Neurology® Neuroimmunology & Neuroinflammation最新文献

{"title":"<i>Neurology® Neuroimmunology and Neuroinflammation</i> Enters Its Second Decade.","authors":"Scott S Zamvil","doi":"10.1212/NXI.0000000000200385","DOIUrl":"10.1212/NXI.0000000000200385","url":null,"abstract":"","PeriodicalId":19472,"journal":{"name":"Neurology® Neuroimmunology & Neuroinflammation","volume":"12 2","pages":"e200385"},"PeriodicalIF":7.8,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11813232/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143391391","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multiple Sclerosis: A Virus-Induced Gliopathy?","authors":"Joseph J Sabatino, Lawrence Steinman","doi":"10.1212/NXI.0000000000200383","DOIUrl":"10.1212/NXI.0000000000200383","url":null,"abstract":"","PeriodicalId":19472,"journal":{"name":"Neurology® Neuroimmunology & Neuroinflammation","volume":"12 2","pages":"e200383"},"PeriodicalIF":7.8,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11820804/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143399341","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Management of Autoimmune Encephalitis in a 7-Year-Old Child With CTLA-4 Haploinsufficiency and AMPA Receptor Antibodies: A Case Report.","authors":"Marjolijn S W Quaak, Michiel S J Buijze, Virginie J M Verhoeven, Clementien Vermont, Emilie P Buddingh, Maud Heredia, Janneke N Samsom, Maarten J Titulaer, Annemarie M C van Rossum, Sylvia Kamphuis, Rinze Frederik Neuteboom","doi":"10.1212/NXI.0000000000200381","DOIUrl":"10.1212/NXI.0000000000200381","url":null,"abstract":"","PeriodicalId":19472,"journal":{"name":"Neurology® Neuroimmunology & Neuroinflammation","volume":"12 2","pages":"e200381"},"PeriodicalIF":7.8,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11825085/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143409516","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fluorescein Angiography as a Surrogate Marker of Disease Activity in Susac Syndrome.","authors":"Laura Guttieres, Lea Vannelli, Sarah Demortiere, Marine Perriguey, Maya Elziere, Pierre Durozard, Clemence Boutiere, Audrey Rico, Frederic Hilezian, Jan-Patrick Stellmann, Jean Pelletier, Adil Maarouf, Natacha Stolowy, Bertrand Audoin","doi":"10.1212/NXI.0000000000200379","DOIUrl":"10.1212/NXI.0000000000200379","url":null,"abstract":"<p><strong>Objectives: </strong>To evaluate the sensitivity of fluorescein angiography (FA) in detecting disease activity in Susac syndrome.</p><p><strong>Methods: </strong>We conducted a blinded analysis of all FA, brain MRI, and audiogram examinations performed throughout the follow-up of patients with Susac syndrome.</p><p><strong>Results: </strong>A total of 79 FA examinations, 85 brain MRI scans, and 49 audiograms were analyzed from 9 patients followed for a mean (SD) period of 6 (4) years. Disease activity was detected in 41.5% of FA examinations, 10.5% of MRI scans, and 25% of audiograms (FA vs MRI, <i>p</i> < 0.0001; FA vs audiogram, <i>p</i> = 0.06; audiogram vs MRI, <i>p</i> < 0.05). Within 3 months of clinical relapses, activity was observed in 57%, 24%, and 27% of FA, MRI, and audiogram examinations, respectively (FA vs MRI, <i>p</i> < 0.05; FA vs audiogram, <i>p</i> = 0.09; audiogram vs MRI, <i>p</i> = 1). Quantitative analysis of FA showed a mean (SD) of 2.5 (2.5) leakages (both eyes) during relapses compared with 1.2 (1.4) during remission (<i>p</i> < 0.05).</p><p><strong>Discussion: </strong>FA, particularly arterial leakage, demonstrated the highest sensitivity in detecting disease activity and may be a valuable tool for treatment management in Susac syndrome. Future studies with larger samples should aim to identify the optimal threshold of FA changes associated with an increased risk of relapse.