酶在线粒体氧化磷酸化过程中催化电子转移到氧的最后一步。Cu2+ 的平衡至关重要,它在中枢神经系统中的紊乱与许多神经退行性疾病和其他脑部疾病的发病机制有关。本研究旨在评估无毒铜离子水平对与脂多糖(LPS;体外炎症模型)或叠氮化钠(NaN3;细胞色素с氧化酶抑制剂)相关的小脑颗粒神经元死亡的影响。材料和方法在体外培养大鼠小脑细胞 24 小时的第 7 至第 8 天,将 LPS(10 μg/mL)或 NaN3(250 μM)加入培养基中。亚硝酸盐的浓度用格里丝测定法测量;吸光度用分光光度计在 540 纳米波长处记录,形态完整的细胞计数为存活的神经元。结果与对照组相比,加入培养基的 LPS 或 NaN3 可使神经元存活率分别降至 15 ± 2% 或 20 ± 3%。Cu2+(0.5 至 5.0 μM)以剂量依赖的方式提高了神经元的存活率,毒性水平的 LPS 为 78 ± 4%,5 μM Cu2+ 的 NaN3 为 86 ± 6%。对照培养基中亚硝酸盐的浓度为 2.0 ± 0.2 μM。向细胞培养物中添加 LPS 后,亚硝酸盐的浓度增至 8.5 ± 0.5 μM。Cu2+ 5 μM 对亚硝酸盐在培养基中的积累没有明显影响。结论我们的研究表明,铜离子可对神经元产生保护作用,使其免受 LPS 诱导或 NaN3 诱导的毒性的影响。这种保护作用可能与 Cu2+ 与线粒体中电子传递链的复合体 IV 的相互作用有关,而不是与抑制 NO 的产生有关。也不能排除 Cu2+ 对细胞凋亡途径蛋白的影响。
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引用次数: 0
Assessment of Mitochondrial Gene Activity in Dopaminergic Neuron Cultures Derived from Induced Pluripotent Stem Cells Obtained from Parkinson's Disease Patients 评估帕金森病患者诱导多能干细胞多巴胺能神经元培养物中线粒体基因的活性
Q3 Multidisciplinary Pub Date : 2024-01-05 DOI: 10.54101/acen.2023.4.7
A. Vetchinova, M. R. Kapkaeva, N. Mudzhiri, S. N. Illarioshkin
Introduction. Induced pluripotent stem cells (iPSCs) culturing allows modelling of neurodegenerative diseases in vitro and discovering its early biomarkers. Our objective was to evaluate the activity of genes involved in mitochondrial dynamics and functions in genetic forms of Parkinson's disease (PD) using cultures of dopaminergic neurons derived from iPSCs. Materials and methods. Dopaminergic neuron cultures were derived by reprogramming of the cells obtained from PD patients with SNCA and LRRK2 gene mutations, as well as from a healthy donor for control. Expression levels of 112 genes regulating mitochondrial structure, dynamics, and functions were assessed by multiplex gene expression profiling using NanoString nCounter custom mitochondrial gene expression panel. Results. When comparing the characteristics of the neurons from patients with genetic forms of PD to those of the control, we observed variations in the gene activity associated with the mitochondrial respiratory chain, the tricarboxylic acid cycle enzyme activities, biosynthesis of amino acids, oxidation of fatty acids, steroid metabolism, calcium homeostasis, and free radical quenching. Several genes in the cell cultures with SNCA and LRRK2 gene mutations exhibited differential expression. Moreover, these genes regulate mitophagy, mitochondrial DNA synthesis, redox reactions, cellular detoxification, apoptosis, as well as metabolism of proteins and nucleotides. Conclusions. The changes in gene network expression found in this pilot study confirm the role of disrupted mitochondrial homeostasis in the molecular pathogenesis of PD. These findings may contribute to the development of biomarkers and to the search for new therapeutic targets for the treatment of SNCA- and LRRK2-associated forms of the disease.
