Neurology® Neuroimmunology & Neuroinflammation最新文献

{"title":"Impact of Immune Checkpoint Inhibitors on the Course of Multiple Sclerosis.","authors":"","doi":"10.1212/NXI.0000000000200245","DOIUrl":"10.1212/NXI.0000000000200245","url":null,"abstract":"","PeriodicalId":19472,"journal":{"name":"Neurology® Neuroimmunology & Neuroinflammation","volume":"11 3","pages":"e200245"},"PeriodicalIF":8.8,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11073866/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140132238","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":"Complement Activation Is Associated With Disease Severity in Multiple Sclerosis.","authors":"","doi":"10.1212/NXI.0000000000200246","DOIUrl":"10.1212/NXI.0000000000200246","url":null,"abstract":"","PeriodicalId":19472,"journal":{"name":"Neurology® Neuroimmunology & Neuroinflammation","volume":"11 3","pages":"e200246"},"PeriodicalIF":8.8,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10959166/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140175831","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":"Safety and Dose-Response of Vidofludimus Calcium in Relapsing Multiple Sclerosis: Extended Results of a Placebo-Controlled Phase 2 Trial.","authors":"Robert J Fox, Heinz Wiendl, Christian Wolf, Nicola De Stefano, Johann Sellner, Viktoriia Gryb, Konrad Rejdak, Plamen S Bozhinov, Daniel Vitt, Hella Kohlhof, Jason Slizgi, Matej Ondrus, Valentina Sciacca, Andreas R Muehler","doi":"10.1212/NXI.0000000000200208","DOIUrl":"10.1212/NXI.0000000000200208","url":null,"abstract":"<p><strong>Background and objectives: </strong>Vidofludimus calcium suppressed MRI disease activity compared with placebo in patients with relapsing-remitting multiple sclerosis (RRMS) in the first cohort of the phase 2 EMPhASIS study. Because 30 mg and 45 mg showed comparable activity on multiple end points, the study enrolled an additional low-dose cohort to further investigate a dose-response relationship.</p><p><strong>Methods: </strong>In a randomized, placebo-controlled, phase 2 trial, patients with RRMS, aged 18-55 years, and with ≥2 relapses in the last 2 years or ≥1 relapse in the last year, and ≥1 gadolinium-enhancing brain lesion in the last 6 months. Patients were randomly assigned (1:1:1) vidofludimus calcium (30 or 45 mg) or placebo in cohort 1 and vidofludimus calcium (10 mg) or placebo (4:1) in cohort 2 for 24 weeks. The primary end point was the cumulative number of combined unique active (CUA) lesions at week 24. Secondary end points were clinical outcomes and safety.</p><p><strong>Results: </strong>Across cohorts 1 and 2, 268 patients were randomized to placebo (n = 81), 10 mg (n = 47) vidofludimus calcium, 30 mg (n = 71) vidofludimus calcium, or 45 mg (n = 69) vidofludimus calcium. The mean cumulative CUA lesions over 24 weeks was 5.8 (95% CI 4.1-8.2) for placebo, 5.9 (95% CI 3.9-9.0) for 10 mg treatment group, 1.4 (95% CI 0.9-2.1) for 30 mg treatment group, and 1.7 (95% CI 1.1-2.5) for 45 mg treatment group. Serum neurofilament light chain decreased in a dose-dependent manner. The number of patients with confirmed disability worsening after 24 weeks was 3 (3.7%) patients receiving placebo and 3 (1.6%) patients receiving any dose of vidofludimus calcium. Treatment-emergent adverse events occurred in 35 (43%) placebo patients compared with 11 (23%) and 71 (37%) patients in the 10 mg or any dose of vidofludimus calcium groups, respectively. The incidence of liver enzyme elevations and infections were similar between placebo and any dose of vidofludimus calcium. No new safety signals were observed.</p><p><strong>Discussion: </strong>Compared with placebo, vidofludimus calcium suppressed the development of new brain lesions with daily doses of 30 mg and 45 mg, but not 10 mg, establishing the lowest efficacious dose is 30 mg.</p><p><strong>Classification of evidence: </strong>This study provides Class II evidence that among adults with active RRMS and ≥1 Gd+ brain lesion in the past 6 months, the cumulative number of active lesions decreased with vidofludimus calcium.</p><p><strong>Trial registration information: </strong>ClinicalTrials.gov (NCT03846219) and EudraCT (2018-001896-19).