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Socioeconomic status moderates associations between hippocampal development and cognition in preterms 社会经济地位可调节早产儿海马体发育与认知能力之间的关系。
IF 4.4 2区 医学 Q1 CLINICAL NEUROLOGY Pub Date : 2024-08-08 DOI: 10.1002/acn3.52168
Julia Konrad, Ting Guo, Steven Ufkes, Thiviya Selvanathan, Min Sheng, Eiman Al-Ajmi, Helen M. Branson, Vann Chau, Linh G. Ly, Edmond N. Kelly, Ruth E. Grunau, Steven P. Miller

Objective

The hippocampus plays a critical role in cognitive networks. The anterior hippocampus is vulnerable to early-life stress and socioeconomic status (SES) with alterations persisting beyond childhood. How SES modifies the relationship between early hippocampal development and cognition remains poorly understood. This study examined associations between SES, structural and functional development of neonatal hippocampus, and 18-month cognition in very preterm neonates.

Methods

In total, 179 preterm neonates were followed prospectively. Structural and resting-state functional MRI were obtained early-in-life and at term-equivalent age (median 32.9 and 41.1 weeks post-menstrual age) to calculate anterior and posterior hippocampal volumes and hippocampal functional connectivity strength. Eighteen-month cognition was assessed via Bayley-III. Longitudinal statistical analysis using generalized estimating equations, accounting for birth gestational age, post-menstrual age at scan, sex, and motion, was performed.

Results

SES, measured as maternal education level, modified associations between anterior but not posterior hippocampal volumes and 18-month cognition (interaction term p = 0.005), and between hippocampal connectivity and cognition (interaction term p = 0.05). Greater anterior hippocampal volumes and hippocampal connectivity were associated with higher cognitive scores only in the lowest SES group. Maternal education alone did not predict neonatal hippocampal volume from early-in-life and term.

Interpretation

SES modified the relationship between neonatal hippocampal development and 18-month cognition in very preterm neonates. The lack of direct association between maternal education and neonatal hippocampal volumes indicates that socio-environmental factors beyond the neonatal period contribute to modifying the relationship between hippocampal development and cognition. These findings point toward opportunities to more equitably promote optimal neurodevelopmental outcomes in very preterm infants.

目的海马在认知网络中发挥着关键作用。海马前部容易受到早期生活压力和社会经济地位(SES)的影响,这种改变会持续到童年之后。人们对社会经济地位如何改变早期海马发育与认知之间的关系仍然知之甚少。本研究探讨了社会经济地位、新生儿海马结构和功能发育与极早产新生儿18个月认知能力之间的关系:共对179名早产新生儿进行了前瞻性随访。研究人员在新生儿早期和足月新生儿(月经后中位数分别为32.9周和41.1周)进行了结构和静息状态功能磁共振成像,以计算海马前部和后部体积以及海马功能连接强度。通过 Bayley-III 评估了 18 个月的认知能力。使用广义估计方程进行了纵向统计分析,并考虑了出生胎龄、扫描时的月经后年龄、性别和运动:以母亲教育水平衡量的社会经济地位改变了海马前部体积(而非后部体积)与 18 个月认知能力之间的关系(交互项 p = 0.005),以及海马连接性与认知能力之间的关系(交互项 p = 0.05)。只有在社会经济地位最低的组别中,海马前部体积和海马连通性越大,认知得分越高。单凭母亲的教育程度并不能预测新生儿海马体积从出生初期到足月的变化:SES改变了极早产新生儿海马体发育与18个月认知能力之间的关系。母亲教育程度与新生儿海马体积之间缺乏直接联系,这表明新生儿期以外的社会环境因素有助于改变海马发育与认知之间的关系。这些发现为更公平地促进早产儿获得最佳神经发育结果提供了机会。
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引用次数: 0
Application of the international criteria for optic neuritis in the Acute Optic Neuritis Network 在急性视神经炎网络中应用视神经炎国际标准。
IF 4.4 2区 医学 Q1 CLINICAL NEUROLOGY Pub Date : 2024-08-04 DOI: 10.1002/acn3.52166
Philipp Klyscz, Susanna Asseyer, Ricardo Alonso, Charlotte Bereuter, Omer Bialer, Atira Bick, Sara Carta, John J. Chen, Leila Cohen, Yamit Cohen-Tayar, Edgar Carnero Contentti, Russell C. Dale, Eoin P. Flanagan, Jonathan A. Gernert, Julian Haas, Joachim Havla, Christoph Heesen, Mark Hellmann, Netta Levin, Pablo Lopez, Itay Lotan, Maria Belen Luis, Sara Mariotto, Christina Mayer, Alvaro Jose Mejia Vergara, Cassandra Ocampo, Susana Ochoa, Frederike C. Oertel, Maja Olszewska, José Luis Peralta Uribe, Jaume Sastre-Garriga, Dario Scocco, Sudarshini Ramanathan, Natthapon Rattanathamsakul, Fu-Dong Shi, Jemal Shifa, Ilya Simantov, Sasitorn Siritho, Alon Tiosano, Nanthaya Tisavipat, Isabel Torres, Adi Vaknin Dembinsky, Angela Vidal-Jordana, Adi Wilf-Yarkoni, Ti Wu, Sol Zamir, Luis Alfonso Zarco, Hanna G. Zimmermann, Axel Petzold, Friedemann Paul, Hadas Stiebel-Kalish

Objective

The first international consensus criteria for optic neuritis (ICON) were published in 2022. We applied these criteria to a prospective, global observational study of acute optic neuritis (ON).