</p>","PeriodicalId":19472,"journal":{"name":"Neurology® Neuroimmunology & Neuroinflammation","volume":"12 2","pages":"e200379"},"PeriodicalIF":7.8,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11805606/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143256299","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Progressive Myelitis in a 63-Year-Old Woman: A Case Report From the National Multiple Sclerosis Society Case Conference Proceedings.","authors":"Kimberly A DiMauro, Morgan E Heber, Jonathan Lee, Jeffrey A Cohen, Eoin P Flanagan, Claire Riley, Myla D Goldman, Scott S Zamvil, Amy C Kunchok","doi":"10.1212/NXI.0000000000200382","DOIUrl":"10.1212/NXI.0000000000200382","url":null,"abstract":"<p><p>We present a case of myelitis in a 63-year-old woman with breast adenocarcinoma treated with pembrolizumab. MRI showed multiple T2-hyperintense lesions throughout the spinal cord, and CSF demonstrated lymphocytic pleocytosis. We discuss the differential diagnosis of myelitis in the setting of cancer and immune checkpoint inhibitors.</p>","PeriodicalId":19472,"journal":{"name":"Neurology® Neuroimmunology & Neuroinflammation","volume":"12 2","pages":"e200382"},"PeriodicalIF":7.8,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11813231/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143391392","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dysregulation of the Kynurenine Pathway in Relapsing Remitting Multiple Sclerosis and Its Correlations With Progressive Neurodegeneration.","authors":"Ananda Staats Pires, Shivani Krishnamurthy, Samridhi Sharma, Sharron Chow, Samuel Klistorner, Gilles J Guillemin, Alexander Klistorner, Yuyi You, Benjamin Heng","doi":"10.1212/NXI.0000000000200372","DOIUrl":"10.1212/NXI.0000000000200372","url":null,"abstract":"<p><strong>Background and objectives: </strong>Despite the absence of acute lesion activity in multiple sclerosis (MS), chronic neurodegeneration continues to progress, and a potential underlying mechanism could be the kynurenine pathway (KP). Prolonged activation of the KP from chronic inflammation is known to exacerbate the progression of neurodegenerative diseases through the production of neurotoxic metabolites. Among the 8 KP metabolites, six of them, namely kynurenine (KYN), 3-hydroxylkynurenine (3HK), anthranilic acid (AA), kynurenic acid (KYNA), and quinolinic acid (QUIN), have been associated with neurodegeneration.</p><p><strong>Methods: </strong>To gain insights into the links between the KP and neurodegeneration in MS, we investigated the KP metabolomics profile of relapsing remitting MS (RRMS) patients and their correlation with parameters of neurodegeneration in brain and retinal. Outpatients with a clinical diagnosis of RRMS (n = 98) or age-matched and sex-matched healthy controls (n = 39) were included. MS participants undertook yearly evaluation of MRI and optical coherence tomography scan to evaluate neuroaxonal loss. Blood samples were collected at the baseline from all participants for the biochemical analysis of KP metabolites.</p><p><strong>Results: </strong>We identified increased plasma levels of AA and 3HAA in the MS group, indicating an anti-inflammatory response alongside active neurodegeneration. By contrast, plasma levels of KYNA and 3HK were lower in the MS group than in healthy controls. Our analysis revealed a higher KYN:tryptophan (TRP) and QUIN:KYNA ratios in the MS cohort, suggesting activation of the pathway toward the production of neurotoxic QUIN. Another important finding was that KP metabolites were correlated with measures of axonal degeneration in patients with MS. Notably, central brain atrophy positively correlated with the TRP levels, but negatively correlated with KYN and level KYN:TRP ratio. Finally, the choroid plexus volume was inversely correlated with KYNA plasma levels.</p><p><strong>Discussion: </strong>These findings highlight changes in the biosynthesis of KP during the progression of RRMS and its correlation with axonal loss. This study underscores the potential of targeting the KP in developing novel treatments for neuroaxonal damage in MS and warrants future research in greater depth.