</p>","PeriodicalId":19472,"journal":{"name":"Neurology® Neuroimmunology & Neuroinflammation","volume":"11 3","pages":"e200208"},"PeriodicalIF":8.8,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11087024/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140853771","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":"Effect of Prior Treatment With Fingolimod on Early and Late Response to Rituximab/Ocrelizumab in Patients With Multiple Sclerosis.","authors":"Lisa Graille-Avy, Clemence Boutiere, Camille Rigollet, Marine Perriguey, Audrey Rico, Sarah Demortiere, Pierre Durozard, Frederic Hilezian, Frederic Vely, Pierre Bertault-Peres, Jean Pelletier, Adil Maarouf, Bertrand Audoin","doi":"10.1212/NXI.0000000000200231","DOIUrl":"10.1212/NXI.0000000000200231","url":null,"abstract":"<p><strong>Background and objectives: </strong>Real-life studies noted that the risk of disease activity in multiple sclerosis (MS) after switching to rituximab (RTX) or ocrelizumab (OCR) may be unequal depending on prior disease-modifying therapy (DMT), with a higher risk associated with fingolimod (FING).</p><p><strong>Methods: </strong>We performed a retrospective analysis of a structured prospective data collection including all consecutive patients with relapsing MS who were prescribed RTX/OCR in the MS center of Marseille. Cox proportional hazards models were applied to clinical and MRI outcomes.</p><p><strong>Results: </strong>We included 321 patients with a median (interquartile range [IQR]) follow-up of 3.5 years (1.5-5) after RTX/OCR initiation. At the first RTX/OCR infusion, the mean (SD) age of patients was 37 (10) years, and the median (IQR) disease duration was 8 years (3-15): 68 patients did not receive treatment before RTX/OCR and 108 switched from FING, 47 from low efficacy therapy, and 98 from natalizumab. For statistical analysis, the group \"FING\" was divided into \"short-FING\" and \"long-FING\" groups according to the median value of the group's washout period (27 days). On Cox proportional hazards analysis, for only the \"long-FING\" group, the risk of relapse within the first 6 months of RTX/OCR was increased as compared with patients without previous DMT (hazard ratio [HR]: 8.78; 95% CI 1.72-44.86; <i>p</i> < 0.01). Previous DMT and washout period duration of FING had no effect on B-cell levels at 6 months. Beyond the first 6 months of RTX/OCR, age <40 years was associated with increased risk of relapse (HR: 3.93; 95% CI 1.30-11.89; <i>p</i> = 0.01), male sex with increased risk of new T2 lesions (HR: 2.26; 95% CI 1.08-4.74; <i>p</i> = 0.03), and EDSS ≥2 with increased risk of disability accumulation (HR: 3.01; 95% CI 1.34-6.74; <i>p</i> < 0.01). Previous DMT had no effect on the effectiveness of RTX/OCR beyond 6 months after initiation.</p><p><strong>Discussion: </strong>For patients switching from FING to RTX/OCR, the risk of disease reactivation within the first 6 months of treatment was increased as compared with patients with other DMT or no previous DMT only when the washout period exceeded 26 days. Neither FING nor other previous DMT reduced the effectiveness of RTX/OCR beyond the first 6 months of treatment.</p>","PeriodicalId":19472,"journal":{"name":"Neurology® Neuroimmunology & Neuroinflammation","volume":"11 3","pages":"e200231"},"PeriodicalIF":8.8,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11090020/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140855670","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":"Comparative Study of Paraneoplastic and Nonparaneoplastic Autoimmune Encephalitis With GABA_BR Antibodies.","authors":"Florian Lamblin, Jeroen Kerstens, Sergio Muñiz-Castrillo, Alberto Vogrig, David Goncalves, Veronique Rogemond, Geraldine Picard, Marine Villard, Anne-Laurie Pinto, Marleen H Van Coevorden-Hameete, Marienke A De Bruijn, Juna M De Vries, Marco Schreurs, Louise Tyvaert, Lucie Hopes, Jerome Aupy, Cecile Marchal, Dimitri Psimaras, Laurent Kremer, Veronique Bourg, Jean-Christophe G Antoine, Adrien Wang, Philippe Kahane, Sophie Demeret, Guido Ahle, Vicente Peris Sempere, Noemie Timestit, Mikail Nourredine, Aurelien Maureille, Marie Benaiteau, Bastien Joubert, Emmanuel Mignot, Maarten J Titulaer, Jerome Honnorat","doi":"10.1212/NXI.0000000000200229","DOIUrl":"10.1212/NXI.0000000000200229","url":null,"abstract":"<p><strong>Background and objectives: </strong>While patients with paraneoplastic autoimmune encephalitis (AE) with gamma-aminobutyric-acid B receptor antibodies (GABA_BR-AE) have poor functional outcomes and high mortality, the prognosis of nonparaneoplastic cases has not been well studied.