Neurology® Neuroimmunology & Neuroinflammation最新文献

{"title":"Amaurosis Fugax Dolorosa: A Prodromal Syndrome in Optic Neuritis Associated With Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease.","authors":"Andreu Vilaseca, Stephanie B Syc-Mazurek, Nisa Vorasoot, Deena A Tajfirouz, Eric Eggenberger, Kevin D Chodnicki, Sean J Pittock, John J Chen, Eoin P Flanagan","doi":"10.1212/NXI.0000000000200471","DOIUrl":"10.1212/NXI.0000000000200471","url":null,"abstract":"<p><strong>Objectives: </strong>Amaurosis fugax (AF) is typically vascular but can rarely be associated with optic neuritis (ON). We describe AF preceding myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) ON.</p><p><strong>Methods: </strong>We retrospectively reviewed our MOGAD cohort (July 2024-April 2024). Inclusion criteria were (1) AF-defined as transient visual loss <24 hours without retinal ischemic lesions-before first ON and (2) fulfilled international MOGAD 2023 diagnostic criteria. Demographics, symptoms/signs, MRI, and optical coherence tomography (OCT) data were collected. Descriptive statistics summarized the findings.</p><p><strong>Results: </strong>In total, 8 of 350 (2.3%) MOGAD patients with ON experienced AF. Most patients (7/8, 87.5%) were women, and all reported periocular pain. Transient visual episodes were typically brief (median, 15 minutes; range, 1-300 minutes) and usually less than 1 hour (6/8, 75.0%). Amaurosis fugax affected the right (n = 4), left (n = 3), or both (n = 1) eyes. Within 1 week, 7 developed ON. MRI showed optic nerve enhancement in involved eye in 8 of 8 (100%). OCT completed in 1 patient at the time of AF showed increased peripapillary retinal nerve fiber layer thickness. No alternative diagnoses emerged during follow-up.</p><p><strong>Discussion: </strong>Painful AF is a previously unrecognized and specific prodrome of MOGAD-associated ON; identifying this rare presentation may enable earlier diagnosis and treatment.</p>","PeriodicalId":19472,"journal":{"name":"Neurology® Neuroimmunology & Neuroinflammation","volume":"12 6","pages":"e200471"},"PeriodicalIF":7.5,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12456432/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145125271","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":"Temporal Association Between Dengue Outbreaks and Neurologic Autoimmune Diseases in French Guiana.","authors":"Nathalie Deschamps, Mathieu Nacher, Hugo Chaumont, Alexis Montcuquet, Clementine Montagnac, Tiphanie Succo, Loic Epelboin, Sophie Devos, Bertrand De Toffol","doi":"10.1212/NXI.0000000000200501","DOIUrl":"https://doi.org/10.1212/NXI.0000000000200501","url":null,"abstract":"<p><strong>Background and objectives: </strong>Recent decades have witnessed the emergence of arbovirus infections, such as dengue, chikungunya, and Zika viruses, which are responsible for neurologic complications such as Guillain-Barré syndrome (GBS). To date, it has mainly been demonstrated that these neurologic complications occur concomitantly with infectious processes. We hypothesized that arbovirus infections may also influence the incidence of autoimmune diseases of the central or peripheral nervous system.</p><p><strong>Methods: </strong>This was a retrospective, observational, single-center study conducted between January 2002 and January 2024 at the Cayenne Hospital in French Guiana including patients with autoimmune encephalitis, neuromyelitis optica spectrum disorders (NMOSDs), GBS, chronic inflammatory demyelinating polyneuropathy, and myasthenia gravis (MG). This series was compared with the incidence of arbovirus infections recorded by the French Public Health Agency during the same period.</p><p><strong>Results: </strong>We observed a significant correlation between dengue infection and the incidence of NMOSD (Spearman rho = 0.88 [<i>p</i> = 0.03]) and MG (Spearman rho = 0.82 [<i>p</i> = 0.048]). GBS was significantly associated with chikungunya (Spearman rho = 0.97 [<i>p</i> = 0.01]), but not with other arbovirus infections. In addition, the mean estimated incidence of NMOSD was high at 5.08 (95% CI 3.03-7.13) per million person-year, approaching the world's highest incidence observed in the French West Indies.