</p>","PeriodicalId":19472,"journal":{"name":"Neurology® Neuroimmunology & Neuroinflammation","volume":"12 2","pages":"e200372"},"PeriodicalIF":7.8,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11744609/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143009112","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impaired Presynaptic Function Contributes Significantly to the Pathology of Glycine Receptor Autoantibodies.","authors":"Anna-Lena Wiessler, Fang Zheng, Christian Werner, Margarita Habib, Erdem Tuzun, Christian Alzheimer, Claudia Sommer, Carmen Villmann","doi":"10.1212/NXI.0000000000200364","DOIUrl":"10.1212/NXI.0000000000200364","url":null,"abstract":"<p><strong>Background and objectives: </strong>Autoantibodies (aAbs) against glycine receptors (GlyRs) are mainly associated with the rare neurologic diseases stiff person syndrome (SPS) and progressive encephalomyelitis with rigidity and myoclonus (PERM). GlyR aAbs are also found in other neurologic diseases such as epilepsy. The aAbs bind to different GlyR α-subunits and, more rarely, also to the GlyR β-subunit. So far, studies on the pathogenic effects of the aAbs have focused on postsynaptic, heteromeric GlyRs, reporting a loss of ion channel function and receptor internalization upon aAb binding. We asked whether the aAbs also affect expression and functionality of presynaptic homomeric GlyRs.</p><p><strong>Methods: </strong>We established interneuron cultures from mouse embryonic spinal cord neurons and used protein biochemistry and super-resolution microscopy to determine aAb binding to presynaptic GlyRs in a uniform neuronal subpopulation. Brainstem slice recordings were used to detect functional alterations.</p><p><strong>Results: </strong>Several days-long exposure of spinal cord cultures with GlyR aAbs did not change expression levels of proteins building a functional glycinergic synapse. A notable exception was the enhanced expression of presynaptic glycine transporter 2 (GlyT2), possibly reflecting an adaptation to altered synaptic properties. Super-resolution microscopy revealed rather similar binding of patient-derived aAbs to postsynaptic vs presynaptic sites with individual binding preferences. Although characterization of interneurons showed absence of GlyRα1 in some interneuron subpopulations, GlyRα2 and patient serum signals exhibited a significantly higher colocalization in samples with presynaptic preference. This finding identifies GlyRα2 as the hitherto unknown predominant presynaptic GlyR subunit in the spinal cord and a target of patient aAbs. Whole-cell recordings from glycinergic neurons in mouse brainstem slices underscored the functional relevance of presynaptic aAb binding demonstrated by a significant reduction in the frequency of spontaneous and miniature inhibitory postsynaptic potentials.</p><p><strong>Discussion: </strong>In summary, our study is the first to implicate presynaptic defects in the pathophysiology of autoimmune diseases such as SPS and PERM, which are associated with GlyR aAbs. Individually tuned binding preferences for presynaptic and postsynaptic targets thus underlie the rather diverse appearance of clinical symptoms and different therapeutic responses in patients suffering from GlyR autoimmunity.</p>","PeriodicalId":19472,"journal":{"name":"Neurology® Neuroimmunology & Neuroinflammation","volume":"12 2","pages":"e200364"},"PeriodicalIF":7.8,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11741293/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143009113","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immunogenetic Studies in Patients With GAD-Positive Stiff-Person Syndrome Reveal Novel Lymphocytic Genes and <i>KLK10</i>-Gene Variants.","authors":"Popianna Tsiortou, Harry Alexopoulos, Konstantinos Kyriakidis, Michalis Kosmidis, Chrysanthi Barba, Sofia Akrivou, Ioannis Michalopoulos, Panagiotis Politis, Marinos C Dalakas","doi":"10.1212/NXI.0000000000200373","DOIUrl":"10.1212/NXI.0000000000200373","url":null,"abstract":"<p><strong>Background and objectives: </strong>The aim of this study was to identify genetic markers and immunologic characteristics of glutamic acid decarboxylase (GAD) antibody-positive patients with stiff-person syndrome (SPS).