Methods

We included 160 patients with a first-ever acute ON suggestive of a demyelinating CNS disease from the Acute Optic Neuritis Network (ACON). We applied the 2022 ICON to all participants and subsequently adjusted the ICON by replacing a missing relative afferent pupillary defect (RAPD) or dyschromatopsia if magnetic resonance imaging pathology of the optical nerve plus optical coherence tomography abnormalities or certain biomarkers are present.

Results

According to the 2022 ICON, 80 (50%) patients were classified as definite ON, 12 (7%) patients were classified as possible ON, and 68 (43%) as not ON (NON). The main reasons for classification as NON were absent RAPD (52 patients, 76%) or dyschromatopsia (49 patients, 72%). Distribution of underlying ON etiologies was as follows: 78 (49%) patients had a single isolated ON, 41 (26%) patients were diagnosed with multiple sclerosis, 25 (16%) patients with myelin oligodendrocyte glycoprotein antibody-associated disease, and 15 (9%) with neuromyelitis optica spectrum disorder. The application of the adjusted ON criteria yielded a higher proportion of patients classified as ON (126 patients, 79%).

Interpretation

According to the 2022 ICON, almost half of the included patients in ACON did not fulfill the requirements for classification of definite or possible ON, particularly due to missing RAPD and dyschromatopsia. Thorough RAPD examination and formal color vision testing are critical to the application of the 2022 ICON.

目的:2022 年发布了首个视神经炎(ICON)国际共识标准。我们将这些标准应用于一项关于急性视神经炎(ON)的前瞻性全球观察研究:我们从急性视神经炎网络(ACON)中纳入了 160 名首次患急性视神经炎并提示患有脱髓鞘性中枢神经系统疾病的患者。我们对所有参与者应用了2022年ICON,随后对ICON进行了调整,如果存在视神经磁共振成像病理学、光学相干断层扫描异常或某些生物标志物,则替换缺失的相对传入性瞳孔缺损(RAPD)或色觉障碍:根据 2022 ICON,80 例(50%)患者被归类为明确的视神经缺损,12 例(7%)患者被归类为可能的视神经缺损,68 例(43%)患者被归类为非视神经缺损(NON)。被归类为非ON的主要原因是RAPD缺失(52名患者,76%)或色觉障碍(49名患者,72%)。潜在 ON 病因的分布情况如下:78名患者(49%)有单个孤立的ON,41名患者(26%)被诊断为多发性硬化症,25名患者(16%)患有髓鞘少突胶质细胞糖蛋白抗体相关疾病,15名患者(9%)患有神经脊髓炎视神经频谱紊乱。应用调整后的ON标准,被归类为ON的患者比例更高(126例,79%):根据2022年的ICON,ACON中几乎一半的患者不符合明确或可能的ON分类要求,特别是由于RAPD缺失和色觉异常。彻底的 RAPD 检查和正规的色觉测试对于 2022 ICON 的应用至关重要。
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引用次数: 0
Diflunisal versus tafamidis on neuropathy and cardiomyopathy in hereditary transthyretin amyloidosis 二氟尼柳与他法米对遗传性转甲状腺素淀粉样变性的神经病变和心肌病的影响
IF 4.4 2区 医学 Q1 CLINICAL NEUROLOGY Pub Date : 2024-08-02 DOI: 10.1002/acn3.52158
Chi-Chao Chao, Shiou-Ru Tzeng, Ming-Chang Chiang, Hsueh-Wen Hsueh, Wan-Jen Hsieh, Yuan-Chun Chao, Mei-Fang Cheng, Yen-Hung Lin, Mao-Yuan Su, Chun-Hsiang Huang, Yi-Shiang Wang, Ming-Fang Hsieh, Ping-Huei Tseng, Sung-Tsang Hsieh

Objectives

Hereditary transthyretin (TTR) amyloidosis (ATTRv) is frequently complicated by polyneuropathy (ATTRv-PN) and cardiomyopathy (ATTRv-CM). The long-term efficacy of diflunisal on both polyneuropathy and cardiomyopathy in ATTRv patients, especially those with non-V30M genotypes, has not been fully investigated and compared with that of tafamidis.

Methods

We compared the structural and biochemical characteristics of A97S-TTR complexed with tafamidis with those of diflunisal, and prospectively followed up and compared the progression of polyneuropathy and cardiomyopathy between ATTRv-PN patients taking diflunisal and those taking tafamidis.

Results

Both diflunisal and tafamidis effectively bind to the two thyroxine-binding sites at the A97S-TTR dimer–dimer interface and equally and almost sufficiently reduce amyloid fibril formation. Thirty-five ATTRv-PN patients receiving diflunisal and 22 patients receiving tafamidis were enrolled. Compared with no treatment, diflunisal treatment significantly delayed the transition of FAP Stage 1 to 2 and Stage 2 to 3 and decreased the deterioration in parameters of the ulnar nerve conduction study (NCS). The progression of FAP stage or NCS parameters did not differ between patients treated with diflunisal and those treated with tafamidis. Both diflunisal and tafamidis treatments significantly decreased radiotracer uptake on 99mTc-PYP SPECT and stabilized cardiac wall thickness and blood pro-B-type natriuretic peptide levels. No significant adverse events occurred during diflunisal or tafamidis treatment.