</p><p><strong>Discussion: </strong>This study reports the epidemiology of neurologic autoimmune diseases in French Guiana. We found a high incidence of NMOSD, like that reported in the French West Indies. Multicenter studies involving countries in the tropical zone are needed to better elucidate the relationship between dengue outbreak and NMOSD and MG.</p>","PeriodicalId":19472,"journal":{"name":"Neurology® Neuroimmunology & Neuroinflammation","volume":"12 6","pages":"e200501"},"PeriodicalIF":7.5,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145275416","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Proinflammatory Effect of Mesenchymal Stem Cells From Patients With Multiple Sclerosis: Potential Modulation Targets.","authors":"Radu Tanasescu, Nanci Frakich, Kiranmai Gumireddy, Sonali Majumdar, Sarah Thevathas, Rhodri Jones, Bruno Gran, David Onion, Pryiankara Jayamanna Wickramasinghe, Cherry Chang, Andrew V Kossenkov, Ian Spendlove, Sergio L Colombo, Louise C Showe, Cris S Constantinescu","doi":"10.1212/NXI.0000000000200444","DOIUrl":"10.1212/NXI.0000000000200444","url":null,"abstract":"<p><strong>Background and objectives: </strong>Mesenchymal stem cells (MSCs) represent a potential cellular therapy for multiple sclerosis (MS). It has been suggested that MSCs from patients with MS have lower immunomodulatory properties than those from healthy controls (HCs). The aims of this study were to compare the immunomodulatory abilities of MSCs from patients with MS and HCs against autologous immune cells and to identify potential targets affecting this ability.</p><p><strong>Methods: </strong>MSCs were obtained by bone marrow aspiration from 5 people with MS and 7 HCs. Autologous peripheral blood mononuclear cells (PBMCs) were stimulated in monoculture or co-culture with MSCs and tested for T-cell expression of IL-17, IFN-γ, and granulocyte-macrophage colony-stimulating factor (GM-CSF) by flow cytometry. Supernatants of monoculture unstimulated MSCs were tested for a panel of cytokines and chemokines using multiplex array or individual ELISA. Gene expression profiling in MSCs was studied using Lexogen QuantSeq RNA-seq platform and subsequent Ingenuity Pathway Analysis.</p><p><strong>Results: </strong>The MSCs from HCs reduced the proportion of autologous T cells expressing IL-17 (Th17, <i>p</i> = 0.046), IFN-γ (Th1, <i>p</i> = 0.03), and GM-CSF (<i>p</i> = 0.012), whereas MSCs from patients with MS had an opposite effect, increasing both autologous Th17 cells (<i>p</i> = 0.01) and GM-CSF-expressing T cells (<i>p</i> = 0.03), with no changes in Th1 cell abundance. Unstimulated MSCs from patients with MS produced less IL-10 (<i>p</i> = 0.03) and more osteopontin (OPN) (<i>p</i> = 0.002) than those from HCs. Gene expression profiling suggested an increase of ADAM28 in the MS MSCs. This was further confirmed at mRNA (by quantitative polymerase chain reaction [qPCR]) and protein (by flow cytometry) levels. Co-cultures of MS MSCs and autologous PBMCs in the presence of natalizumab, a monoclonal antibody that binds α4β1 and blocks its interaction with both ADAM28 and OPN, resulted in a reduction of Th17 cells. In addition, adding IL-10 to the co-cultures abrogated the increase in Th17 cells, potentially interfering with MS MSC inflammatory effect.</p><p><strong>Discussion: </strong>Our results suggest that blocking ADAM-28 and OPN interaction with cognate receptors or increasing IL-10 reduces the proinflammatory potential of MSCs from people with MS. Similar approaches could be used in clinical MSC treatments.