简介诱导多能干细胞(iPSCs)培养可在体外模拟神经退行性疾病并发现其早期生物标志物。我们的目的是利用从 iPSCs 中提取的多巴胺能神经元培养物,评估帕金森病(PD)遗传形式中涉及线粒体动力学和功能的基因的活性。材料与方法多巴胺能神经元培养物是通过对SNCA和LRRK2基因突变的帕金森病患者以及健康供体的细胞进行重编程而获得的。使用 NanoString nCounter 定制线粒体基因表达谱面板,通过多重基因表达谱分析评估了 112 个调控线粒体结构、动力学和功能的基因的表达水平。结果显示在比较遗传型帕金森病患者和对照组神经元的特征时,我们观察到与线粒体呼吸链、三羧酸循环酶活性、氨基酸的生物合成、脂肪酸的氧化、类固醇代谢、钙平衡和自由基淬灭相关的基因活性存在差异。在 SNCA 和 LRRK2 基因突变的细胞培养物中,一些基因表现出不同的表达。此外,这些基因还调控有丝分裂、线粒体 DNA 合成、氧化还原反应、细胞解毒、细胞凋亡以及蛋白质和核苷酸的代谢。结论本试验研究发现的基因网络表达变化证实了线粒体平衡紊乱在帕金森病分子发病机制中的作用。这些发现可能有助于开发生物标记物,并为治疗 SNCA- 和 LRRK2- 相关疾病寻找新的治疗靶点。
{"title":"Assessment of Mitochondrial Gene Activity in Dopaminergic Neuron Cultures Derived from Induced Pluripotent Stem Cells Obtained from Parkinson's Disease Patients","authors":"A. Vetchinova, M. R. Kapkaeva, N. Mudzhiri, S. N. Illarioshkin","doi":"10.54101/acen.2023.4.7","DOIUrl":"https://doi.org/10.54101/acen.2023.4.7","url":null,"abstract":"Introduction. Induced pluripotent stem cells (iPSCs) culturing allows modelling of neurodegenerative diseases in vitro and discovering its early biomarkers. \u0000Our objective was to evaluate the activity of genes involved in mitochondrial dynamics and functions in genetic forms of Parkinson's disease (PD) using cultures of dopaminergic neurons derived from iPSCs. \u0000Materials and methods. Dopaminergic neuron cultures were derived by reprogramming of the cells obtained from PD patients with SNCA and LRRK2 gene mutations, as well as from a healthy donor for control. Expression levels of 112 genes regulating mitochondrial structure, dynamics, and functions were assessed by multiplex gene expression profiling using NanoString nCounter custom mitochondrial gene expression panel. \u0000Results. When comparing the characteristics of the neurons from patients with genetic forms of PD to those of the control, we observed variations in the gene activity associated with the mitochondrial respiratory chain, the tricarboxylic acid cycle enzyme activities, biosynthesis of amino acids, oxidation of fatty acids, steroid metabolism, calcium homeostasis, and free radical quenching. Several genes in the cell cultures with SNCA and LRRK2 gene mutations exhibited differential expression. Moreover, these genes regulate mitophagy, mitochondrial DNA synthesis, redox reactions, cellular detoxification, apoptosis, as well as metabolism of proteins and nucleotides. \u0000Conclusions. The changes in gene network expression found in this pilot study confirm the role of disrupted mitochondrial homeostasis in the molecular pathogenesis of PD. These findings may contribute to the development of biomarkers and to the search for new therapeutic targets for the treatment of SNCA- and LRRK2-associated forms of the disease.","PeriodicalId":36946,"journal":{"name":"Annals of Clinical and Experimental Neurology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-01-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139383340","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Long-term Intracerebroventricular Administration of Ouabain Causes Motor Impairments in C57Bl/6 Mice 长期脑室内注射欧贝因会导致 C57Bl/6 小鼠运动障碍
Q3 Multidisciplinary Pub Date : 2024-01-05 DOI: 10.54101/acen.2023.4.5
Y. Timoshina, R. Kazanskaya, Vladislav A. Zavialov, A. Volnova, Alexander V. Latanov, Tatiana N. Fedorova, R. Gainetdinov, A. Lopachev