Interpretations

The binding patterns of both tafamidis and diflunisal to A97S-TTR closely resembled those observed in the wild type. Diflunisal can effectively delay the progression of polyneuropathy and cardiomyopathy with similar efficacy to tafamidis and may become a cost-effective alternative treatment for late-onset ATTRv-PN.

目的:遗传性转甲状腺素(TTR)淀粉样变性(ATTRv)经常并发多发性神经病(ATTRv-PN)和心肌病(ATTRv-CM)。目前尚未全面研究二氟尼柳对 ATTRv 患者,尤其是非 V30M 基因型患者的多发性神经病变和心肌病的长期疗效,也未将其与他法米迪进行比较:我们比较了A97S-TTR与他非米迪复合物和二氟尼沙的结构和生化特征,并对服用二氟尼沙和他非米迪的ATTRv-PN患者的多发性神经病和心肌病进展进行了前瞻性随访和比较:结果:二氟尼沙和他伐米迪都能有效地与A97S-TTR二聚体界面上的两个甲状腺素结合位点结合,并同样几乎充分地减少淀粉样纤维的形成。35名ATTRv-PN患者接受了地氟尼沙治疗,22名患者接受了他法米迪治疗。与未接受治疗相比,地氟尼沙治疗明显延缓了FAP 1期向2期和2期向3期的转变,并减少了尺神经传导研究(NCS)参数的恶化。使用地氟尼沙和他氟米特治疗的患者在FAP分期或NCS参数的进展方面没有差异。地氟尼萨和他法米迪治疗均可显著降低 99mTc-PYP SPECT 的放射性示踪剂摄取量,并稳定心肌壁厚度和血液中前 B 型钠尿肽的水平。在二氟尼柳或他法米迪治疗期间未发生重大不良事件:他非米迪和地氟尼萨与A97S-TTR的结合模式与野生型非常相似。地氟尼沙能有效延缓多发性神经病和心肌病的进展,其疗效与他法米地相似,可能成为晚发型ATTRv-PN的一种经济有效的替代治疗方法。
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引用次数: 0
Protein-extending ACTN2 frameshift variants cause variable myopathy phenotypes by protein aggregation 蛋白扩展 ACTN2 框移变体通过蛋白聚集导致不同的肌病表型。
IF 4.4 2区 医学 Q1 CLINICAL NEUROLOGY Pub Date : 2024-08-02 DOI: 10.1002/acn3.52154
Johanna Ranta-aho, Kevin J. Felice, Per Harald Jonson, Jaakko Sarparanta, Cédric Yvorel, Ines Harzallah, Renaud Touraine, Lynn Pais, Christina A. Austin-Tse, Vijay S. Ganesh, Melanie C. O'Leary, Heidi L. Rehm, Michael K. Hehir, Sub Subramony, Qian Wu, Bjarne Udd, Marco Savarese

Objective

The objective of the study is to characterize the pathomechanisms underlying actininopathies.

Distal myopathies are a group of rare, inherited muscular disorders characterized by progressive loss of muscle fibers that begin in the distal parts of arms and legs. Recently, variants in a new disease gene, ACTN2, have been shown to cause distal myopathy. ACTN2, a gene previously only associated with cardiomyopathies, encodes alpha-actinin-2, a protein expressed in both cardiac and skeletal sarcomeres. The primary function of alpha-actinin-2 is to link actin and titin to the sarcomere Z-disk. New ACTN2 variants are continuously discovered; however, the clinical significance of many variants remains unknown. Thus, lack of clear genotype–phenotype correlations in ACTN2-related diseases, actininopathies, persists.

Methods

Functional characterization in C2C12 cell model of several ACTN2 variants is conducted, including frameshift and missense variants associated with dominant and recessive actininopathies. We assess the genotype–phenotype correlations of actininopathies using clinical data from several patients carrying these variants.

Results

The results show that the missense variants associated with a recessive form of actininopathy do not cause detectable alpha-actinin-2 aggregates in the cell model. Conversely, dominant frameshift variants causing a protein extension do form alpha-actinin-2 aggregates.

Interpretation

The results suggest that alpha-actinin-2 aggregation is the disease mechanism underlying some dominant actininopathies, and thus, we recommend that protein-extending frameshift variants in ACTN2 should be classified as pathogenic. However, this mechanism is likely elicited by only a limited number of variants. Alternative functional characterization methods should be explored to further investigate other molecular mechanisms underlying actininopathies.