</p>","PeriodicalId":19472,"journal":{"name":"Neurology® Neuroimmunology & Neuroinflammation","volume":"12 6","pages":"e200444"},"PeriodicalIF":7.5,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12403300/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144963439","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":"Angiogenesis and Hypoxia Biomarkers Are Dysregulated in Progressive Multiple Sclerosis.","authors":"Heather Y F Yong, Rajiv W Jain, Maria Goiko, Nicholas J Batty, Serena Phillips, Mankarman Ghuman, Marcus Werner Koch, Carlos Camara-Lemarroy","doi":"10.1212/NXI.0000000000200477","DOIUrl":"10.1212/NXI.0000000000200477","url":null,"abstract":"<p><strong>Background and objectives: </strong>Multiple sclerosis (MS) is a neuroinflammatory and neurodegenerative CNS disorder characterized by a state of \"virtual hypoxia.\" Angiogenesis, one of the main homeostatic responses to hypoxia, has been implicated in the pathophysiology of MS. The study objective was to determine whether angiogenic and hypoxia-related molecules are dysregulated in the serum and CNS of patients with progressive multiple sclerosis (PMS).</p><p><strong>Methods: </strong>Baseline serum samples were obtained from a phase II trial of Ibudilast in PMS (n = 203 analyzed) and matched to healthy controls (n = 53). Participants on previous therapeutics (interferons or glatiramer acetate) were excluded from analysis (n = 131). Angiogenic factors were measured using a commercially available bead-based multiplex assay, and hypoxia biomarkers were measured using a custom bead-based multiplex assay. To interrogate the expression of selected hypoxia and angiogenic markers in the CNS, we analyzed publicly available transcriptomic databases and in-house generated data from normal appearing white matter of 2 SPMS donors and 2 nonneurologic disease controls.</p><p><strong>Results: </strong>Circulating markers of hypoxia (such as hypoxia inducible factor-1-a, heme oxygenase-1, and heat shock protein-90) were increased in serum. Conversely, markers of angiogenesis (such as vascular endothelial growth factor-A [VEGF-A], heparin-binding epidermal growth factor, and hepatocyte growth factor) were reduced suggesting a blunting of the angiogenic response. Several of these changes were confirmed in the PMS CNS transcriptome. Lower levels of VEGF-A were associated with disability worsening on the timed-25 foot-walk test at 24 (<i>p</i> = 0.02) and 48 (<i>p</i> = 0.02) weeks and predicted disability worsening (hazard ratio 0.31, 95% CI 0.14-0.69, <i>p</i> = 0.034). Conversely, higher leptin levels trended to predict cognitive worsening on the symbol digit modalities test.</p><p><strong>Discussion: </strong>Hypoxia-angiogenesis signals are dysregulated in PMS. Increased hypoxia and an insufficient angiogenic adaptive response may play a role in PMS pathophysiology and be a relevant pathway, both in understanding disease mechanisms and as a possible therapeutic target.</p>","PeriodicalId":19472,"journal":{"name":"Neurology® Neuroimmunology & Neuroinflammation","volume":"12 6","pages":"e200477"},"PeriodicalIF":7.5,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12448328/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145086845","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":"IV Immunoglobulin Is Associated With Epigenetic, Ribosomal, and Immune Changes in Pediatric Acute-Onset Neuropsychiatric Syndrome.","authors":"Velda X Han, Hiroya Nishida, Brooke A Keating, Brian S Gloss, Xianzhong Lau, Ruwani Dissanayake, Jessica Hayes, Shekeeb S Mohammad, Shrujna Patel, Russell C Dale","doi":"10.1212/NXI.0000000000200467","DOIUrl":"10.1212/NXI.0000000000200467","url":null,"abstract":"<p><strong>Objectives: </strong>Pediatric acute-onset neuropsychiatric syndrome (PANS) is characterized by infection-provoked abrupt-onset obsessive compulsive disorder (OCD) and neurodevelopmental regression. Owing to the neuroimmune hypothesis, we investigated the effects of IV immunoglobulin (IVIg) on cell-specific gene expression.</p><p><strong>Methods: </strong>Single-cell RNA sequencing of peripheral immune cells was performed in 5 children with PANS (median age 8 (5.5-16) years), before and after administering open-label IVIg, compared with 4 controls (median age 13.5 [IQR 12-15] years).