</p><p><strong>Methods: </strong>Patients with GABA_BR-AE from the French and the Dutch Paraneoplastic Neurologic Syndromes Reference Centers databases were retrospectively included and their data collected; the neurologic outcomes of paraneoplastic and nonparaneoplastic cases were compared. Immunoglobulin G (IgG) isotyping and human leukocyte antigen (HLA) genotyping were performed in patients with available samples.</p><p><strong>Results: </strong>A total of 111 patients (44/111 [40%] women) were enrolled, including 84 of 111 (76%) paraneoplastic and 18 of 111 (16%) nonparaneoplastic cases (cancer status was undetermined for 9 patients). Patients presented with seizures (88/111 [79%]), cognitive impairment (54/111 [49%]), and/or behavioral disorders (34/111 [31%]), and 54 of 111 (50%) were admitted in intensive care unit (ICU). Nonparaneoplastic patients were significantly younger (median age 54 years [range 19-88] vs 67 years [range 50-85] for paraneoplastic cases, <i>p</i> < 0.001) and showed a different demographic distribution. Nonparaneoplastic patients more often had CSF pleocytosis (17/17 [100%] vs 58/78 [74%], <i>p</i> = 0.02), were almost never associated with KTCD16-abs (1/16 [6%] vs 61/70 [87%], <i>p</i> < 0.001), and were more frequently treated with second-line immunotherapy (11/18 [61%] vs 18/82 [22%], <i>p</i> = 0.003). However, no difference of IgG subclass or HLA association was observed, although sample size was small (10 and 26 patients, respectively). After treatment, neurologic outcome was favorable (mRS ≤2) for 13 of 16 (81%) nonparaneoplastic and 37 of 84 (48%) paraneoplastic cases (<i>p</i> = 0.03), while 3 of 18 (17%) and 42 of 83 (51%) patients had died at last follow-up (<i>p</i> = 0.008), respectively. Neurologic outcome no longer differed after adjustment for confounding factors but seemed to be negatively associated with increased age and ICU admission. A better survival was associated with nonparaneoplastic cases, a younger age, and the use of immunosuppressive drugs.</p><p><strong>Discussion: </strong>Nonparaneoplastic GABA_BR-AE involved younger patients without associated KCTD16-abs and carried better neurologic and vital prognoses than paraneoplastic GABA_BR-AE, which might be due to a more intensive treatment strategy. A better understanding of immunologic mechanisms underlying both forms is needed.</p>","PeriodicalId":19472,"journal":{"name":"Neurology® Neuroimmunology & Neuroinflammation","volume":"11 3","pages":"e200229"},"PeriodicalIF":8.8,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11087025/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140857337","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":"Case-Control Study of Individuals With Small Fiber Neuropathy After COVID-19.","authors":"Lindsay McAlpine, Adeel S Zubair, Phillip Joseph, Serena Spudich","doi":"10.1212/NXI.0000000000200244","DOIUrl":"10.1212/NXI.0000000000200244","url":null,"abstract":"<p><strong>Objectives: </strong>To report a case-control study of new-onset small fiber neuropathy (SFN) after COVID-19 with invasive cardiopulmonary exercise testing (iCPET). SFN is a critical objective finding in long COVID and amenable to treatment.</p><p><strong>Methods: </strong>A retrospective chart review was conducted on patients seen in the NeuroCOVID Clinic at Yale who developed new-onset SFN after a documented COVID-19 illness. We collected demographics, symptoms, skin biopsy, iCPET testing, treatments, and clinical response to treatment or no intervention.</p><p><strong>Results: </strong>Sixteen patients were diagnosed with SFN on skin biopsy (median age 47, 75% female, 75% White). 92% of patients reported postexertional malaise characteristic of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), and 7 patients underwent iCPET, which demonstrated neurovascular dysregulation and dysautonomia consistent with ME/CFS. Nine patients underwent treatment with IVIG, and 7 were not treated with IVIG. The IVIG group experienced significant clinical response in their neuropathic symptoms (9/9) compared with those who did not receive IVIG (3/7; <i>p</i> = 0.02).