研究目的这项研究的目的是确定肌动蛋白病的病理机制。远端肌病是一组罕见的遗传性肌肉疾病,其特征是肌肉纤维从手臂和腿的远端部位开始逐渐丧失。最近,一种新的疾病基因 ACTN2 的变异被证明可导致远端肌病。ACTN2 基因以前只与心肌病有关,它编码α-肌动蛋白-2,这是一种在心脏和骨骼肌肌节中都有表达的蛋白质。α-肌动蛋白-2的主要功能是将肌动蛋白和泰汀蛋白连接到肌节Z盘上。新的 ACTN2 变体不断被发现,但许多变体的临床意义仍不清楚。因此,ACTN2相关疾病(肌动蛋白病)的基因型与表型之间仍然缺乏明确的相关性:方法:我们在 C2C12 细胞模型中对几种 ACTN2 变异进行了功能表征,包括与显性和隐性肌动蛋白病相关的框移位和错义变异。我们利用携带这些变体的几名患者的临床数据评估了肌动蛋白病的基因型与表型的相关性:结果表明,与隐性肌动蛋白病相关的错义变体在细胞模型中不会导致可检测到的α-肌动蛋白-2聚集。相反,导致蛋白质延伸的显性框架移位变体却能形成α-actin-2聚集体:结果表明,α-肌动蛋白-2聚集是某些显性肌动蛋白病的疾病机制,因此,我们建议将ACTN2中的蛋白延伸框架移位变体归类为致病变体。然而,这种机制可能只由数量有限的变异体引起。应探索其他功能表征方法,进一步研究肌动蛋白病的其他分子机制。
{"title":"Protein-extending ACTN2 frameshift variants cause variable myopathy phenotypes by protein aggregation","authors":"Johanna Ranta-aho,&nbsp;Kevin J. Felice,&nbsp;Per Harald Jonson,&nbsp;Jaakko Sarparanta,&nbsp;Cédric Yvorel,&nbsp;Ines Harzallah,&nbsp;Renaud Touraine,&nbsp;Lynn Pais,&nbsp;Christina A. Austin-Tse,&nbsp;Vijay S. Ganesh,&nbsp;Melanie C. O'Leary,&nbsp;Heidi L. Rehm,&nbsp;Michael K. Hehir,&nbsp;Sub Subramony,&nbsp;Qian Wu,&nbsp;Bjarne Udd,&nbsp;Marco Savarese","doi":"10.1002/acn3.52154","DOIUrl":"10.1002/acn3.52154","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>The objective of the study is to characterize the pathomechanisms underlying actininopathies.</p>\u0000 \u0000 <p>Distal myopathies are a group of rare, inherited muscular disorders characterized by progressive loss of muscle fibers that begin in the distal parts of arms and legs. Recently, variants in a new disease gene, <i>ACTN2</i>, have been shown to cause distal myopathy. <i>ACTN2</i>, a gene previously only associated with cardiomyopathies, encodes alpha-actinin-2, a protein expressed in both cardiac and skeletal sarcomeres. The primary function of alpha-actinin-2 is to link actin and titin to the sarcomere Z-disk. New <i>ACTN2</i> variants are continuously discovered; however, the clinical significance of many variants remains unknown. Thus, lack of clear genotype–phenotype correlations in <i>ACTN2</i>-related diseases, actininopathies, persists.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Functional characterization in C2C12 cell model of several <i>ACTN2</i> variants is conducted, including frameshift and missense variants associated with dominant and recessive actininopathies. We assess the genotype–phenotype correlations of actininopathies using clinical data from several patients carrying these variants.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The results show that the missense variants associated with a recessive form of actininopathy do not cause detectable alpha-actinin-2 aggregates in the cell model. Conversely, dominant frameshift variants causing a protein extension do form alpha-actinin-2 aggregates.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Interpretation</h3>\u0000 \u0000 <p>The results suggest that alpha-actinin-2 aggregation is the disease mechanism underlying some dominant actininopathies, and thus, we recommend that protein-extending frameshift variants in <i>ACTN2</i> should be classified as pathogenic. However, this mechanism is likely elicited by only a limited number of variants. Alternative functional characterization methods should be explored to further investigate other molecular mechanisms underlying actininopathies.</p>\u0000 </section>\u0000 </div>","PeriodicalId":126,"journal":{"name":"Annals of Clinical and Translational Neurology","volume":"11 9","pages":"2392-2405"},"PeriodicalIF":4.4,"publicationDate":"2024-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/acn3.52154","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141877984","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Mitochondrial DNA disorders in neuromuscular diseases in diverse populations. 不同人群神经肌肉疾病中的线粒体 DNA 紊乱。
IF 4.4 2区 医学 Q1 CLINICAL NEUROLOGY Pub Date : 2024-08-02 DOI: 10.1002/acn3.52141
Fei Gao, Katherine R Schon, Jana Vandrovcova, Lindsay Wilson, Michael G Hanna, Büşranur Çavdarlı, Jeannine Heckmann, Patrick F Chinnery, Rita Horvath

Neuromuscular features are common in mitochondrial DNA (mtDNA) disorders. The genetic architecture of mtDNA disorders in diverse populations is poorly understood. We analysed mtDNA variants from whole-exome sequencing data in neuromuscular patients from South Africa, Brazil, India, Turkey and Zambia. In 998 individuals, there were two definite diagnoses, two possible diagnoses and eight secondary findings. Surprisingly, common pathogenic mtDNA variants found in people of European ancestry were very rare. Whole-exome or -genome sequencing from undiagnosed patients with neuromuscular symptoms should be re-analysed for mtDNA variants, but the landscape of pathogenic mtDNA variants differs around the world.