Introduction. Cardiac glycosides are natural ligands of Na+/K+-ATPase, which regulate its activity and signaling. Intracerebroventricular administration of ouabain has been previously shown to induce hyperlocomotion in C57Bl/6 mice via a decrease in the rate of dopamine reuptake from the synaptic cleft. Materials and methods. This study involved forty C57BL/6 mice. 1.5 μL of 50 μM ouabain was administered daily into the left lateral cerebral ventricle over the course of 4 days. On day 5, open field, beam balance, and ladder rung walking tests were performed to assess the locomotor activity and motor impairments in the mice. We evaluated changes in the activation of signaling cascades, ratios of proapoptotic and antiapoptotic proteins, and the amount of α1 and α3 isoforms of the Na+/K+-ATPase α-subunit in brain tissue using Western blotting. Na+/K+-ATPase activity was evaluated in the crude synaptosomal fractions of the brain tissues. Results. We observed hyperlocomotion and stereotypic behavior during the open field test 24 hours after the last injection of ouabain. On day 5, the completion time and the number of errors made in the beam balance and ladder rung walking tests increased in the mice that received ouabain. Akt kinase activity decreased in the striatum, whereas the ratio of proapoptotic and antiapoptotic proteins and the number of Na+/K+-ATPase α-subunits did not change. Na+/K+-ATPase activity increased in the striatum and decreased in the brainstem. Conclusions. Long-term exposure to ouabain causes motor impairments mediated by changes in the activation of signaling cascades in dopaminergic neurons.
导言强心苷是 Na+/K+-ATP 酶的天然配体,可调节其活性和信号传导。以前曾有研究表明,脑室内给药乌巴因可通过降低突触间隙的多巴胺再摄取率来诱导 C57Bl/6 小鼠的过度运动。材料和方法。本研究涉及 40 只 C57BL/6 小鼠。每天在左侧脑室注射 1.5 μL 50 μM 的欧阿巴因,连续注射 4 天。第5天,进行开阔地、横梁平衡和梯级行走测试,以评估小鼠的运动活动和运动障碍。我们使用 Western 印迹技术评估了脑组织中信号级联的激活、促凋亡蛋白和抗凋亡蛋白的比例以及 Na+/K+-ATPase α 亚基的 α1 和 α3 异构体数量的变化。对脑组织粗突触体部分的Na+/K+-ATP酶活性进行了评估。结果在最后一次注射乌苯那敏24小时后,我们观察到大鼠在开阔地试验中出现过度运动和刻板行为。第5天,接受乌巴因注射的小鼠在横梁平衡和梯级行走测试中的完成时间和错误次数均有所增加。纹状体中的Akt激酶活性降低,而促凋亡蛋白和抗凋亡蛋白的比例以及Na+/K+-ATPase α亚基的数量没有变化。纹状体的Na+/K+-ATP酶活性增加,而脑干的活性降低。结论长期暴露于欧巴马因会导致多巴胺能神经元信号级联激活发生变化,从而引起运动障碍。
{"title":"Long-term Intracerebroventricular Administration of Ouabain Causes Motor Impairments in C57Bl/6 Mice","authors":"Y. Timoshina, R. Kazanskaya, Vladislav A. Zavialov, A. Volnova, Alexander V. Latanov, Tatiana N. Fedorova, R. Gainetdinov, A. Lopachev","doi":"10.54101/acen.2023.4.5","DOIUrl":"https://doi.org/10.54101/acen.2023.4.5","url":null,"abstract":"Introduction. Cardiac glycosides are natural ligands of Na+/K+-ATPase, which regulate its activity and signaling. Intracerebroventricular administration of ouabain has been previously shown to induce hyperlocomotion in C57Bl/6 mice via a decrease in the rate of dopamine reuptake from the synaptic cleft. \u0000Materials and methods. This study involved forty C57BL/6 mice. 1.5 μL of 50 μM ouabain was administered daily into the left lateral cerebral ventricle over the course of 4 days. On day 5, open field, beam balance, and ladder rung walking tests were performed to assess the locomotor activity and motor impairments in the mice. We evaluated changes in the activation of signaling cascades, ratios of proapoptotic and antiapoptotic proteins, and the amount of α1 and α3 isoforms of the Na+/K+-ATPase α-subunit in brain tissue using Western blotting. Na+/K+-ATPase activity was evaluated in the crude synaptosomal fractions of the brain tissues. \u0000Results. We observed hyperlocomotion and stereotypic behavior during the open field test 24 hours after the last injection of ouabain. On day 5, the completion time and the number of errors made in the beam balance and ladder rung walking tests increased in the mice that received ouabain. Akt kinase activity decreased in the striatum, whereas the ratio of proapoptotic and antiapoptotic proteins and the number of Na+/K+-ATPase α-subunits