</p><p><strong>Discussion: </strong>Here, we present preliminary evidence that after COVID-19, SFN is responsive to treatment with IVIG and linked with neurovascular dysregulation and dysautonomia on iCPET. A larger clinical trial is indicated to further demonstrate the clinical utility of IVIG in treating postinfectious SFN.</p><p><strong>Classification of evidence: </strong>This study provides Class III evidence. It is a retrospective cohort study.</p>","PeriodicalId":19472,"journal":{"name":"Neurology® Neuroimmunology & Neuroinflammation","volume":"11 3","pages":"e200244"},"PeriodicalIF":8.8,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11087026/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140862979","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":"Genome-Wide Association Study Identifies IFIH1 and HLA-DQB1*05:02 Loci Associated With Anti-NMDAR Encephalitis.","authors":"Xu Liu, Xiaodong Zheng, Yaqing Shu, Xiao Qu, Qun Wang, Xiao Liu, Fa-Yun Hu, Jie Liu, Yajun Lian, Bao-Ming He, Caihua Li, Dong Zhou, Wei Qiu, Liangdan Sun, Zhen Hong","doi":"10.1212/NXI.0000000000200221","DOIUrl":"https://doi.org/10.1212/NXI.0000000000200221","url":null,"abstract":"<p><strong>Background and objectives: </strong>Anti-N-methyl-d-aspartate receptor (NMDAR) encephalitis is a rare autoimmune neurologic disorder, the genetic etiology of which remains poorly understood. Our study aims to investigate the genetic basis of this disease in the Chinese Han population.</p><p><strong>Methods: </strong>We performed a genome-wide association study and fine-mapping study within the major histocompatibility complex (MHC) region of 413 Chinese patients with anti-NMDAR encephalitis recruited from 6 large tertiary hospitals and 7,127 healthy controls.</p><p><strong>Results: </strong>Our genome-wide association analysis identified a strong association at the IFIH1 locus on chromosome 2q24.2 (rs3747517, <i>p</i> = 1.06 × 10^-8, OR = 1.55, 95% CI, 1.34-1.80), outside of the human leukocyte antigen (HLA) region. Furthermore, through a fine-mapping study of the MHC region, we discovered associations for 3 specific HLA class I and II alleles. Notably, HLA-DQB1*05:02 (<i>p</i> = 1.43 × 10^-12; OR, 2.10; 95% CI 1.70-2.59) demonstrates the strongest association among classical HLA alleles, closely followed by HLA-A*11:01 (<i>p</i> = 4.36 × 10^-7; OR, 1.52; 95% CI 1.29-1.79) and HLA-A*02:07 (<i>p</i> = 1.28 × 10^-8; OR, 1.87; 95% CI 1.50-2.31). In addition, we uncovered 2 main HLA amino acid variation associated with anti-NMDAR encephalitis including HLA-DQβ1-126H (<i>p</i> = 1.43 × 10^-12; OR, 2.10; 95% CI 1.70-2.59), exhibiting a predisposing effect, and HLA-B-97R (<i>p</i> = 3.40 × 10^-8; OR, 0.63; 95% CI 0.53-0.74), conferring a protective effect. Computational docking analysis suggested a close relationship between the NR1 subunit of NMDAR and DQB1*05:02.</p><p><strong>Discussion: </strong>Our findings indicate that genetic variation in IFIH1, involved in the type I interferon signaling pathway and innate immunity, along with variations in the HLA class I and class II genes, has substantial implications for the susceptibility to anti-NMDAR encephalitis in the Chinese Han population.</p>","PeriodicalId":19472,"journal":{"name":"Neurology® Neuroimmunology & Neuroinflammation","volume":"11 3","pages":"e200221"},"PeriodicalIF":8.8,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11010247/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140863055","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":"Post-COVID Small Fiber Neuropathy, Implications of Innate Immunity, and Challenges on IVIG Therapy.","authors":"Marinos C Dalakas","doi":"10.1212/NXI.0000000000200248","DOIUrl":"10.1212/NXI.0000000000200248","url":null,"abstract":"","PeriodicalId":19472,"journal":{"name":"Neurology® Neuroimmunology & Neuroinflammation","volume":"11 3","pages":"e200248"},"PeriodicalIF":8.8,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11087046/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140874756","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":"CD138 as a Specific CSF Biomarker of Multiple Sclerosis.","authors":"Geoffrey Hinsinger, Lucile Du Trieu De Terdonck, Serge Urbach, Nicolas Salvetat, Manon Rival, Manon Galoppin, Chantal Ripoll, Renaud Cezar, Sabine Laurent-Chabalier, Christophe Demattei, Hanane Agherbi, Giovanni Castelnovo, Sylvain Lehmann, Valérie Rigau, Philippe Marin, Eric Thouvenot","doi":"10.1212/NXI.0000000000200230","DOIUrl":"https://doi.org/10.1212/NXI.0000000000200230","url":null,"abstract":"<p><strong>Background and objectives: </strong>The aim of this study was to identify novel biomarkers for multiple sclerosis (MS) diagnosis and prognosis, addressing the critical need for specific and prognostically valuable markers in the field.