</p><p><strong>Methods: </strong>We conducted systemic immunogenetic studies in 11 GAD-positive patients: 8 with sporadic SPS and 3 from a three-generation family with very high GAD-ab titers but diverse symptomatology (one with GAD-epilepsy and SPS and 2 only with diabetes), by performing complete immunologic profile and whole-exome sequencing analysis.</p><p><strong>Results: </strong>Two genes expressed in immune and neuronal tissues were identified: the <i>ORAI1</i> that codes for a calcium release-activated channel protein with a role in the activation of T lymphocytes and the <i>LILRA4</i> that encodes an IgG-like cell surface protein expressed in plasmacytoid dendritic cells. An important finding was the identification of 7 genetic polymorphisms in the novel <i>Kallikrein 10</i> (<i>KLK10)</i> gene, shared by all 9 typical patients with SPS, as verified by Sanger sequencing, but not in the 2 GAD-positive family members with diabetes or the GAD-negative controls. To further verify these findings, Sanger sequencing was performed in 10 more patients with SPS and 15 autoimmune controls collectively confirmed that among a total of 39 tested samples, 95% of the 19 patients with SPS were homozygous or heterozygous for all 7 KLK10 variants while 90% of the 20 controls had the wild type or were heterozygous. <i>KLK10</i> is a peptidase expressed in the choroid plexus epithelium and neuroendocrine organs and participates in the initiation of systemic inflammatory responses and immune-modulated disorders through proteolytic cascades.</p><p><strong>Discussion: </strong>KLK10 is a novel and potentially key genetic marker in patients with SPS that can contribute to disease pathogenesis by altering protease activity or the expression of neuron-to-immune cell signaling facilitating GAD autoimmunity. Along with the 2 newly identified immune-related genes, KLK10 is likely an interplay between genetic predisposition and immune dysregulation, necessitating the need to explore their significance as susceptibility disease factors and possibly as novel therapeutic targets.</p>","PeriodicalId":19472,"journal":{"name":"Neurology® Neuroimmunology & Neuroinflammation","volume":"12 2","pages":"e200373"},"PeriodicalIF":7.8,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11820810/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143399320","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Long-Term Clinical and Biological Prognostic Factors of Anti-NMDA Receptor Encephalitis in Children.","authors":"Maxime Mazowiecki, Lorraine Flet-Berliac, Julia Roux, Anne Lépine, Pascale Chretien, Salima Hacein-Bey-Abina, Laetitia Giorgi, Frederic Villega, Emmanuel Cheuret, Marie Benaiteau, Veronique Rogemond, Geraldine Picard, Sarah Baer, Pierre Cleuziou, Elodie Lametery, Isabelle Desguerre, Mélodie Aubart, Mathilde Chevignard, Roger Le Grand, Philippe Horellou, Carole Leroy, Bastien Joubert, Jerome Honnorat, Kumaran Deiva","doi":"10.1212/NXI.0000000000200346","DOIUrl":"10.1212/NXI.0000000000200346","url":null,"abstract":"<p><strong>Background and objectives: </strong>Anti-NMDAR encephalitis (NMDARE) is a severe neurologic condition, and recently, the NMDAR Encephalitis One-Year Functional Status (NEOS) score has emerged as a 1-year prognostic tool. This study aimed to evaluate NEOS score and biomarker (neurofilament light chains [NfL], total-Tau protein, glial fibrillary acidic protein, and serum cytokines) correlation with modified Rankin Scale (mRS), cognitive impairment, and clinical recovery in pediatric NMDARE over 2 years.</p><p><strong>Methods: </strong>In this French multicenter observational study, 104 pediatric patients with NMDARE were followed for a minimum of 2 years. Clinical data and serum/plasma samples were collected. Biomarker levels, measured using electroluminescence mesoscale discovery (MSD) S-PLEX, were compared between patients and controls and assessed for correlations with disease activity, mRS, cognitive/language impairment, and recovery status at 2 years.