神经肌肉特征在线粒体 DNA(mtDNA)紊乱中很常见。人们对不同人群中 mtDNA 疾病的遗传结构知之甚少。我们分析了来自南非、巴西、印度、土耳其和赞比亚的神经肌肉患者的全外显子测序数据中的 mtDNA 变异。在 998 人中,有 2 人确诊,2 人可能确诊,8 人继发。令人惊讶的是,在欧洲血统人群中发现的常见致病 mtDNA 变异非常罕见。应重新分析未确诊的神经肌肉症状患者的全外显子组或基因组测序,以发现mtDNA变体,但世界各地致病性mtDNA变体的情况各不相同。
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引用次数: 0
True first-pass effect in patients undergoing thrombectomy for acute large core strokes 对急性大面积脑卒中患者进行血栓切除术的真正首通效应。
IF 4.4 2区 医学 Q1 CLINICAL NEUROLOGY Pub Date : 2024-08-02 DOI: 10.1002/acn3.52155
Shitao Fan, Changwei Guo, Jiacheng Huang, Zhouzhou Peng, Chengsong Yue, Jie Yang, Linyu Li, Dongjing Xie, Nizhen Yu, Shihai Yang, Xiaolei Shi, Dahong Yang, Fengli Li, Qingwu Yang

Objective

The impact of true first-pass effect (T-FPE, achieving substantial recanalization with extended thrombolysis in cerebral infarction; eTICI 3 after 1 thrombectomy) and outcomes on acute ischemic stroke (AIS) with large ischemic core remains uncertain. We aimed to study the association between T-FPE and outcomes in AIS patients with large core infarct through a real-world multicenter study.

Methods

From a prospective multicentric registry, we collected the data of all consecutive acute stroke patients with a large ischemic core who underwent thrombectomy and compared the outcomes of patients who achieved T-FPE and those who did not. In addition, we compared the outcomes of patients with different numbers of thrombectomy pass to identify the effectiveness of T-FPE. Multivariate analysis was performed to determine the predictors of T-FPE. The primary outcome was good functional outcome (modified Rankin Scale score; mRS 0–3) at 90 days. Safety outcomes included a 90-day mortality and symptomatic intracerebral hemorrhage within 48 hours after thrombectomy.

Results

Between November 2021 and February 2023, 447 eligible patients at 38 stroke centers were enrolled. Out of 447 thrombectomy patients, T-FPE was achieved in 102 individuals (22.8%). T-FPE was significantly associated with a higher proportion of good functional outcome (mRS 0–3 at 3 months, OR 2.221, 95% CI 1.418–3.479, p < 0.001) and lower mortality than non-T-FPE patients (31.4% vs. 45.5%, p = 0.012). The occlusion sites and lower DBP were strong predictors of T-FPE.

Interpretation

T-FPE was associated with favorable outcomes at 90 days in AIS patients with a large ischemic core who underwent EVT.

目的:真正的首通效应(T-FPE,通过脑梗塞扩大溶栓治疗实现实质性再通畅;eTICI 3 后 1 次血栓切除术)与大面积缺血核心急性缺血性卒中(AIS)预后的影响仍不确定。我们旨在通过一项真实世界的多中心研究,研究T-FPE与大核心梗死AIS患者的预后之间的关系:方法:我们从一个前瞻性多中心登记处收集了所有连续接受血栓切除术的大核心缺血急性卒中患者的数据,并比较了获得 T-FPE 和未获得 T-FPE 患者的预后。此外,我们还比较了不同血栓切除次数患者的预后,以确定 T-FPE 的有效性。我们进行了多变量分析,以确定 T-FPE 的预测因素。主要结果是 90 天后的良好功能预后(改良 Rankin 量表评分;mRS 0-3)。安全性结果包括90天死亡率和血栓切除术后48小时内无症状性脑内出血:结果:2021 年 11 月至 2023 年 2 月期间,38 个卒中中心的 447 名符合条件的患者入选。在 447 名血栓切除术患者中,有 102 人(22.8%)达到了 T-FPE。T-FPE与较高比例的良好功能预后(3 个月时 mRS 0-3,OR 2.221,95% CI 1.418-3.479,P 解释:T-FPE 与良好预后相关:T-FPE与接受EVT治疗的大面积缺血核心AIS患者90天后的良好预后相关。
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引用次数: 0
The impact of diagnosis delay on European patients with generalised myasthenia gravis 诊断延误对欧洲全身性肌无力患者的影响。
IF 4.4 2区 医学 Q1 CLINICAL NEUROLOGY Pub Date : 2024-08-01 DOI: 10.1002/acn3.52122
Elena Cortés-Vicente, Andras J. Borsi, Charlotte Gary, Wim G.J. Noel, Jennifer M.S. Lee, Wisam Karmous, Qiaoyi Zhang, Kavita H. Gandhi, Alberto E. Batista, Jonathan J. DeCourcy, Sophie G. Barlow, Shiva L. Birija, Gregor A. Gibson

Objective

The objective was to determine the mean duration of diagnosis delay for patients with myasthenia gravis from five European countries and explore the impact of >1 year diagnosis delay.

Methods

Patients with myasthenia gravis (N = 387) from Europe (France/Germany/Italy/Spain/United Kingdom) and their physicians participated in the Adelphi Real World Myasthenia Gravis Disease Specific Programme™. Diagnosis delay (time from symptom onset to diagnosis) was calculated and characteristics described for patients experiencing >1 year and ≤1 year diagnosis delay. Denominators varied according to outcome as missing data were not imputed.

Results

Mean (standard deviation) diagnosis delay was 363.1 (520.9) days, and 27.1% (105 out of 387) of patients experienced diagnosis delay >1 year. Among patients with >1 year and ≤1 year diagnosis delay, respectively, 69.2% (72 out of 104) and 17.4% [45 out of 259] had initially received a different diagnosis (physician-reported); 40.0% (42 out of 105) and 24.1% (68 out of 282) were Myasthenia Gravis Foundation of America class III at the time of the survey (physician-reported); 72.4% (76 out of 105) and 61.3% (173 out of 282) had fatigue (subjective physician reporting from a pre-selected list of symptoms); 30.5% (32 out of 105) and 17.4% (49 out of 282) had anxiety and 21.9% (23 out of 105) and 13.1% (37 out of 282) had depression (both subjective physician reporting from a pre-selected list, Likert-style); and mean (standard deviation) MG-QoL-15r score was 14.4 (5.50) and 12.6 (7.84) (self-reported by N = 43 and N = 74 patients, respectively).