did not change. Na+/K+-ATPase activity increased in the striatum and decreased in the brainstem. \u0000Conclusions. Long-term exposure to ouabain causes motor impairments mediated by changes in the activation of signaling cascades in dopaminergic neurons.","PeriodicalId":36946,"journal":{"name":"Annals of Clinical and Experimental Neurology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-01-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139381044","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Poststroke Asthenic Disorder 中风后衰弱症
Q3 Multidisciplinary Pub Date : 2024-01-05 DOI: 10.54101/acen.2023.4.8
M. Kutlubaev, A. I. Akhmetova
Asthenic disorders are seen in approximately half of poststroke patients. The mechanisms underlying poststroke asthenia (PSA) are related to brain connectome damage, as well as neuroinflammatory and neuroendocrine mechanisms. PSA is associated with a lack of energy, lassitude, and fatigue that do not improve after rest or sleep; it is differentiated from depression, apathy, and daytime drowsiness. Risk factors for PSA include female gender, anxiety and depressive disorders, severe neurological deficit, sleep disorders, diabetes etc. Treatment of PSA includes cognitive behavioral therapy graded physical activity, and pharmacotherapy.
约有一半的卒中后患者会出现气喘症状。脑卒中后虚弱症(PSA)的发病机制与大脑连接体损伤以及神经炎症和神经内分泌机制有关。PSA 与乏力、倦怠和疲劳有关,休息或睡眠后症状不会改善;它与抑郁、冷漠和白天嗜睡有所区别。PSA 的风险因素包括女性性别、焦虑和抑郁障碍、严重的神经系统缺陷、睡眠障碍、糖尿病等。PSA 的治疗包括认知行为疗法、分级体力活动和药物疗法。
{"title":"Poststroke Asthenic Disorder","authors":"M. Kutlubaev, A. I. Akhmetova","doi":"10.54101/acen.2023.4.8","DOIUrl":"https://doi.org/10.54101/acen.2023.4.8","url":null,"abstract":"Asthenic disorders are seen in approximately half of poststroke patients. The mechanisms underlying poststroke asthenia (PSA) are related to brain connectome damage, as well as neuroinflammatory and neuroendocrine mechanisms. PSA is associated with a lack of energy, lassitude, and fatigue that do not improve after rest or sleep; it is differentiated from depression, apathy, and daytime drowsiness. Risk factors for PSA include female gender, anxiety and depressive disorders, severe neurological deficit, sleep disorders, diabetes etc. Treatment of PSA includes cognitive behavioral therapy graded physical activity, and pharmacotherapy.","PeriodicalId":36946,"journal":{"name":"Annals of Clinical and Experimental Neurology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-01-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139381116","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
A Clinical Case of Corticospinal Tract Reorganization of Supplementary Motor Area in a Child After Acute Hypoxic Brain Injury 急性缺氧性脑损伤后儿童补充运动区皮质脊髓束重组的临床病例
Q3 Multidisciplinary Pub Date : 2024-01-05 DOI: 10.54101/acen.2023.4.12
D. S. Kanshina, I. Melnikov, Maksim V. Ublinsky, S. S. Nikitin, Svetlana A. Valliulina, Tolibdzhon A. Akhadov, M. Surma
We present clinical observation of a 3-year-old child during recovery after acute hypoxic brain injury (freshwater drowning). Using diagnostic transcranial magnetic stimulation and magnetic resonance tractography with reconstruction of the corticospinal tract (CST) originated from the primary motor cortex and supplementary motor area (SMA), we determined that hypoxic brain injury induced activation of CST from the SMA. The period of reorganization was associated with the development of epileptiform patterns, that confirms the transient hyperexcitability of cortical neurons. Our findings indicate no recovery of motor function after acute hypoxic brain injury when CST originated only from SMA.