</p><p><strong>Results: </strong>At a median follow-up of 39.5 months, 68 percent of patients had unfavorable recovery and 54% had significant cognitive impairment. Both outcomes were strongly associated with younger age at diagnosis (OR 6.10 [1.91-27.3] <i>p</i> < 0.01 and 5.69 [1.46-27.7] <i>p</i> = 0.02, respectively). A higher NEOS score was significantly correlated with increased cognitive impairment (OR 2.53 [1.52-4.21], <i>p</i> < 0.001), higher mRS scores (OR 2.12 [1.34-3.57], <i>p</i> < 0.01), and unfavorable recovery at 2 years (OR 2.00 [1.30-3.06], <i>p</i> = 0.015). Elevated NfL levels were significantly associated with unfavorable recovery (OR 3.62 [1.29-10.9] <i>p</i> = 0.012) and severe cognitive impairment (OR 3.77 [1.38-10.9] <i>p</i> = 0.012) at 2 years. The combined area under the curve (AUC) for NfL and NEOS was significantly higher than the AUCs of NEOS and NfL alone <i>(p</i> = 0.01).</p><p><strong>Discussion: </strong>The NEOS score strongly predicts long-term outcomes in NMDARE, with its predictive value extending beyond the first-year mR prediction. NfL levels at disease onset seem to improve accuracy in predicting poor outcomes, providing valuable information for treatment decisions and future clinical trials.</p>","PeriodicalId":19472,"journal":{"name":"Neurology® Neuroimmunology & Neuroinflammation","volume":"12 2","pages":"e200346"},"PeriodicalIF":7.8,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12231184/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142882632","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Assessing the Risk of Relapse After In Vitro Fertilization in Women With Multiple Sclerosis.","authors":"Marie Mainguy, Romain Casey, Sandra Vukusic, Christine Lebrun-Frenay, Eric Berger, Anne Kerbrat, Abdullatif Al Khedr, Bertrand Bourre, Jonathan Ciron, Pierre Clavelou, Jerome De Seze, Gilles Defer, Ines Doghri, Amélie Dos Santos, Karolina Hankiewicz, Pierre M Labauge, Emmanuelle Le Page, Laurent Magy, Elisabeth Maillart, Eric Manchon, Laure Michel, Thibault Moreau, Solène Moulin, Jean Pelletier, Corinne Pottier, Aurélie Ruet, Mariana Sarov, Bruno Stankoff, Eric Thouvenot, Abir Wahab, Helene Zephir, Emmanuelle Leray, David Axel Laplaud","doi":"10.1212/NXI.0000000000200371","DOIUrl":"10.1212/NXI.0000000000200371","url":null,"abstract":"<p><strong>Background and objectives: </strong>Older studies reported an increased risk of relapse after in vitro fertilization (IVF) in women with multiple sclerosis (MS), which has not been confirmed by more recent works. All these studies had several limitations, such as small sample sizes, absence of a control population, or lack of neurologic validation of the relapses. The aim of this study was to determine the risk of relapse after IVF in women with MS.</p><p><strong>Methods: </strong>This retrospective cohort study included all women with MS who underwent IVF between 2009 and 2019 and a control group of women with MS who did not undergo IVF matched on age, MS duration, number of relapses, and MS-specific treatments in the previous year. Data on MS (disease duration, treatments, and relapses) were from the French MS Registry (OFSEP), whereas data on IVF (number of procedures, stimulation protocol type, and outcomes) were from the French national health insurance database. For this, the 2 databases were linked by indirect matching.</p><p><strong>Results: </strong>In total, 115 women with MS underwent 199 IVF procedures (mean age at first IVF: 33.9 ± 4.0 years; 45.2% had ≥2 IVF procedures), and 175 IVFs (88.0%) could be matched to specific patients. The risk of relapse in the 3 months after index date was the same in both IVF group and control group (0.06 relapse per patient-year), as confirmed also by the before-after analysis in the IVF group (0.06 vs 0.08).</p><p><strong>Discussion: </strong>This study, using a 10-year clinical and administrative dataset, did not find any increased risk of relapse after IVF. The maintenance of disease-modifying therapies until IVF was a determining factor in reducing the risk of relapse.</p>","PeriodicalId":19472,"journal":{"name":"Neurology® Neuroimmunology & Neuroinflammation","volume":"12 2","pages":"e200371"},"PeriodicalIF":7.8,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11820809/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143399317","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}