Interpretation

More than a quarter of patients with myasthenia gravis experienced diagnosis delay of >1 year. These patients had a different clinical profile with regards to severity, symptoms, comorbidities and MG-QoL-15r score, compared with patients experiencing ≤1 year diagnosis delay.

目的目的是确定欧洲五国肌无力患者的平均诊断延迟时间,并探讨诊断延迟超过一年的影响:来自欧洲(法国/德国/意大利/西班牙/英国)的重症肌无力患者(N = 387)及其医生参加了阿德尔菲真实世界重症肌无力疾病专项计划(Adelphi Real World Myasthenia Gravis Disease Specific Programme™)。对诊断延迟(从症状出现到确诊的时间)进行了计算,并描述了诊断延迟>1年和≤1年的患者的特征。由于缺失数据未进行归类,因此分母因结果而异:平均(标准差)诊断延迟时间为 363.1 (520.9) 天,27.1% 的患者(387 人中有 105 人)诊断延迟时间超过 1 年。在诊断延迟>1年和≤1年的患者中,分别有69.2%(104人中有72人)和17.4%[259人中有45人]最初接受过不同的诊断(医生报告);40.0%(105人中有42人)和24.1%(282人中有68人)在调查时属于美国肌无力症基金会III级(医生报告);72.4%(105人中有76人)和61.3%(282 人中有 173 人)有疲劳感(医生从预先选定的症状清单中主观报告);30.5%(105 人中有 32 人)和 17.4%(282 人中有 49 人)有焦虑感,21.9%(105 人中有 23 人)和 13.1%(282 人中有 37 人)有焦虑感。平均(标准差)MG-QoL-15r 得分为 14.4(5.50)和 12.6(7.84)(分别由 N = 43 和 N = 74 名患者自我报告):超过四分之一的重症肌无力患者的诊断延迟时间超过一年。与诊断延迟≤1年的患者相比,这些患者在严重程度、症状、并发症和MG-QoL-15r评分方面的临床特征有所不同。
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引用次数: 0
MRI evidence of gray matter loss in COVID-19 patients with cognitive and olfactory disorders COVID-19认知和嗅觉障碍患者灰质丢失的核磁共振成像证据。
IF 4.4 2区 医学 Q1 CLINICAL NEUROLOGY Pub Date : 2024-07-30 DOI: 10.1002/acn3.52164
Serena Capelli, Alberto Arrigoni, Angela Napolitano, Giulio Pezzetti, Andrea Remuzzi, Rosalia Zangari, Ferdinando Luca Lorini, Maria Sessa, Anna Caroli, Simonetta Gerevini

Objective

The aim of this study was to assess COVID-19-related gray matter (GM) structural alterations in two distinct groups of patients presenting with the prevailing and distinctive COVID-19-related neurological symptoms – isolated olfactory disorders as sole neurological manifestation (COVID-OD) and cognitive disorders (COVID-CD) – as compared to a control group of unaffected individuals.

Methods

The study included 61 COVID-CD patients (57 [60–63] years, 62% females), 84 COVID-OD patients (49 [35–57] years, 60% females), and 17 controls (51 [41–52] years, 41% females). Region-based morphometry (RBM) and voxel-based morphometry (VBM) were performed on T1-weighted MRI scans to assess GM regional volume and voxel-wise density differences between COVID-19 patients and controls. Surface-based morphometry (SBM) was applied to investigate cortical thickness alterations. The statistical models built to assess GM structural differences among groups included total intracranial volume and age as nuisance variables.

Results

The multi-morphometric analysis revealed statistically significant (p < 0.05 corrected for multiple comparisons) reduction in GM regional volumes, in voxel-wise GM density and in cortical thickness in both COVID-CD and COVID-OD patient groups as compared to controls. Across all three analyses, COVID-CD patients showed more distributed and severe GM loss than COVID-OD patients. The most prominently affected GM regions in the COVID-CD group included the hippocampus, putamen, cingulate gyrus, precuneus, precentral and postcentral gyri, amygdala, lingual gyrus, and caudate nucleus.

Interpretation

Our MRI findings show that COVID-19-related olfactory and cognitive disorders both induce GM atrophy, although at different degrees of severity, likely indicative of neurodegeneration and neuroinflammation.