我们对一名 3 岁儿童急性缺氧性脑损伤(淡水溺水)后的恢复过程进行了临床观察。我们利用诊断性经颅磁刺激和磁共振束成像技术重建了源自初级运动皮层和辅助运动区(SMA)的皮质脊髓束(CST),确定缺氧性脑损伤诱发了来自 SMA 的 CST 激活。重组期与癫痫样模式的发展相关,这证实了皮质神经元的短暂过度兴奋性。我们的研究结果表明,当 CST 仅来自 SMA 时,急性缺氧性脑损伤后运动功能无法恢复。
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引用次数: 0
The Long-Term Course of Chronic Inflammatory Demyelinating Polyneuropathy: a Retrospective Study 慢性炎症性脱髓鞘多发性神经病的长期病程:一项回顾性研究
Q3 Multidisciplinary Pub Date : 2024-01-05 DOI: 10.54101/acen.2023.4.1
Evgeniya A. Melnik, A. S. Arestova, Irina A. Berdalina, E. Gnedovskaya, Darya A. Grishinа, N. Suponeva, M. Piradov
Introduction. Chronic inflammatory demyelinating polyneuropathy (CIDP) is characterized by long-term progressive or relapsing course, neurological deficit, and disability of varied severity. The course of CIDP after specific therapy and, if necessary, long-term maintenance treatment are to be studied. Objective: To evaluate CIDP clinical and history characteristics over the long-term follow-up ( 5 years), to compare long-term CIDP course in a number of clinical variants and onset types, and to determine clinical predictors of unfavorable CIDP course. Materials and methods. The study included 45 patients diagnosed with CIDP based on EAN/PNS 2021 criteria lasting for 5 or more years. Retrospective collection and analysis of medical records and clinical history were performed. Internationally accepted scales were used to assess neurological deficit (NIS, MRCss), disability (INCAT), and disease activity status (CDAS). The criteria of unfavorable course were developed to evaluate factors affecting CIDP course. Results. Among the patients with CIDP history of 5 years, each third (34%) had no neurological deficit and remained in long-term clinical remission (CDAS 1). The vast majority (90%) responded to first-line therapy in early disease, while only 53% of patients required maintenance treatment in 5 or more years of the onset. With the developed criteria (poor response to glucocorticosteroids (GCS), need for maintenance therapy, and CDAS 3–5), unfavourable CIDP course was detected in 24 (53.3%) participants. Its probability increased in later onset (47 [30; 50] years), the chronic type of onset, and delayed specific therapy. The most significant predictors included low total NIS score at onset (60 points) and multifocal CIDP. Conclusions. The course of typical CIDP is relatively favorable if timely diagnosed, and pathogenetic treatment initiated. Patients with acute and subacute onset demonstrate the best long-term status. The predictors of unfavourable disease course include mild neurological deficit at onset (NIS total score 60 points) and multifocal CIDP.