</p><p><strong>Methods: </strong>We conducted an extensive proteomic investigation, combining analysis of (1) CSF proteome from symptomatic controls, fast and slow converters after clinically isolated syndromes, and patients with relapsing-remitting MS (n = 10 per group) using label-free quantitative proteomics and (2) oligodendrocyte secretome changes under proinflammatory or proapoptotic conditions using stable isotope labeling by amino acids in cell culture. Proteins exhibiting differential abundance in both proteomic analyses were combined with other putative MS biomarkers, yielding a comprehensive list of 87 proteins that underwent quantification through parallel reaction monitoring (PRM) in a novel cohort, comprising symptomatic controls, inflammatory neurologic disease controls, and patients with MS at various disease stages (n = 10 per group). The 11 proteins that passed this qualification step were subjected to a new PRM assay within an expanded cohort comprising 158 patients with either MS at different disease stages or other inflammatory or noninflammatory neurologic disease controls.</p><p><strong>Results: </strong>This study unveiled a promising biomarker signature for MS, including previously established candidates, such as chitinase 3-like protein 1, chitinase 3-like protein 2, chitotriosidase, immunoglobulin kappa chain region C, neutrophil gelatinase-associated lipocalin, and CD27. In addition, we identified novel markers, namely cat eye syndrome critical region protein 1 (adenosine deaminase 2, a therapeutic target in multiple sclerosis) and syndecan-1, a proteoglycan, also known as plasma cell surface marker CD138 and acting as chitinase 3-like protein 1 receptor implicated in inflammation and cancer signaling. CD138 exhibited good diagnostic accuracy in distinguishing MS from inflammatory neurologic disorders (area under the curve [AUC] = 0.85, CI 0.75-0.95). CD138 immunostaining was also observed in the brains of patients with MS and cultured oligodendrocyte precursor cells but was absent in astrocytes.</p><p><strong>Discussion: </strong>These findings identify CD138 as a specific CSF biomarker for MS and suggest the selective activation of the chitinase 3-like protein 1/CD138 pathway within the oligodendrocyte lineage in MS. They offer promising prospects for improving MS diagnosis and prognosis by providing much-needed specificity and clinical utility.</p><p><strong>Classification of evidence: </strong>This study provides Class II evidence that CD138 distinguishes multiple sclerosis from other inflammatory neurologic disorders with an AUC of 0.85 (95% CI 0.75-0.95).</p>","PeriodicalId":19472,"journal":{"name":"Neurology® Neuroimmunology & Neuroinflammation","volume":"11 3","pages":"e200230"},"PeriodicalIF":8.8,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11057439/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140864730","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":"A 42-Year-Old Woman With Rapidly Expanding White Matter Lesions: From the National Multiple Sclerosis Society Case Conference Proceedings.","authors":"Tolulope O Amiola, Unsong Oh, Hope Richard, Scott D Newsome, Jennifer Graves, Scott S Zamvil, Myla D Goldman","doi":"10.1212/NXI.0000000000200201","DOIUrl":"10.1212/NXI.0000000000200201","url":null,"abstract":"<p><p>A 42-year-old woman and active cocaine user complained of subacutely worsening blurred vision and imbalance. Examination of the brain MRI showed rapidly expanding white matter lesions. Brain biopsy was consistent with inflammatory demyelination. Given an unusual presentation and a history of cocaine use, a broad differential diagnosis was considered including neurologic toxidromes.</p>","PeriodicalId":19472,"journal":{"name":"Neurology® Neuroimmunology & Neuroinflammation","volume":"11 3","pages":"e200201"},"PeriodicalIF":8.8,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11073887/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139575974","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}