研究目的本研究的目的是评估两组不同患者与 COVID-19 相关的灰质(GM)结构改变,这两组患者均表现出与 COVID-19 相关的普遍而独特的神经症状,即作为唯一神经表现的孤立嗅觉障碍(COVID-OD)和认知障碍(COVID-CD),并与未受影响的对照组进行比较:研究对象包括 61 名 COVID-CD 患者(57 [60-63] 岁,62% 为女性)、84 名 COVID-OD 患者(49 [35-57] 岁,60% 为女性)和 17 名对照组(51 [41-52] 岁,41% 为女性)。对T1加权磁共振成像扫描进行了基于区域的形态测量(RBM)和基于体素的形态测量(VBM),以评估COVID-19患者和对照组之间的GM区域体积和体素密度差异。基于表面的形态测量法(SBM)用于研究皮质厚度的改变。为评估各组间的基因组结构差异而建立的统计模型将颅内总容积和年龄作为干扰变量:结果:多形态计量学分析表明,各组间的皮质厚度差异具有显著的统计学意义(P我们的磁共振成像研究结果表明,COVID-19相关的嗅觉和认知障碍都会诱发基因组萎缩,只是严重程度不同,这可能表明神经变性和神经炎症。
{"title":"MRI evidence of gray matter loss in COVID-19 patients with cognitive and olfactory disorders","authors":"Serena Capelli,&nbsp;Alberto Arrigoni,&nbsp;Angela Napolitano,&nbsp;Giulio Pezzetti,&nbsp;Andrea Remuzzi,&nbsp;Rosalia Zangari,&nbsp;Ferdinando Luca Lorini,&nbsp;Maria Sessa,&nbsp;Anna Caroli,&nbsp;Simonetta Gerevini","doi":"10.1002/acn3.52164","DOIUrl":"10.1002/acn3.52164","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>The aim of this study was to assess COVID-19-related gray matter (GM) structural alterations in two distinct groups of patients presenting with the prevailing and distinctive COVID-19-related neurological symptoms – isolated olfactory disorders as sole neurological manifestation (COVID-OD) and cognitive disorders (COVID-CD) – as compared to a control group of unaffected individuals.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>The study included 61 COVID-CD patients (57 [60–63] years, 62% females), 84 COVID-OD patients (49 [35–57] years, 60% females), and 17 controls (51 [41–52] years, 41% females). Region-based morphometry (RBM) and voxel-based morphometry (VBM) were performed on T1-weighted MRI scans to assess GM regional volume and voxel-wise density differences between COVID-19 patients and controls. Surface-based morphometry (SBM) was applied to investigate cortical thickness alterations. The statistical models built to assess GM structural differences among groups included total intracranial volume and age as nuisance variables.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The multi-morphometric analysis revealed statistically significant (<i>p</i> &lt; 0.05 corrected for multiple comparisons) reduction in GM regional volumes, in voxel-wise GM density and in cortical thickness in both COVID-CD and COVID-OD patient groups as compared to controls. Across all three analyses, COVID-CD patients showed more distributed and severe GM loss than COVID-OD patients. The most prominently affected GM regions in the COVID-CD group included the hippocampus, putamen, cingulate gyrus, precuneus, precentral and postcentral gyri, amygdala, lingual gyrus, and caudate nucleus.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Interpretation</h3>\u0000 \u0000 <p>Our MRI findings show that COVID-19-related olfactory and cognitive disorders both induce GM atrophy, although at different degrees of severity, likely indicative of neurodegeneration and neuroinflammation.</p>\u0000 </section>\u0000 </div>","PeriodicalId":126,"journal":{"name":"Annals of Clinical and Translational Neurology","volume":"11 9","pages":"2457-2472"},"PeriodicalIF":4.4,"publicationDate":"2024-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/acn3.52164","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141854330","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Improving criteria for dissemination in space in multiple sclerosis by including additional regions 通过纳入更多区域,改进多发性硬化症空间播散的标准。
IF 4.4 2区 医学 Q1 CLINICAL NEUROLOGY Pub Date : 2024-07-30 DOI: 10.1002/acn3.52170
Michael A. Foster, Giuseppe Pontillo, Indran Davagnanam, Sara Collorone, Ferran Prados, Baris Kanber, Marios C. Yiannakas, Lola Ogunbowale, Ailbhe Burke, Claudia A. M. Gandini Wheeler-Kingshott, Olga Ciccarelli, Wallace Brownlee, Frederik Barkhof, Ahmed T. Toosy

Objective

We investigated the effects of adding regions to current dissemination in space (DIS) criteria for multiple sclerosis (MS).

Methods

Participants underwent brain, optic nerve, and spinal cord MRI. Baseline DIS was assessed by 2017 McDonald criteria and versions including optic nerve, temporal lobe, or corpus callosum as a fifth region (requiring 2/5), a version with all regions (requiring 3/7) and optic nerve variations requiring 3/5 and 4/5 regions. Performance was evaluated against MS diagnosis (2017 McDonald criteria) during follow-up.

Results

Eighty-four participants were recruited (53F, 32.8 ± 7.1 years). 2017 McDonald DIS criteria were 87% sensitive (95% CI: 76–94), 73% specific (50–89), and 83% accurate (74–91) in identifying MS. Modified criteria with optic nerve improved sensitivity to 98% (91–100), with specificity 33% (13–59) and accuracy 84% (74–91). Criteria including temporal lobe showed sensitivity 94% (84–98), specificity 50% (28–72), and accuracy 82% (72–90); criteria including corpus callosum showed sensitivity 90% (80–96), specificity 68% (45–86), and accuracy 85% (75–91). Criteria adding all three regions (3/7 required) had sensitivity 95% (87–99), specificity 55% (32–76), and accuracy 85% (75–91). When requiring 3/5 regions (optic nerve as the fifth), sensitivity was 82% (70–91), specificity 77% (55–92), and accuracy 81% (71–89); with 4/5 regions, sensitivity was 56% (43–69), specificity 95% (77–100), and accuracy 67% (56–77).