简介慢性炎症性脱髓鞘性多发性神经病(CIDP)的特点是长期进展性或复发性病程、神经功能缺损和不同程度的残疾。我们需要研究 CIDP 在接受特定治疗后的病程,以及必要时的长期维持治疗。目的:评估 CIDP 的临床和病史:评估 CIDP 长期随访(5 年)的临床和病史特征,比较多种临床变异和发病类型的 CIDP 长期病程,并确定不利 CIDP 病程的临床预测因素。材料和方法研究纳入了 45 名根据 EAN/PNS 2021 标准确诊为 CIDP 的患者,病程均在 5 年或 5 年以上。研究人员对病历和临床病史进行了回顾性收集和分析。采用国际公认的量表评估神经功能缺损(NIS、MRCss)、残疾(INCAT)和疾病活动状态(CDAS)。制定了不利病程标准,以评估影响 CIDP 病程的因素。结果在病史长达 5 年的 CIDP 患者中,三分之一(34%)的患者没有神经功能缺损,并保持长期临床缓解(CDAS 1)。绝大多数患者(90%)对疾病早期的一线治疗有反应,只有 53% 的患者需要在发病后 5 年或更长时间内接受维持治疗。根据已制定的标准(对糖皮质激素(GCS)反应不佳、需要维持治疗和 CDAS 3-5),有 24 名(53.3%)参与者发现了 CIDP 病程不利。如果发病年龄较晚(47 [30; 50]岁)、发病类型为慢性和延迟接受特定治疗,则出现不利病程的概率会增加。最重要的预测因素包括发病时 NIS 总分低(60 分)和多灶性 CIDP。结论如果及时诊断并开始病因治疗,典型的CIDP病程相对较好。急性和亚急性发病患者的长期状况最好。预示不良病程的因素包括发病时轻度神经功能缺损(NIS总分60分)和多灶性CIDP。
{"title":"The Long-Term Course of Chronic Inflammatory Demyelinating Polyneuropathy: a Retrospective Study","authors":"Evgeniya A. Melnik, A. S. Arestova, Irina A. Berdalina, E. Gnedovskaya, Darya A. Grishinа, N. Suponeva, M. Piradov","doi":"10.54101/acen.2023.4.1","DOIUrl":"https://doi.org/10.54101/acen.2023.4.1","url":null,"abstract":"Introduction. Chronic inflammatory demyelinating polyneuropathy (CIDP) is characterized by long-term progressive or relapsing course, neurological deficit, and disability of varied severity. The course of CIDP after specific therapy and, if necessary, long-term maintenance treatment are to be studied. \u0000Objective: To evaluate CIDP clinical and history characteristics over the long-term follow-up ( 5 years), to compare long-term CIDP course in a number of clinical variants and onset types, and to determine clinical predictors of unfavorable CIDP course. \u0000Materials and methods. The study included 45 patients diagnosed with CIDP based on EAN/PNS 2021 criteria lasting for 5 or more years. Retrospective collection and analysis of medical records and clinical history were performed. Internationally accepted scales were used to assess neurological deficit (NIS, MRCss), disability (INCAT), and disease activity status (CDAS). The criteria of unfavorable course were developed to evaluate factors affecting CIDP course. \u0000Results. Among the patients with CIDP history of 5 years, each third (34%) had no neurological deficit and remained in long-term clinical remission (CDAS 1). The vast majority (90%) responded to first-line therapy in early disease, while only 53% of patients required maintenance treatment in 5 or more years of the onset. With the developed criteria (poor response to glucocorticosteroids (GCS), need for maintenance therapy, and CDAS 3–5), unfavourable CIDP course was detected in 24 (53.3%) participants. Its probability increased in later onset (47 [30; 50] years), the chronic type of onset, and delayed specific therapy. The most significant predictors included low total NIS score at onset (60 points) and multifocal CIDP. \u0000Conclusions. The course of typical CIDP is relatively favorable if timely diagnosed, and pathogenetic treatment initiated. Patients with acute and subacute onset demonstrate the best long-term status. The predictors of unfavourable disease course include mild neurological deficit at onset (NIS total score 60 points) and multifocal CIDP.","PeriodicalId":36946,"journal":{"name":"Annals of Clinical and Experimental Neurology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-01-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139383542","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Long-Term Outcomes of Management of Inferior Alveolar Neuropathy Following Orthognatic Surgeries in Patients with Mandibular Anomalies and Deformities 下颌骨异常和畸形患者正颌手术后下牙槽神经病变的长期治疗效果
Q3 Multidisciplinary Pub Date : 2024-01-05 DOI: 10.54101/acen.2023.4.4
M. Tanashyan, M. Maximova, Pavel A. Fedin, T. Noskova
Introduction. Orthognatic surgery is a routine method to manage mandibular anomalies and deformities. Objective: To assess long-term outcomes of rhythmic peripheral magnetic stimulation (rPMS) in patients with neuropathy of the inferior alveolar nerve (IAN) resulting from the surgical treatment of mandibular anomalies and deformities. Materials and methods. The study included 8 males and 16 females aged 32 ± 12 years with IAN neuropathy following the surgical treatment of mandibular anomalies and deformities. Therapeutic rPMS was performed with the Neuro-MS magnetic stimulator (Neurosoft, Ivanovo, Ivanovo Region, Russian Federation). Trigeminal and brainstem acoustic evoked potentials (EPs) were registered with Neuro-MVP (Neurosoft) to assess rPMS both at baseline (in 10 days) and in long term (in 18 ± 2 months). Results. Sensory disorders and pain prevailed in postoperative IAN neuropathy. Sensory disorders improved in 20 patients following 10-day rPMS. The clinical effect persisted in re-assessment. In long term, acoustic brainstem EPs normalized and trigeminal EPs did not change negatively. Conclusion. The use of rPMS in IAN neuropathy following orthognatic surgeries contributes to the functional improvement and stabilization of the peripheral and central brainstem and the trigeminal system.