</p><p><strong>Results: </strong>The index PANS event (age 1.8-13 years) involved abrupt eating restriction (n = 5), developmental regression (n = 4), and OCD (n = 3). A total of 144,470 cells were sequenced and clustered into 11 cell types. Children with PANS before IVIg compared with controls showed downregulated immune pathways (defense response, innate immunity, secretory granules) in most cell types, with natural killer (NK) cells showing upregulated immune pathways (response to corticosteroid), supporting baseline \"immune dysregulation.\" Ribosomal pathways were upregulated in neutrophils and CD8 T cells but downregulated in NK cells. In children with PANS after IVIg, the baseline immune and ribosomal pathway abnormalities were reversed and histone modification pathways (histone methyltransferase, chromatin) were downregulated in neutrophils and NK cells.</p><p><strong>Discussion: </strong>We propose that PANS is an epigenetic immune brain disorder with cellular epigenetic, ribosomal, and immune dysregulation. Epigenetic and immune-modulating therapies, such as IVIg, may have disease-modifying effects.</p>","PeriodicalId":19472,"journal":{"name":"Neurology® Neuroimmunology & Neuroinflammation","volume":"12 6","pages":"e200467"},"PeriodicalIF":7.5,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12440302/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145069938","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 Efficacy and Safety of Satralizumab in Patients With Neuromyelitis Optica Spectrum Disorder From the SAkuraMoon Open-Label Extension Study.","authors":"Jeffrey L Bennett, Kazuo Fujihara, Albert Saiz, Anthony L Traboulsee, Benjamin M Greenberg, Brian G Weinshenker, Francesco Patti, Ingo Kleiter, Jacqueline Palace, Jerome De Seze, Rachael Evans, Kathleen Blondeau, Gaëlle Klingelschmitt, Ivana Vodopivec, Masouda Rahim, Takashi Yamamura","doi":"10.1212/NXI.0000000000200494","DOIUrl":"10.1212/NXI.0000000000200494","url":null,"abstract":"","PeriodicalId":19472,"journal":{"name":"Neurology® Neuroimmunology & Neuroinflammation","volume":"12 6","pages":"e200494"},"PeriodicalIF":7.5,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12507440/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145239318","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":"Correlation of C-Reactive Protein With Severe Fatigue in Patients With Myasthenia Gravis.","authors":"Annabel M Ruiter, Krista E van Meijgaarden, Simone A Joosten, Pietro Spitali, Maartje G Huijbers, Erik W van Zwet, Umesh A Badrising, Martijn Tannemaat, Jan J Verschuuren","doi":"10.1212/NXI.0000000000200468","DOIUrl":"10.1212/NXI.0000000000200468","url":null,"abstract":"<p><strong>Background and objectives: </strong>Most patients with myasthenia gravis (MG) suffer from fatigue, which can be defined as a subjective lack of energy and difficulty in initiating or sustaining voluntary activities. This is conceptually different from muscle weakness or muscle fatigability. Fatigue is one of the most reported symptoms in MG and has been hypothesized to be an innate mechanism to minimize muscle activity in order to protect muscles from (further) damage. The exact pathophysiology of fatigue remains unclear, and it is very likely a multifactorial phenomenon. The aim of this study was to provide a better understanding on the pathophysiology of fatigue in MG.</p><p><strong>Methods: </strong>We analyzed 38 serum biomarkers including various cytokines and myokines in a cohort of 116 anti-acetylcholine receptor-positive patients with MG. A multivariate linear regression analysis for each biomarker was performed in search for a correlation with fatigue. The following preselected covariates were included in the primary analysis: sex, age, disease severity, depression and anxiety scores, nonsteroid immune suppressive medication, and cumulative prednisone dosage in the past 6 months.</p><p><strong>Results: </strong>Severe fatigue was present in 64% of patients. Results show a robust correlation between fatigue and C-reactive protein (CRP) in the primary analysis. This correlation persisted when additionally adjusting for BMI, strenuous physical activities, and hemoglobulin levels.