Interpretation

Optic nerve inclusion increased sensitivity while lowering specificity. Increasing required regions in optic nerve criteria increased specificity and decreased sensitivity. Results suggest considering the optic nerve for DIS. An option of 3/5 or 4/5 regions preserved specificity, and criteria adding all three regions had highest accuracy.

目的我们研究了在目前多发性硬化症(MS)的空间播散(DIS)标准中增加区域的影响:参与者接受脑、视神经和脊髓 MRI 检查。根据 2017 年麦克唐纳标准和包括视神经、颞叶或胼胝体作为第五个区域(要求 2/5)的版本、包含所有区域(要求 3/7)的版本以及要求 3/5 和 4/5 区域的视神经变异版本对基线 DIS 进行评估。在随访过程中,根据多发性硬化症诊断(2017 年麦克唐纳标准)对结果进行了评估:共招募了 84 名参与者(53 名女性,32.8 ± 7.1 岁)。2017 年麦克唐纳 DIS 标准在识别 MS 方面的敏感度为 87%(95% CI:76-94),特异度为 73%(50-89),准确度为 83%(74-91)。包含视神经的修改标准将敏感性提高到 98% (91-100),特异性为 33% (13-59),准确性为 84% (74-91)。包括颞叶的标准显示灵敏度为 94% (84-98),特异性为 50% (28-72),准确率为 82% (72-90);包括胼胝体的标准显示灵敏度为 90% (80-96),特异性为 68% (45-86),准确率为 85% (75-91)。加入所有三个区域(要求 3/7)的标准灵敏度为 95% (87-99),特异性为 55% (32-76),准确率为 85% (75-91)。要求 3/5 个区域(视神经为第五个区域)时,灵敏度为 82% (70-91),特异性为 77% (55-92),准确率为 81% (71-89);要求 4/5 个区域时,灵敏度为 56% (43-69),特异性为 95% (77-100),准确率为 67% (56-77):视神经的加入提高了灵敏度,同时降低了特异性。视神经标准中所需区域的增加提高了特异性,降低了敏感性。结果表明,DIS应考虑视神经。3/5或4/5个区域的选择保留了特异性,增加所有三个区域的标准具有最高的准确性。
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引用次数: 0
Analyzing post-endovascular treatment stroke prognosis with transcranial Doppler and quantitative electroencephalography 利用经颅多普勒和定量脑电图分析血管内治疗后中风的预后。
IF 4.4 2区 医学 Q1 CLINICAL NEUROLOGY Pub Date : 2024-07-28 DOI: 10.1002/acn3.52157
Yajie Qi, Yingqi Xing, Qingduo Wang, Yanting Cao, Hongxiu Chen, Ying Chen

Objective

Despite successful recanalization following acute ischemic stroke, patients may have a poor prognosis. We investigated whether transcranial Doppler combined with quantitative electroencephalography can identify patients with a poor prognosis at an early stage.

Methods

Prospectively recruited patients with successful recanalization after endovascular treatment for acute ischemic stroke were assessed for prognosis at 90 days using the modified Rankin Scale. Clinical information and National Institute of Health Stroke Scale scores were recorded. Transcranial Doppler combined with quantitative electroencephalography was used to evaluate brain function.

Results

Of the 37 patients (63.5 ± 11.7 years) studied, 18 had a poor prognosis at 90 days (modified Rankin Scale >3). Multivariable analysis revealed that transcranial Doppler indicators of the pulsatility index of the unaffected side, quantitative electroencephalography indicators of the pairwise-derived Brain Symmetry Index, and National Institute of Health Stroke Scale score were independent prognostic indicators. Modeling indicated that combining these independent predictors yielded superior accuracy and net clinical benefit to any single variable. With the final predictive model presented as a nomogram, internal validation by bootstrap resampling showed good discrimination with a concordance index of 0.961. The calibration curve displayed good agreement of predicted and actual probabilities.

Interpretation

The nomogram prediction model combining transcranial Doppler with quantitative electroencephalography and National Institute of Health Stroke Scale scores can provide guidance for individualized risk prediction in patients with acute ischemic stroke after revascularization.

目的:尽管急性缺血性脑卒中患者的再通术取得了成功,但他们的预后可能很差。我们研究了经颅多普勒与定量脑电图相结合能否在早期识别预后不良的患者:方法:对前瞻性招募的急性缺血性脑卒中血管内治疗后成功再通的患者,使用改良的 Rankin 量表评估其 90 天后的预后。记录临床信息和美国国立卫生研究院卒中量表评分。经颅多普勒结合定量脑电图用于评估脑功能:结果:在接受研究的 37 名患者(63.5 ± 11.7 岁)中,18 名患者在 90 天后预后较差(修正的 Rankin 量表>3)。多变量分析表明,经颅多普勒非受影响侧搏动指数指标、定量脑电图对源脑对称性指数指标和美国国立卫生研究院卒中量表评分是独立的预后指标。建模结果表明,与任何单一变量相比,将这些独立预测指标结合在一起可获得更高的准确性和净临床效益。最终的预测模型以提名图的形式呈现,通过引导重采样进行的内部验证显示出良好的区分度,一致性指数为 0.961。校准曲线显示预测概率和实际概率的一致性良好:经颅多普勒与定量脑电图和美国国立卫生研究院卒中量表评分相结合的提名图预测模型可为血管重建术后急性缺血性卒中患者的个体化风险预测提供指导。
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引用次数: 0
期刊
Annals of Clinical and Translational Neurology
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