简介正颌手术是治疗下颌骨异常和畸形的常规方法。目的评估因下颌骨异常和畸形手术治疗导致下牙槽神经(IAN)病变的患者接受节律性外周磁刺激(rPMS)的长期疗效。材料和方法。研究对象包括下颌骨异常和畸形手术治疗后导致下牙槽神经病变的 8 名男性和 16 名女性,年龄为 32 ± 12 岁。使用 Neuro-MS 磁刺激器(Neurosoft,伊万诺沃,伊万诺沃州,俄罗斯联邦)进行治疗性 rPMS。使用Neuro-MVP(Neurosoft)记录三叉神经和脑干声诱发电位(EPs),以评估基线(10天)和长期(18 ± 2个月)的rPMS。结果显示术后 IAN 神经病变主要表现为感觉障碍和疼痛。20 名患者在接受为期 10 天的 rPMS 治疗后,感觉障碍有所改善。再次评估时,临床效果依然存在。从长远来看,听性脑干 EPs 恢复正常,三叉神经 EPs 没有发生负面变化。结论在正颌手术后的 IAN 神经病变中使用 rPMS 有助于改善和稳定周围脑干、中枢脑干和三叉神经系统的功能。
{"title":"Long-Term Outcomes of Management of Inferior Alveolar Neuropathy Following Orthognatic Surgeries in Patients with Mandibular Anomalies and Deformities","authors":"M. Tanashyan, M. Maximova, Pavel A. Fedin, T. Noskova","doi":"10.54101/acen.2023.4.4","DOIUrl":"https://doi.org/10.54101/acen.2023.4.4","url":null,"abstract":"Introduction. Orthognatic surgery is a routine method to manage mandibular anomalies and deformities. \u0000Objective: To assess long-term outcomes of rhythmic peripheral magnetic stimulation (rPMS) in patients with neuropathy of the inferior alveolar nerve (IAN) resulting from the surgical treatment of mandibular anomalies and deformities. \u0000Materials and methods. The study included 8 males and 16 females aged 32 ± 12 years with IAN neuropathy following the surgical treatment of mandibular anomalies and deformities. Therapeutic rPMS was performed with the Neuro-MS magnetic stimulator (Neurosoft, Ivanovo, Ivanovo Region, Russian Federation). Trigeminal and brainstem acoustic evoked potentials (EPs) were registered with Neuro-MVP (Neurosoft) to assess rPMS both at baseline (in 10 days) and in long term (in 18 ± 2 months). \u0000Results. Sensory disorders and pain prevailed in postoperative IAN neuropathy. Sensory disorders improved in 20 patients following 10-day rPMS. The clinical effect persisted in re-assessment. In long term, acoustic brainstem EPs normalized and trigeminal EPs did not change negatively. \u0000Conclusion. The use of rPMS in IAN neuropathy following orthognatic surgeries contributes to the functional improvement and stabilization of the peripheral and central brainstem and the trigeminal system.","PeriodicalId":36946,"journal":{"name":"Annals of Clinical and Experimental Neurology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-01-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139382029","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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Annals of Clinical and Experimental Neurology
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