</p><p><strong>Discussion: </strong>Our findings suggest that chronic low-grade inflammation, mediated by CRP, contributes to the pathogenesis of fatigue in MG. This aligns with the hypothesis that local peripheral inflammatory processes induce systemic inflammatory cascades responsible for fatigue.</p>","PeriodicalId":19472,"journal":{"name":"Neurology® Neuroimmunology & Neuroinflammation","volume":"12 6","pages":"e200468"},"PeriodicalIF":7.5,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12448326/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145086816","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":"Hiding in Plain Sight: Inflammation in Iatrogenic Cerebral Amyloid Angiopathy.","authors":"Gargi Banerjee, David John Werring","doi":"10.1212/NXI.0000000000200493","DOIUrl":"https://doi.org/10.1212/NXI.0000000000200493","url":null,"abstract":"","PeriodicalId":19472,"journal":{"name":"Neurology® Neuroimmunology & Neuroinflammation","volume":"12 6","pages":"e200493"},"PeriodicalIF":7.5,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145258638","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Extensive Corticospinal Tract Involvement in a Patient With Autoimmune Glial Fibrillary Acidic Protein Astrocytopathy.","authors":"Shumpei Murakami, Keigo Kihrara, Kotaro Ogawa, Hideki Mochizuki","doi":"10.1212/NXI.0000000000200464","DOIUrl":"https://doi.org/10.1212/NXI.0000000000200464","url":null,"abstract":"","PeriodicalId":19472,"journal":{"name":"Neurology® Neuroimmunology & Neuroinflammation","volume":"12 6","pages":"e200464"},"PeriodicalIF":7.5,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12396745/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144963343","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":"Unique Polysomnography Pattern Leading to the Diagnosis of Anti-Ma2 Encephalitis.","authors":"Guillermo Nuñez-Manjarres, Ane Mínguez-Olaondo, Tamara Castillo-Triviño, Ana Vinagre-Aragon, Amaia Muñoz-Lopetegi","doi":"10.1212/NXI.0000000000200465","DOIUrl":"https://doi.org/10.1212/NXI.0000000000200465","url":null,"abstract":"<p><strong>Background and objectives: </strong>Anti-Ma2 encephalitis is a rare autoimmune paraneoplastic syndrome that can present as secondary narcolepsy due to hypothalamic involvement.</p><p><strong>Methods: </strong>We present a case of anti-Ma2 encephalitis in which polysomnography was key to suspect the final diagnosis.</p><p><strong>Results: </strong>A 72-year-old man presented with progressive hypersomnia and recurrent falls, initially misinterpreted as secondary to obstructive sleep apnea and cardiogenic syncope, respectively. Symptoms continued to worsen, prompting hospital admission. Video-polysomnography revealed a previously unreported sleep pattern, characterized by an abnormally increased proportion of REM sleep (approximately 3 times the expected), with sleep-onset REM periods occurring every time sleep was resumed after nocturnal awakenings. In addition, non-REM sleep was undifferentiated, without sleep spindles, K complexes, or slow-wave sleep. The recurrent SOREMPs raised suspicion of secondary narcolepsy. MRI showed T2 hyperintensities in different brain regions, including the hypothalamus, and CSF analysis confirmed anti-Ma2 antibodies and decreased hypocretin-1 levels. Symptoms only partially improved after immunotherapy, and malignancy screening remained inconclusive.</p><p><strong>Discussion: </strong>This case illustrates the diagnostic challenge of autoimmune encephalitis, especially in the older population, and adds to the growing evidence on the value of sleep studies in these conditions. We describe a unique polysomnography pattern in anti-Ma2 encephalitis that could guide the diagnosis of this entity.</p>","PeriodicalId":19472,"journal":{"name":"Neurology® Neuroimmunology & Neuroinflammation","volume":"12 6","pages":"e200465"},"PeriodicalIF":7.5,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12396744/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144963357","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}